Azar I

Background: Immune checkpoint inhibitors (ICI) have tremendously changed the paradigm of management for advanced stage cancers such as lung malignancies. Two unique patterns of response to immunotherapy have recently been described: pseudoprogression and hyperprogression. Hyperprogression is defined as a 2-fold increase in the tumor growth rate within 8 weeks of ICI administration.

Case Presentation: A 58-year-old female presented with left-sided chest pain for two weeks. CT-chest with contrast showed an 8.6 × 6.1 × 7.6 cm3 left upper lobe mass. An endobronchial ultrasound (EBUS)-guided biopsy revealed poorly differentiated adenocarcinoma. Staging FDG-18 PET scan revealed no metastases, resulting in a stage IIIA Non-Small Cell Lung Cancer (T4N0M0) on presentation. Per NCCN guidelines, she received standard of care definitive concurrent chemoradiation. Follow-up scans showed significant response in local disease without distant metastases. The patient then received cycle 1 consolidation immunotherapy with Durvalumab. Two weeks after, she complained of fatigue, new-onset headache and worsening dyspnea. CT-chest revealed development of a right upper lobe opacity, MRI brain showed the development of multiple brain metastases and PET scan uncovered hypermetabolic activity in a left adrenal nodule. Biopsy of the adrenal nodule confirmed metastatic adenocarcinoma, consistent with hyperprogression. Molecular testing of the standard lung tumor markers was negative (EGFR(-) ALK(-) BRAF(-) ROS-1 (-) PD-L1 <1%). Given her hyperprogression on ICIs, we opted to treat her with systemic chemotherapy with Carboplatin and Pemetrexed.

Conclusion: We herein report the first case report of hyperprogression in the non-metastatic setting. As ICIs become more incorporated in oncology practice, physicians should be aware of hyperprogression and its diagnostic criteria. Current molecular predictors of hyperprogression include MDM2/4 and EGFR mutations. Further elucidation of predictors of hyperprogressive disease will help guide better selection of ICI candidates.

Background: Immune checkpoint inhibitors (ICI) have tremendously changed the paradigm of management for advanced stage cancers such as lung malignancies. Two unique patterns of response to immunotherapy have recently been described: pseudoprogression and hyperprogression. Hyperprogression is defined as a 2-fold increase in the tumor growth rate within 8 weeks of ICI administration.

Case Presentation: A 58-year-old female presented with left-sided chest pain for two weeks. CT-chest with contrast showed an 8.6 × 6.1 × 7.6 cm3 left upper lobe mass. An endobronchial ultrasound (EBUS)-guided biopsy revealed poorly differentiated adenocarcinoma. Staging FDG-18 PET scan revealed no metastases, resulting in a stage IIIA Non-Small Cell Lung Cancer (T4N0M0) on presentation. Per NCCN guidelines, she received standard of care definitive concurrent chemoradiation. Follow-up scans showed significant response in local disease without distant metastases. The patient then received cycle 1 consolidation immunotherapy with Durvalumab. Two weeks after, she complained of fatigue, new-onset headache and worsening dyspnea. CT-chest revealed development of a right upper lobe opacity, MRI brain showed the development of multiple brain metastases and PET scan uncovered hypermetabolic activity in a left adrenal nodule. Biopsy of the adrenal nodule confirmed metastatic adenocarcinoma, consistent with hyperprogression. Molecular testing of the standard lung tumor markers was negative (EGFR(-) ALK(-) BRAF(-) ROS-1 (-) PD-L1 <1%). Given her hyperprogression on ICIs, we opted to treat her with systemic chemotherapy with Carboplatin and Pemetrexed.

Conclusion: We herein report the first case report of hyperprogression in the non-metastatic setting. As ICIs become more incorporated in oncology practice, physicians should be aware of hyperprogression and its diagnostic criteria. Current molecular predictors of hyperprogression include MDM2/4 and EGFR mutations. Further elucidation of predictors of hyperprogressive disease will help guide better selection of ICI candidates.

