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Foot Rash + Gnarly Toenails = Man in Need of a Diagnosis
ANSWER
The correct answer is to perform a KOH examination (choice “b”), which takes just five minutes and offers the chance to establish the fungal origin of the rash. Although the patient’s skin is quite dry, the use of a moisturizer (choice “a”) is unlikely to address the overall problem. A punch biopsy (choice “c”) would be a logical choice if the KOH failed to solve the mystery. The use of combination creams (choice “d”) that contain a steroid (triamcinolone) and an antifungal (nystatin) is essentially an admission of the lack of a definitive diagnosis. For reasons discussed below, this strategy has almost no chance of helping.
DISCUSSION
In this case, the KOH prep showed numerous hyphal elements, confirming suspicions of a fungal origin. One potential source of these organisms was the patient’s feet, where fungal infection had been present for years (“more than 30,” questioning revealed).
A common scenario is one in which the patient applies a steroid cream to a bit of dry skin just above the feet, which allows the fungi to gain a “foothold” from which to spread upward onto the leg; this progress is assisted through scratching and additional steroid application. If no firm diagnosis is ever established, definitive treatment cannot be undertaken and the problem never resolves.
In my opinion, there is never a reason to prescribe a product containing nystatin. In 1950, when it was discovered by researchers working in New York State laboratories (after which it was named), its efficacy against Candida species represented a notable advance, given the limited drug choices available for that purpose. But it has little, if any, activity against the dermatophytes causing our patient’s problems. And the steroid (triamcinolone) in this combination product, far from adding any therapeutic benefit, effectively diminishes any natural immune response.
The other reason to refrain from prescribing nystatin is that, since its discovery, at least three generations of products that treat both fungi and yeast (the azoles, such as clotrimazole, econazole, and fluconazole) have become available and have been found to be very effective.
The more important issue in this case, however, is finally having an accurate diagnosis: tinea corporis, probably caused by the most common dermatophyte, Trichophyton rubrum. The patient’s body is obviously a very happy home for this ubiquitous organism, to the extent that our chances of eliminating it are quite small. But we can at least make the patient more comfortable.
Treatment entailed ketoconazole foam (applied bid to his legs) and a two-month course of oral terbinafine (250 mg/d), which cleared up most of the skin problem. For his overgrown toenails, the patient was advised to establish care with a podiatrist for regular trimming.
In terms of a differential, this patient might have had psoriasis or eczema—and may still have one or both, since there’s no law against having more than one condition in the same location. In time, we may have to reconsider our solitary diagnosis.
ANSWER
The correct answer is to perform a KOH examination (choice “b”), which takes just five minutes and offers the chance to establish the fungal origin of the rash. Although the patient’s skin is quite dry, the use of a moisturizer (choice “a”) is unlikely to address the overall problem. A punch biopsy (choice “c”) would be a logical choice if the KOH failed to solve the mystery. The use of combination creams (choice “d”) that contain a steroid (triamcinolone) and an antifungal (nystatin) is essentially an admission of the lack of a definitive diagnosis. For reasons discussed below, this strategy has almost no chance of helping.
DISCUSSION
In this case, the KOH prep showed numerous hyphal elements, confirming suspicions of a fungal origin. One potential source of these organisms was the patient’s feet, where fungal infection had been present for years (“more than 30,” questioning revealed).
A common scenario is one in which the patient applies a steroid cream to a bit of dry skin just above the feet, which allows the fungi to gain a “foothold” from which to spread upward onto the leg; this progress is assisted through scratching and additional steroid application. If no firm diagnosis is ever established, definitive treatment cannot be undertaken and the problem never resolves.
In my opinion, there is never a reason to prescribe a product containing nystatin. In 1950, when it was discovered by researchers working in New York State laboratories (after which it was named), its efficacy against Candida species represented a notable advance, given the limited drug choices available for that purpose. But it has little, if any, activity against the dermatophytes causing our patient’s problems. And the steroid (triamcinolone) in this combination product, far from adding any therapeutic benefit, effectively diminishes any natural immune response.
The other reason to refrain from prescribing nystatin is that, since its discovery, at least three generations of products that treat both fungi and yeast (the azoles, such as clotrimazole, econazole, and fluconazole) have become available and have been found to be very effective.
The more important issue in this case, however, is finally having an accurate diagnosis: tinea corporis, probably caused by the most common dermatophyte, Trichophyton rubrum. The patient’s body is obviously a very happy home for this ubiquitous organism, to the extent that our chances of eliminating it are quite small. But we can at least make the patient more comfortable.
Treatment entailed ketoconazole foam (applied bid to his legs) and a two-month course of oral terbinafine (250 mg/d), which cleared up most of the skin problem. For his overgrown toenails, the patient was advised to establish care with a podiatrist for regular trimming.
In terms of a differential, this patient might have had psoriasis or eczema—and may still have one or both, since there’s no law against having more than one condition in the same location. In time, we may have to reconsider our solitary diagnosis.
ANSWER
The correct answer is to perform a KOH examination (choice “b”), which takes just five minutes and offers the chance to establish the fungal origin of the rash. Although the patient’s skin is quite dry, the use of a moisturizer (choice “a”) is unlikely to address the overall problem. A punch biopsy (choice “c”) would be a logical choice if the KOH failed to solve the mystery. The use of combination creams (choice “d”) that contain a steroid (triamcinolone) and an antifungal (nystatin) is essentially an admission of the lack of a definitive diagnosis. For reasons discussed below, this strategy has almost no chance of helping.
DISCUSSION
In this case, the KOH prep showed numerous hyphal elements, confirming suspicions of a fungal origin. One potential source of these organisms was the patient’s feet, where fungal infection had been present for years (“more than 30,” questioning revealed).
A common scenario is one in which the patient applies a steroid cream to a bit of dry skin just above the feet, which allows the fungi to gain a “foothold” from which to spread upward onto the leg; this progress is assisted through scratching and additional steroid application. If no firm diagnosis is ever established, definitive treatment cannot be undertaken and the problem never resolves.
In my opinion, there is never a reason to prescribe a product containing nystatin. In 1950, when it was discovered by researchers working in New York State laboratories (after which it was named), its efficacy against Candida species represented a notable advance, given the limited drug choices available for that purpose. But it has little, if any, activity against the dermatophytes causing our patient’s problems. And the steroid (triamcinolone) in this combination product, far from adding any therapeutic benefit, effectively diminishes any natural immune response.
The other reason to refrain from prescribing nystatin is that, since its discovery, at least three generations of products that treat both fungi and yeast (the azoles, such as clotrimazole, econazole, and fluconazole) have become available and have been found to be very effective.
The more important issue in this case, however, is finally having an accurate diagnosis: tinea corporis, probably caused by the most common dermatophyte, Trichophyton rubrum. The patient’s body is obviously a very happy home for this ubiquitous organism, to the extent that our chances of eliminating it are quite small. But we can at least make the patient more comfortable.
Treatment entailed ketoconazole foam (applied bid to his legs) and a two-month course of oral terbinafine (250 mg/d), which cleared up most of the skin problem. For his overgrown toenails, the patient was advised to establish care with a podiatrist for regular trimming.
In terms of a differential, this patient might have had psoriasis or eczema—and may still have one or both, since there’s no law against having more than one condition in the same location. In time, we may have to reconsider our solitary diagnosis.
For several years, a 66-year-old man has had an itchy rash on his right leg; recently, it has become more bothersome. In general, he has noticed that when cold weather arrives, the rash improves slightly, but it inevitably worsens again as winter progresses. Over the years, the providers he has consulted have prescribed a number of topical products—among them, antifungal and steroid creams. Each of these products seems to help for a short period, then stops; at that point, the patient switches to a different product, with similar mixed results. The patient says he doesn’t have any other skin problems. Examination reveals patches of dry skin scattered from the knee to the top of the patient’s foot. Most have a faintly erythematous surface and arciform borders. These patches blend into a similar rash that covers the sides of both feet. All 10 toenails are grossly dystrophic, yellowed, and overgrown. The skin on the patient’s other leg is somewhat dry but otherwise unaffected.
Cystic Nodule on the Palm
The Diagnosis: Nodular Hidradenoma
Nodular hidradenomas (NHs) are rare benign cutaneous adnexal neoplasms first described in 1949 as clear cell papillary carcinomas.1 Since then, various terms have been used to describe this entity, such as eccrine acrospiroma, solid-cystic hidradenoma, and clear cell hidradenoma.2 Review of the literature revealed a female predominance (2:1 ratio) and a mean age at presentation of 37.2 years.3,4 Nodular hidradenoma presents as an asymptomatic, solitary, mobile, firm nodule with intact overlying skin. Rarely, multiple nodules may occur.3 Some tumors display ulceration and serous fluid leakage.5 They occur most commonly on the scalp, face, and upper extremities with an average size of 2 cm.3 Rapid growth of the tumor may signal a malignant change.6
Histopathology reveals a lobulated, circumscribed, symmetrical tumor with dermal nests of epithelial cells that are polygonal with eosinophilic cytoplasm forming ductlike spaces (Figure). However, clear cell changes and squamous differentiation may be prominent features. Cystic spaces may result from tumor cell degeneration. Most tumors are encased by collagenous fibrous tissue and rarely have epidermal attachments.3
  Anastomosing aggregates of squamous cells forming ductlike spaces were viewed on low-power magnification (A)(H&E, original magnification ×10). On higher power there were ductlike spaces and eosinophilic hyalinized stroma entrapped by the bland-appearing squamous proliferation (B)(H&E, original magnification ×20). |
Nodular hidradenoma traditionally has been considered to be of eccrine origin, but more recent literature indicates that the majority of NHs are of apocrine origin. Histologically, apocrine tumors display eosinophilic secretion, mucinous epithelium, squamous or sebaceous differentiation, and decapitation secretion, whereas eccrine tumors are identified by their lack of specific features.3
Nodular hidradenoma may recur after excision. Malignant transformation is rare. In one review, 6.7% (6/89) of NHs were malignant, characterized by abnormal mitoses, nuclear atypia, and necrosis.4 Malignant NH or nodular hidradenocarcinoma behaves aggressively with up to an 86% local recurrence and 60% rate of metastasis within 2 years.6 Survival time is inversely proportional to the size of the tumor and is generally poor, with a 5-year disease-free survival of less than 30%.6,7
Treatment of NH is achieved through primary excision or Mohs micrographic surgery; however, treatment of nodular hidradenocarcinoma is controversial and typically begins with wide local excision but may involve lymph node dissection if necessary. Use of adjuvant chemotherapy and radiation therapy for metastases warrants more clinical studies, as it is a rare occurrence.6 Our patient planned to undergo a total excision of the benign nodule once she healed from the biopsy; however, she was lost to follow-up, as she moved out of state.
1. Lui Y. The histogenesis of clear cell papillary carcinoma of the skin. Am J Pathol. 1949;25:93-103.
2. Obaidat NA, Khaled OA, Ghazarian D. Skin adnexal neoplasms–part 2: an approach to tumours of cutaneous sweat glands. J Clin Pathol. 2007;60:145-159.
3. Nandeesh BN, Rajalakshmi T. A study of histopathologic spectrum of nodular hidradenoma. Am J Dermatopathol. 2012;34:461-470.
4. Hernández-Pérez E, Cestoni-Parducci R. Nodular hidradenoma and hidradenocarcinoma: a 10-year review. J Am Acad Dermatol. 1985;12:15-20.
5. Sirinoglu H, Celebiler O. Benign nodular hidradenoma of the face. J Craniofac Surg. 2011;22:750-751.
6. Souvatzidis P, Sbano P, Mandato F, et al. Malignant nodular hidradenoma of the skin: report of seven cases. J Eur Acad Dermatol Venereol. 2008;22:549-554.
7. Ko CJ, Cochran AJ, Eng W, et al. Hidradenocarcinoma: a histological and immunohistochemical study. J Cutan Pathol. 2006;33:726-730.
