Medication risks in older patients (70 +) with cancer and their association with therapy-related toxicity.

BACKGROUND: To evaluate medication-related risks in older patients with cancer and their association with severe toxicity during antineoplastic therapy. METHODS: This is a secondary analysis of two prospective, single-center observational studies which included patients ≥ 70 years with cancer. The patients' medication lists were investigated regarding possible risks: polymedication (defined as the use of ≥ 5 drugs), potentially inappropriate medication (PIM), and relevant potential drug-drug interactions (rPDDI). The risks were analyzed before and after start of cancer therapy. Severe toxicity during antineoplastic therapy was captured from medical records according to the Common Terminology Criteria for Adverse Events (CTCAE). The association between grade ≥ 3 toxicity and medication risks was evaluated by univariate as well as multivariate regression adjusted by ECOG and age. RESULTS: The study cohort comprised 136 patients (50% female, mean age 77 years, 42% hematological malignancies). Before the start of cancer therapy, patients took on average 5 drugs as long-term medication and 52% of patients were exposed to polymedication. More than half of patients used at least one PIM. Approximately one third of patients exhibited rPDDI. The prevalence of medication risks increased after start of cancer therapy. rPDDI were significantly associated with severe overall toxicity (OR, 5.07; p = 0.036; 95% Confidence Interval (CI) 1.11-23.14; toxicity in patients with rPDDI 94.1% (32/34) vs 75.9% (60/79) in patients without rPDDI) and hematological toxicity (OR, 3.95; p = 0.010; 95% CI 1.38-11.29; hematological toxicity in patients with rPDDI 85.3% (29/34) vs 59.5% (47/79) in patients without rPDDI). In the multivariate analysis adjusted by ECOG and age, only the association for rPDDI with hematological toxicity remained statistically significant (OR, 4.51; p = 0.007; 95% CI 1.52-13.38). These findings should be further investigated in larger studies. CONCLUSION: Medication risks are common in older patients with cancer and might be associated with toxicity. This raises the need for tailored interventions to ensure medication safety in this patient cohort.

[BCG-therapy as a rare reason for postrenal failure]. / Seltene Ursache für ein postrenales Nierenversagen.

HISTORY AND CLINICAL FINDINGS: In the following case report, we describe a patient with acute renal failure due to an urinary congestion level II-III under BCG-(Bacillus Calmette-Guérin)-therapy because of bladder cancer. Cystoscopy revealed the diagnosis of BCG-induced intramural narrowing of distal ureters bilaterally. THERAPY AND FURTHER DEVELOPMENT: After receiving a double-J-catheter the renal function returned to normal. CONCLUSIONS: Although postrenal failure is relatively rare (5 %), also seldom causes such as medication-induced (e. g. BCG) ureter stenosis has to be included into the differential diagnosis.

[Polycythemia vera as a cause for progressive cognitive impairment]. / Polycythämia vera in der differenzialdiagnostischen Abklärung kognitiver Defizite.

HISTORY: A 82-years old woman was admitted with a progressive cognitive decline for further investigations and treatment. FINDINGS AND DIAGNOSIS: In the computed tomography of the brain findings of subcortical artherosclerotic encephalopathy (SAE) were present. Laboratory findings revealed elevated hemoglobin-levels (19.9 g/dl). In further investigations we found a mutation in JAK-2 as diagnostic sign for polycythemia vera (Pv). After specific treatment of the Pv cognition improved significantly. DISCUSSION: In this case report we were able to relate the progressive cognitive impairment in the context of newly diagnosed Pv in conjunction with pre-existing SAE. After Pv-directed therapy cognition improved. This case report underlines the importance of a good diagnostic work-up of patients with cognitive impairment to rule out secondary and possible treatable causes.

Comparing the performance of the CARG and the CRASH score for predicting toxicity in older patients with cancer.