Background: Immune checkpoint inhibitors (ICI) have tremendously changed the paradigm of management for advanced stage cancers such as lung malignancies. Two unique patterns of response to immunotherapy have recently been described: pseudoprogression and hyperprogression. Hyperprogression is defined as a 2-fold increase in the tumor growth rate within 8 weeks of ICI administration.

Case Presentation: A 58-year-old female presented with left-sided chest pain for two weeks. CT-chest with contrast showed an 8.6 × 6.1 × 7.6 cm3 left upper lobe mass. An endobronchial ultrasound (EBUS)-guided biopsy revealed poorly differentiated adenocarcinoma. Staging FDG-18 PET scan revealed no metastases, resulting in a stage IIIA Non-Small Cell Lung Cancer (T4N0M0) on presentation. Per NCCN guidelines, she received standard of care definitive concurrent chemoradiation. Follow-up scans showed significant response in local disease without distant metastases. The patient then received cycle 1 consolidation immunotherapy with Durvalumab. Two weeks after, she complained of fatigue, new-onset headache and worsening dyspnea. CT-chest revealed development of a right upper lobe opacity, MRI brain showed the development of multiple brain metastases and PET scan uncovered hypermetabolic activity in a left adrenal nodule. Biopsy of the adrenal nodule confirmed metastatic adenocarcinoma, consistent with hyperprogression. Molecular testing of the standard lung tumor markers was negative (EGFR(-) ALK(-) BRAF(-) ROS-1 (-) PD-L1 <1%). Given her hyperprogression on ICIs, we opted to treat her with systemic chemotherapy with Carboplatin and Pemetrexed.

Conclusion: We herein report the first case report of hyperprogression in the non-metastatic setting. As ICIs become more incorporated in oncology practice, physicians should be aware of hyperprogression and its diagnostic criteria. Current molecular predictors of hyperprogression include MDM2/4 and EGFR mutations. Further elucidation of predictors of hyperprogressive disease will help guide better selection of ICI candidates.

Background: Sarcomatoid carcinoma is an unusual form of non-small cell lung cancer (NSCLC) that comprises 0.1% to 0.4% of all pulmonary malignancy. Mean age of onset is around 65 years of age, male to female ratio is almost 4-to-1, and it is associated with a poor prognosis.

Case Report: We present a case of sarcomatoid carcinoma in a 37-year-old patient, with a history of Hodgkin’s lymphoma, treated with chemotherapy, and uncontrolled HIV, initially presenting with unresponsiveness, tachycardia, and hypoxia after several days of vaginal bleeding. Her serum beta-HCG was 93.0 on admission. Her obstetric vaginal ultrasound did not identify an intrauterine pregnancy but did not rule out an ectopic pregnancy. A follow-up Beta-HCG in 1 week showed B-HCG rising to 163. Chest CT on admission revealed a cavitary lesion in the right upper lobe, suspicious for tuberculosis. A lung biopsy performed revealed highly atypical spindle epithelial cells suspicious for sarcomatoid carcinoma. A week later, biopsy of the left iliac bone of a lesion identified on CT scan of the pelvis on admission revealed cells similar in morphology and immunohistochemistry to the lung specimen, consistent with metastatic sarcomatoid carcinoma. After lengthy discussions, the patient opted for hospice care secondary to her poor functional status.

Conclusions: This case highlighted the importance of a broad differential in the approach to patients with unconfirmed diagnosis and expands the metastatic profile of sarcomatoid carcinoma. This is, also to the best of our knowledge, the first case of metastatic sarcomatoid carcinoma in a young female patient and the second in a HIV patients.

Background: Sarcomatoid carcinoma is an unusual form of non-small cell lung cancer (NSCLC) that comprises 0.1% to 0.4% of all pulmonary malignancy. Mean age of onset is around 65 years of age, male to female ratio is almost 4-to-1, and it is associated with a poor prognosis.