The Diagnosis: Nodular Hidradenoma
Nodular hidradenomas (NHs) are rare benign cutaneous adnexal neoplasms first described in 1949 as clear cell papillary carcinomas.1 Since then, various terms have been used to describe this entity, such as eccrine acrospiroma, solid-cystic hidradenoma, and clear cell hidradenoma.2 Review of the literature revealed a female predominance (2:1 ratio) and a mean age at presentation of 37.2 years.3,4 Nodular hidradenoma presents as an asymptomatic, solitary, mobile, firm nodule with intact overlying skin. Rarely, multiple nodules may occur.3 Some tumors display ulceration and serous fluid leakage.5 They occur most commonly on the scalp, face, and upper extremities with an average size of 2 cm.3 Rapid growth of the tumor may signal a malignant change.6
Histopathology reveals a lobulated, circumscribed, symmetrical tumor with dermal nests of epithelial cells that are polygonal with eosinophilic cytoplasm forming ductlike spaces (Figure). However, clear cell changes and squamous differentiation may be prominent features. Cystic spaces may result from tumor cell degeneration. Most tumors are encased by collagenous fibrous tissue and rarely have epidermal attachments.3
Anastomosing aggregates of squamous cells forming ductlike spaces were viewed on low-power magnification (A)(H&E, original magnification ×10). On higher power there were ductlike spaces and eosinophilic hyalinized stroma entrapped by the bland-appearing squamous proliferation (B)(H&E, original magnification ×20). |
Nodular hidradenoma traditionally has been considered to be of eccrine origin, but more recent literature indicates that the majority of NHs are of apocrine origin. Histologically, apocrine tumors display eosinophilic secretion, mucinous epithelium, squamous or sebaceous differentiation, and decapitation secretion, whereas eccrine tumors are identified by their lack of specific features.3
Nodular hidradenoma may recur after excision. Malignant transformation is rare. In one review, 6.7% (6/89) of NHs were malignant, characterized by abnormal mitoses, nuclear atypia, and necrosis.4 Malignant NH or nodular hidradenocarcinoma behaves aggressively with up to an 86% local recurrence and 60% rate of metastasis within 2 years.6 Survival time is inversely proportional to the size of the tumor and is generally poor, with a 5-year disease-free survival of less than 30%.6,7
Treatment of NH is achieved through primary excision or Mohs micrographic surgery; however, treatment of nodular hidradenocarcinoma is controversial and typically begins with wide local excision but may involve lymph node dissection if necessary. Use of adjuvant chemotherapy and radiation therapy for metastases warrants more clinical studies, as it is a rare occurrence.6 Our patient planned to undergo a total excision of the benign nodule once she healed from the biopsy; however, she was lost to follow-up, as she moved out of state.
The Diagnosis: Nodular Hidradenoma
Nodular hidradenomas (NHs) are rare benign cutaneous adnexal neoplasms first described in 1949 as clear cell papillary carcinomas.1 Since then, various terms have been used to describe this entity, such as eccrine acrospiroma, solid-cystic hidradenoma, and clear cell hidradenoma.2 Review of the literature revealed a female predominance (2:1 ratio) and a mean age at presentation of 37.2 years.3,4 Nodular hidradenoma presents as an asymptomatic, solitary, mobile, firm nodule with intact overlying skin. Rarely, multiple nodules may occur.3 Some tumors display ulceration and serous fluid leakage.5 They occur most commonly on the scalp, face, and upper extremities with an average size of 2 cm.3 Rapid growth of the tumor may signal a malignant change.6
Histopathology reveals a lobulated, circumscribed, symmetrical tumor with dermal nests of epithelial cells that are polygonal with eosinophilic cytoplasm forming ductlike spaces (Figure). However, clear cell changes and squamous differentiation may be prominent features. Cystic spaces may result from tumor cell degeneration. Most tumors are encased by collagenous fibrous tissue and rarely have epidermal attachments.3
Anastomosing aggregates of squamous cells forming ductlike spaces were viewed on low-power magnification (A)(H&E, original magnification ×10). On higher power there were ductlike spaces and eosinophilic hyalinized stroma entrapped by the bland-appearing squamous proliferation (B)(H&E, original magnification ×20). |
Nodular hidradenoma traditionally has been considered to be of eccrine origin, but more recent literature indicates that the majority of NHs are of apocrine origin. Histologically, apocrine tumors display eosinophilic secretion, mucinous epithelium, squamous or sebaceous differentiation, and decapitation secretion, whereas eccrine tumors are identified by their lack of specific features.3
Nodular hidradenoma may recur after excision. Malignant transformation is rare. In one review, 6.7% (6/89) of NHs were malignant, characterized by abnormal mitoses, nuclear atypia, and necrosis.4 Malignant NH or nodular hidradenocarcinoma behaves aggressively with up to an 86% local recurrence and 60% rate of metastasis within 2 years.6 Survival time is inversely proportional to the size of the tumor and is generally poor, with a 5-year disease-free survival of less than 30%.6,7
Treatment of NH is achieved through primary excision or Mohs micrographic surgery; however, treatment of nodular hidradenocarcinoma is controversial and typically begins with wide local excision but may involve lymph node dissection if necessary. Use of adjuvant chemotherapy and radiation therapy for metastases warrants more clinical studies, as it is a rare occurrence.6 Our patient planned to undergo a total excision of the benign nodule once she healed from the biopsy; however, she was lost to follow-up, as she moved out of state.
1. Lui Y. The histogenesis of clear cell papillary carcinoma of the skin. Am J Pathol. 1949;25:93-103.
2. Obaidat NA, Khaled OA, Ghazarian D. Skin adnexal neoplasms–part 2: an approach to tumours of cutaneous sweat glands. J Clin Pathol. 2007;60:145-159.
3. Nandeesh BN, Rajalakshmi T. A study of histopathologic spectrum of nodular hidradenoma. Am J Dermatopathol. 2012;34:461-470.
4. Hernández-Pérez E, Cestoni-Parducci R. Nodular hidradenoma and hidradenocarcinoma: a 10-year review. J Am Acad Dermatol. 1985;12:15-20.
5. Sirinoglu H, Celebiler O. Benign nodular hidradenoma of the face. J Craniofac Surg. 2011;22:750-751.
6. Souvatzidis P, Sbano P, Mandato F, et al. Malignant nodular hidradenoma of the skin: report of seven cases. J Eur Acad Dermatol Venereol. 2008;22:549-554.
7. Ko CJ, Cochran AJ, Eng W, et al. Hidradenocarcinoma: a histological and immunohistochemical study. J Cutan Pathol. 2006;33:726-730.
1. Lui Y. The histogenesis of clear cell papillary carcinoma of the skin. Am J Pathol. 1949;25:93-103.
2. Obaidat NA, Khaled OA, Ghazarian D. Skin adnexal neoplasms–part 2: an approach to tumours of cutaneous sweat glands. J Clin Pathol. 2007;60:145-159.
3. Nandeesh BN, Rajalakshmi T. A study of histopathologic spectrum of nodular hidradenoma. Am J Dermatopathol. 2012;34:461-470.
4. Hernández-Pérez E, Cestoni-Parducci R. Nodular hidradenoma and hidradenocarcinoma: a 10-year review. J Am Acad Dermatol. 1985;12:15-20.
5. Sirinoglu H, Celebiler O. Benign nodular hidradenoma of the face. J Craniofac Surg. 2011;22:750-751.
6. Souvatzidis P, Sbano P, Mandato F, et al. Malignant nodular hidradenoma of the skin: report of seven cases. J Eur Acad Dermatol Venereol. 2008;22:549-554.
7. Ko CJ, Cochran AJ, Eng W, et al. Hidradenocarcinoma: a histological and immunohistochemical study. J Cutan Pathol. 2006;33:726-730.
A 73-year-old woman with a history of multiple strokes with residual left-sided motor deficits and resultant left-hand contracture, type 2 diabetes mellitus, hypertension, and a remote history of treated colon cancer and breast cancer presented with hypertensive urgency and neck pain. Upon admission, the nursing staff found an “unusual growth” on the patient’s left hand. Dermatology was consulted and a 2×1.5×1.5-cm multilobulated, malodorous, slightly tender, nonfluctuant, gelatinous, mobile, cystic nodule overlying the fourth metacarpal palmar head was examined. The patient reported the lesion was present for more than a year. Imaging was pursued, but radiography, ultrasonography, and magnetic resonance imaging could not be performed adequately due to the patient’s severe contracture. Given the extensive differential diagnoses, an orthopedic hand surgeon performed a large incisional biopsy to obtain tissue diagnosis.
Firm Plaques and Nodules Over the Body
The Diagnosis: Pancreatic Panniculitis
The biopsy specimen revealed necrosis of the panniculus with “ghost” cells (Figure). Calcification was encountered. Changes of vasculitis were not identified and fungal organisms were not noted. The histopathologic findings supported a diagnosis of pancreatic panniculitis.
Pancreatic panniculitis has been associated with pancreatitis, pancreatic carcinoma, pancreatic pseudocysts, congenital abnormalities of the pancreas, and drug-induced pancreatitis.1 Skin lesions may herald a diagnosis of pancreatic disease in an outpatient and should prompt thorough clinical evaluation when encountered in an outpatient setting. Our patient first developed tender nodules on the left shin 2 to 3 weeks prior to presentation. She reported that her initial nodules were flesh colored but then became erythematous and tender over 1 week’s time. The patient’s history was remarkable for ovarian cancer. She had been hospitalized 2 weeks prior to presentation for abdominal pain and ascites. Imaging studies revealed a cystic lesion in the head of the pancreas. The pancreas was traumatized during a peritoneal tap. Her nodules developed shortly thereafter and were distributed on the arms, legs, back, and abdomen.
Pancreatic tumors or inflammation are thought to trigger pancreatic panniculitis by releasing enzymes. Pancreatic enzymes such as lipase are thought to play a role in the development of pancreatic panniculitis by entering the vascular system and leading to fat necrosis.2,3 Biopsy reveals necrosis of adipocytes in the center of fat lobules.4 Ghost cells result from hydrolytic activity of enzymes on the fat cells followed by calcium deposition. A report indicates that fungal infection or gout also can cause changes that mimic pancreatic panniculitis.5
Other entities in the differential diagnosis can be excluded by biopsy. Polyarteritis nodosa is a vasculitis. Although panniculitis may be seen in polyarteritis as a secondary phenomenon, lesions are centered around blood vessels and often eventuate in ulceration.6 Subcutaneous fungal infection typically reveals organisms on periodic acid–Schiff stain.7 Pyoderma gangrenosum is associated with ulceration and a neutrophilic infiltrate that is often centered around a central pilosebaceous unit in developing lesions.8 Erythema nodosum is a panniculitis in which septal inflammation predominates.9 These differential diagnoses of pancreatic panniculitis are summarized in the Table.
Pancreatic panniculitis can be associated with acute arthritis and inflammation of periarticular fat.10 Treatment of pancreatic panniculitis is usually focused on the underlying pancreatic disease.11,12 Our patient benefited from analgesic therapy and her lesions improved on follow-up. Clinicians encountering a patient with new tender nodules should be prompted to perform a biopsy. When histopathologic evaluation reveals ghosted adipocytes, pancreatic panniculitis should be suspected and clinical evaluation undertaken.
1. Garcia-Romero D, Vanaclocha F. Pancreatic panniculitis. Dermatol Clin. 2008;26:465-470.
2. Berman B, Conteas C, Smith B, et al. Fatal pancreatitis presenting with subcutaneous fat necrosis. J Am Acad Dermatol. 1987;17:359-364.
3. Dhawan SS, Jimenez-Acosta F, Poppiti RJ Jr, et al. Subcutaneous fat necrosis associated with pancreatitis: histochemical and electron microscopic findings. Am J Gastroenterol. 1990;85:1025-1028.
4. Cannon JR, Pitha JV, Everett MA. Subcutaneous fat necrosis in pancreatitis. J Cutan Pathol. 1979;6:501-506.
5. Requena L, Sitthinamsuwan P, Santonja C, et al. Cutaneous and mucosal mucormycosis mimicking pancreatic panniculitis and gouty panniculitis. J Am Acad Dermatol. 2012;66:975-984.
6. Grattan CEH. Polyarteritis nodosa. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 1. 3rd ed. China: Elsevier Saunders; 2012:405-407.
7. Millett CR, Halpern AV, Heymann WR. Subcutaneous mycoses. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 2. 3rd ed. China: Elsevier Saunders; 2012:1266-1273.
8. Moschella SL, Davis MDP. Pyoderma gangrenosum. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 1. 3rd ed. China: Elsevier Saunders; 2012:427-431.
9. Patterson JW. Erythema nodosum. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 2. 3rd ed. China: Elsevier Saunders; 2012:1641-1645.
10. Patterson JW. Pancreatic panniculitis. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 2. 3rd ed. China: Elsevier Saunders; 2012:1649-1650.
