Mehdi S

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: USPSTF recommends against continuing screening for colorectal cancer (CRC) past 75 years in adequately screened individuals. Research has shown that onetime screening for elderly who have never been screened appears to be cost effective until 86 years of age. Survival and staging data that compare elderly vs younger populations has not been published.

Objective: (1) To compare staging (0-4) of CRC in groups of 60-69, 70-79, and 80 to 89-year-olds; (2) To compare survival outcomes (5-10 years) in stages 0-2 for these age groups after treatment (ie, surgery); (3) To compare surgical and no treatment (ie, no surgery) survival outcomes in these age groups

Methods: Male veterans were selected from Veterans Affairs National Cancer Cube Registry. 22,735 patients within 60-69, 18,390 within 70-79 and 10,057 within 80-89 years were diagnosed with CRC within years 2000-2015 with majority being stages 1 and 2. Surgical and survival data were obtained only for stage 0-2 as surgery is currently the standard of treatment for these stages.

Results: After surgery, 5- to 10-year survival for 60-69 age group averaged about 34.4% (95% CI, 31.94-36.85) for stage 0-2. Similarly, for 70-79 and 80-89 age group it was 30.86% (95% CI, 29.54-32.19) and 25.45% (95% CI, 24.77-25.69), respectively. The 5- to 10-year survival data for patients not undergoing surgery was 1.03%, 0.81%, and 0.95% for age groups 60-69, 70-79 and 80-89, respectively.

Conclusions: The highest number of CRC cases diagnosed across each age group was stage 1 with stage 2 being second. In the surgical treatment group survival was statistically different for 80-89 age group as compared to 60-69 and 70-79, though octogenarians did have a surprisingly high mean of 25.45% suggesting early detection and treatment will help survival. Survival data from no-treatment cases showed an immense drop in survival for patients not undergoing surgery, suggesting that these candidates may have other reasons or comorbid conditions leading to their demise.

Background: USPSTF recommends against continuing screening for colorectal cancer (CRC) past 75 years in adequately screened individuals. Research has shown that onetime screening for elderly who have never been screened appears to be cost effective until 86 years of age. Survival and staging data that compare elderly vs younger populations has not been published.

Objective: (1) To compare staging (0-4) of CRC in groups of 60-69, 70-79, and 80 to 89-year-olds; (2) To compare survival outcomes (5-10 years) in stages 0-2 for these age groups after treatment (ie, surgery); (3) To compare surgical and no treatment (ie, no surgery) survival outcomes in these age groups

Methods: Male veterans were selected from Veterans Affairs National Cancer Cube Registry. 22,735 patients within 60-69, 18,390 within 70-79 and 10,057 within 80-89 years were diagnosed with CRC within years 2000-2015 with majority being stages 1 and 2. Surgical and survival data were obtained only for stage 0-2 as surgery is currently the standard of treatment for these stages.

Results: After surgery, 5- to 10-year survival for 60-69 age group averaged about 34.4% (95% CI, 31.94-36.85) for stage 0-2. Similarly, for 70-79 and 80-89 age group it was 30.86% (95% CI, 29.54-32.19) and 25.45% (95% CI, 24.77-25.69), respectively. The 5- to 10-year survival data for patients not undergoing surgery was 1.03%, 0.81%, and 0.95% for age groups 60-69, 70-79 and 80-89, respectively.

Conclusions: The highest number of CRC cases diagnosed across each age group was stage 1 with stage 2 being second. In the surgical treatment group survival was statistically different for 80-89 age group as compared to 60-69 and 70-79, though octogenarians did have a surprisingly high mean of 25.45% suggesting early detection and treatment will help survival. Survival data from no-treatment cases showed an immense drop in survival for patients not undergoing surgery, suggesting that these candidates may have other reasons or comorbid conditions leading to their demise.

Background: USPSTF recommends against continuing screening for colorectal cancer (CRC) past 75 years in adequately screened individuals. Research has shown that onetime screening for elderly who have never been screened appears to be cost effective until 86 years of age. Survival and staging data that compare elderly vs younger populations has not been published.

Objective: (1) To compare staging (0-4) of CRC in groups of 60-69, 70-79, and 80 to 89-year-olds; (2) To compare survival outcomes (5-10 years) in stages 0-2 for these age groups after treatment (ie, surgery); (3) To compare surgical and no treatment (ie, no surgery) survival outcomes in these age groups

Methods: Male veterans were selected from Veterans Affairs National Cancer Cube Registry. 22,735 patients within 60-69, 18,390 within 70-79 and 10,057 within 80-89 years were diagnosed with CRC within years 2000-2015 with majority being stages 1 and 2. Surgical and survival data were obtained only for stage 0-2 as surgery is currently the standard of treatment for these stages.

Results: After surgery, 5- to 10-year survival for 60-69 age group averaged about 34.4% (95% CI, 31.94-36.85) for stage 0-2. Similarly, for 70-79 and 80-89 age group it was 30.86% (95% CI, 29.54-32.19) and 25.45% (95% CI, 24.77-25.69), respectively. The 5- to 10-year survival data for patients not undergoing surgery was 1.03%, 0.81%, and 0.95% for age groups 60-69, 70-79 and 80-89, respectively.

Conclusions: The highest number of CRC cases diagnosed across each age group was stage 1 with stage 2 being second. In the surgical treatment group survival was statistically different for 80-89 age group as compared to 60-69 and 70-79, though octogenarians did have a surprisingly high mean of 25.45% suggesting early detection and treatment will help survival. Survival data from no-treatment cases showed an immense drop in survival for patients not undergoing surgery, suggesting that these candidates may have other reasons or comorbid conditions leading to their demise.

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.