Case Report: We present a case of sarcomatoid carcinoma in a 37-year-old patient, with a history of Hodgkin’s lymphoma, treated with chemotherapy, and uncontrolled HIV, initially presenting with unresponsiveness, tachycardia, and hypoxia after several days of vaginal bleeding. Her serum beta-HCG was 93.0 on admission. Her obstetric vaginal ultrasound did not identify an intrauterine pregnancy but did not rule out an ectopic pregnancy. A follow-up Beta-HCG in 1 week showed B-HCG rising to 163. Chest CT on admission revealed a cavitary lesion in the right upper lobe, suspicious for tuberculosis. A lung biopsy performed revealed highly atypical spindle epithelial cells suspicious for sarcomatoid carcinoma. A week later, biopsy of the left iliac bone of a lesion identified on CT scan of the pelvis on admission revealed cells similar in morphology and immunohistochemistry to the lung specimen, consistent with metastatic sarcomatoid carcinoma. After lengthy discussions, the patient opted for hospice care secondary to her poor functional status.

Conclusions: This case highlighted the importance of a broad differential in the approach to patients with unconfirmed diagnosis and expands the metastatic profile of sarcomatoid carcinoma. This is, also to the best of our knowledge, the first case of metastatic sarcomatoid carcinoma in a young female patient and the second in a HIV patients.

Background: Sarcomatoid carcinoma is an unusual form of non-small cell lung cancer (NSCLC) that comprises 0.1% to 0.4% of all pulmonary malignancy. Mean age of onset is around 65 years of age, male to female ratio is almost 4-to-1, and it is associated with a poor prognosis.

Case Report: We present a case of sarcomatoid carcinoma in a 37-year-old patient, with a history of Hodgkin’s lymphoma, treated with chemotherapy, and uncontrolled HIV, initially presenting with unresponsiveness, tachycardia, and hypoxia after several days of vaginal bleeding. Her serum beta-HCG was 93.0 on admission. Her obstetric vaginal ultrasound did not identify an intrauterine pregnancy but did not rule out an ectopic pregnancy. A follow-up Beta-HCG in 1 week showed B-HCG rising to 163. Chest CT on admission revealed a cavitary lesion in the right upper lobe, suspicious for tuberculosis. A lung biopsy performed revealed highly atypical spindle epithelial cells suspicious for sarcomatoid carcinoma. A week later, biopsy of the left iliac bone of a lesion identified on CT scan of the pelvis on admission revealed cells similar in morphology and immunohistochemistry to the lung specimen, consistent with metastatic sarcomatoid carcinoma. After lengthy discussions, the patient opted for hospice care secondary to her poor functional status.

Conclusions: This case highlighted the importance of a broad differential in the approach to patients with unconfirmed diagnosis and expands the metastatic profile of sarcomatoid carcinoma. This is, also to the best of our knowledge, the first case of metastatic sarcomatoid carcinoma in a young female patient and the second in a HIV patients.

Background: The translocation t(11;14)(q13;q32) typically considered a hallmark of mantle cell lymphoma(MCL), has also been implicated in some cases of non-MCL lymphoproliferative disorders. Although uncommon, it has been reported in 2-5% of chronic lymphocytic leukemia (CLL) cases. Most of the cases identified have been observed mostly in relapsed CLL. This genetic aberration can be considered a significant prognostic indicator for CLL. t(11;14) positive CLL at the time of diagnosis has been rarely reported. We describe a case of a patient
diagnosed with CLL who was positive for this genetic abnormality.

Case Report: A 64-year-old white male presented with absolute lymphocytosis of 7 years. Lymphocyte immunophenotype detected a CD5(+) CD10(-) CD23(+) CD38(-) CD43(+) FMC7(partial dim) kappa-restricted B-cell population consistent with CLL. CT chest, abdomen, pelvis showed mildly prominent mediastinal and hilar lymph nodes only and was thus classified as Rai stage I. Peripheral FISH came back positive for t(11:14), cyclin D1-IgH translocation. His EPO, Jak2 and BCR-ABL mutation were all negative (done for mild erythrocytosis). Immunoglobulin and SPEP were negative. UPEP showed high Kappa/Lambda ratio. Although this tumor carries t(11;14) (q13;q32) translocation, immunostaining for BCL-1 was negative. It is possible that the gene is not expressed. Based on the staining and the clinical presentation, MCL was excluded. Per NCCN guidelines, patient is receiving clinical monitoring for stage I CLL.