11. Requena L, Sanchez Yus E. Panniculitis. part II. mostly lobular panniculitis. J Am Acad Dermatol. 2001;45:325-361.
12. Dahl PR, Su WP, Cullimore KC, et al. Pancreatic panniculitis. J Am Acad Dermatol. 1995;33:413-417.
The Diagnosis: Pancreatic Panniculitis
The biopsy specimen revealed necrosis of the panniculus with “ghost” cells (Figure). Calcification was encountered. Changes of vasculitis were not identified and fungal organisms were not noted. The histopathologic findings supported a diagnosis of pancreatic panniculitis.
Pancreatic panniculitis has been associated with pancreatitis, pancreatic carcinoma, pancreatic pseudocysts, congenital abnormalities of the pancreas, and drug-induced pancreatitis.1 Skin lesions may herald a diagnosis of pancreatic disease in an outpatient and should prompt thorough clinical evaluation when encountered in an outpatient setting. Our patient first developed tender nodules on the left shin 2 to 3 weeks prior to presentation. She reported that her initial nodules were flesh colored but then became erythematous and tender over 1 week’s time. The patient’s history was remarkable for ovarian cancer. She had been hospitalized 2 weeks prior to presentation for abdominal pain and ascites. Imaging studies revealed a cystic lesion in the head of the pancreas. The pancreas was traumatized during a peritoneal tap. Her nodules developed shortly thereafter and were distributed on the arms, legs, back, and abdomen.
Pancreatic tumors or inflammation are thought to trigger pancreatic panniculitis by releasing enzymes. Pancreatic enzymes such as lipase are thought to play a role in the development of pancreatic panniculitis by entering the vascular system and leading to fat necrosis.2,3 Biopsy reveals necrosis of adipocytes in the center of fat lobules.4 Ghost cells result from hydrolytic activity of enzymes on the fat cells followed by calcium deposition. A report indicates that fungal infection or gout also can cause changes that mimic pancreatic panniculitis.5
Other entities in the differential diagnosis can be excluded by biopsy. Polyarteritis nodosa is a vasculitis. Although panniculitis may be seen in polyarteritis as a secondary phenomenon, lesions are centered around blood vessels and often eventuate in ulceration.6 Subcutaneous fungal infection typically reveals organisms on periodic acid–Schiff stain.7 Pyoderma gangrenosum is associated with ulceration and a neutrophilic infiltrate that is often centered around a central pilosebaceous unit in developing lesions.8 Erythema nodosum is a panniculitis in which septal inflammation predominates.9 These differential diagnoses of pancreatic panniculitis are summarized in the Table.
Pancreatic panniculitis can be associated with acute arthritis and inflammation of periarticular fat.10 Treatment of pancreatic panniculitis is usually focused on the underlying pancreatic disease.11,12 Our patient benefited from analgesic therapy and her lesions improved on follow-up. Clinicians encountering a patient with new tender nodules should be prompted to perform a biopsy. When histopathologic evaluation reveals ghosted adipocytes, pancreatic panniculitis should be suspected and clinical evaluation undertaken.
The Diagnosis: Pancreatic Panniculitis
The biopsy specimen revealed necrosis of the panniculus with “ghost” cells (Figure). Calcification was encountered. Changes of vasculitis were not identified and fungal organisms were not noted. The histopathologic findings supported a diagnosis of pancreatic panniculitis.
Pancreatic panniculitis has been associated with pancreatitis, pancreatic carcinoma, pancreatic pseudocysts, congenital abnormalities of the pancreas, and drug-induced pancreatitis.1 Skin lesions may herald a diagnosis of pancreatic disease in an outpatient and should prompt thorough clinical evaluation when encountered in an outpatient setting. Our patient first developed tender nodules on the left shin 2 to 3 weeks prior to presentation. She reported that her initial nodules were flesh colored but then became erythematous and tender over 1 week’s time. The patient’s history was remarkable for ovarian cancer. She had been hospitalized 2 weeks prior to presentation for abdominal pain and ascites. Imaging studies revealed a cystic lesion in the head of the pancreas. The pancreas was traumatized during a peritoneal tap. Her nodules developed shortly thereafter and were distributed on the arms, legs, back, and abdomen.
Pancreatic tumors or inflammation are thought to trigger pancreatic panniculitis by releasing enzymes. Pancreatic enzymes such as lipase are thought to play a role in the development of pancreatic panniculitis by entering the vascular system and leading to fat necrosis.2,3 Biopsy reveals necrosis of adipocytes in the center of fat lobules.4 Ghost cells result from hydrolytic activity of enzymes on the fat cells followed by calcium deposition. A report indicates that fungal infection or gout also can cause changes that mimic pancreatic panniculitis.5
Other entities in the differential diagnosis can be excluded by biopsy. Polyarteritis nodosa is a vasculitis. Although panniculitis may be seen in polyarteritis as a secondary phenomenon, lesions are centered around blood vessels and often eventuate in ulceration.6 Subcutaneous fungal infection typically reveals organisms on periodic acid–Schiff stain.7 Pyoderma gangrenosum is associated with ulceration and a neutrophilic infiltrate that is often centered around a central pilosebaceous unit in developing lesions.8 Erythema nodosum is a panniculitis in which septal inflammation predominates.9 These differential diagnoses of pancreatic panniculitis are summarized in the Table.
Pancreatic panniculitis can be associated with acute arthritis and inflammation of periarticular fat.10 Treatment of pancreatic panniculitis is usually focused on the underlying pancreatic disease.11,12 Our patient benefited from analgesic therapy and her lesions improved on follow-up. Clinicians encountering a patient with new tender nodules should be prompted to perform a biopsy. When histopathologic evaluation reveals ghosted adipocytes, pancreatic panniculitis should be suspected and clinical evaluation undertaken.
1. Garcia-Romero D, Vanaclocha F. Pancreatic panniculitis. Dermatol Clin. 2008;26:465-470.
2. Berman B, Conteas C, Smith B, et al. Fatal pancreatitis presenting with subcutaneous fat necrosis. J Am Acad Dermatol. 1987;17:359-364.
3. Dhawan SS, Jimenez-Acosta F, Poppiti RJ Jr, et al. Subcutaneous fat necrosis associated with pancreatitis: histochemical and electron microscopic findings. Am J Gastroenterol. 1990;85:1025-1028.
4. Cannon JR, Pitha JV, Everett MA. Subcutaneous fat necrosis in pancreatitis. J Cutan Pathol. 1979;6:501-506.
5. Requena L, Sitthinamsuwan P, Santonja C, et al. Cutaneous and mucosal mucormycosis mimicking pancreatic panniculitis and gouty panniculitis. J Am Acad Dermatol. 2012;66:975-984.
6. Grattan CEH. Polyarteritis nodosa. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 1. 3rd ed. China: Elsevier Saunders; 2012:405-407.
7. Millett CR, Halpern AV, Heymann WR. Subcutaneous mycoses. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 2. 3rd ed. China: Elsevier Saunders; 2012:1266-1273.
8. Moschella SL, Davis MDP. Pyoderma gangrenosum. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 1. 3rd ed. China: Elsevier Saunders; 2012:427-431.
9. Patterson JW. Erythema nodosum. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 2. 3rd ed. China: Elsevier Saunders; 2012:1641-1645.
10. Patterson JW. Pancreatic panniculitis. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 2. 3rd ed. China: Elsevier Saunders; 2012:1649-1650.
11. Requena L, Sanchez Yus E. Panniculitis. part II. mostly lobular panniculitis. J Am Acad Dermatol. 2001;45:325-361.
12. Dahl PR, Su WP, Cullimore KC, et al. Pancreatic panniculitis. J Am Acad Dermatol. 1995;33:413-417.
1. Garcia-Romero D, Vanaclocha F. Pancreatic panniculitis. Dermatol Clin. 2008;26:465-470.
2. Berman B, Conteas C, Smith B, et al. Fatal pancreatitis presenting with subcutaneous fat necrosis. J Am Acad Dermatol. 1987;17:359-364.
3. Dhawan SS, Jimenez-Acosta F, Poppiti RJ Jr, et al. Subcutaneous fat necrosis associated with pancreatitis: histochemical and electron microscopic findings. Am J Gastroenterol. 1990;85:1025-1028.
4. Cannon JR, Pitha JV, Everett MA. Subcutaneous fat necrosis in pancreatitis. J Cutan Pathol. 1979;6:501-506.
5. Requena L, Sitthinamsuwan P, Santonja C, et al. Cutaneous and mucosal mucormycosis mimicking pancreatic panniculitis and gouty panniculitis. J Am Acad Dermatol. 2012;66:975-984.
6. Grattan CEH. Polyarteritis nodosa. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 1. 3rd ed. China: Elsevier Saunders; 2012:405-407.
7. Millett CR, Halpern AV, Heymann WR. Subcutaneous mycoses. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 2. 3rd ed. China: Elsevier Saunders; 2012:1266-1273.
8. Moschella SL, Davis MDP. Pyoderma gangrenosum. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 1. 3rd ed. China: Elsevier Saunders; 2012:427-431.
9. Patterson JW. Erythema nodosum. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 2. 3rd ed. China: Elsevier Saunders; 2012:1641-1645.
10. Patterson JW. Pancreatic panniculitis. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. Vol 2. 3rd ed. China: Elsevier Saunders; 2012:1649-1650.
11. Requena L, Sanchez Yus E. Panniculitis. part II. mostly lobular panniculitis. J Am Acad Dermatol. 2001;45:325-361.
12. Dahl PR, Su WP, Cullimore KC, et al. Pancreatic panniculitis. J Am Acad Dermatol. 1995;33:413-417.
A 52-year-old woman presented with painful erythematous nodules of 2 weeks’ duration that began as a single lesion on the left shin and spread rapidly to involve the trunk, arms, and legs. A punch biopsy was performed. Pertinent history included a recent hospitalization for drainage of malignant ascites secondary to metastatic ovarian cancer. The lesions did not drain and were not pruritic. The patient did not have a history of fever, night sweats, nausea, headache, neurologic change, muscle aching, or recent weight loss.
Indurated Erythematous Papules and Plaques on the Forearm
The Diagnosis: Mycobacterium chelonae Arising Within a Tattoo
A 3-mm punch biopsy specimen was obtained from one of the plaques. Histopathology revealed an unremarkable epidermis with granulomatous collections of epithelioid histiocytes in association with neutrophils and lymphocytes in the dermis (Figure 1). Periodic acid–Schiff stain was negative for fungal organisms. Gram stain was negative for bacteria. Fite stain was positive for acid-fast bacilli (Figure 2). Clinical and histopathologic findings led to the initial diagnosis of a mycobacterial infection within the tattoo. The patient was empirically started on oral doxycycline 100 mg twice daily and oral clarithromycin 500 mg twice daily with mild improvement of the lesions over the next month. After 6 weeks the mycobacterial cultures were persistently negative and high-performance liquid chromatography was performed verifying the presence of Mycobacterium chelonae. Clarithromycin was continued and the doxycycline was replaced with oral trimethoprim-sulfamethoxazole (double strength) twice daily due to resistance. The patient was referred to an infectious disease specialist who concurred with the treatment regimen for a duration of 6 months to a year. A chest radiograph also was performed to rule out disseminated disease. Several months later the patient’s close friend presented with a similar infection that was acquired on the same day as our patient at the same tattoo parlor. The New York City Department of Health and Mental Hygiene was notified about these cases and informed us of other cases in New York State linked to contaminated tattoo ink.
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Mycobacterium chelonae is a rapidly growing nontuberculous mycobacteria (Runyon group IV) that is found in nature and contaminated sources such as soil, lakes, sewage, and tap water.1 Inoculation ofM chelonae through contaminated instruments leads to the formation of painful lesions, abscesses, fistulas, and granulomas that are extremely difficult to treat.2 In our patient, M chelonae was most likely transmitted via contaminated tap water that was used to dilute the black tattoo ink to yield a gray color. Alternative sources are the ink itself or the container used to mix the ink.3Mycobacterium chelonae can cause infections in the skin, lungs, joints, bones, and eyes.4 With the exception of lung disease, trauma is the usual inciting factor. Disseminated infections are almost exclusively found in immunosuppressed individuals. Mycobacterium chelonae is typically found to grow on culture within 7 days. However, in our case there was no growth after 6 weeks of incubation. High-performance liquid chromatography analysis of mycolic acid is an alternative method of identifying mycobacteria. This technique verified the presence of M chelonae in our case when cultures were persistently negative.5
Mycobacterium chelonae is difficult to treat. The most common antibiotics used for treatment are clarithromycin, azithromycin, doxycycline, and linezolid.6 Studies of various antibiotics have shown that clarithromycin is the most effective macrolide against M chelonae.7 Tetracyclines also were studied in their effectiveness at treating nontuberculous mycobacteria infections but were found to have increased resistance to M chelonae.8 Although treatment regimens vary, the highest success rates are achieved with a minimum of 6 months of therapy using at least 2 drugs. Longer treatment is recommended for immunocompromised individuals.9
The case we present is important from a public health perspective. The tattoo industry and ink manufacturers should bemade aware of the risks of various infections from nonsterile techniques. Tattoo parlor employees should be advised of the risks of using nonsterile water for ink dilution and cleaning tattoo equipment. They also should be continuously educated on aseptic techniques.
