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July 11, 2002 Vol. 347 No. 2
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In a double-blind trial, 180 patients with osteoarthritis of the knee were randomly assigned to undergo arthroscopy with débridement, arthroscopic lavage, or a placebo procedure on the knee. The outcomes in terms of pain and physical function were assessed at multiple points over a 24-month period and remained similar in the three groups.
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Nine patients who had splenic lymphoma with villous lymphocytes were treated with interferon alfa for hepatitis C virus (HCV) infection. Seven patients subsequently had no evidence of HCV infection and had remission of the lymphoma. In two patients the lymphoma regressed only after additional antiviral treatment. A similar treatment had no effect in six patients with splenic lymphoma with villous lymphocytes who had no evidence of HCV infection.
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Untreated congenital hypothyroidism leads to severe developmental difficulties. The authors of this report sought to identify defects in the thyroid oxidase system in infants with iodide-organification defects because two proteins, thyroid oxidase 1 and thyroid oxidase 2, are involved in that process. Biallelic loss-of-function mutations in THOX2, the gene for thyroid oxidase 2, were found in one patient with permanent congenital hypothyroidism, and monoallelic mutations were found in three patients with transient congenital hypothyroidism.
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Recurrent glomerulonephritis after renal transplantation is a serious complication that can result in allograft loss. This study, based on data from the Australia and New Zealand Dialysis and Transplant Registry, determined the incidence and timing of risk factors for allograft loss due to recurrent glomerulonephritis in 1505 patients with biopsy-proved glomerulonephritis that had led to end-stage renal disease and primary transplantation. Allograft loss due to a recurrence of glomerulonephritis occurred in 52 recipients. Ten years after transplantation, recurrence was the third most frequent cause of allograft loss, after chronic rejection and death with a functioning renal transplant.
Cystinosis, a rare autosomal recessive lysosomal storage disease, is due to impaired transport of cystine from lysosomes. The disease results in deposition of crystals throughout the body; if untreated, it leads to failure to thrive, profound metabolic imbalance, early end-stage renal disease, thyroid failure, and multiorgan dysfunction. As this review describes, substantial progress has been made in our understanding and treatment of this disorder. The administration of cysteamine, each molecule of which can combine with a half-molecule of cystine (cysteine) to facilitate the exit of cystine from the lysosome, has greatly improved the course of the disease. In addition, the gene for cystinosis, CTNS, which encodes a protein called cystinosin, was isolated in 1998, opening new avenues for understanding this condition.
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