Conclusions: Translocations involving the immunoglobulin genes are commonly identified. Uncommon genomic abnormalities in CLL should be recognized as significant independent predictors of disease progression and survival. It is important to recognize cases of CLL with t(11;14) translocation to achieve risk-adapted treatment strategies, which might be required to treat such patients.

Background: The translocation t(11;14)(q13;q32) typically considered a hallmark of mantle cell lymphoma(MCL), has also been implicated in some cases of non-MCL lymphoproliferative disorders. Although uncommon, it has been reported in 2-5% of chronic lymphocytic leukemia (CLL) cases. Most of the cases identified have been observed mostly in relapsed CLL. This genetic aberration can be considered a significant prognostic indicator for CLL. t(11;14) positive CLL at the time of diagnosis has been rarely reported. We describe a case of a patient
diagnosed with CLL who was positive for this genetic abnormality.

Case Report: A 64-year-old white male presented with absolute lymphocytosis of 7 years. Lymphocyte immunophenotype detected a CD5(+) CD10(-) CD23(+) CD38(-) CD43(+) FMC7(partial dim) kappa-restricted B-cell population consistent with CLL. CT chest, abdomen, pelvis showed mildly prominent mediastinal and hilar lymph nodes only and was thus classified as Rai stage I. Peripheral FISH came back positive for t(11:14), cyclin D1-IgH translocation. His EPO, Jak2 and BCR-ABL mutation were all negative (done for mild erythrocytosis). Immunoglobulin and SPEP were negative. UPEP showed high Kappa/Lambda ratio. Although this tumor carries t(11;14) (q13;q32) translocation, immunostaining for BCL-1 was negative. It is possible that the gene is not expressed. Based on the staining and the clinical presentation, MCL was excluded. Per NCCN guidelines, patient is receiving clinical monitoring for stage I CLL.

Conclusions: Translocations involving the immunoglobulin genes are commonly identified. Uncommon genomic abnormalities in CLL should be recognized as significant independent predictors of disease progression and survival. It is important to recognize cases of CLL with t(11;14) translocation to achieve risk-adapted treatment strategies, which might be required to treat such patients.

Background: The translocation t(11;14)(q13;q32) typically considered a hallmark of mantle cell lymphoma(MCL), has also been implicated in some cases of non-MCL lymphoproliferative disorders. Although uncommon, it has been reported in 2-5% of chronic lymphocytic leukemia (CLL) cases. Most of the cases identified have been observed mostly in relapsed CLL. This genetic aberration can be considered a significant prognostic indicator for CLL. t(11;14) positive CLL at the time of diagnosis has been rarely reported. We describe a case of a patient
diagnosed with CLL who was positive for this genetic abnormality.

Case Report: A 64-year-old white male presented with absolute lymphocytosis of 7 years. Lymphocyte immunophenotype detected a CD5(+) CD10(-) CD23(+) CD38(-) CD43(+) FMC7(partial dim) kappa-restricted B-cell population consistent with CLL. CT chest, abdomen, pelvis showed mildly prominent mediastinal and hilar lymph nodes only and was thus classified as Rai stage I. Peripheral FISH came back positive for t(11:14), cyclin D1-IgH translocation. His EPO, Jak2 and BCR-ABL mutation were all negative (done for mild erythrocytosis). Immunoglobulin and SPEP were negative. UPEP showed high Kappa/Lambda ratio. Although this tumor carries t(11;14) (q13;q32) translocation, immunostaining for BCL-1 was negative. It is possible that the gene is not expressed. Based on the staining and the clinical presentation, MCL was excluded. Per NCCN guidelines, patient is receiving clinical monitoring for stage I CLL.