1. Lee RP, Cheung KW, Chiu KH, et al. Mycobacterium chelonae infection after total knee arthroplasty: a case report. J Orthop Surg (Hong Kong). 2012;20:134-136.
2. Camargo D, Saad C, Ruiz F, et al. latrogenic outbreak of M. chelonae skin abscesses. Epidemiol Infect. 1996;117:113-119.
3. Rodríguez-Blanco I, Fernández LC, Suárez-Peñaranda JM, et al. Mycobacterium chelonae infection associated with tattoos. Acta Derm Venereol. 2011;91:61-62.
4. Karak K, Bhattacharyya S, Majumdar S, et al. Pulmonary infections caused by mycobacteria other than M. tuberculosis in and around Calcutta. Indian J Pathol Microbiol. 1996;39:131-134.
5. Butler WR, Floyd MM, Silcox V, et al. Standardized Method for HPLC Identification of Mycobacteria. Atlanta, GA: Centers for Disease Control and Prevention, US Department of Health and Human Services; 1996.
6. Brown-Elliot BA, Wallace RJ Jr, Blinkhorn R, et al. Successful treatment of disseminated Mycobacterium chelonae infection with linezolid. Clin Infect Dis. 2001;33:1433-1434.
7. Brown BA, Wallace RJ Jr, Onyi GO, et al. Activities of four macrolides, including clarithromycin, against Mycobacterium fortuitum, Mycobacterium chelonae, and Mycobacterium chelonae-like organisms. Antimicrob Agents Chemother. 1992;36:180-184.
8. Swenson JM, Wallace RJ Jr, Silcox VA, et al. Antimicrobial susceptibility of five subgroups of Mycobacterium fortuitum and Mycobacterium chelonae. Antimicrob Agents Chemother. 1985;28:807-811.
9. Leung YY, Choi KW, Ho KM, et al. Disseminated cutaneous infection with Mycobacterium chelonae mimicking panniculitis in a patient with dermatomyositis. Hong Kong Med J. 2005;11:515-519.
The Diagnosis: Mycobacterium chelonae Arising Within a Tattoo
A 3-mm punch biopsy specimen was obtained from one of the plaques. Histopathology revealed an unremarkable epidermis with granulomatous collections of epithelioid histiocytes in association with neutrophils and lymphocytes in the dermis (Figure 1). Periodic acid–Schiff stain was negative for fungal organisms. Gram stain was negative for bacteria. Fite stain was positive for acid-fast bacilli (Figure 2). Clinical and histopathologic findings led to the initial diagnosis of a mycobacterial infection within the tattoo. The patient was empirically started on oral doxycycline 100 mg twice daily and oral clarithromycin 500 mg twice daily with mild improvement of the lesions over the next month. After 6 weeks the mycobacterial cultures were persistently negative and high-performance liquid chromatography was performed verifying the presence of Mycobacterium chelonae. Clarithromycin was continued and the doxycycline was replaced with oral trimethoprim-sulfamethoxazole (double strength) twice daily due to resistance. The patient was referred to an infectious disease specialist who concurred with the treatment regimen for a duration of 6 months to a year. A chest radiograph also was performed to rule out disseminated disease. Several months later the patient’s close friend presented with a similar infection that was acquired on the same day as our patient at the same tattoo parlor. The New York City Department of Health and Mental Hygiene was notified about these cases and informed us of other cases in New York State linked to contaminated tattoo ink.
|
Mycobacterium chelonae is a rapidly growing nontuberculous mycobacteria (Runyon group IV) that is found in nature and contaminated sources such as soil, lakes, sewage, and tap water.1 Inoculation ofM chelonae through contaminated instruments leads to the formation of painful lesions, abscesses, fistulas, and granulomas that are extremely difficult to treat.2 In our patient, M chelonae was most likely transmitted via contaminated tap water that was used to dilute the black tattoo ink to yield a gray color. Alternative sources are the ink itself or the container used to mix the ink.3Mycobacterium chelonae can cause infections in the skin, lungs, joints, bones, and eyes.4 With the exception of lung disease, trauma is the usual inciting factor. Disseminated infections are almost exclusively found in immunosuppressed individuals. Mycobacterium chelonae is typically found to grow on culture within 7 days. However, in our case there was no growth after 6 weeks of incubation. High-performance liquid chromatography analysis of mycolic acid is an alternative method of identifying mycobacteria. This technique verified the presence of M chelonae in our case when cultures were persistently negative.5
Mycobacterium chelonae is difficult to treat. The most common antibiotics used for treatment are clarithromycin, azithromycin, doxycycline, and linezolid.6 Studies of various antibiotics have shown that clarithromycin is the most effective macrolide against M chelonae.7 Tetracyclines also were studied in their effectiveness at treating nontuberculous mycobacteria infections but were found to have increased resistance to M chelonae.8 Although treatment regimens vary, the highest success rates are achieved with a minimum of 6 months of therapy using at least 2 drugs. Longer treatment is recommended for immunocompromised individuals.9
The case we present is important from a public health perspective. The tattoo industry and ink manufacturers should bemade aware of the risks of various infections from nonsterile techniques. Tattoo parlor employees should be advised of the risks of using nonsterile water for ink dilution and cleaning tattoo equipment. They also should be continuously educated on aseptic techniques.
The Diagnosis: Mycobacterium chelonae Arising Within a Tattoo
A 3-mm punch biopsy specimen was obtained from one of the plaques. Histopathology revealed an unremarkable epidermis with granulomatous collections of epithelioid histiocytes in association with neutrophils and lymphocytes in the dermis (Figure 1). Periodic acid–Schiff stain was negative for fungal organisms. Gram stain was negative for bacteria. Fite stain was positive for acid-fast bacilli (Figure 2). Clinical and histopathologic findings led to the initial diagnosis of a mycobacterial infection within the tattoo. The patient was empirically started on oral doxycycline 100 mg twice daily and oral clarithromycin 500 mg twice daily with mild improvement of the lesions over the next month. After 6 weeks the mycobacterial cultures were persistently negative and high-performance liquid chromatography was performed verifying the presence of Mycobacterium chelonae. Clarithromycin was continued and the doxycycline was replaced with oral trimethoprim-sulfamethoxazole (double strength) twice daily due to resistance. The patient was referred to an infectious disease specialist who concurred with the treatment regimen for a duration of 6 months to a year. A chest radiograph also was performed to rule out disseminated disease. Several months later the patient’s close friend presented with a similar infection that was acquired on the same day as our patient at the same tattoo parlor. The New York City Department of Health and Mental Hygiene was notified about these cases and informed us of other cases in New York State linked to contaminated tattoo ink.
|
Mycobacterium chelonae is a rapidly growing nontuberculous mycobacteria (Runyon group IV) that is found in nature and contaminated sources such as soil, lakes, sewage, and tap water.1 Inoculation ofM chelonae through contaminated instruments leads to the formation of painful lesions, abscesses, fistulas, and granulomas that are extremely difficult to treat.2 In our patient, M chelonae was most likely transmitted via contaminated tap water that was used to dilute the black tattoo ink to yield a gray color. Alternative sources are the ink itself or the container used to mix the ink.3Mycobacterium chelonae can cause infections in the skin, lungs, joints, bones, and eyes.4 With the exception of lung disease, trauma is the usual inciting factor. Disseminated infections are almost exclusively found in immunosuppressed individuals. Mycobacterium chelonae is typically found to grow on culture within 7 days. However, in our case there was no growth after 6 weeks of incubation. High-performance liquid chromatography analysis of mycolic acid is an alternative method of identifying mycobacteria. This technique verified the presence of M chelonae in our case when cultures were persistently negative.5
Mycobacterium chelonae is difficult to treat. The most common antibiotics used for treatment are clarithromycin, azithromycin, doxycycline, and linezolid.6 Studies of various antibiotics have shown that clarithromycin is the most effective macrolide against M chelonae.7 Tetracyclines also were studied in their effectiveness at treating nontuberculous mycobacteria infections but were found to have increased resistance to M chelonae.8 Although treatment regimens vary, the highest success rates are achieved with a minimum of 6 months of therapy using at least 2 drugs. Longer treatment is recommended for immunocompromised individuals.9
The case we present is important from a public health perspective. The tattoo industry and ink manufacturers should bemade aware of the risks of various infections from nonsterile techniques. Tattoo parlor employees should be advised of the risks of using nonsterile water for ink dilution and cleaning tattoo equipment. They also should be continuously educated on aseptic techniques.
1. Lee RP, Cheung KW, Chiu KH, et al. Mycobacterium chelonae infection after total knee arthroplasty: a case report. J Orthop Surg (Hong Kong). 2012;20:134-136.
2. Camargo D, Saad C, Ruiz F, et al. latrogenic outbreak of M. chelonae skin abscesses. Epidemiol Infect. 1996;117:113-119.
3. Rodríguez-Blanco I, Fernández LC, Suárez-Peñaranda JM, et al. Mycobacterium chelonae infection associated with tattoos. Acta Derm Venereol. 2011;91:61-62.
4. Karak K, Bhattacharyya S, Majumdar S, et al. Pulmonary infections caused by mycobacteria other than M. tuberculosis in and around Calcutta. Indian J Pathol Microbiol. 1996;39:131-134.
5. Butler WR, Floyd MM, Silcox V, et al. Standardized Method for HPLC Identification of Mycobacteria. Atlanta, GA: Centers for Disease Control and Prevention, US Department of Health and Human Services; 1996.
6. Brown-Elliot BA, Wallace RJ Jr, Blinkhorn R, et al. Successful treatment of disseminated Mycobacterium chelonae infection with linezolid. Clin Infect Dis. 2001;33:1433-1434.
7. Brown BA, Wallace RJ Jr, Onyi GO, et al. Activities of four macrolides, including clarithromycin, against Mycobacterium fortuitum, Mycobacterium chelonae, and Mycobacterium chelonae-like organisms. Antimicrob Agents Chemother. 1992;36:180-184.
8. Swenson JM, Wallace RJ Jr, Silcox VA, et al. Antimicrobial susceptibility of five subgroups of Mycobacterium fortuitum and Mycobacterium chelonae. Antimicrob Agents Chemother. 1985;28:807-811.
9. Leung YY, Choi KW, Ho KM, et al. Disseminated cutaneous infection with Mycobacterium chelonae mimicking panniculitis in a patient with dermatomyositis. Hong Kong Med J. 2005;11:515-519.
1. Lee RP, Cheung KW, Chiu KH, et al. Mycobacterium chelonae infection after total knee arthroplasty: a case report. J Orthop Surg (Hong Kong). 2012;20:134-136.
2. Camargo D, Saad C, Ruiz F, et al. latrogenic outbreak of M. chelonae skin abscesses. Epidemiol Infect. 1996;117:113-119.
3. Rodríguez-Blanco I, Fernández LC, Suárez-Peñaranda JM, et al. Mycobacterium chelonae infection associated with tattoos. Acta Derm Venereol. 2011;91:61-62.
4. Karak K, Bhattacharyya S, Majumdar S, et al. Pulmonary infections caused by mycobacteria other than M. tuberculosis in and around Calcutta. Indian J Pathol Microbiol. 1996;39:131-134.
5. Butler WR, Floyd MM, Silcox V, et al. Standardized Method for HPLC Identification of Mycobacteria. Atlanta, GA: Centers for Disease Control and Prevention, US Department of Health and Human Services; 1996.
6. Brown-Elliot BA, Wallace RJ Jr, Blinkhorn R, et al. Successful treatment of disseminated Mycobacterium chelonae infection with linezolid. Clin Infect Dis. 2001;33:1433-1434.
7. Brown BA, Wallace RJ Jr, Onyi GO, et al. Activities of four macrolides, including clarithromycin, against Mycobacterium fortuitum, Mycobacterium chelonae, and Mycobacterium chelonae-like organisms. Antimicrob Agents Chemother. 1992;36:180-184.