OBJECTIVES: To compare the CARG (Cancer and Aging Research Group) and CRASH (Chemotherapy Risk Assessment Scale for High-Age Patients) score regarding the predictive performance for severe toxicity in older patients with cancer. METHODS: We recruited patients ≥70 years and applied the CARG and CRASH score before the start of systemic cancer treatment. The CARG predicts severe overall toxicity; the CRASH additionally predicts hematologic and nonhematologic toxicity. We captured ≥ grade 3 toxicity according to Common Terminology Criteria for Adverse Events (CTCAE) from medical records. Predictive performance was assessed using logistic regression and the area under the receiver operating characteristic curve (ROC-AUC). RESULTS: The study cohort comprised 120 patients (50% female, mean age 77.2 years, 57% solid tumors). The median of the CARG (range 0-23) and the combined CRASH (range 0-12) were 9 and 8, respectively. 81% of patients experienced toxicity; 67% showed hematologic toxicity. The predictive performance of the CARG and the combined CRASH was similar for overall toxicity (CARG: Odds ratio per unit increase (OR) 1.266, P = .015; ROC-AUC 0.681, P = .010; combined CRASH: OR 1.337, P = .029; ROC-AUC 0.650, P = .032). For hematologic toxicity, the hematologic CRASH was a significant predictor and showed numerically a higher ROC-AUC than the CARG which was not statistically different (CARG: OR 1.048, P = .462; ROC-AUC 0.564, P = .271; hematologic CRASH: OR 1.602, P = .007; ROC-AUC 0.665, P = .005). CONCLUSION: Both scores exhibited similar predictive performance for toxicity in older patients with cancer.

[Simvastatin-Induced Myopathy after Dose Increase]. / Simvastatin-induzierte Myopathie nach Dosiserhöhung.

HISTORY AND CLINICAL FINDINGS: We present a 86-year-old patient who suffered from progressive weakness in his right leg. Due to a hypercholesterinemia he had received Simvastatin for a few years. Because of higher cholesterine levels the dosis had been increased from 40 to 80 mg 6 months ago. INVESTIGATIONS AND DIAGNOSIS: We saw elevated levels of creatinine kinase and creatinine. In the EMG, a neuromuscular impairment was detected. In context with the medical history we could make the diagnosis of a statin-induced myopathy with rhabdomyolysis. TREATMENT AND COURSE: After stopping the medication with statin and under liquid substitution, creatinine kinase and creatinine levels dropped. After therapy the weakness of the leg was totally recurrent. CONCLUSION: In case of unclear neurological symptoms and under therapy with statins, a myopathy should be considered.

[Pregabalin as a rare cause of liver disease]. / Pregabalin als seltene Ursache einer Hepatopathie.

UNLABELLED: In this report we describe a patient who developed liver failure due to new administration of pregabaline. HISTORY AND ADMISSION FINDINGS: A 76-year old woman was admitted with a sacral fracture after conservative treatment in a trauma surgery ward for further rehabilitative treatment. INVESTIGATIONS: At admittance the patient complaint of lower back pain. Physical examination revealed unsteadiness in walking tests. Laboratory tests revealed mildly elevated infection parameters (CRP 0.67 mg / dl) and alkaline phosphatase (191U / I). TREATMENT AND COURSE: Physical training was initiated. Multimodal therapy for pain was continued with tilidin / naloxon, which had been started at the trauma surgery ward. Due to persistent pain and its radicular nature additional pregabaline treatment was initiated. Ten days thereafter the patient developed nausea without vomiting and subsequently (day 15) jaundice. Blood examination revealed elevated liver enzymes (ALT 246U / I, AST 86U / I, GGT 2068U / I and bilirubine 6 mg / dl). Abdominal sonography and MRCP were normal. After discontinuation of pregabaline treatment nausea disappeared within several days and liver enzymes declined to normal values within several weaks. CONCLUSION: Pregabaline should be taken into account as cause of acute liver failure.