Arthroscopy for Osteoarthritis of the Knee?

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.

Although arthroscopy is commonly performed for osteoarthritis of the knee, this carefully blinded and controlled study found no evidence of any improvement from either arthroscopic débridement or arthroscopic lavage. The moderate improvements observed in all three groups may reflect either the effects of medical therapy or the natural history of the osteoarthritis.

Related Editorial

Regression of Splenic Lymphoma after Treatment for Hepatitis C

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.

This study was undertaken after a patient with this chronic B-cell lymphoproliferative disorder had a hematologic response after treatment with interferon alfa for cryoglobulinemia and HCV infection. These findings suggest that HCV infection may be involved in the pathogenesis of this subtype of lymphoma.

Related Perspective

THOX2-Inactivating Mutations and Congenital Hypothyroidism

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.

Inactivating mutations in the THOX2 gene that result in total disruption of thyroid hormone synthesis are associated with severe, permanent congenital hypothyroidism, whereas monoallelic mutations lead to a milder, transient form of the disease. This may represent the first genetic mutation causing transient congenital hypothyroidism that has been discovered.

Risk of Allograft Loss from Recurrent Glomerulonephritis

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.

No risk factors were identified that warrant changing the approach to renal transplantation in patients with primary glomerulonephritides.

Medical Progress: Cystinosis

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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