Introduction: Acyclovir (ACV)-associated encephalopathy is related to an increase in plasma levels of 9-carboxymethoxymethylguanine, an ACV metabolite, and is often reported in patients with renal dysfunction. We report a case of ACV-associated encephalopathy with rapid progression of renal dysfunction after oral administration of valacyclovir (VACV) and review literature of previous ACV-associated encephalopathy cases.Patient concerns: An 88-year-old man was diagnosed with herpes zoster. VACV (3000 mg/day) treatment was initiated. Serum creatinine (Cr) level was 0.80 mg/dL. However, irritability, memory impairment, and decreased responsiveness occurred after 3 days. The Cr level was 6.76 mg/dL on admission.Diagnosis: He was diagnosed with ACV-associated encephalopathy with acute kidney injury.Interventions: VACV was discontinued, hemodialysis was initiated on the day of admission, and then the signs and symptoms improved approximately 72 hours after the admission. Conclusion:Worsening of renal function and encephalopathy should be a focus when using VACV or ACV, regardless of age and original renal function. Acute kidney injury and ACV-associated encephalopathy may particularly occur in the elderly even when renal function is normal. Therefore, regular monitoring of renal function and consciousness is necessary during VACV treatment.
Background Acyclovir (ACV) neurotoxicity is a neuropsychiatric condition induced by the anti-herpetic drugs ACV and valacyclovir (VACV). It is presumed that elevated blood levels of ACV and its metabolite 9-carboxymethoxymethylguanine are involved in the development of ACV-induced encephalopathy; age and renal dysfunction are risk factors. Here, we report a case of encephalopathy caused by the administration of VACV for herpes zoster prophylaxis in a patient with renal dysfunction owing to multiple myeloma. Case Presentation Renal dysfunction was diagnosed in a 70-year-old man visiting our hospital for a medical checkup. His creatinine clearance rate was 8 mL/min. He was diagnosed with symptomatic multiple myeloma, and bortezomib/dexamethasone (BD) therapy for multiple myeloma and VACV for herpes zoster prophylaxis were initiated. We administered 500 mg/day of VACV three times a week, a lower dosage than recommended, after adjusting for his renal impairment. His renal function was monitored twice per week during therapy. During the second course of BD therapy, 6 weeks after starting treatment, he was hospitalized owing to impaired consciousness (Glasgow Coma Scale score: E2, V4, M4), and his BD and VACV therapy were suspended. Brain magnetic resonance imaging and cerebrospinal fluid analysis showed no abnormalities. Three days after discontinuing BD and VACV therapy, his consciousness recovered completely, and impaired consciousness did not recur after resuming BD therapy. His clinical diagnosis was thus ACV-induced encephalopathy. Conclusion VACV is often prescribed to patients with multiple myeloma receiving BD therapy to prevent herpes zoster. ACV-induced encephalopathy is commonly observed in patients with renal dysfunction; especially among patients with multiple myeloma with Bence–Jones proteinuria, renal tubules are easily damaged and plasma ACV concentrations are likely to increase and induce ACV-induced encephalopathy. Careful monitoring of the level of consciousness is necessary during preventive ACV therapy in patients with renal dysfunction.
Paralytic ileus as tuberculosis-immune reconstitution inflammatory syndrome (TB-IRIS) is extremely rare. We herein report a 44-year-old man with pulmonary and renal tuberculosis who developed paralytic ileus 14 days after starting antituberculosis therapy (ATT) despite an initial favorable response to ATT. Paralytic ileus was successfully managed with conservative care. He initially required hemodialysis because of obstructive uropathy due to renal tuberculosis, but he was able to withdraw from dialysis after placement of ureteral stents. TB-IRIS can affect organs other than the original sites of tuberculosis, and the combined use of steroids may be effective for its prevention and treatment.
Objective To examine the association between hospital volume and postoperative 5‐year survival for patients with prostate, kidney, and bladder cancer. Method Using Osaka Cancer Registry data, we identified 9285 patients who were diagnosed as having prostate, kidney, or bladder cancer and who underwent surgery between 2007 and 2011 in Osaka, Japan. The surgical hospital volume of each hospital was calculated and then divided into quartiles (high, medium, low, very low). We estimated the hazard ratios of hospital volume (quartiles) for 5‐year survival using Cox proportional hazard models. Results For all three cancer sites, the mortality hazard of hospitals with the lowest hospital volume was significantly higher than that of hospitals with the highest volume. The difference in adjusted 5‐year survival rates between hospitals with the highest and lowest hospital volume was 3.6% for prostate cancer, 6.6% for kidney cancer, and 13.3% for bladder cancer. Conclusion Hospital surgical volume seems to affect 5‐year survival for patients with urological cancers, especially kidney and bladder cancer.
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