Shane E. Zainab, MBBS

Background

CML is usually classified in chronic phase (CP), accelerated phase (AP) and/or Blast phase (BP). Studies have described another provisional entity as Preleukemic phase of CML which precedes CP and is without leukocytosis and blood features of CP phase of CML. Here we will present a case of metastatic prostate cancer, where next-generation sequencing showed BCR-ABL1 but no overt leukocytosis and then later developed clinical CML after 11 months.

Case Presentation

Our patient was 87-yr-old male with history of metastatic prostate cancer, who presented with elevated PSA levels and new bony metastasis. He underwent next-generation-sequencing (foundation one liquid cdx) in April 2022. It did not show reportable alterations related to prostate cancer but BCR-ABL1 (p210) fusion was detected. It also showed ASXL1-S846fs5 and TET2-Q1548 that are also markers of clonal hematopoiesis. In March 2023 (11 months after the finding of BCR-ABL1), he developed asymptomatic leukocytosis, Workup showed BCR-ABL1(210) of 44% in peripheral blood and bone marrow showed 9% blasts. He was started on Imatinib after shared decision-making and considering the toxicity profile and comorbidities. He followed up regularly with improvement in leukocytosis.

Discussion

The diagnosis of CML is first suspected by typical findings in blood and/or bone marrow and then confirmed by presence of Philadelphia chromosome. Along with chronic and accelerated phases, there is another term described in few cases called “preleukemic or smoldering or aleukemic phase.” This is not a wellestablished term but mostly defined as normal leukocyte count with presence of BCR/ABL1 fusion gene/ ph chromosome. Preleukemic phase of CML is mostly underdiagnosed or misdiagnosed. Our case is unique in that BCR/ABL1 fusion was detected incidentally on next-generation sequencing and patient progressed to chronic phase of CML 11 months later. Upon literature review, few case reports and case series documenting aleukemic/preleukemic phase of CML but timing from the appearance of BCR/ABL1 mutation to actual development to leukocytosis is not well documented. Especially in the era of NGS testing, patients with incidental BCR-ABL1 should be evaluated further irrespective of normal WBC. Further studies need to be done to recognize this early and decrease the delay in treatment.

Background

CML is usually classified in chronic phase (CP), accelerated phase (AP) and/or Blast phase (BP). Studies have described another provisional entity as Preleukemic phase of CML which precedes CP and is without leukocytosis and blood features of CP phase of CML. Here we will present a case of metastatic prostate cancer, where next-generation sequencing showed BCR-ABL1 but no overt leukocytosis and then later developed clinical CML after 11 months.

Case Presentation

Our patient was 87-yr-old male with history of metastatic prostate cancer, who presented with elevated PSA levels and new bony metastasis. He underwent next-generation-sequencing (foundation one liquid cdx) in April 2022. It did not show reportable alterations related to prostate cancer but BCR-ABL1 (p210) fusion was detected. It also showed ASXL1-S846fs5 and TET2-Q1548 that are also markers of clonal hematopoiesis. In March 2023 (11 months after the finding of BCR-ABL1), he developed asymptomatic leukocytosis, Workup showed BCR-ABL1(210) of 44% in peripheral blood and bone marrow showed 9% blasts. He was started on Imatinib after shared decision-making and considering the toxicity profile and comorbidities. He followed up regularly with improvement in leukocytosis.

Discussion

The diagnosis of CML is first suspected by typical findings in blood and/or bone marrow and then confirmed by presence of Philadelphia chromosome. Along with chronic and accelerated phases, there is another term described in few cases called “preleukemic or smoldering or aleukemic phase.” This is not a wellestablished term but mostly defined as normal leukocyte count with presence of BCR/ABL1 fusion gene/ ph chromosome. Preleukemic phase of CML is mostly underdiagnosed or misdiagnosed. Our case is unique in that BCR/ABL1 fusion was detected incidentally on next-generation sequencing and patient progressed to chronic phase of CML 11 months later. Upon literature review, few case reports and case series documenting aleukemic/preleukemic phase of CML but timing from the appearance of BCR/ABL1 mutation to actual development to leukocytosis is not well documented. Especially in the era of NGS testing, patients with incidental BCR-ABL1 should be evaluated further irrespective of normal WBC. Further studies need to be done to recognize this early and decrease the delay in treatment.