Conclusions: Translocations involving the immunoglobulin genes are commonly identified. Uncommon genomic abnormalities in CLL should be recognized as significant independent predictors of disease progression and survival. It is important to recognize cases of CLL with t(11;14) translocation to achieve risk-adapted treatment strategies, which might be required to treat such patients.

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: We present a case of a 69-year-old male with a past medical history of RA, Afib, COPD, and DVT with pulmonary embolism. He presented to the emergency department with encephalopathy and severe abdominal pain. On exam the patient was septic with a diffusely tender abdominal exam with peritoneal signs. The CT scan showed pneumoperitoneum. The patient underwent emergent laparotomy which revealed fecal peritonitis from a cecal perforation. After washout, patient had bowel resection of the involved intestine with a primary anastomosis. Biopsy of his resected small bowel and cecum showed submucosal blood vessels with numerous lymphoid cells. Immunohistochemical staining showed aberrant expression for CD43 and CD30 with an increased proliferation index (Ki67 80-90%). Molecular studies of both the lymphoid aggregates
and the atypical intravascular cells were negative for Ig heavy chain, t(11:18) & t(14,19). A diagnosis of intravascular lymphoma was still made. Patient underwent four further abdominal washouts with reconstruction of anterior abdominal wall with Permacol™ biological mesh. The patient condition continued to deteriorate, and he was transitioned to palliative care. He died a month after. An autopsy was not performed.

Discussion: Intravascular lymphoma is a rare and very aggressive malignancy characterized by proliferation of atypical B cell confined mostly to the vascular lumen. Its presentation is protean depending on the organs involved. It has been referred to as “the oncologists great imitator.” In a series of 38 patients by Ferreri et al, the most common symptoms were fever, cutaneous symptoms, neurological symptoms followed by abdominal pain. Most patients present in an advanced state, one series of 96 patients by Murase et al, 91% of the patient presenting with clinical stage III or stage IV disease.

There remain no standard diagnostic criteria for intravascular lymphoma. First step is demonstration of lymphoma cells in small- and medium-sized blood vessels with characteristic sparing of surrounding tissue. B cell clones are most common, but T and NK cells have also been reported. Molecular, immune histochemical and flow cytometry techniques may aid in establishing diagnosis. Prognosis remains poor even with aggressive treatment, the largest series by Murase et al, with mean survival of just 13 months with treatment.

Background: We present a case of a 69-year-old male with a past medical history of RA, Afib, COPD, and DVT with pulmonary embolism. He presented to the emergency department with encephalopathy and severe abdominal pain. On exam the patient was septic with a diffusely tender abdominal exam with peritoneal signs. The CT scan showed pneumoperitoneum. The patient underwent emergent laparotomy which revealed fecal peritonitis from a cecal perforation. After washout, patient had bowel resection of the involved intestine with a primary anastomosis. Biopsy of his resected small bowel and cecum showed submucosal blood vessels with numerous lymphoid cells. Immunohistochemical staining showed aberrant expression for CD43 and CD30 with an increased proliferation index (Ki67 80-90%). Molecular studies of both the lymphoid aggregates
and the atypical intravascular cells were negative for Ig heavy chain, t(11:18) & t(14,19). A diagnosis of intravascular lymphoma was still made. Patient underwent four further abdominal washouts with reconstruction of anterior abdominal wall with Permacol™ biological mesh. The patient condition continued to deteriorate, and he was transitioned to palliative care. He died a month after. An autopsy was not performed.

Discussion: Intravascular lymphoma is a rare and very aggressive malignancy characterized by proliferation of atypical B cell confined mostly to the vascular lumen. Its presentation is protean depending on the organs involved. It has been referred to as “the oncologists great imitator.” In a series of 38 patients by Ferreri et al, the most common symptoms were fever, cutaneous symptoms, neurological symptoms followed by abdominal pain. Most patients present in an advanced state, one series of 96 patients by Murase et al, 91% of the patient presenting with clinical stage III or stage IV disease.

