Cisplatin is known to induce Fanconi syndrome and renal salt wasting (RSW). RSW typically only requires transient normal saline (NS) support. We report a severe RSW case that required 12 liters of 3% saline. A 57-year-old woman with limited stage small cell cancer was admitted for cisplatin (80 mg/m2) and etoposide (100 mg/m2) therapy. Patient's serum sodium (SNa) decreased from 138 to 133 and 125 mEq/L within 24 and 48 hours of cisplatin therapy, respectively. A diagnosis of syndrome of inappropriate antidiuretic hormone secretion (SIADH) was initially made. Despite free water restriction, patient's SNa continued to decrease in association with acute onset of headaches, nausea, and dizziness. Three percent saline (3%S) infusion with rates up to 1400 mL/day was required to correct and maintain SNa at 135 mEq/L. Studies to evaluate Fanconi syndrome revealed hypophosphatemia and glucosuria in the absence of serum hyperglycemia. The natriuresis slowed down by 2.5 weeks, but 3%S support was continued for a total volume of 12 liters over 3.5 weeks. Attempts of questionable benefits to slow down glomerular filtration included the administration of ibuprofen and benazepril. To our knowledge, this is the most severe case of RSW ever reported with cisplatin.
A 50-year-old female with a prolonged history of untreated human immunodeficiency virus (HIV) presented with a large vaginal mass. During workup, the mass was found to be vaginal squamous cell carcinoma. Imaging suggested stage IV disease, but a biopsy of liver lesions demonstrated synchronous diffuse large B-cell lymphoma. Her treatment course was notable for complete remission of her lymphoma with lymphoma-directed chemotherapy and complete clinical response of her squamous cell carcinoma to lymphoma-directed therapy. She tolerated intensive chemotherapy despite her HIV but eventually died due to infectious complications during surgery to address a vaginal fistula. The case is demonstrative of several important diagnostic and therapeutic principles in the management of HIV-associated malignancies. Thorough consideration and testing must be performed to ensure accurate staging, as synchronous malignancies and infections can distort standard clinical testing. Further, standard chemotherapeutic regimens often must be tailored and specially sequenced when dealing with severely immunocompromised patients with multiple synchronous processes.
The purpose of this study was to determine FDG PET/CT utility in predicting patient outcome undergoing Y RE for metastatic liver tumors.Thirty-one patients with metastatic tumors to the liver underwent Y RE between March 15, 2007, and May 5, 2011, at our institution. FDG PET/CT imaging was performed on each patient within 3 months before and after undergoing Y RE. Pretreatment and posttreatment FDG PET/CT were evaluated for SUV, number of liver lesions, and presence of disease outside the liver. The Kaplan-Meier method and Cox proportional hazard modeling was used to evaluate if SUV was a predictor of overall survival.Of the 31 patients, 12 were alive at the end of the study; median survival was 9 months (95% confidence interval, 7-18 months). The 24-month survival rate was 0.28 (95% confidence interval, 0.12-0.48). Kaplan-Meier analysis of preprocedure FDG PET/CT imaging showed no difference in rates of survival by number of lesions observed in the liver (P = 0.114) or presence of disease observed outside the liver (P = 0.719). Cases with new lesions outside the liver after treatment had significantly shorter survival times than cases without new lesions outside the liver (P = 0.002). Cox proportional hazard model showed that SUV levels before and after treatment were not significant predictors of overall survival.The appearance of new lesions outside the liver on FDG PET/CT within 3 months after Y RE was the only statistically significant variable in predicting poor outcome. Absence of new lesions outside the liver on postprocedure FDG PET/CT imaging helps identify patients achieving long-term survival.
Primary Effusion Lymphoma (PEL) is a unique immunodeficiency-associated malignancy that requires infection with Kaposi sarcoma herpesvirus/human herpesvirus 8 (KSHV/HHV8). Although thought to arise from mature B-lymphocytes, PEL typically has a null Immunophenotype but can very rarely show lineage specific aberrancies, including aberrant T-cell markers.Here we present one such case of PEL where aberrant T-cell markers led to a misdiagnosis of peripheral T-cell lymphoma. We performed a review of the literature to identify similar cases of PEL with strong T-cell antigen expression. Most cases occurred in men who were HIV positive or otherwise immunodeficient. Many were EBV positive. Rare cases demonstrated T-cell receptor gene rearrangements. Postulated theories for the cause of disordered differentiation include immunodeficiency and/or EBV infection. The expression of T-cell antigens on PELs may be a source for error in diagnosis and awareness of this correlation is of practical diagnostic relevance.
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