8. Swenson JM, Wallace RJ Jr, Silcox VA, et al. Antimicrobial susceptibility of five subgroups of Mycobacterium fortuitum and Mycobacterium chelonae. Antimicrob Agents Chemother. 1985;28:807-811.
9. Leung YY, Choi KW, Ho KM, et al. Disseminated cutaneous infection with Mycobacterium chelonae mimicking panniculitis in a patient with dermatomyositis. Hong Kong Med J. 2005;11:515-519.
A 21-year-old man presented with growing, mildly pruritic, cutaneous papules and plaques on the right extensor forearm of 3 weeks’ duration. The lesions appeared 1 week after receiving a tattoo on the arm. One year prior the patient had a similar tattoo placed on another section of the right arm without any complications. The patient was afebrile and denied a history of sarcoidosis. Physical examination revealed indurated erythematous papules and plaques on the right extensor forearm that were most prominent in the gray-colored areas of the tattoo.
Hole in Jaw Has Drained Fluid for 20 Years
ANSWER
The correct answer is all of the above (choice “d”). The patient’s actual diagnosis, sinus tract of odontogenic origin (choice “a”), will be discussed further.
Branchial cleft cyst (choice “b”) is always in the differential for neck masses, and squamous cell carcinoma (choice “c”) should always be considered in cases of nonhealing lesions—although 20 years is an unlikely timeframe for that diagnosis! Additional differential possibilities include thyroglossal duct cyst and pyogenic granuloma.
DISCUSSION
Sinus tracts of odontogenic origin, also called dentocutaneous sinus tracts, are primarily caused by periapical abscesses. As the purulent material accumulates in the confined space around the apical area, pressure increases; this sets in motion a tunneling process that terminates in an outlet, often inside the mouth but also (often enough) on the skin.
In the latter instance, known as extraoral sinus, the opening forms along the chin or submental area. In 80% of cases, the source is the mandibular teeth.
Dermocutaneous sinuses of maxillary origin, though not unknown, are decidedly unusual. They can drain anywhere on the maxilla, including around the nose. In edentulous patients, retained tooth fragments or segments of apical abscesses can act as the nidus for this process.
When a draining sinus manifests more acutely or occurs in a patient from a high-risk area (eg, Mexico or Central America), other diagnoses must be considered. These include scrofula, in which regional nymph nodes, infected by Mycobacterium tuberculosis or atypical mycobacterial organism, break down and drain. The indolent nature and chronicity of this patient’s problem effectively ruled out this diagnosis.
Culture of the fluid draining from the abscess would reveal a number of organisms (mostly of the strep family) but would not show the actual causative bacteria, since they are typically anaerobic. Biopsy of the surrounding tissue is occasionally necessary, when squamous cell carcinoma or other neoplastic process is suspected.
TREATMENT
The patient was advised to see a dentist, who will likely obtain a panoramic radiograph of her teeth, with particular attention to the affected area.
If an abscess is identified, as expected, treatment would entail root canal or extraction. The sinus tract would then heal rather quickly.
Antibiotics would be of limited use without elimination of the pocket. However, when patients complain of discomfort or outright pain, antibiotics (eg, penicillin V potassium or amoxicillin/clavulanate) can help to reduce the inflammation and offer some relief.
ANSWER
The correct answer is all of the above (choice “d”). The patient’s actual diagnosis, sinus tract of odontogenic origin (choice “a”), will be discussed further.
Branchial cleft cyst (choice “b”) is always in the differential for neck masses, and squamous cell carcinoma (choice “c”) should always be considered in cases of nonhealing lesions—although 20 years is an unlikely timeframe for that diagnosis! Additional differential possibilities include thyroglossal duct cyst and pyogenic granuloma.
DISCUSSION
Sinus tracts of odontogenic origin, also called dentocutaneous sinus tracts, are primarily caused by periapical abscesses. As the purulent material accumulates in the confined space around the apical area, pressure increases; this sets in motion a tunneling process that terminates in an outlet, often inside the mouth but also (often enough) on the skin.
In the latter instance, known as extraoral sinus, the opening forms along the chin or submental area. In 80% of cases, the source is the mandibular teeth.
Dermocutaneous sinuses of maxillary origin, though not unknown, are decidedly unusual. They can drain anywhere on the maxilla, including around the nose. In edentulous patients, retained tooth fragments or segments of apical abscesses can act as the nidus for this process.
When a draining sinus manifests more acutely or occurs in a patient from a high-risk area (eg, Mexico or Central America), other diagnoses must be considered. These include scrofula, in which regional nymph nodes, infected by Mycobacterium tuberculosis or atypical mycobacterial organism, break down and drain. The indolent nature and chronicity of this patient’s problem effectively ruled out this diagnosis.
Culture of the fluid draining from the abscess would reveal a number of organisms (mostly of the strep family) but would not show the actual causative bacteria, since they are typically anaerobic. Biopsy of the surrounding tissue is occasionally necessary, when squamous cell carcinoma or other neoplastic process is suspected.
TREATMENT
The patient was advised to see a dentist, who will likely obtain a panoramic radiograph of her teeth, with particular attention to the affected area.
If an abscess is identified, as expected, treatment would entail root canal or extraction. The sinus tract would then heal rather quickly.
Antibiotics would be of limited use without elimination of the pocket. However, when patients complain of discomfort or outright pain, antibiotics (eg, penicillin V potassium or amoxicillin/clavulanate) can help to reduce the inflammation and offer some relief.
ANSWER
The correct answer is all of the above (choice “d”). The patient’s actual diagnosis, sinus tract of odontogenic origin (choice “a”), will be discussed further.
Branchial cleft cyst (choice “b”) is always in the differential for neck masses, and squamous cell carcinoma (choice “c”) should always be considered in cases of nonhealing lesions—although 20 years is an unlikely timeframe for that diagnosis! Additional differential possibilities include thyroglossal duct cyst and pyogenic granuloma.
DISCUSSION
Sinus tracts of odontogenic origin, also called dentocutaneous sinus tracts, are primarily caused by periapical abscesses. As the purulent material accumulates in the confined space around the apical area, pressure increases; this sets in motion a tunneling process that terminates in an outlet, often inside the mouth but also (often enough) on the skin.
In the latter instance, known as extraoral sinus, the opening forms along the chin or submental area. In 80% of cases, the source is the mandibular teeth.
Dermocutaneous sinuses of maxillary origin, though not unknown, are decidedly unusual. They can drain anywhere on the maxilla, including around the nose. In edentulous patients, retained tooth fragments or segments of apical abscesses can act as the nidus for this process.
When a draining sinus manifests more acutely or occurs in a patient from a high-risk area (eg, Mexico or Central America), other diagnoses must be considered. These include scrofula, in which regional nymph nodes, infected by Mycobacterium tuberculosis or atypical mycobacterial organism, break down and drain. The indolent nature and chronicity of this patient’s problem effectively ruled out this diagnosis.
Culture of the fluid draining from the abscess would reveal a number of organisms (mostly of the strep family) but would not show the actual causative bacteria, since they are typically anaerobic. Biopsy of the surrounding tissue is occasionally necessary, when squamous cell carcinoma or other neoplastic process is suspected.
TREATMENT
The patient was advised to see a dentist, who will likely obtain a panoramic radiograph of her teeth, with particular attention to the affected area.
If an abscess is identified, as expected, treatment would entail root canal or extraction. The sinus tract would then heal rather quickly.
Antibiotics would be of limited use without elimination of the pocket. However, when patients complain of discomfort or outright pain, antibiotics (eg, penicillin V potassium or amoxicillin/clavulanate) can help to reduce the inflammation and offer some relief.
A 74-year-old woman is referred to dermatology by the primary care provider at her nursing home. She has a small hole on her left jaw that has drained foul-smelling material for more than 20 years. Although the site has never been painful, it occasionally swells and becomes slightly sensitive before slowly returning to its usual small size over a period of weeks. The patient is in generally poor health, with early dementia, chronic congestive heart failure, and diabetes. All her teeth were removed almost 30 years ago. She is afebrile and in no acute distress. On the submental aspect of her left jaw, there is a round, 6-cm area of skin that is retracted and fixed around a centrally placed sinus opening (measuring about 2 to 3 mm). A scant amount of purulent-looking fluid can be expressed from the spot. The area is faintly pink, but there is no evidence of increased warmth or tenderness on palpation.
Woman Complains of Knee Pain Following Fight
ANSWER
The radiograph shows a small calcification along the medial aspect of the medial collateral ligament. This finding is known as a Pellegrini-Stieda lesion. While it certainly could represent a small avulsion fracture, the lack of joint fluid and soft-tissue swelling makes this diagnosis less likely. The patient was treated symptomatically with anti-inflammatory medications.
ANSWER
The radiograph shows a small calcification along the medial aspect of the medial collateral ligament. This finding is known as a Pellegrini-Stieda lesion. While it certainly could represent a small avulsion fracture, the lack of joint fluid and soft-tissue swelling makes this diagnosis less likely. The patient was treated symptomatically with anti-inflammatory medications.
ANSWER
The radiograph shows a small calcification along the medial aspect of the medial collateral ligament. This finding is known as a Pellegrini-Stieda lesion. While it certainly could represent a small avulsion fracture, the lack of joint fluid and soft-tissue swelling makes this diagnosis less likely. The patient was treated symptomatically with anti-inflammatory medications.
A 35-year-old woman presents for evaluation of left knee pain secondary to an assault. She says she was involved in a fight and was struck multiple times throughout her whole body. She states she is “sore all over,” but her knee bothers her the most, as it is difficult and painful to bear weight. The patient’s medical history is unremarkable. Physical exam shows a young female who is uncomfortable but in no obvious distress. Her vital signs are normal. You note bruises throughout her body. Inspection of her left knee shows no obvious deformity or swelling. There is some mild bruising and pain present to palpation. She has limited flexion and extension secondary to pain. However, the joint itself appears stable. Radiographs of the knee are obtained. What is your impression?
Neighbor Finds Man on Knees, Vomiting
ANSWER
The correct interpretation of this ECG includes atrial fibrillation and ST- and T-wave changes consistent with a central nervous system hemorrhage, as well as a markedly prolonged QT interval.
The most common ECG alterations seen in cases of acute subarachnoid hemorrhage include repolarization abnormalities due to imbalance of autonomic cardiovascular control. While ST depression is more common in patients with poor outcomes, it is not predictive.
ANSWER
The correct interpretation of this ECG includes atrial fibrillation and ST- and T-wave changes consistent with a central nervous system hemorrhage, as well as a markedly prolonged QT interval.
The most common ECG alterations seen in cases of acute subarachnoid hemorrhage include repolarization abnormalities due to imbalance of autonomic cardiovascular control. While ST depression is more common in patients with poor outcomes, it is not predictive.
ANSWER
The correct interpretation of this ECG includes atrial fibrillation and ST- and T-wave changes consistent with a central nervous system hemorrhage, as well as a markedly prolonged QT interval.
The most common ECG alterations seen in cases of acute subarachnoid hemorrhage include repolarization abnormalities due to imbalance of autonomic cardiovascular control. While ST depression is more common in patients with poor outcomes, it is not predictive.
A 68-year-old man was found on his knees, vomiting, in his backyard by a neighbor early this morning. When asked if he was OK, the patient responded that he suddenly felt nauseated and had a headache. The neighbor helped him to his feet and, noticing that his left leg and arm were weak, called 911. During that time, the neighbor observed slurred speech. As they waited for the ambulance to arrive, the patient was able to say that this was the worst headache he’d ever had. When the paramedics arrived, they recorded a blood pressure of 198/120 mm Hg, consistent in both arms. Medical history is remarkable for hypertension, paroxysmal atrial fibrillation, adult-onset diabetes, and nephrolithiasis. Surgical history is remarkable for appendectomy, cholecystectomy, and lithotripsy. The patient is a retired civil engineer who lives at home alone. His wife died three years ago of complications from uterine cancer. He has one adult son who is in excellent health but lives on the opposite coast. The patient has never smoked and drinks approximately one six-pack of beer per month. Current medications include hydrochlorothiazide, metformin, and rivaroxaban. He is allergic to sulfa-containing medications. A complete review of systems is not obtained, given the patient’s slurred speech and progressive aphasia. He is able to nod yes or no to specific questions, and no significant symptoms or findings are identified. At the hospital, the patient is agitated and in apparent distress, with severe headache and aphasia. Vital signs include a blood pressure of 180/110 mm Hg; pulse, 60 beats/min; respiratory rate, 14 breaths/min; and temperature, 98.4°F. The O2 saturation is 96.4% on room air. Pertinent physical findings include aphasia, oculomotor nerve palsy, nuchal rigidity, and findings of a left-sided (right hemispheric) progressive hemiparesis. The remainder of the physical examination is noncontributory. Samples are drawn for laboratory testing, and an ECG is obtained prior to the patient’s transfer to radiology for CT of the head. The ECG findings include a ventricular rate of 62 beats/min; QRS duration, 88 ms; QT/QTc interval, 718/728 ms; P axis, not measured; R axis, 35°; and T axis, 209°. What is your interpretation of this ECG?