Background

CML is usually classified in chronic phase (CP), accelerated phase (AP) and/or Blast phase (BP). Studies have described another provisional entity as Preleukemic phase of CML which precedes CP and is without leukocytosis and blood features of CP phase of CML. Here we will present a case of metastatic prostate cancer, where next-generation sequencing showed BCR-ABL1 but no overt leukocytosis and then later developed clinical CML after 11 months.

Case Presentation

Our patient was 87-yr-old male with history of metastatic prostate cancer, who presented with elevated PSA levels and new bony metastasis. He underwent next-generation-sequencing (foundation one liquid cdx) in April 2022. It did not show reportable alterations related to prostate cancer but BCR-ABL1 (p210) fusion was detected. It also showed ASXL1-S846fs5 and TET2-Q1548 that are also markers of clonal hematopoiesis. In March 2023 (11 months after the finding of BCR-ABL1), he developed asymptomatic leukocytosis, Workup showed BCR-ABL1(210) of 44% in peripheral blood and bone marrow showed 9% blasts. He was started on Imatinib after shared decision-making and considering the toxicity profile and comorbidities. He followed up regularly with improvement in leukocytosis.

Discussion

The diagnosis of CML is first suspected by typical findings in blood and/or bone marrow and then confirmed by presence of Philadelphia chromosome. Along with chronic and accelerated phases, there is another term described in few cases called “preleukemic or smoldering or aleukemic phase.” This is not a wellestablished term but mostly defined as normal leukocyte count with presence of BCR/ABL1 fusion gene/ ph chromosome. Preleukemic phase of CML is mostly underdiagnosed or misdiagnosed. Our case is unique in that BCR/ABL1 fusion was detected incidentally on next-generation sequencing and patient progressed to chronic phase of CML 11 months later. Upon literature review, few case reports and case series documenting aleukemic/preleukemic phase of CML but timing from the appearance of BCR/ABL1 mutation to actual development to leukocytosis is not well documented. Especially in the era of NGS testing, patients with incidental BCR-ABL1 should be evaluated further irrespective of normal WBC. Further studies need to be done to recognize this early and decrease the delay in treatment.

Background

Monoclonal B cell lymphocytosis (MBL) is defined as presence of clonal b cell population that is fewer than 5 × 10(9)/L B-cells in peripheral blood and no other signs of a lymphoproliferative disorder. Patients with MBL are usually monitored with periodic history, physical exam and blood counts. Here we presented a case of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) in breast in a patient with a history of MBL.

Case Presentation

68-year-old male with history of MBL underwent mammogram for breast mass. It showed suspicious 4.4 x 1.6 cm solid and cystic lesion containing a 1.7 x 0.9 x 1.8 cm solid hypervascular mass. Patient underwent left breast mass excision. Histologic sections focus of ADH involving papilloma with uninvolved margins. Lymphoid infiltrates noted had CLL/SLL immunophenotype and that it consists mostly of small B cells positive for CD5, CD20, CD23, CD43, Bcl-2, LEF1. CT CAP and PET/CT were negative for lymphadenopathy. Bone marrow biopsy showed marrow involvement by mature B-cell lymphoproliferative process, immunophenotypically consistent with CLL/SLL. As intra-ductal papilloma completely excised and hemogram was normal tumor board recommended surveillance only for CLL/SLL.

Discussion

MBL can progress to CLL, but it can rarely be presented as an extra-nodal mass in solid organs. We described a case of MBL that progressed to CLL/ SLL in breast mass in a male patient. This is the first reported case in literature where MBL progressed to CLL/ SLL of breast without lymphadenopathy. Upon literature review 8 case reports were found where CLL/SLL were described in breast tissue. 7 of them were in females and 1 one was in male. Two patients had CLL before breast mass but none of them had a history of MBL. 3 described cases in females had CLL/SLL infiltration of breast along with invasive ductal carcinoma. So, a patient with MBL can progress to involve solid organs despite no absolute lymphocytosis and should be considered in differentials of a new mass. Although more common in females, but it can occur in males as well. It’s important to consider the possibility of both CLL/SLL and breast cancer existing simultaneously.

Background

Monoclonal B cell lymphocytosis (MBL) is defined as presence of clonal b cell population that is fewer than 5 × 10(9)/L B-cells in peripheral blood and no other signs of a lymphoproliferative disorder. Patients with MBL are usually monitored with periodic history, physical exam and blood counts. Here we presented a case of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) in breast in a patient with a history of MBL.

