Esfandiarifard S

Background: Right-sided colon cancer (RC) is derived from the mid-gut, while left-sided colon cancer (LC) originates from the hindgut. LC has been associated with better survival compared to RC. The effect of primary tumor sidedness on colorectal cancer (CRC) survival rates has not been studied in VA hospitals.

Methods: Data from the National VA Cancer Cube Registry was studied. 65,940 cases of CRC were diagnosed between 2001 and 2015. ICD codes C18 to C20 were used to delineate patients with RC vs. LC. RC was defined as cancer from the cecum to the hepatic flexure, LC from the splenic flexure to the rectum with transverse cancer in between flexures. Local IRB approval was obtained.

Results: Of the total number of CRC, 30.3% were RC and 58.8% were LC. RC constituted 36.3% of cases in women and 30.1% of cases in men. RC was diagnosed after the age of 70 years in 51.8% of cases, compared with 38.5% of LC. LC constituted 56.0% of CRC in blacks, and 59.4% in whites. RC was more likely to be diagnosed at more advanced stage, with 60.84% of cases diagnosed at stage II-IV, compared to 51.82% of LC. Stage IV RC has worse one year survival as compared with LC (50.5% vs 42.2% surviving less than one year, respectively)

Conclusions: RC is associated with female gender, older age, poorer functional status, and more advanced stage at diagnosis. LC was associated with white race. Stage IV RC had worse one-year survival than LC colon cancer.

Background: Right-sided colon cancer (RC) is derived from the mid-gut, while left-sided colon cancer (LC) originates from the hindgut. LC has been associated with better survival compared to RC. The effect of primary tumor sidedness on colorectal cancer (CRC) survival rates has not been studied in VA hospitals.

Methods: Data from the National VA Cancer Cube Registry was studied. 65,940 cases of CRC were diagnosed between 2001 and 2015. ICD codes C18 to C20 were used to delineate patients with RC vs. LC. RC was defined as cancer from the cecum to the hepatic flexure, LC from the splenic flexure to the rectum with transverse cancer in between flexures. Local IRB approval was obtained.

Results: Of the total number of CRC, 30.3% were RC and 58.8% were LC. RC constituted 36.3% of cases in women and 30.1% of cases in men. RC was diagnosed after the age of 70 years in 51.8% of cases, compared with 38.5% of LC. LC constituted 56.0% of CRC in blacks, and 59.4% in whites. RC was more likely to be diagnosed at more advanced stage, with 60.84% of cases diagnosed at stage II-IV, compared to 51.82% of LC. Stage IV RC has worse one year survival as compared with LC (50.5% vs 42.2% surviving less than one year, respectively)

Conclusions: RC is associated with female gender, older age, poorer functional status, and more advanced stage at diagnosis. LC was associated with white race. Stage IV RC had worse one-year survival than LC colon cancer.

Background: Right-sided colon cancer (RC) is derived from the mid-gut, while left-sided colon cancer (LC) originates from the hindgut. LC has been associated with better survival compared to RC. The effect of primary tumor sidedness on colorectal cancer (CRC) survival rates has not been studied in VA hospitals.

Methods: Data from the National VA Cancer Cube Registry was studied. 65,940 cases of CRC were diagnosed between 2001 and 2015. ICD codes C18 to C20 were used to delineate patients with RC vs. LC. RC was defined as cancer from the cecum to the hepatic flexure, LC from the splenic flexure to the rectum with transverse cancer in between flexures. Local IRB approval was obtained.

Results: Of the total number of CRC, 30.3% were RC and 58.8% were LC. RC constituted 36.3% of cases in women and 30.1% of cases in men. RC was diagnosed after the age of 70 years in 51.8% of cases, compared with 38.5% of LC. LC constituted 56.0% of CRC in blacks, and 59.4% in whites. RC was more likely to be diagnosed at more advanced stage, with 60.84% of cases diagnosed at stage II-IV, compared to 51.82% of LC. Stage IV RC has worse one year survival as compared with LC (50.5% vs 42.2% surviving less than one year, respectively)

Conclusions: RC is associated with female gender, older age, poorer functional status, and more advanced stage at diagnosis. LC was associated with white race. Stage IV RC had worse one-year survival than LC colon cancer.