There remain no standard diagnostic criteria for intravascular lymphoma. First step is demonstration of lymphoma cells in small- and medium-sized blood vessels with characteristic sparing of surrounding tissue. B cell clones are most common, but T and NK cells have also been reported. Molecular, immune histochemical and flow cytometry techniques may aid in establishing diagnosis. Prognosis remains poor even with aggressive treatment, the largest series by Murase et al, with mean survival of just 13 months with treatment.

Background: We present a case of a 69-year-old male with a past medical history of RA, Afib, COPD, and DVT with pulmonary embolism. He presented to the emergency department with encephalopathy and severe abdominal pain. On exam the patient was septic with a diffusely tender abdominal exam with peritoneal signs. The CT scan showed pneumoperitoneum. The patient underwent emergent laparotomy which revealed fecal peritonitis from a cecal perforation. After washout, patient had bowel resection of the involved intestine with a primary anastomosis. Biopsy of his resected small bowel and cecum showed submucosal blood vessels with numerous lymphoid cells. Immunohistochemical staining showed aberrant expression for CD43 and CD30 with an increased proliferation index (Ki67 80-90%). Molecular studies of both the lymphoid aggregates
and the atypical intravascular cells were negative for Ig heavy chain, t(11:18) & t(14,19). A diagnosis of intravascular lymphoma was still made. Patient underwent four further abdominal washouts with reconstruction of anterior abdominal wall with Permacol™ biological mesh. The patient condition continued to deteriorate, and he was transitioned to palliative care. He died a month after. An autopsy was not performed.

Discussion: Intravascular lymphoma is a rare and very aggressive malignancy characterized by proliferation of atypical B cell confined mostly to the vascular lumen. Its presentation is protean depending on the organs involved. It has been referred to as “the oncologists great imitator.” In a series of 38 patients by Ferreri et al, the most common symptoms were fever, cutaneous symptoms, neurological symptoms followed by abdominal pain. Most patients present in an advanced state, one series of 96 patients by Murase et al, 91% of the patient presenting with clinical stage III or stage IV disease.

There remain no standard diagnostic criteria for intravascular lymphoma. First step is demonstration of lymphoma cells in small- and medium-sized blood vessels with characteristic sparing of surrounding tissue. B cell clones are most common, but T and NK cells have also been reported. Molecular, immune histochemical and flow cytometry techniques may aid in establishing diagnosis. Prognosis remains poor even with aggressive treatment, the largest series by Murase et al, with mean survival of just 13 months with treatment.

Background: Under-treatment of metastatic pancreatic cancer (MPC) continues to be a problem. Recent data presented at AVAHO 2016 (poster 21) by Ahmed et al showed patients in the VA system with MPC had treatment rates substantially lower than ACOS certified hospitals (41.5% vs 53.2%).

Objective: We aim to determine the treatment rate of MPC at the Stratton VA Medical Center (SVAMC), an ACOS-certified VA hospital, compare it with the national VAH and ACOS hospitals, and conduct a root-cause analysis for this under-treatment.

Methods: We retrospectively reviewed the medical records of MPC patients at the SVAMC between January 2010 and December 2016. All patients who presented to SVAMC with biopsy-proven MPC were included. Charts were reviewed to determine whether patients received systemic therapy, the specific type of therapy each patient received, survival rates, and the stated reason for not receiving chemotherapy.

Results: Thirty-five patients were identified to have had likely MPC. Three were excluded as they did not have a tissue biopsy. Of the remaining 32, 19 (59.4%) received systemic therapy. Thirteen (40.6%) were found not to have been treated with systemic chemotherapy. The stated reasons for non-treatment were low functional status (8 patients, 61.5%), patient refusal (3 patients, 23.1%) and other reasons (2 patients, 15.4%). Median survival of metastatic pancreatic adenocarcinoma was 233 days in the Chemotherapy group vs 60 days in the group that did not receive systemic therapy (P = .012 for mean survival). The treatment rate for MPC at SVAMC was determined to be 59.4%, which is higher than both VAH (41.5%) and ACOS certified hospitals (53.2%).

