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A case of misdiagnosis and therapeutic misadventure is presented. The misdiagnosis resulted from the coincidental intake of mackerel and poor history taking. The therapeutic misadventure resulted from treatment with allopurinol and thiazide, which may not have been indicated. Dietary regulations for the treatment of certain biochemical abnormalities may be more desirable than therapeutic interventions. Use of allopurinol for hyperuricemia, if indicated, should be reserved for overproducers and not undersecretors.
Cellular survival and death are at least partially regulated by the phosphorylation of proteins. A chaperon protein, 14-3-3ζ, regulates the activity of many proteins by covering the phosphorylation site within a 14-3-3 binding motif. Therefore, regulation of 14-3-3ζ activity may affect the fate of cells subjected to cold preservation and/or hypothermic oxygenated conditions. The present study assessed whether 14-3-3ζ protects cells from hypothermic oxygenation-induced injury and clarified its role in mitochondrial functions. Human renal tubular cell line HK-2 or 14-3-3ζ-overexpressed HK-2 (ζHK-2) cells were subjected to 72 hours of normoxic cold preservation in UW solution with or without antioxidants and hydroperoxides. Cellular death, adenosine triphosphate (ATP) content, and MTT catabolism were evaluated. Deferoxamine treatment reduced cellular death and augmented ATP content in both cell types. These indices were higher in ζHK-2, regardless of deferoxamine treatment. Exposure to hydroperoxides did not affect cellular death in either cell type, whereas hydroperoxide supplementation significantly reduced ATP content, except for low-dose hydrogen peroxide in HK-2 cells. MTT assay at normal state showed higher values in ζHK-2 cells, whereas it was impaired by hydroperoxides in both cell types. These results suggest that accumulation of hydroperoxides as a byproduct of the augmented oxidative phosphorylation by 14-3-3ζ overexpression causes mitochondrial dysfunction. In conclusion, despite possessing many potentially protective functions, 14-3-3ζ exacerbates cellular injury under hypothermic oxygenated conditions. 14-3-3ζ accelerates mitochondrial functions together with iron-dependent oxidative damage. Although further investigations are necessary, upregulation of 14-3-3ζ could be a method to maintain mitochondrial function under hypothermic oxygenated conditions, as shown in hypothermic machine preservation of renal grafts, when appropriate antioxidant treatment is administered.
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ANCA is detected in several vasculitic diseases, including drug-induced systemic vasculitis: propylthiouracil (PTU), hydralazine, minocycline, penicillamine, allopurinol, procainamide, carbimazole, thiamazole, clozapine and phenytoin. All have been known to induce ANCA positive vasculitis in adult patients.
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IEA were remarkably more prevalent in DN (41%), when compared with IgAN (7%, P = 0.001), MN (8%, P = 0.017) or MPGN (14%, P = 0.013), but not FSGS (26%, P = 0.18). In DN cases, univariate analysis revealed that IEA were associated with greater IFTA severity, but not with the percentage of glomerulosclerosis, mesangial expansion, history of drug allergy, number of prescribed medications or particular class of medications (antibiotics, NSAIDs, aspirin, thiazide, loop diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, insulin, sulfonylurea, metformin or allopurinol). Multivariate analysis showed that the severity of IFTA was the only significant predictor for IEA (P < 0.01) after stepwise adjustment for age, number of medications, drug allergy, diabetes type, % global glomerulosclerosis and mesangial expansion.
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Neutrophils are a major source of radical production during reperfusion after ischemia. Radicals formed in the xanthine oxidase reaction seem to function as a primer for the neutrophils. The nonsignificant linear correlation between radical formation and morphological appearance suggests that factors other than free radicals are important for the development of intestinal damage after a period of ischemia.
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Chronic tophaceous gout is a disabling erosive arthritis characterized by an elevated serum urate concentration, recurrent attacks of arthritis, and deposits of monosodium urate crystals in synovial fluids. Tophi, ulcerations of the overlying skin, and fissures of the interarticular cartilage may occur in advanced stages, combined with deformities of the joints and decreased active joint flexion and extension. Although the timely use of allopurinol is associated with a decrease in the frequency of deposits of the tophaceous substance, however, surgical management is necessary to restore and improve the cosmesis and joint function, to alleviate symptomatic discomfort, and to reduce the risk of infection when the overlying skin becomes ulcerated. The authors present their experience in the surgical management of the chronic tophaceous gout in the hand.
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A patient with allopurinol hypersensitivity, manifested by fever, lymphadenopathy and a severe erythematous, morbilliform, maculopapular rash was studied. On immunofluorescent staining of the patient's skin, heavy granular deposits of immunoglobulin M (IgM) were found at the dermal-epidermal junction. Transformation of the patient's lymphocytes could not be effected by a variety of combinations of allopurinol, allopurinol metabolites and serum. These data suggested that the hypersensitivity reaction caused by allopurinol had immune complex deposition as the central feature in pathogenesis. The predominance of IgM may provide a distinctive feature from the deposits generally seen in systemic and discoid lupus erythematosus.
Acute tumor lysis syndrome (TLS) is a condition that results from the rapid destruction of tumor cells accompanied with a massive release of cellular breakdown products. Acute renal failure resulting from TLS has been reported in cases of hematologic malignancies, spontaneous or treatment induced, the latter especially by chemotherapy. We present the case of a patient with diffuse large B-cell lymphoma who developed radiotherapy-induced TLS and subsequently acute renal failure. He presented with a large mediastinal tumor compressing the airway, thus causing dyspnea. After 6 Gy/3 fractions/3 days of palliative radiotherapy for the tumor, a decrease in urine volume was noted as well as rapid tumor shrinking. Because this patient died despite previous prophylaxic anti-uric acid treatment and hemodialysis, his case illustrates the need to anticipate the development of acute renal failure, even though there may be no remarkable serum uric acid elevation after the initiation of radiotherapy.
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One hundred and seventy patients were enrolled and randomized to two groups: a study group (n = 85) who received 300 mg of oral allopurinol at 15 h and 3 h before endoscopic retrograde cholangiopancreatography (ERCP) and a control group (n = 85) receiving an oral placebo at the same times. Main Outcome Measurements included serum amylase levels and the number severity of the episodes of pancreatitis. Serum amylase levels were classified as normal (< 150 IU/L) or hyperamylasemia (> 151 IU/L). Episodes of PEP were classified following Ranson's criteria and CT severity index.