Backgroud: Metastatic pancreatic cancer (MPC) is associated with an extremely high mortality. Current NCCN guidelines recommend systemic therapy, as it is superior to best supportive care. Undertreatment of MPC continues to be an issue. Recent treatment and survival data of MPC in VA hospitals have not been published. The relationship between MPC treatment and survival and the American College of Surgeons’ (ACS) Committee on Cancer (CoC) accreditation in VA hospitals has not been studied.

Methods: Nationwide data from the National VA Cancer Cube Registry was analyzed. 6,775 patients were diagnosed with MPC between 2000 and 2014. CoC accreditation of each VA hospital was obtained using the ACS website.

Results: MPC constitutes 52.31% of all pancreatic cancer diagnosed (6,775/12,951 cases). The near totality were men (97.44%). The > 70-years age group and the 60-70-years age group were the most common ages at diagnosis with 39.39% and 38.02%, respectively. The proportion of early-onset pancreatic cancer was 2.84%. When compared to all stages of pancreatic cancer, stage IV pancreatic cancer had a lower proportion of cancer originating from the head of the pancreas (39.44% versus 50.63%) and more originating from the tail (17.99% versus 13.39%). Tumors originating from head of the pancreas are more likely to cause biliary symptoms and thus are more likely to be caught at an earlier stage. Overall, treatment rate in the VA at the national level with first-line chemotherapy was 37.61%. The rate of treatment over the years has increased in a linear fashion from 33.01% in 2000 to 41.95% in 2014. This has corresponded with an increase of 1-5 years survival of 9.29% in 2000 to 22.99% in 2014 and 5-10 years survival from 0.96% in 2000 to 6.00% in 2012. Treatment rates in CoC accredited and non-CoC accredited VA hospitals were similar (38.94% and 38.12%, respectively). Survival rates in CoC accredited and non-COC accredited VAs were similar with a 1-5 years survival rate of
8.89% and 8.57%, respectively.

Conclusions: Treatment and survival of MPC have risen significantly in the past decade at VA hospitals. CoC accreditation is not associated with a change in treatment or survival rates.

Backgroud: Metastatic pancreatic cancer (MPC) is associated with an extremely high mortality. Current NCCN guidelines recommend systemic therapy, as it is superior to best supportive care. Undertreatment of MPC continues to be an issue. Recent treatment and survival data of MPC in VA hospitals have not been published. The relationship between MPC treatment and survival and the American College of Surgeons’ (ACS) Committee on Cancer (CoC) accreditation in VA hospitals has not been studied.

Methods: Nationwide data from the National VA Cancer Cube Registry was analyzed. 6,775 patients were diagnosed with MPC between 2000 and 2014. CoC accreditation of each VA hospital was obtained using the ACS website.

Results: MPC constitutes 52.31% of all pancreatic cancer diagnosed (6,775/12,951 cases). The near totality were men (97.44%). The > 70-years age group and the 60-70-years age group were the most common ages at diagnosis with 39.39% and 38.02%, respectively. The proportion of early-onset pancreatic cancer was 2.84%. When compared to all stages of pancreatic cancer, stage IV pancreatic cancer had a lower proportion of cancer originating from the head of the pancreas (39.44% versus 50.63%) and more originating from the tail (17.99% versus 13.39%). Tumors originating from head of the pancreas are more likely to cause biliary symptoms and thus are more likely to be caught at an earlier stage. Overall, treatment rate in the VA at the national level with first-line chemotherapy was 37.61%. The rate of treatment over the years has increased in a linear fashion from 33.01% in 2000 to 41.95% in 2014. This has corresponded with an increase of 1-5 years survival of 9.29% in 2000 to 22.99% in 2014 and 5-10 years survival from 0.96% in 2000 to 6.00% in 2012. Treatment rates in CoC accredited and non-CoC accredited VA hospitals were similar (38.94% and 38.12%, respectively). Survival rates in CoC accredited and non-COC accredited VAs were similar with a 1-5 years survival rate of
8.89% and 8.57%, respectively.

Conclusions: Treatment and survival of MPC have risen significantly in the past decade at VA hospitals. CoC accreditation is not associated with a change in treatment or survival rates.