Papules on the Face and Body
The Diagnosis: Lichen Spinulosus
Lichen spinulosus, also referred to as keratosis spinulosa, is a disorder of keratinization characterized by grouped 1- to 3-mm papules with a horny spine localized to follicles (Figure).1 These lesions most commonly occur in the first through third decades of life, presenting as 2- to 6-cm patches on the neck, buttocks, thighs, abdomen, or extensor surfaces.1-4 Some patients report mild pruritus.1 The cause is unknown.1-3,5-7 Several proposed but unproven explanations include atopy,2,4 genetic predisposition,1,2 toxins,3,5 infection,5 abnormal immune response,8 and vitamin deficiency.1,6,7
Our patient’s presentation is atypical due to her age and the involvement of her face. Generalized lichen spinulosus in adults likely is rare. A few similar cases have been reported: a 61-year-old woman with Crohn disease and lichen spinulosus affecting the groin, inframammary region, and back8; 2 case reports linked to alcoholism-associated nutritional deficiency6,7; and generalized lichen spinulosus–like eruptions in 2 patients with human immuno-deficiency virus infection.9,10 Our patient’s medical history indicated an extensive smoking history; thiamine deficiency 5 years prior treated with vitamin B complex supplements, which she still takes; and a recent diagnosis of vitamin D deficiency. She had no evidence of immunodeficiency or systemic illness on routine screening.
The disorders of follicular keratinization are lichen spinulosus, keratosis pilaris, keratosis pilaris atrophicans, pityriasis rubra pilaris, lichen planopilaris, erythromelanosis follicularis faciei, and phrynoderma.11 The clinical differential diagnosis of lichen spinulosus includes keratosis pilaris, phrynoderma, pityriasis rubra pilaris, and frictional lichenoid eruption. Lichen spinulosus can be distinguished from keratosis pilaris by 4 factors1,11: (1) keratosis pilaris lesions develop slowly over time as opposed to the rapid onset in lichen spinulosus; (2) keratosis pilaris is preferentially located on the upper arms and legs; (3) keratosis pilaris does not develop in small clusters; (4) keratosis pilaris, unlike lichen spinulosus, often has a thin outline of perifollicular erythema. Histopathologically, lichen spinulosus is similar to keratosis pilaris, showing dilated hair follicles with a keratin plug and perifollicular and perivascular dermal lymphocytic infiltrate.1 A punch biopsy from our patient’s cheek demonstrated focal follicular hyperkeratosis with dermal perivascular inflammation. Periodic acid–Schiff with diastase stain was negative for pathogenic fungal organisms.
Treatment of lichen spinulosus is initiated to address cosmetic concerns. Traditionally, keratolytics and emollients are utilized. Success has been described with salicylic acid gel 6% without occlusion for 8 weeks12 or with occlusion for 2 weeks.13 Tar preparations and mid-potency topical corticosteroids may be used on lesions not located on the face.2,4,15 Topical vitamin A,2 lactic acid,4 and ammonium lactate lotion2 have been therapeutic in some cases. Facial lesions have been successfully treated with tacalcitol14 or tretinoin gel 0.04% in combination with hydroactive adhesive applications.15 In the case of lichen spinulosus accompanying alcoholism, oral vitamin supplementation has been sufficient for resolution.6,7
Our patient was initially prescribed ammonium lactate lotion twice daily and tretinoin cream 0.025% for facial application nightly. She only used the tretinoin briefly due to skin irritation, and she discontinued use of ammonium lactate due to lotion texture. Three months of vitamin A and vitamin B complex supplementation did not lead to any improvement. She believed the papules softened by scrubbing them with a loofah in the shower and then moisturizing. Malignancy workup, including a colonoscopy, mammography, chest radiograph, and basic blood tests, were negative. No remarkable change was noted by the patient at 1-year follow-up.
1. Friedman SJ. Lichen spinulosus. clinicopathologic review of thirty-five cases. J Am Acad Dermatol. 1990;22:261-264.
2. Boyd AS. Lichen spinulosus: case report and overview. Cutis. 1989;43:557-560.
3. Adamson H. Lichen pilaris, seu spinulosis. Br J Dermatol. 1905;17:39-54.
4. Strickling WA, Norton SA. Spiny eruption on the neck. diagnosis: lichen spinulosus (LS). Arch Dermatol. 2000;136:1165-1170.
5. Becker S. Lichen spinulosus following intradermal application of diphtheria toxin. Arch Dermatol Syph. 1930;21:839-840.
6. Irgang S. Lichen spinulosus responsive to ascorbic acid (vitamin C). case in an alcoholic adult. Skin. 1964;3:145-146.
7. Kabashima R, Sugita K, Kabashima K, et al. Lichen spinulosus in an alcoholic patient. Acta Derm Venereol. 2009;89:311-312.
8. Kano Y, Orihara M, Yagita A, et al. Lichen spinulosus in a patient with Crohn disease. Int J Dermatol. 1995;34:670-671.
9. Cohen SJ, Dicken CH. Generalized lichen spinulosus in an HIV-positive man. J Am Acad Dermatol. 1991;25:116-118.
10. Resnick SD, Murrell DF, Woosley J. Acne conglobata and a generalized lichen spinulosus-like eruption in a man seropositive for human immunodeficiency virus. J Am Acad Dermatol. 1992;26:1013-1014.
11. McMichael A, Curtis A, Guzman-Sanchez D, et al. Folliculitis and other follicular disorders. In: Bolognia J, Jorizzo J, Rapini R, eds. Dermatology. Vol 1. 3rd ed. New York, NY: Elsevier; 2012:571-586.
12. Tuyp E, McLeod WA, Boyko W. Lichen spinulosus with immunofluorescent studies. Cutis. 1984;33:197-200.
13. Maiocco KJ, Miller OF. Lichen spinulosus: response to therapy. Cutis. 1976;17:294-299.
14. Kim SH, Kang JH, Seo JK, et al. Successful treatment of lichen spinulosus with topical tacalcitol cream. Pediatr Dermatol. 2010;27:546-547.
15. Forman SB, Hudgins EM, Blaylock WK. Lichen spinulosus: excellent response to tretinoin gel and hydroactive adhesive applications. Arch Dermatol. 2007;143:122-123.
The Diagnosis: Lichen Spinulosus
Lichen spinulosus, also referred to as keratosis spinulosa, is a disorder of keratinization characterized by grouped 1- to 3-mm papules with a horny spine localized to follicles (Figure).1 These lesions most commonly occur in the first through third decades of life, presenting as 2- to 6-cm patches on the neck, buttocks, thighs, abdomen, or extensor surfaces.1-4 Some patients report mild pruritus.1 The cause is unknown.1-3,5-7 Several proposed but unproven explanations include atopy,2,4 genetic predisposition,1,2 toxins,3,5 infection,5 abnormal immune response,8 and vitamin deficiency.1,6,7
Our patient’s presentation is atypical due to her age and the involvement of her face. Generalized lichen spinulosus in adults likely is rare. A few similar cases have been reported: a 61-year-old woman with Crohn disease and lichen spinulosus affecting the groin, inframammary region, and back8; 2 case reports linked to alcoholism-associated nutritional deficiency6,7; and generalized lichen spinulosus–like eruptions in 2 patients with human immuno-deficiency virus infection.9,10 Our patient’s medical history indicated an extensive smoking history; thiamine deficiency 5 years prior treated with vitamin B complex supplements, which she still takes; and a recent diagnosis of vitamin D deficiency. She had no evidence of immunodeficiency or systemic illness on routine screening.
The disorders of follicular keratinization are lichen spinulosus, keratosis pilaris, keratosis pilaris atrophicans, pityriasis rubra pilaris, lichen planopilaris, erythromelanosis follicularis faciei, and phrynoderma.11 The clinical differential diagnosis of lichen spinulosus includes keratosis pilaris, phrynoderma, pityriasis rubra pilaris, and frictional lichenoid eruption. Lichen spinulosus can be distinguished from keratosis pilaris by 4 factors1,11: (1) keratosis pilaris lesions develop slowly over time as opposed to the rapid onset in lichen spinulosus; (2) keratosis pilaris is preferentially located on the upper arms and legs; (3) keratosis pilaris does not develop in small clusters; (4) keratosis pilaris, unlike lichen spinulosus, often has a thin outline of perifollicular erythema. Histopathologically, lichen spinulosus is similar to keratosis pilaris, showing dilated hair follicles with a keratin plug and perifollicular and perivascular dermal lymphocytic infiltrate.1 A punch biopsy from our patient’s cheek demonstrated focal follicular hyperkeratosis with dermal perivascular inflammation. Periodic acid–Schiff with diastase stain was negative for pathogenic fungal organisms.
Treatment of lichen spinulosus is initiated to address cosmetic concerns. Traditionally, keratolytics and emollients are utilized. Success has been described with salicylic acid gel 6% without occlusion for 8 weeks12 or with occlusion for 2 weeks.13 Tar preparations and mid-potency topical corticosteroids may be used on lesions not located on the face.2,4,15 Topical vitamin A,2 lactic acid,4 and ammonium lactate lotion2 have been therapeutic in some cases. Facial lesions have been successfully treated with tacalcitol14 or tretinoin gel 0.04% in combination with hydroactive adhesive applications.15 In the case of lichen spinulosus accompanying alcoholism, oral vitamin supplementation has been sufficient for resolution.6,7
Our patient was initially prescribed ammonium lactate lotion twice daily and tretinoin cream 0.025% for facial application nightly. She only used the tretinoin briefly due to skin irritation, and she discontinued use of ammonium lactate due to lotion texture. Three months of vitamin A and vitamin B complex supplementation did not lead to any improvement. She believed the papules softened by scrubbing them with a loofah in the shower and then moisturizing. Malignancy workup, including a colonoscopy, mammography, chest radiograph, and basic blood tests, were negative. No remarkable change was noted by the patient at 1-year follow-up.
The Diagnosis: Lichen Spinulosus
Lichen spinulosus, also referred to as keratosis spinulosa, is a disorder of keratinization characterized by grouped 1- to 3-mm papules with a horny spine localized to follicles (Figure).1 These lesions most commonly occur in the first through third decades of life, presenting as 2- to 6-cm patches on the neck, buttocks, thighs, abdomen, or extensor surfaces.1-4 Some patients report mild pruritus.1 The cause is unknown.1-3,5-7 Several proposed but unproven explanations include atopy,2,4 genetic predisposition,1,2 toxins,3,5 infection,5 abnormal immune response,8 and vitamin deficiency.1,6,7
Our patient’s presentation is atypical due to her age and the involvement of her face. Generalized lichen spinulosus in adults likely is rare. A few similar cases have been reported: a 61-year-old woman with Crohn disease and lichen spinulosus affecting the groin, inframammary region, and back8; 2 case reports linked to alcoholism-associated nutritional deficiency6,7; and generalized lichen spinulosus–like eruptions in 2 patients with human immuno-deficiency virus infection.9,10 Our patient’s medical history indicated an extensive smoking history; thiamine deficiency 5 years prior treated with vitamin B complex supplements, which she still takes; and a recent diagnosis of vitamin D deficiency. She had no evidence of immunodeficiency or systemic illness on routine screening.
The disorders of follicular keratinization are lichen spinulosus, keratosis pilaris, keratosis pilaris atrophicans, pityriasis rubra pilaris, lichen planopilaris, erythromelanosis follicularis faciei, and phrynoderma.11 The clinical differential diagnosis of lichen spinulosus includes keratosis pilaris, phrynoderma, pityriasis rubra pilaris, and frictional lichenoid eruption. Lichen spinulosus can be distinguished from keratosis pilaris by 4 factors1,11: (1) keratosis pilaris lesions develop slowly over time as opposed to the rapid onset in lichen spinulosus; (2) keratosis pilaris is preferentially located on the upper arms and legs; (3) keratosis pilaris does not develop in small clusters; (4) keratosis pilaris, unlike lichen spinulosus, often has a thin outline of perifollicular erythema. Histopathologically, lichen spinulosus is similar to keratosis pilaris, showing dilated hair follicles with a keratin plug and perifollicular and perivascular dermal lymphocytic infiltrate.1 A punch biopsy from our patient’s cheek demonstrated focal follicular hyperkeratosis with dermal perivascular inflammation. Periodic acid–Schiff with diastase stain was negative for pathogenic fungal organisms.