Case Presentation

68-year-old male with history of MBL underwent mammogram for breast mass. It showed suspicious 4.4 x 1.6 cm solid and cystic lesion containing a 1.7 x 0.9 x 1.8 cm solid hypervascular mass. Patient underwent left breast mass excision. Histologic sections focus of ADH involving papilloma with uninvolved margins. Lymphoid infiltrates noted had CLL/SLL immunophenotype and that it consists mostly of small B cells positive for CD5, CD20, CD23, CD43, Bcl-2, LEF1. CT CAP and PET/CT were negative for lymphadenopathy. Bone marrow biopsy showed marrow involvement by mature B-cell lymphoproliferative process, immunophenotypically consistent with CLL/SLL. As intra-ductal papilloma completely excised and hemogram was normal tumor board recommended surveillance only for CLL/SLL.

Discussion

MBL can progress to CLL, but it can rarely be presented as an extra-nodal mass in solid organs. We described a case of MBL that progressed to CLL/ SLL in breast mass in a male patient. This is the first reported case in literature where MBL progressed to CLL/ SLL of breast without lymphadenopathy. Upon literature review 8 case reports were found where CLL/SLL were described in breast tissue. 7 of them were in females and 1 one was in male. Two patients had CLL before breast mass but none of them had a history of MBL. 3 described cases in females had CLL/SLL infiltration of breast along with invasive ductal carcinoma. So, a patient with MBL can progress to involve solid organs despite no absolute lymphocytosis and should be considered in differentials of a new mass. Although more common in females, but it can occur in males as well. It’s important to consider the possibility of both CLL/SLL and breast cancer existing simultaneously.

Background

Monoclonal B cell lymphocytosis (MBL) is defined as presence of clonal b cell population that is fewer than 5 × 10(9)/L B-cells in peripheral blood and no other signs of a lymphoproliferative disorder. Patients with MBL are usually monitored with periodic history, physical exam and blood counts. Here we presented a case of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) in breast in a patient with a history of MBL.

Case Presentation

68-year-old male with history of MBL underwent mammogram for breast mass. It showed suspicious 4.4 x 1.6 cm solid and cystic lesion containing a 1.7 x 0.9 x 1.8 cm solid hypervascular mass. Patient underwent left breast mass excision. Histologic sections focus of ADH involving papilloma with uninvolved margins. Lymphoid infiltrates noted had CLL/SLL immunophenotype and that it consists mostly of small B cells positive for CD5, CD20, CD23, CD43, Bcl-2, LEF1. CT CAP and PET/CT were negative for lymphadenopathy. Bone marrow biopsy showed marrow involvement by mature B-cell lymphoproliferative process, immunophenotypically consistent with CLL/SLL. As intra-ductal papilloma completely excised and hemogram was normal tumor board recommended surveillance only for CLL/SLL.

Discussion

MBL can progress to CLL, but it can rarely be presented as an extra-nodal mass in solid organs. We described a case of MBL that progressed to CLL/ SLL in breast mass in a male patient. This is the first reported case in literature where MBL progressed to CLL/ SLL of breast without lymphadenopathy. Upon literature review 8 case reports were found where CLL/SLL were described in breast tissue. 7 of them were in females and 1 one was in male. Two patients had CLL before breast mass but none of them had a history of MBL. 3 described cases in females had CLL/SLL infiltration of breast along with invasive ductal carcinoma. So, a patient with MBL can progress to involve solid organs despite no absolute lymphocytosis and should be considered in differentials of a new mass. Although more common in females, but it can occur in males as well. It’s important to consider the possibility of both CLL/SLL and breast cancer existing simultaneously.

Background

Pancreatic cancer stands as a prominent contributor to cancer-related mortality in the United States. In this abstract, we reviewed the SEER database to uncover the latest trends in pancreatic cancer among individuals diagnosed under the age of 50.

Methods

Information was obtained from the SEER database November 2023 which covers 22 national cancer registries. Only patients with age < 50 years were included. Age adjusted incidence and 5-year relative survival were compared between different ethnic groups.