Backgroud: Metastatic pancreatic cancer (MPC) is associated with an extremely high mortality. Current NCCN guidelines recommend systemic therapy, as it is superior to best supportive care. Undertreatment of MPC continues to be an issue. Recent treatment and survival data of MPC in VA hospitals have not been published. The relationship between MPC treatment and survival and the American College of Surgeons’ (ACS) Committee on Cancer (CoC) accreditation in VA hospitals has not been studied.

Methods: Nationwide data from the National VA Cancer Cube Registry was analyzed. 6,775 patients were diagnosed with MPC between 2000 and 2014. CoC accreditation of each VA hospital was obtained using the ACS website.

Results: MPC constitutes 52.31% of all pancreatic cancer diagnosed (6,775/12,951 cases). The near totality were men (97.44%). The > 70-years age group and the 60-70-years age group were the most common ages at diagnosis with 39.39% and 38.02%, respectively. The proportion of early-onset pancreatic cancer was 2.84%. When compared to all stages of pancreatic cancer, stage IV pancreatic cancer had a lower proportion of cancer originating from the head of the pancreas (39.44% versus 50.63%) and more originating from the tail (17.99% versus 13.39%). Tumors originating from head of the pancreas are more likely to cause biliary symptoms and thus are more likely to be caught at an earlier stage. Overall, treatment rate in the VA at the national level with first-line chemotherapy was 37.61%. The rate of treatment over the years has increased in a linear fashion from 33.01% in 2000 to 41.95% in 2014. This has corresponded with an increase of 1-5 years survival of 9.29% in 2000 to 22.99% in 2014 and 5-10 years survival from 0.96% in 2000 to 6.00% in 2012. Treatment rates in CoC accredited and non-CoC accredited VA hospitals were similar (38.94% and 38.12%, respectively). Survival rates in CoC accredited and non-COC accredited VAs were similar with a 1-5 years survival rate of
8.89% and 8.57%, respectively.

Conclusions: Treatment and survival of MPC have risen significantly in the past decade at VA hospitals. CoC accreditation is not associated with a change in treatment or survival rates.

Background: CONCORD is a global program for worldwide surveillance of cancer survival. A recent analysis of the CONCORD-2 study shows a 9-10% lower survival rates for blacks affected by colon cancer (CC) as compared to whites in the US between 2001 and 2009.

Methods: We aim to investigate the differences in the survival of blacks and whites affected by CC in the National VA Cancer Cube Database in the same time-period. Overall, 30,196 CC cases between 2001 and 2009 were examined.

Results: 66.12% (19,967) of CC patients identified as white and 16.32% (4929) identified as black. The distribution of stages in blacks was the following: Stage 0: 10.49% (517), I: 25.10% (1237), II: 18.58% (916), III: 17.73% (874) and IV: 17.91% (883). By comparison, CC cases in whites presented as Stage 0: 8.92% (1781), I: 26.62% (5316), II: 22.29% (4450), III 18.75% (3744) and IV 13.71% (2738) (P value for X2 trend test = .021). Interestingly, in contrast to the results of the CONCORD study, the overall 5-year survival for all stages of CC in blacks and whites was similar [blacks: 2,854 (57.90%); whites 11,897 (59.58%); P = .2750]. The same holds true for the 5-year survival for Stage 0 [blacks: 423 (81.82%) whites: 1391 (78.10%); P = .5338], Stage I [blacks: 932 (75.34%) whites: 3973 (74.74%); P = .8667], Stage II [blacks: 605(66.05%) whites:2927 (65.78%); P = .9427], Stage III [blacks:509 (58.24%) whites:2138 (57.10%); P = .7513], Stage IV blacks:101 (11.44%) whites:364 (13.29%); P = .2058].

Conclusions: The racial disparity in survival highlighted in CONCORD-2 (9-10% lower 5-year survival for blacks) is not replicable in the VA system. This difference is likely due to the uniformity of the VA in providing screening and treatment services and in leveling the playing field in terms of access to care. We believe these results should be taken into consideration in the current discussion of the shape of the healthcare system the US should adopt.