Treatment of lichen spinulosus is initiated to address cosmetic concerns. Traditionally, keratolytics and emollients are utilized. Success has been described with salicylic acid gel 6% without occlusion for 8 weeks12 or with occlusion for 2 weeks.13 Tar preparations and mid-potency topical corticosteroids may be used on lesions not located on the face.2,4,15 Topical vitamin A,2 lactic acid,4 and ammonium lactate lotion2 have been therapeutic in some cases. Facial lesions have been successfully treated with tacalcitol14 or tretinoin gel 0.04% in combination with hydroactive adhesive applications.15 In the case of lichen spinulosus accompanying alcoholism, oral vitamin supplementation has been sufficient for resolution.6,7
Our patient was initially prescribed ammonium lactate lotion twice daily and tretinoin cream 0.025% for facial application nightly. She only used the tretinoin briefly due to skin irritation, and she discontinued use of ammonium lactate due to lotion texture. Three months of vitamin A and vitamin B complex supplementation did not lead to any improvement. She believed the papules softened by scrubbing them with a loofah in the shower and then moisturizing. Malignancy workup, including a colonoscopy, mammography, chest radiograph, and basic blood tests, were negative. No remarkable change was noted by the patient at 1-year follow-up.
1. Friedman SJ. Lichen spinulosus. clinicopathologic review of thirty-five cases. J Am Acad Dermatol. 1990;22:261-264.
2. Boyd AS. Lichen spinulosus: case report and overview. Cutis. 1989;43:557-560.
3. Adamson H. Lichen pilaris, seu spinulosis. Br J Dermatol. 1905;17:39-54.
4. Strickling WA, Norton SA. Spiny eruption on the neck. diagnosis: lichen spinulosus (LS). Arch Dermatol. 2000;136:1165-1170.
5. Becker S. Lichen spinulosus following intradermal application of diphtheria toxin. Arch Dermatol Syph. 1930;21:839-840.
6. Irgang S. Lichen spinulosus responsive to ascorbic acid (vitamin C). case in an alcoholic adult. Skin. 1964;3:145-146.
7. Kabashima R, Sugita K, Kabashima K, et al. Lichen spinulosus in an alcoholic patient. Acta Derm Venereol. 2009;89:311-312.
8. Kano Y, Orihara M, Yagita A, et al. Lichen spinulosus in a patient with Crohn disease. Int J Dermatol. 1995;34:670-671.
9. Cohen SJ, Dicken CH. Generalized lichen spinulosus in an HIV-positive man. J Am Acad Dermatol. 1991;25:116-118.
10. Resnick SD, Murrell DF, Woosley J. Acne conglobata and a generalized lichen spinulosus-like eruption in a man seropositive for human immunodeficiency virus. J Am Acad Dermatol. 1992;26:1013-1014.
11. McMichael A, Curtis A, Guzman-Sanchez D, et al. Folliculitis and other follicular disorders. In: Bolognia J, Jorizzo J, Rapini R, eds. Dermatology. Vol 1. 3rd ed. New York, NY: Elsevier; 2012:571-586.
12. Tuyp E, McLeod WA, Boyko W. Lichen spinulosus with immunofluorescent studies. Cutis. 1984;33:197-200.
13. Maiocco KJ, Miller OF. Lichen spinulosus: response to therapy. Cutis. 1976;17:294-299.
14. Kim SH, Kang JH, Seo JK, et al. Successful treatment of lichen spinulosus with topical tacalcitol cream. Pediatr Dermatol. 2010;27:546-547.
15. Forman SB, Hudgins EM, Blaylock WK. Lichen spinulosus: excellent response to tretinoin gel and hydroactive adhesive applications. Arch Dermatol. 2007;143:122-123.
1. Friedman SJ. Lichen spinulosus. clinicopathologic review of thirty-five cases. J Am Acad Dermatol. 1990;22:261-264.
2. Boyd AS. Lichen spinulosus: case report and overview. Cutis. 1989;43:557-560.
3. Adamson H. Lichen pilaris, seu spinulosis. Br J Dermatol. 1905;17:39-54.
4. Strickling WA, Norton SA. Spiny eruption on the neck. diagnosis: lichen spinulosus (LS). Arch Dermatol. 2000;136:1165-1170.
5. Becker S. Lichen spinulosus following intradermal application of diphtheria toxin. Arch Dermatol Syph. 1930;21:839-840.
6. Irgang S. Lichen spinulosus responsive to ascorbic acid (vitamin C). case in an alcoholic adult. Skin. 1964;3:145-146.
7. Kabashima R, Sugita K, Kabashima K, et al. Lichen spinulosus in an alcoholic patient. Acta Derm Venereol. 2009;89:311-312.
8. Kano Y, Orihara M, Yagita A, et al. Lichen spinulosus in a patient with Crohn disease. Int J Dermatol. 1995;34:670-671.
9. Cohen SJ, Dicken CH. Generalized lichen spinulosus in an HIV-positive man. J Am Acad Dermatol. 1991;25:116-118.
10. Resnick SD, Murrell DF, Woosley J. Acne conglobata and a generalized lichen spinulosus-like eruption in a man seropositive for human immunodeficiency virus. J Am Acad Dermatol. 1992;26:1013-1014.
11. McMichael A, Curtis A, Guzman-Sanchez D, et al. Folliculitis and other follicular disorders. In: Bolognia J, Jorizzo J, Rapini R, eds. Dermatology. Vol 1. 3rd ed. New York, NY: Elsevier; 2012:571-586.
12. Tuyp E, McLeod WA, Boyko W. Lichen spinulosus with immunofluorescent studies. Cutis. 1984;33:197-200.
13. Maiocco KJ, Miller OF. Lichen spinulosus: response to therapy. Cutis. 1976;17:294-299.
14. Kim SH, Kang JH, Seo JK, et al. Successful treatment of lichen spinulosus with topical tacalcitol cream. Pediatr Dermatol. 2010;27:546-547.
15. Forman SB, Hudgins EM, Blaylock WK. Lichen spinulosus: excellent response to tretinoin gel and hydroactive adhesive applications. Arch Dermatol. 2007;143:122-123.
A 65-year-old woman presented for evaluation of papules on the face and body that had developed over a short period of time approximately 1.5 years prior. The papules were entirely asymptomatic. She had no prior treatment. On physical examination multiple flesh-colored papules with a central keratotic spicule were noted on the face, neck, arms, and legs.
Erythematous Friable Papule Under the Great Toenail
The Diagnosis: Subungual Eccrine Poroma
Histologic examination revealed a solitary papule (Figure 1). The epidermis was replaced with a well-defined proliferation of cuboidal and poroid cells. These cells demonstrated a downgrowth into the dermis in broad anastomosing bands that were surrounded by a fibrovascular stroma. Notably, there were few scattered foci of maturation into the ductal lumina of eccrine origin, which confirmed the diagnosis (Figure 2).
|
First described in 1956 by Goldman et al,1 eccrine poromas are benign, slow-growing tumors that account for approximately 10% of sweat gland neoplasms.2 Onset is typically in mid to late adulthood, and there is no ethnic or gender predilection. Classically, eccrine poromas present as soft, sessile, reddish papules or nodules measuring less than 2 cm that protrude from a well-circumscribed depression.
Although eccrine poromas can develop on hair-bearing regions, they most commonly arise on acral skin. In acral locations, bleeding, discharge, rapid growth, and localized pain can occur. These symptoms are even more common in this lesion’s malignant counterpart, eccrine porocarcinoma.3
Solar damage, radiation exposure, trauma, and human papillomavirus have been indicated in the pathogenesis of eccrine poroma; however, the exact etiology has yet to be defined.2,4 The differential diagnosis includes nevus, pyogenic granu-loma, acrochordon, basal cell carcinoma, and verruca vulgaris.5
Histologically, eccrine poromas consist of a combination of 5 distinct features: poroid cells, cuticular cells, intracytoplasmic or intercellular vacuolization en route to duct formation, massive necrosis or necrosis en masse, and nuclear monomorphism of the poroid and cuticular cells.6 However, all 5 histologic features do not have to be present for the diagnosis. Classically, there is a sharp demarcation of the lesion from the surrounding epidermis.7
Treatment of choice is complete excision to prevent recurrence and risk for malignant transformation in long-standing lesions. One study of eccrine porocarcinomas found that 18% (11/62) arose from a benign preexistent poroma.8 These malignant lesions are found more commonly on the extremities and tend to show a slight female predominance.9
Although there have been 2 reported cases of subungual eccrine porocarcinomas9,10 and 1 case of periungual eccrine porocarcinoma,11 according to an Ovid search using the terms porocarcinoma and nail, the benign subungual eccrine poroma is more rare.
1. Goldman P, Pinkus H, Rogin JR. Eccrine poroma; tumors exhibiting features of the epidermal sweat duct unit. AMA Arch Derm. 1956;74:511-521.
2. Orlandi C, Arcangeli F, Patrizi A, et al. Eccrine poroma in a child. Pediatr Dermatol. 2005;22:279-280.
3. Casper DJ, Glass LF, Shenefelt PD. An unusually large eccrine poroma: a case report and review of the literature. Cutis. 2011;88:227-229.
4. Kang MC, Kim SA, Lee KS, et al. A case of an unusual eccrine poroma on the left forearm area. Ann Dermatol. 2011;23:250-253.
5. Moore TO, Orman HL, Orman SK, et al. Poromas of the head and neck. J Am Acad Dermatol. 2001;44:48-52.
6. Chen CC, Chang YT, Liu HN. Clinical and histological characteristics of poroid neoplasms: a study of 25 cases in Taiwan. Int J Dermatol. 2006;45:722-727.
7. Smith EV, Madan V, Joshi A, et al. A pigmented lesion on the foot. Clin Exp Dermatol. 2012;37:84-86.
8. Robson A, Greene J, Ansari N, et al. Eccrine porocarcinoma (malignant eccrine poroma): a clinicopathologic study of 69 cases. Am J Surg Pathol. 2001;25:710-720.
9. Moussallem CD, Abi Hatem NE, El-Khoury ZN.Malignant porocarcinoma of the nail fold: a tricky diagnosis. Dermatol Online J. 2008;14:10.
10. Requena L, Sánchez M, Aguilar A, et al. Periungual porocarcinoma. Dermatologica. 1990;180:177-180.
11. van Gorp J, van der Putte SC. Periungual eccrine porocarcinoma. Dermatology. 1993;187:67-70.
The Diagnosis: Subungual Eccrine Poroma
Histologic examination revealed a solitary papule (Figure 1). The epidermis was replaced with a well-defined proliferation of cuboidal and poroid cells. These cells demonstrated a downgrowth into the dermis in broad anastomosing bands that were surrounded by a fibrovascular stroma. Notably, there were few scattered foci of maturation into the ductal lumina of eccrine origin, which confirmed the diagnosis (Figure 2).
|
First described in 1956 by Goldman et al,1 eccrine poromas are benign, slow-growing tumors that account for approximately 10% of sweat gland neoplasms.2 Onset is typically in mid to late adulthood, and there is no ethnic or gender predilection. Classically, eccrine poromas present as soft, sessile, reddish papules or nodules measuring less than 2 cm that protrude from a well-circumscribed depression.
Although eccrine poromas can develop on hair-bearing regions, they most commonly arise on acral skin. In acral locations, bleeding, discharge, rapid growth, and localized pain can occur. These symptoms are even more common in this lesion’s malignant counterpart, eccrine porocarcinoma.3
Solar damage, radiation exposure, trauma, and human papillomavirus have been indicated in the pathogenesis of eccrine poroma; however, the exact etiology has yet to be defined.2,4 The differential diagnosis includes nevus, pyogenic granu-loma, acrochordon, basal cell carcinoma, and verruca vulgaris.5
Histologically, eccrine poromas consist of a combination of 5 distinct features: poroid cells, cuticular cells, intracytoplasmic or intercellular vacuolization en route to duct formation, massive necrosis or necrosis en masse, and nuclear monomorphism of the poroid and cuticular cells.6 However, all 5 histologic features do not have to be present for the diagnosis. Classically, there is a sharp demarcation of the lesion from the surrounding epidermis.7
Treatment of choice is complete excision to prevent recurrence and risk for malignant transformation in long-standing lesions. One study of eccrine porocarcinomas found that 18% (11/62) arose from a benign preexistent poroma.8 These malignant lesions are found more commonly on the extremities and tend to show a slight female predominance.9
Although there have been 2 reported cases of subungual eccrine porocarcinomas9,10 and 1 case of periungual eccrine porocarcinoma,11 according to an Ovid search using the terms porocarcinoma and nail, the benign subungual eccrine poroma is more rare.