Results

We identified 124691 patients with pancreatic cancer diagnosed between 2017-2021, among them 6477 were with age less than 50 years at the time of diagnosis. 3074 were male and 3403 were male. Age adjusted incidence rate was 1.2/100,000 in females and 1.4/100,000 in males. Overall, Average Annual Percent Change (AAPC) of 2.6% (95% CI: 1.9 – 4.3) was noticed between 2017-2021 when compared to previously reported rates. AAPC among different ethnic groups were Hispanics, any race: 5.3% (CI: 4-7.5), Non-Hispanic American Indian/Alaska Native: 1.1 (CI: -2.7-5.1), Non-Hispanic Asian/Pacific Islander: 1.9 (CI: 1.1-2.9), Non-Hispanic Black: 1.0 (CI: 0.3-1.7), and Non-Hispanic White: 1.6 (CI: 1.1-2.1). Stage 4 was the most common stage. Overall, the 5-year relative survival from 2014- 2020 was 37.4% (CI: 36.1-38.7). 5-year relative survival among ethnic groups from 2014-2020 were: Hispanics, any race: 40.3% (CI: 37.6-43.0), Non-Hispanic American Indian/Alaska Native: 21.4 (CI: 8.5-38.2), Non-Hispanic Asian/Pacific Islander: 40.2 (CI: 35.7-44.7), Non-Hispanic Black: 33.1 (CI: 29.9-36.3), and Non-Hispanic White: 36.6 (CI: 34.8-38.4).

Conclusions

Our analysis reveals a rise in the ageadjusted incidence of pancreatic cancer among younger demographics. Particularly noteworthy is the sharp increase observed over the past five years among Hispanics when compared to other ethnic populations. This rise is observed in both males and females. Further studies need to be done to study the risk factors associated with this increase in trend of pancreatic cancer at young age specifically in Hispanic population.

Background

Pancreatic cancer stands as a prominent contributor to cancer-related mortality in the United States. In this abstract, we reviewed the SEER database to uncover the latest trends in pancreatic cancer among individuals diagnosed under the age of 50.

Methods

Information was obtained from the SEER database November 2023 which covers 22 national cancer registries. Only patients with age < 50 years were included. Age adjusted incidence and 5-year relative survival were compared between different ethnic groups.

Results

We identified 124691 patients with pancreatic cancer diagnosed between 2017-2021, among them 6477 were with age less than 50 years at the time of diagnosis. 3074 were male and 3403 were male. Age adjusted incidence rate was 1.2/100,000 in females and 1.4/100,000 in males. Overall, Average Annual Percent Change (AAPC) of 2.6% (95% CI: 1.9 – 4.3) was noticed between 2017-2021 when compared to previously reported rates. AAPC among different ethnic groups were Hispanics, any race: 5.3% (CI: 4-7.5), Non-Hispanic American Indian/Alaska Native: 1.1 (CI: -2.7-5.1), Non-Hispanic Asian/Pacific Islander: 1.9 (CI: 1.1-2.9), Non-Hispanic Black: 1.0 (CI: 0.3-1.7), and Non-Hispanic White: 1.6 (CI: 1.1-2.1). Stage 4 was the most common stage. Overall, the 5-year relative survival from 2014- 2020 was 37.4% (CI: 36.1-38.7). 5-year relative survival among ethnic groups from 2014-2020 were: Hispanics, any race: 40.3% (CI: 37.6-43.0), Non-Hispanic American Indian/Alaska Native: 21.4 (CI: 8.5-38.2), Non-Hispanic Asian/Pacific Islander: 40.2 (CI: 35.7-44.7), Non-Hispanic Black: 33.1 (CI: 29.9-36.3), and Non-Hispanic White: 36.6 (CI: 34.8-38.4).

Conclusions

Our analysis reveals a rise in the ageadjusted incidence of pancreatic cancer among younger demographics. Particularly noteworthy is the sharp increase observed over the past five years among Hispanics when compared to other ethnic populations. This rise is observed in both males and females. Further studies need to be done to study the risk factors associated with this increase in trend of pancreatic cancer at young age specifically in Hispanic population.

Background

Pancreatic cancer stands as a prominent contributor to cancer-related mortality in the United States. In this abstract, we reviewed the SEER database to uncover the latest trends in pancreatic cancer among individuals diagnosed under the age of 50.

Methods

Information was obtained from the SEER database November 2023 which covers 22 national cancer registries. Only patients with age < 50 years were included. Age adjusted incidence and 5-year relative survival were compared between different ethnic groups.