Background: CONCORD is a global program for worldwide surveillance of cancer survival. A recent analysis of the CONCORD-2 study shows a 9-10% lower survival rates for blacks affected by colon cancer (CC) as compared to whites in the US between 2001 and 2009.

Methods: We aim to investigate the differences in the survival of blacks and whites affected by CC in the National VA Cancer Cube Database in the same time-period. Overall, 30,196 CC cases between 2001 and 2009 were examined.

Results: 66.12% (19,967) of CC patients identified as white and 16.32% (4929) identified as black. The distribution of stages in blacks was the following: Stage 0: 10.49% (517), I: 25.10% (1237), II: 18.58% (916), III: 17.73% (874) and IV: 17.91% (883). By comparison, CC cases in whites presented as Stage 0: 8.92% (1781), I: 26.62% (5316), II: 22.29% (4450), III 18.75% (3744) and IV 13.71% (2738) (P value for X2 trend test = .021). Interestingly, in contrast to the results of the CONCORD study, the overall 5-year survival for all stages of CC in blacks and whites was similar [blacks: 2,854 (57.90%); whites 11,897 (59.58%); P = .2750]. The same holds true for the 5-year survival for Stage 0 [blacks: 423 (81.82%) whites: 1391 (78.10%); P = .5338], Stage I [blacks: 932 (75.34%) whites: 3973 (74.74%); P = .8667], Stage II [blacks: 605(66.05%) whites:2927 (65.78%); P = .9427], Stage III [blacks:509 (58.24%) whites:2138 (57.10%); P = .7513], Stage IV blacks:101 (11.44%) whites:364 (13.29%); P = .2058].

Conclusions: The racial disparity in survival highlighted in CONCORD-2 (9-10% lower 5-year survival for blacks) is not replicable in the VA system. This difference is likely due to the uniformity of the VA in providing screening and treatment services and in leveling the playing field in terms of access to care. We believe these results should be taken into consideration in the current discussion of the shape of the healthcare system the US should adopt.

Background: CONCORD is a global program for worldwide surveillance of cancer survival. A recent analysis of the CONCORD-2 study shows a 9-10% lower survival rates for blacks affected by colon cancer (CC) as compared to whites in the US between 2001 and 2009.

Methods: We aim to investigate the differences in the survival of blacks and whites affected by CC in the National VA Cancer Cube Database in the same time-period. Overall, 30,196 CC cases between 2001 and 2009 were examined.

Results: 66.12% (19,967) of CC patients identified as white and 16.32% (4929) identified as black. The distribution of stages in blacks was the following: Stage 0: 10.49% (517), I: 25.10% (1237), II: 18.58% (916), III: 17.73% (874) and IV: 17.91% (883). By comparison, CC cases in whites presented as Stage 0: 8.92% (1781), I: 26.62% (5316), II: 22.29% (4450), III 18.75% (3744) and IV 13.71% (2738) (P value for X2 trend test = .021). Interestingly, in contrast to the results of the CONCORD study, the overall 5-year survival for all stages of CC in blacks and whites was similar [blacks: 2,854 (57.90%); whites 11,897 (59.58%); P = .2750]. The same holds true for the 5-year survival for Stage 0 [blacks: 423 (81.82%) whites: 1391 (78.10%); P = .5338], Stage I [blacks: 932 (75.34%) whites: 3973 (74.74%); P = .8667], Stage II [blacks: 605(66.05%) whites:2927 (65.78%); P = .9427], Stage III [blacks:509 (58.24%) whites:2138 (57.10%); P = .7513], Stage IV blacks:101 (11.44%) whites:364 (13.29%); P = .2058].

Conclusions: The racial disparity in survival highlighted in CONCORD-2 (9-10% lower 5-year survival for blacks) is not replicable in the VA system. This difference is likely due to the uniformity of the VA in providing screening and treatment services and in leveling the playing field in terms of access to care. We believe these results should be taken into consideration in the current discussion of the shape of the healthcare system the US should adopt.