The Diagnosis: Subungual Eccrine Poroma
Histologic examination revealed a solitary papule (Figure 1). The epidermis was replaced with a well-defined proliferation of cuboidal and poroid cells. These cells demonstrated a downgrowth into the dermis in broad anastomosing bands that were surrounded by a fibrovascular stroma. Notably, there were few scattered foci of maturation into the ductal lumina of eccrine origin, which confirmed the diagnosis (Figure 2).
|
First described in 1956 by Goldman et al,1 eccrine poromas are benign, slow-growing tumors that account for approximately 10% of sweat gland neoplasms.2 Onset is typically in mid to late adulthood, and there is no ethnic or gender predilection. Classically, eccrine poromas present as soft, sessile, reddish papules or nodules measuring less than 2 cm that protrude from a well-circumscribed depression.
Although eccrine poromas can develop on hair-bearing regions, they most commonly arise on acral skin. In acral locations, bleeding, discharge, rapid growth, and localized pain can occur. These symptoms are even more common in this lesion’s malignant counterpart, eccrine porocarcinoma.3
Solar damage, radiation exposure, trauma, and human papillomavirus have been indicated in the pathogenesis of eccrine poroma; however, the exact etiology has yet to be defined.2,4 The differential diagnosis includes nevus, pyogenic granu-loma, acrochordon, basal cell carcinoma, and verruca vulgaris.5
Histologically, eccrine poromas consist of a combination of 5 distinct features: poroid cells, cuticular cells, intracytoplasmic or intercellular vacuolization en route to duct formation, massive necrosis or necrosis en masse, and nuclear monomorphism of the poroid and cuticular cells.6 However, all 5 histologic features do not have to be present for the diagnosis. Classically, there is a sharp demarcation of the lesion from the surrounding epidermis.7
Treatment of choice is complete excision to prevent recurrence and risk for malignant transformation in long-standing lesions. One study of eccrine porocarcinomas found that 18% (11/62) arose from a benign preexistent poroma.8 These malignant lesions are found more commonly on the extremities and tend to show a slight female predominance.9
Although there have been 2 reported cases of subungual eccrine porocarcinomas9,10 and 1 case of periungual eccrine porocarcinoma,11 according to an Ovid search using the terms porocarcinoma and nail, the benign subungual eccrine poroma is more rare.
1. Goldman P, Pinkus H, Rogin JR. Eccrine poroma; tumors exhibiting features of the epidermal sweat duct unit. AMA Arch Derm. 1956;74:511-521.
2. Orlandi C, Arcangeli F, Patrizi A, et al. Eccrine poroma in a child. Pediatr Dermatol. 2005;22:279-280.
3. Casper DJ, Glass LF, Shenefelt PD. An unusually large eccrine poroma: a case report and review of the literature. Cutis. 2011;88:227-229.
4. Kang MC, Kim SA, Lee KS, et al. A case of an unusual eccrine poroma on the left forearm area. Ann Dermatol. 2011;23:250-253.
5. Moore TO, Orman HL, Orman SK, et al. Poromas of the head and neck. J Am Acad Dermatol. 2001;44:48-52.
6. Chen CC, Chang YT, Liu HN. Clinical and histological characteristics of poroid neoplasms: a study of 25 cases in Taiwan. Int J Dermatol. 2006;45:722-727.
7. Smith EV, Madan V, Joshi A, et al. A pigmented lesion on the foot. Clin Exp Dermatol. 2012;37:84-86.
8. Robson A, Greene J, Ansari N, et al. Eccrine porocarcinoma (malignant eccrine poroma): a clinicopathologic study of 69 cases. Am J Surg Pathol. 2001;25:710-720.
9. Moussallem CD, Abi Hatem NE, El-Khoury ZN.Malignant porocarcinoma of the nail fold: a tricky diagnosis. Dermatol Online J. 2008;14:10.
10. Requena L, Sánchez M, Aguilar A, et al. Periungual porocarcinoma. Dermatologica. 1990;180:177-180.
11. van Gorp J, van der Putte SC. Periungual eccrine porocarcinoma. Dermatology. 1993;187:67-70.
1. Goldman P, Pinkus H, Rogin JR. Eccrine poroma; tumors exhibiting features of the epidermal sweat duct unit. AMA Arch Derm. 1956;74:511-521.
2. Orlandi C, Arcangeli F, Patrizi A, et al. Eccrine poroma in a child. Pediatr Dermatol. 2005;22:279-280.
3. Casper DJ, Glass LF, Shenefelt PD. An unusually large eccrine poroma: a case report and review of the literature. Cutis. 2011;88:227-229.
4. Kang MC, Kim SA, Lee KS, et al. A case of an unusual eccrine poroma on the left forearm area. Ann Dermatol. 2011;23:250-253.
5. Moore TO, Orman HL, Orman SK, et al. Poromas of the head and neck. J Am Acad Dermatol. 2001;44:48-52.
6. Chen CC, Chang YT, Liu HN. Clinical and histological characteristics of poroid neoplasms: a study of 25 cases in Taiwan. Int J Dermatol. 2006;45:722-727.
7. Smith EV, Madan V, Joshi A, et al. A pigmented lesion on the foot. Clin Exp Dermatol. 2012;37:84-86.
8. Robson A, Greene J, Ansari N, et al. Eccrine porocarcinoma (malignant eccrine poroma): a clinicopathologic study of 69 cases. Am J Surg Pathol. 2001;25:710-720.
9. Moussallem CD, Abi Hatem NE, El-Khoury ZN.Malignant porocarcinoma of the nail fold: a tricky diagnosis. Dermatol Online J. 2008;14:10.
10. Requena L, Sánchez M, Aguilar A, et al. Periungual porocarcinoma. Dermatologica. 1990;180:177-180.
11. van Gorp J, van der Putte SC. Periungual eccrine porocarcinoma. Dermatology. 1993;187:67-70.
A 20-year-old woman presented with a subungual growth of 1 year’s duration that would intermittently bleed. Despite treatment with silver nitrate in 2 sequential treatments, the lesion continued to increase in size. Physical examination revealed a 6×7-mm erythematous, friable, well-defined papule under the medial aspect of the distal great toenail. Complete surgical excision of the lesion was performed.
Dreadlocks
The Diagnosis: “Pseudonits”
Dreadlocks are matted hairs formed into thick ropelike strands (Figure 1). As a chosen hairstyle dreadlocks are worn by individuals of many different ethnic groups but are most commonly associated with members of the Rastafarian movement, or Rastas. Various techniques are used to form dreadlocks including backcombing (also known as teasing) in which the hair is combed toward the scalp to facilitate tangles and knotting or the neglect method in which the hair is not combed, brushed, or cut, becoming tangled and twisted as it grows long. Manicuring and perming techniques may be used to create the starting point for dreadlocks.
Telogen hairs are the hairs shed as part of normal hair cycling. The average person is estimated to lose 50 telogen hairs per day.1 With dreadlocks, the hairs are entangled distally, so when telogen hairs are released from scalp follicles, the shed hairs remain part of the locks. These “club” hairs have a bulbous white tip situated at the proximal end of the hair shaft (Figure 2) and should not be mistaken for the eggs of Pediculus humanus var capitis, hence the designation pseudonits.2 Hair casts, keratinous material surrounding the hair shafts when there is infundibular or perifollicular hyperkeratosis, also may resemble nits.3 Hair cast pseudonits can be distinguished from true nits by one’s ability to slide the hair casts freely along the hair shaft, whereas lice ova are cemented to the hair shaft and fixed in place.
Figure 2. “Club” hairs with a bulbous white tip situated at the
proximal end of the hair shaft (“pseudonits”).
1. Sperling LC. An Atlas of Hair Pathology with Clinical Correlations. New York, NY: The Parthenon Publishing Group; 2003.
2. Salih S, Bowling JC. Pseudonits in dreadlocked hair: A louse-y case of nits. Dermatology. 2006;213:245.
3. Lam M, Crutchfield CE 3rd, Lewis EJ. Hair casts: a case of pseudonits. Cutis. 1997;60:251-252.
The Diagnosis: “Pseudonits”
Dreadlocks are matted hairs formed into thick ropelike strands (Figure 1). As a chosen hairstyle dreadlocks are worn by individuals of many different ethnic groups but are most commonly associated with members of the Rastafarian movement, or Rastas. Various techniques are used to form dreadlocks including backcombing (also known as teasing) in which the hair is combed toward the scalp to facilitate tangles and knotting or the neglect method in which the hair is not combed, brushed, or cut, becoming tangled and twisted as it grows long. Manicuring and perming techniques may be used to create the starting point for dreadlocks.
Telogen hairs are the hairs shed as part of normal hair cycling. The average person is estimated to lose 50 telogen hairs per day.1 With dreadlocks, the hairs are entangled distally, so when telogen hairs are released from scalp follicles, the shed hairs remain part of the locks. These “club” hairs have a bulbous white tip situated at the proximal end of the hair shaft (Figure 2) and should not be mistaken for the eggs of Pediculus humanus var capitis, hence the designation pseudonits.2 Hair casts, keratinous material surrounding the hair shafts when there is infundibular or perifollicular hyperkeratosis, also may resemble nits.3 Hair cast pseudonits can be distinguished from true nits by one’s ability to slide the hair casts freely along the hair shaft, whereas lice ova are cemented to the hair shaft and fixed in place.
Figure 2. “Club” hairs with a bulbous white tip situated at the
proximal end of the hair shaft (“pseudonits”).
The Diagnosis: “Pseudonits”
Dreadlocks are matted hairs formed into thick ropelike strands (Figure 1). As a chosen hairstyle dreadlocks are worn by individuals of many different ethnic groups but are most commonly associated with members of the Rastafarian movement, or Rastas. Various techniques are used to form dreadlocks including backcombing (also known as teasing) in which the hair is combed toward the scalp to facilitate tangles and knotting or the neglect method in which the hair is not combed, brushed, or cut, becoming tangled and twisted as it grows long. Manicuring and perming techniques may be used to create the starting point for dreadlocks.
Telogen hairs are the hairs shed as part of normal hair cycling. The average person is estimated to lose 50 telogen hairs per day.1 With dreadlocks, the hairs are entangled distally, so when telogen hairs are released from scalp follicles, the shed hairs remain part of the locks. These “club” hairs have a bulbous white tip situated at the proximal end of the hair shaft (Figure 2) and should not be mistaken for the eggs of Pediculus humanus var capitis, hence the designation pseudonits.2 Hair casts, keratinous material surrounding the hair shafts when there is infundibular or perifollicular hyperkeratosis, also may resemble nits.3 Hair cast pseudonits can be distinguished from true nits by one’s ability to slide the hair casts freely along the hair shaft, whereas lice ova are cemented to the hair shaft and fixed in place.
Figure 2. “Club” hairs with a bulbous white tip situated at the
proximal end of the hair shaft (“pseudonits”).
1. Sperling LC. An Atlas of Hair Pathology with Clinical Correlations. New York, NY: The Parthenon Publishing Group; 2003.
2. Salih S, Bowling JC. Pseudonits in dreadlocked hair: A louse-y case of nits. Dermatology. 2006;213:245.
3. Lam M, Crutchfield CE 3rd, Lewis EJ. Hair casts: a case of pseudonits. Cutis. 1997;60:251-252.
1. Sperling LC. An Atlas of Hair Pathology with Clinical Correlations. New York, NY: The Parthenon Publishing Group; 2003.
2. Salih S, Bowling JC. Pseudonits in dreadlocked hair: A louse-y case of nits. Dermatology. 2006;213:245.
3. Lam M, Crutchfield CE 3rd, Lewis EJ. Hair casts: a case of pseudonits. Cutis. 1997;60:251-252.
A 17-year-old adolescent girl presented to our dermatology office with dreadlocks that were unrelated to the reason for her visit. She had mild scalp pruritus. Close inspection of the hair and scalp was performed.