Results

We identified 124691 patients with pancreatic cancer diagnosed between 2017-2021, among them 6477 were with age less than 50 years at the time of diagnosis. 3074 were male and 3403 were male. Age adjusted incidence rate was 1.2/100,000 in females and 1.4/100,000 in males. Overall, Average Annual Percent Change (AAPC) of 2.6% (95% CI: 1.9 – 4.3) was noticed between 2017-2021 when compared to previously reported rates. AAPC among different ethnic groups were Hispanics, any race: 5.3% (CI: 4-7.5), Non-Hispanic American Indian/Alaska Native: 1.1 (CI: -2.7-5.1), Non-Hispanic Asian/Pacific Islander: 1.9 (CI: 1.1-2.9), Non-Hispanic Black: 1.0 (CI: 0.3-1.7), and Non-Hispanic White: 1.6 (CI: 1.1-2.1). Stage 4 was the most common stage. Overall, the 5-year relative survival from 2014- 2020 was 37.4% (CI: 36.1-38.7). 5-year relative survival among ethnic groups from 2014-2020 were: Hispanics, any race: 40.3% (CI: 37.6-43.0), Non-Hispanic American Indian/Alaska Native: 21.4 (CI: 8.5-38.2), Non-Hispanic Asian/Pacific Islander: 40.2 (CI: 35.7-44.7), Non-Hispanic Black: 33.1 (CI: 29.9-36.3), and Non-Hispanic White: 36.6 (CI: 34.8-38.4).

Conclusions

Our analysis reveals a rise in the ageadjusted incidence of pancreatic cancer among younger demographics. Particularly noteworthy is the sharp increase observed over the past five years among Hispanics when compared to other ethnic populations. This rise is observed in both males and females. Further studies need to be done to study the risk factors associated with this increase in trend of pancreatic cancer at young age specifically in Hispanic population.

Background

Metastatic prostate cancer typically manifests with metastases to the lungs, bones, and adrenal glands. Here, we report a unique case where the initial presentation involved pleural nodules, subsequently leading to the discovery of pleural and pericardial metastases. 

Case Presentation

Our patient, a 73-year-old male with a history of active tobacco use disorder, COPD, and right shoulder melanoma (2004), initially presented to his primary care physician for a routine visit. Following a Low Dose Chest CT scan (LDCT), numerous new pleural nodules were identified. Physical examination revealed small nevi and skin tags, but no malignant characteristics. Initial concerns centered on the potential recurrence of malignant melanoma with pleural metastases or an inflammatory condition. Subsequent PET scan results raised significant suspicion of malignancy. PSA was 2.41. Pleuroscopy biopsies revealed invasive nonsmall cell carcinoma, positive for NKX31 and MOC31, but negative for S100, PSA, and synaptophysin. This pattern strongly suggests metastatic prostate cancer despite the absence of PSA staining. (Stage IV B: cTxcN1cM1c). A subsequent PSMA PET highlighted extensive metastatic involvement in the pericardium, posterior and mediastinal pleura, mediastinum, and ribs. Treatment commenced with Degarelix followed by the standard regimen of Docetaxel, Abiraterone, and prednisone. Genetic counseling and palliative care services were additionally recommended.

Discussion

Prostate cancer typically spreads to bones, lungs, liver, and adrenal glands. Rarely, it appears in sites like pericardium and pleura. Pleural metastases are usually found postmortem; clinical diagnosis is rare. Pericardial metastases are exceptionally uncommon, with few documented cases. The precise mechanism of metastatic dissemination remains uncertain, with theories suggesting spread through the vertebral-venous plexus or via the vena cava to distant organs. Treatment approaches vary based on symptomatic effusions, ranging from pericardiocentesis, thoracocentesis to chemotherapy, radiotherapy, and hormone therapy. Studies have shown systemic docetaxel to be effective in managing pleural and pericardial symptoms. Despite their rarity, healthcare providers should consider these possibilities when encountering pleural thickening or pericardial abnormalities on imaging studies.

Conclusions

Pleural and pericardial metastases represent uncommon occurrences in prostate cancer. Continued research efforts can facilitate early detection of metastatic disease, enabling more effective and precisely targeted management strategies when symptoms manifest.

Background

Metastatic prostate cancer typically manifests with metastases to the lungs, bones, and adrenal glands. Here, we report a unique case where the initial presentation involved pleural nodules, subsequently leading to the discovery of pleural and pericardial metastases. 