Background: Small cell lung cancer (SCLC) carries a dismal prognosis with a 5-year survival of about 10%. Progress in treatment of SCLC has been poor and overall survival of SCLC has remained stagnant since the late 1970s. Limited-stage SCLC (LS-SCLC) is defined as a tumor confined into one hemithorax with or without lymphadenopathies included in a single radiation field. LS-SCLC frequently metastasizes to the brain. The administration of preventive radiation to the brain, a process known as prophylactic cranial irradiation (PCI) has been the major change in the management of SCLC. There is currently a paucity of data on sites of metastasis of SCLC after PCI has been performed. We aim to describe the pattern of recurrence post-PCI in SCLC.

Methods: A retrospective chart review of all LS-SCLC (stages IA to IIIB) patients who presented to the Stratton Veteran Affairs Medical Center (SVAMC) between January 2006 and January 2017 was performed. Exclusion criteria included other types of lung cancer and stage IV SCLC.

Results: Of the 31 LS-SCLC patients, 12 received PCI. Reasons for not receiving PCI included rapid progression of the disease/metastasis to the brain (8), patient refusal (5), loss to follow-up (4) and existing co-morbidities/poor performance status (2). Of the 12 that received PCI, 8 patients had recurrences, with most recurrences affecting more than one organ. Sites of recurrences included: lung (6), liver (4), lymph nodes (3), bone (2), soft tissue (1).

Conclusions: Post-PCI, LS-SCLC is likely to recur at the site of the tumor itself or metastasize to the liver and lymph nodes. Given the rarity of SCLC presenting at the limited stage, larger scale studies are needed to further delineate the pattern of metastasis of SCLC.

Background: Small cell lung cancer (SCLC) carries a dismal prognosis with a 5-year survival of about 10%. Progress in treatment of SCLC has been poor and overall survival of SCLC has remained stagnant since the late 1970s. Limited-stage SCLC (LS-SCLC) is defined as a tumor confined into one hemithorax with or without lymphadenopathies included in a single radiation field. LS-SCLC frequently metastasizes to the brain. The administration of preventive radiation to the brain, a process known as prophylactic cranial irradiation (PCI) has been the major change in the management of SCLC. There is currently a paucity of data on sites of metastasis of SCLC after PCI has been performed. We aim to describe the pattern of recurrence post-PCI in SCLC.

Methods: A retrospective chart review of all LS-SCLC (stages IA to IIIB) patients who presented to the Stratton Veteran Affairs Medical Center (SVAMC) between January 2006 and January 2017 was performed. Exclusion criteria included other types of lung cancer and stage IV SCLC.

Results: Of the 31 LS-SCLC patients, 12 received PCI. Reasons for not receiving PCI included rapid progression of the disease/metastasis to the brain (8), patient refusal (5), loss to follow-up (4) and existing co-morbidities/poor performance status (2). Of the 12 that received PCI, 8 patients had recurrences, with most recurrences affecting more than one organ. Sites of recurrences included: lung (6), liver (4), lymph nodes (3), bone (2), soft tissue (1).

Conclusions: Post-PCI, LS-SCLC is likely to recur at the site of the tumor itself or metastasize to the liver and lymph nodes. Given the rarity of SCLC presenting at the limited stage, larger scale studies are needed to further delineate the pattern of metastasis of SCLC.

Background: Small cell lung cancer (SCLC) carries a dismal prognosis with a 5-year survival of about 10%. Progress in treatment of SCLC has been poor and overall survival of SCLC has remained stagnant since the late 1970s. Limited-stage SCLC (LS-SCLC) is defined as a tumor confined into one hemithorax with or without lymphadenopathies included in a single radiation field. LS-SCLC frequently metastasizes to the brain. The administration of preventive radiation to the brain, a process known as prophylactic cranial irradiation (PCI) has been the major change in the management of SCLC. There is currently a paucity of data on sites of metastasis of SCLC after PCI has been performed. We aim to describe the pattern of recurrence post-PCI in SCLC.

Methods: A retrospective chart review of all LS-SCLC (stages IA to IIIB) patients who presented to the Stratton Veteran Affairs Medical Center (SVAMC) between January 2006 and January 2017 was performed. Exclusion criteria included other types of lung cancer and stage IV SCLC.