Conclusions: Our study showed that treatment rates for MPC at the SVAMC was higher than national average VA data. The vast majority of non-treatments (patient refusal, diminished ECOG status) were appropriate and in line with NCCN guidelines. National averaged data may mask regional trends and heterogeneity in practice in various VA centers. Further studies should explore this heterogeneity and identify possible causes.

Background: Under-treatment of metastatic pancreatic cancer (MPC) continues to be a problem. Recent data presented at AVAHO 2016 (poster 21) by Ahmed et al showed patients in the VA system with MPC had treatment rates substantially lower than ACOS certified hospitals (41.5% vs 53.2%).

Objective: We aim to determine the treatment rate of MPC at the Stratton VA Medical Center (SVAMC), an ACOS-certified VA hospital, compare it with the national VAH and ACOS hospitals, and conduct a root-cause analysis for this under-treatment.

Methods: We retrospectively reviewed the medical records of MPC patients at the SVAMC between January 2010 and December 2016. All patients who presented to SVAMC with biopsy-proven MPC were included. Charts were reviewed to determine whether patients received systemic therapy, the specific type of therapy each patient received, survival rates, and the stated reason for not receiving chemotherapy.

Results: Thirty-five patients were identified to have had likely MPC. Three were excluded as they did not have a tissue biopsy. Of the remaining 32, 19 (59.4%) received systemic therapy. Thirteen (40.6%) were found not to have been treated with systemic chemotherapy. The stated reasons for non-treatment were low functional status (8 patients, 61.5%), patient refusal (3 patients, 23.1%) and other reasons (2 patients, 15.4%). Median survival of metastatic pancreatic adenocarcinoma was 233 days in the Chemotherapy group vs 60 days in the group that did not receive systemic therapy (P = .012 for mean survival). The treatment rate for MPC at SVAMC was determined to be 59.4%, which is higher than both VAH (41.5%) and ACOS certified hospitals (53.2%).

Conclusions: Our study showed that treatment rates for MPC at the SVAMC was higher than national average VA data. The vast majority of non-treatments (patient refusal, diminished ECOG status) were appropriate and in line with NCCN guidelines. National averaged data may mask regional trends and heterogeneity in practice in various VA centers. Further studies should explore this heterogeneity and identify possible causes.

Background: Under-treatment of metastatic pancreatic cancer (MPC) continues to be a problem. Recent data presented at AVAHO 2016 (poster 21) by Ahmed et al showed patients in the VA system with MPC had treatment rates substantially lower than ACOS certified hospitals (41.5% vs 53.2%).

Objective: We aim to determine the treatment rate of MPC at the Stratton VA Medical Center (SVAMC), an ACOS-certified VA hospital, compare it with the national VAH and ACOS hospitals, and conduct a root-cause analysis for this under-treatment.

Methods: We retrospectively reviewed the medical records of MPC patients at the SVAMC between January 2010 and December 2016. All patients who presented to SVAMC with biopsy-proven MPC were included. Charts were reviewed to determine whether patients received systemic therapy, the specific type of therapy each patient received, survival rates, and the stated reason for not receiving chemotherapy.

Results: Thirty-five patients were identified to have had likely MPC. Three were excluded as they did not have a tissue biopsy. Of the remaining 32, 19 (59.4%) received systemic therapy. Thirteen (40.6%) were found not to have been treated with systemic chemotherapy. The stated reasons for non-treatment were low functional status (8 patients, 61.5%), patient refusal (3 patients, 23.1%) and other reasons (2 patients, 15.4%). Median survival of metastatic pancreatic adenocarcinoma was 233 days in the Chemotherapy group vs 60 days in the group that did not receive systemic therapy (P = .012 for mean survival). The treatment rate for MPC at SVAMC was determined to be 59.4%, which is higher than both VAH (41.5%) and ACOS certified hospitals (53.2%).

Conclusions: Our study showed that treatment rates for MPC at the SVAMC was higher than national average VA data. The vast majority of non-treatments (patient refusal, diminished ECOG status) were appropriate and in line with NCCN guidelines. National averaged data may mask regional trends and heterogeneity in practice in various VA centers. Further studies should explore this heterogeneity and identify possible causes.

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.