Case Presentation

Our patient, a 73-year-old male with a history of active tobacco use disorder, COPD, and right shoulder melanoma (2004), initially presented to his primary care physician for a routine visit. Following a Low Dose Chest CT scan (LDCT), numerous new pleural nodules were identified. Physical examination revealed small nevi and skin tags, but no malignant characteristics. Initial concerns centered on the potential recurrence of malignant melanoma with pleural metastases or an inflammatory condition. Subsequent PET scan results raised significant suspicion of malignancy. PSA was 2.41. Pleuroscopy biopsies revealed invasive nonsmall cell carcinoma, positive for NKX31 and MOC31, but negative for S100, PSA, and synaptophysin. This pattern strongly suggests metastatic prostate cancer despite the absence of PSA staining. (Stage IV B: cTxcN1cM1c). A subsequent PSMA PET highlighted extensive metastatic involvement in the pericardium, posterior and mediastinal pleura, mediastinum, and ribs. Treatment commenced with Degarelix followed by the standard regimen of Docetaxel, Abiraterone, and prednisone. Genetic counseling and palliative care services were additionally recommended.

Discussion

Prostate cancer typically spreads to bones, lungs, liver, and adrenal glands. Rarely, it appears in sites like pericardium and pleura. Pleural metastases are usually found postmortem; clinical diagnosis is rare. Pericardial metastases are exceptionally uncommon, with few documented cases. The precise mechanism of metastatic dissemination remains uncertain, with theories suggesting spread through the vertebral-venous plexus or via the vena cava to distant organs. Treatment approaches vary based on symptomatic effusions, ranging from pericardiocentesis, thoracocentesis to chemotherapy, radiotherapy, and hormone therapy. Studies have shown systemic docetaxel to be effective in managing pleural and pericardial symptoms. Despite their rarity, healthcare providers should consider these possibilities when encountering pleural thickening or pericardial abnormalities on imaging studies.

Conclusions

Pleural and pericardial metastases represent uncommon occurrences in prostate cancer. Continued research efforts can facilitate early detection of metastatic disease, enabling more effective and precisely targeted management strategies when symptoms manifest.

Background

Metastatic prostate cancer typically manifests with metastases to the lungs, bones, and adrenal glands. Here, we report a unique case where the initial presentation involved pleural nodules, subsequently leading to the discovery of pleural and pericardial metastases. 

Case Presentation

Our patient, a 73-year-old male with a history of active tobacco use disorder, COPD, and right shoulder melanoma (2004), initially presented to his primary care physician for a routine visit. Following a Low Dose Chest CT scan (LDCT), numerous new pleural nodules were identified. Physical examination revealed small nevi and skin tags, but no malignant characteristics. Initial concerns centered on the potential recurrence of malignant melanoma with pleural metastases or an inflammatory condition. Subsequent PET scan results raised significant suspicion of malignancy. PSA was 2.41. Pleuroscopy biopsies revealed invasive nonsmall cell carcinoma, positive for NKX31 and MOC31, but negative for S100, PSA, and synaptophysin. This pattern strongly suggests metastatic prostate cancer despite the absence of PSA staining. (Stage IV B: cTxcN1cM1c). A subsequent PSMA PET highlighted extensive metastatic involvement in the pericardium, posterior and mediastinal pleura, mediastinum, and ribs. Treatment commenced with Degarelix followed by the standard regimen of Docetaxel, Abiraterone, and prednisone. Genetic counseling and palliative care services were additionally recommended.

Discussion

Prostate cancer typically spreads to bones, lungs, liver, and adrenal glands. Rarely, it appears in sites like pericardium and pleura. Pleural metastases are usually found postmortem; clinical diagnosis is rare. Pericardial metastases are exceptionally uncommon, with few documented cases. The precise mechanism of metastatic dissemination remains uncertain, with theories suggesting spread through the vertebral-venous plexus or via the vena cava to distant organs. Treatment approaches vary based on symptomatic effusions, ranging from pericardiocentesis, thoracocentesis to chemotherapy, radiotherapy, and hormone therapy. Studies have shown systemic docetaxel to be effective in managing pleural and pericardial symptoms. Despite their rarity, healthcare providers should consider these possibilities when encountering pleural thickening or pericardial abnormalities on imaging studies.

Conclusions

Pleural and pericardial metastases represent uncommon occurrences in prostate cancer. Continued research efforts can facilitate early detection of metastatic disease, enabling more effective and precisely targeted management strategies when symptoms manifest.