Results: Of the 31 LS-SCLC patients, 12 received PCI. Reasons for not receiving PCI included rapid progression of the disease/metastasis to the brain (8), patient refusal (5), loss to follow-up (4) and existing co-morbidities/poor performance status (2). Of the 12 that received PCI, 8 patients had recurrences, with most recurrences affecting more than one organ. Sites of recurrences included: lung (6), liver (4), lymph nodes (3), bone (2), soft tissue (1).

Conclusions: Post-PCI, LS-SCLC is likely to recur at the site of the tumor itself or metastasize to the liver and lymph nodes. Given the rarity of SCLC presenting at the limited stage, larger scale studies are needed to further delineate the pattern of metastasis of SCLC.

Background: A 69-year-old male with history of stage IV left kidney clear cell carcinoma presented with 4-day history of gross hematuria, fever of 101.4 F and fatigue. He had been started on sunitinib, a VEGF Tyrosine Kinase Inhibitor (TKI) two weeks previously. Vitals were significant
for systolic BP of 160. Renal ultrasound showed perinephric hematoma. Labs were significant for platelets of 68,000, sodium of 120 and creatinine of 2.7 (baseline creatinine of 1.0). Urine sodium was less than 10 and 24 hours urine protein was 484 mg. Peripheral smear was negative for schistocytes. Renal biopsy performed after platelet infusion showed extensive interstitial inflammation with frequent eosinophils and interstitial edema, consistent with druginduced acute interstitial nephritis. He was started on oral steroids and required intermittent hemodialysis.

Discussion: This report describes the second known case of biopsy-proven sunitinib-induced acute interstitial nephritis (AIN). Similar case reports involving the VEGF-targeting drugs sorafenib (TKI), and bevacizumab (monoclonal antibody) imply a class effect. Previously reported renal adverse events of sunitinib include hypertension, proteinuria, renal insufficiency, and thrombotic microangiopathy; all present in this case except thrombotic microangiopathy. Thus, thrombocytopenia in this case may be secondary to bone marrow suppression.

Interestingly, while sunitinib is also used for the treatment of gastrointestinal stromal tumor (GIST) and pancreatic neuroendocrine tumors (PNET); thus far, cases of sunitinib-induced AIN have only been described in patients with metastatic renal cell carcinoma.

Given the risk of bleeding associated with a renal biopsy in the setting of thrombocytopenia on one hand; and the lethal complications that may ensue from delayed diagnosis and the possibility of permanent dialysis associated with AIN on the other, the decision to proceed with a renal biopsy is a controversial one and must be weighed carefully.

Conclusions: While sunitinib-induced AIN is exceedingly rare, it should be considered in patients with acute renal failure. Given the literature implicating VEGF-targeting drugs in cases of AIN, further study is required to elicit the link between the VEGF pathway and AIN.

Background: A 69-year-old male with history of stage IV left kidney clear cell carcinoma presented with 4-day history of gross hematuria, fever of 101.4 F and fatigue. He had been started on sunitinib, a VEGF Tyrosine Kinase Inhibitor (TKI) two weeks previously. Vitals were significant
for systolic BP of 160. Renal ultrasound showed perinephric hematoma. Labs were significant for platelets of 68,000, sodium of 120 and creatinine of 2.7 (baseline creatinine of 1.0). Urine sodium was less than 10 and 24 hours urine protein was 484 mg. Peripheral smear was negative for schistocytes. Renal biopsy performed after platelet infusion showed extensive interstitial inflammation with frequent eosinophils and interstitial edema, consistent with druginduced acute interstitial nephritis. He was started on oral steroids and required intermittent hemodialysis.

Discussion: This report describes the second known case of biopsy-proven sunitinib-induced acute interstitial nephritis (AIN). Similar case reports involving the VEGF-targeting drugs sorafenib (TKI), and bevacizumab (monoclonal antibody) imply a class effect. Previously reported renal adverse events of sunitinib include hypertension, proteinuria, renal insufficiency, and thrombotic microangiopathy; all present in this case except thrombotic microangiopathy. Thus, thrombocytopenia in this case may be secondary to bone marrow suppression.

Interestingly, while sunitinib is also used for the treatment of gastrointestinal stromal tumor (GIST) and pancreatic neuroendocrine tumors (PNET); thus far, cases of sunitinib-induced AIN have only been described in patients with metastatic renal cell carcinoma.

Given the risk of bleeding associated with a renal biopsy in the setting of thrombocytopenia on one hand; and the lethal complications that may ensue from delayed diagnosis and the possibility of permanent dialysis associated with AIN on the other, the decision to proceed with a renal biopsy is a controversial one and must be weighed carefully.

Conclusions: While sunitinib-induced AIN is exceedingly rare, it should be considered in patients with acute renal failure. Given the literature implicating VEGF-targeting drugs in cases of AIN, further study is required to elicit the link between the VEGF pathway and AIN.

Background: A 69-year-old male with history of stage IV left kidney clear cell carcinoma presented with 4-day history of gross hematuria, fever of 101.4 F and fatigue. He had been started on sunitinib, a VEGF Tyrosine Kinase Inhibitor (TKI) two weeks previously. Vitals were significant
for systolic BP of 160. Renal ultrasound showed perinephric hematoma. Labs were significant for platelets of 68,000, sodium of 120 and creatinine of 2.7 (baseline creatinine of 1.0). Urine sodium was less than 10 and 24 hours urine protein was 484 mg. Peripheral smear was negative for schistocytes. Renal biopsy performed after platelet infusion showed extensive interstitial inflammation with frequent eosinophils and interstitial edema, consistent with druginduced acute interstitial nephritis. He was started on oral steroids and required intermittent hemodialysis.

Discussion: This report describes the second known case of biopsy-proven sunitinib-induced acute interstitial nephritis (AIN). Similar case reports involving the VEGF-targeting drugs sorafenib (TKI), and bevacizumab (monoclonal antibody) imply a class effect. Previously reported renal adverse events of sunitinib include hypertension, proteinuria, renal insufficiency, and thrombotic microangiopathy; all present in this case except thrombotic microangiopathy. Thus, thrombocytopenia in this case may be secondary to bone marrow suppression.

Interestingly, while sunitinib is also used for the treatment of gastrointestinal stromal tumor (GIST) and pancreatic neuroendocrine tumors (PNET); thus far, cases of sunitinib-induced AIN have only been described in patients with metastatic renal cell carcinoma.

Given the risk of bleeding associated with a renal biopsy in the setting of thrombocytopenia on one hand; and the lethal complications that may ensue from delayed diagnosis and the possibility of permanent dialysis associated with AIN on the other, the decision to proceed with a renal biopsy is a controversial one and must be weighed carefully.

Conclusions: While sunitinib-induced AIN is exceedingly rare, it should be considered in patients with acute renal failure. Given the literature implicating VEGF-targeting drugs in cases of AIN, further study is required to elicit the link between the VEGF pathway and AIN.

Background: Current NCCN guidelines recommend the use of cetuximab, an EGFR monoclonal antibody, in the treatment of head and neck (H&N) cancers in combination with radiation therapy as initial treatment of locally or regionally advanced disease in patients, who are ineligible
for platinum-based therapy. It is also the standard of care in the treatment of recurrent or persistent disease with distant metastases.

Objective: Hypomagnesemia is a common side effect of cetuximab. Previous studies demonstrated that magnesium reduction was a potential marker of efficacy and outcome in the treatment of advanced colorectal cancer. We hypothesize that hypomagnesemia is also a marker of efficacy of the anti-neoplastic treatment of H&N cancer.

Methods: We retrospectively reviewed the medical records of H&N cancer patients that were treated with cetuximab between January 1, 2006 and January 1, 2016 at the Stratton VA Medical Center. Included in the study were patients aged over 20 years with stage III or IV H&N cancer who received cetuximab. Exclusion criteria included prior magnesium supplementation, history of treatment with anti-EGFR therapy, malabsorption syndromes and genetic magnesium wasting syndrome.

Results: Of the 63 patients studied, 23 developed hypomagnesemia for an overall incidence of 36.5%. The median age of diagnosis was 65 years for the hypomagnesemia group and 66 years for the nonhypomagnesemia. The patients that developed hypomagnesemia had a median survival of 27 months (95% CI, 16.3-37.6) while those that maintained normal magnesium levels had a mean survival of 20 months (95% CI, 12.3-27.7) (P = .583).

Conclusions: To our knowledge, no study has examined the predictive value of hypomagnesemia for the overall survival of H&N cancer patients treated with cetuximab that develop hypomagnesemia vs those that don’t. While data from the colorectal cancer suggest that hypomagnesemia may be used as a surrogate of efficacy for cetuximab, our data negates such correlation. Further study is required to elicit the link between cetuximab and hypomagnesemia.

Background: Current NCCN guidelines recommend the use of cetuximab, an EGFR monoclonal antibody, in the treatment of head and neck (H&N) cancers in combination with radiation therapy as initial treatment of locally or regionally advanced disease in patients, who are ineligible
for platinum-based therapy. It is also the standard of care in the treatment of recurrent or persistent disease with distant metastases.

Objective: Hypomagnesemia is a common side effect of cetuximab. Previous studies demonstrated that magnesium reduction was a potential marker of efficacy and outcome in the treatment of advanced colorectal cancer. We hypothesize that hypomagnesemia is also a marker of efficacy of the anti-neoplastic treatment of H&N cancer.

Methods: We retrospectively reviewed the medical records of H&N cancer patients that were treated with cetuximab between January 1, 2006 and January 1, 2016 at the Stratton VA Medical Center. Included in the study were patients aged over 20 years with stage III or IV H&N cancer who received cetuximab. Exclusion criteria included prior magnesium supplementation, history of treatment with anti-EGFR therapy, malabsorption syndromes and genetic magnesium wasting syndrome.

Results: Of the 63 patients studied, 23 developed hypomagnesemia for an overall incidence of 36.5%. The median age of diagnosis was 65 years for the hypomagnesemia group and 66 years for the nonhypomagnesemia. The patients that developed hypomagnesemia had a median survival of 27 months (95% CI, 16.3-37.6) while those that maintained normal magnesium levels had a mean survival of 20 months (95% CI, 12.3-27.7) (P = .583).

Conclusions: To our knowledge, no study has examined the predictive value of hypomagnesemia for the overall survival of H&N cancer patients treated with cetuximab that develop hypomagnesemia vs those that don’t. While data from the colorectal cancer suggest that hypomagnesemia may be used as a surrogate of efficacy for cetuximab, our data negates such correlation. Further study is required to elicit the link between cetuximab and hypomagnesemia.

Background: Current NCCN guidelines recommend the use of cetuximab, an EGFR monoclonal antibody, in the treatment of head and neck (H&N) cancers in combination with radiation therapy as initial treatment of locally or regionally advanced disease in patients, who are ineligible
for platinum-based therapy. It is also the standard of care in the treatment of recurrent or persistent disease with distant metastases.

Objective: Hypomagnesemia is a common side effect of cetuximab. Previous studies demonstrated that magnesium reduction was a potential marker of efficacy and outcome in the treatment of advanced colorectal cancer. We hypothesize that hypomagnesemia is also a marker of efficacy of the anti-neoplastic treatment of H&N cancer.

Methods: We retrospectively reviewed the medical records of H&N cancer patients that were treated with cetuximab between January 1, 2006 and January 1, 2016 at the Stratton VA Medical Center. Included in the study were patients aged over 20 years with stage III or IV H&N cancer who received cetuximab. Exclusion criteria included prior magnesium supplementation, history of treatment with anti-EGFR therapy, malabsorption syndromes and genetic magnesium wasting syndrome.

Results: Of the 63 patients studied, 23 developed hypomagnesemia for an overall incidence of 36.5%. The median age of diagnosis was 65 years for the hypomagnesemia group and 66 years for the nonhypomagnesemia. The patients that developed hypomagnesemia had a median survival of 27 months (95% CI, 16.3-37.6) while those that maintained normal magnesium levels had a mean survival of 20 months (95% CI, 12.3-27.7) (P = .583).

Conclusions: To our knowledge, no study has examined the predictive value of hypomagnesemia for the overall survival of H&N cancer patients treated with cetuximab that develop hypomagnesemia vs those that don’t. While data from the colorectal cancer suggest that hypomagnesemia may be used as a surrogate of efficacy for cetuximab, our data negates such correlation. Further study is required to elicit the link between cetuximab and hypomagnesemia.