Geographic variation in the use of breast-conserving treatment for breast cancer.

Background: In the past decade there has been an increase in the use of treatment designed to conserve the breast for women with breast cancer. The extent to which such treatment has been adopted in various regions of the country and whether characteristics of hospitals and patients predict its use is not known, however.

Methods: We used national data on Medicare claims for inpatient care provided in 1986 to study 36,982 women 65 to 79 years of age, who had local or regional breast cancer and underwent either mastectomy or breast-conserving treatment (local excision, quadrantectomy, or subtotal mastectomy).

Influence of antihyperuricemic therapy on the clinical and radiographic progression of gout.

Ten years ago, we studied the clinical and radiographic manifestations of gout in 60 patients and described 3 patterns of disease. To determine the consequences of management over a 10-year period, we recently reassessed the 39 available patients of this population. We found that although reduced tophaceous deposition on physical examination correlated with normalization of the serum urate concentration, no correlation existed between radiographic changes and mean serum urate concentrations.

Synovial fluid 5'-nucleotidase activity. Relationship to other purine catabolic enzymes and to arthropathies associated with calcium crystal deposition.

We measured 5'-nucleotidase (5NT) activity in synovial fluid from 159 patients with various diagnoses. The activity of 5NT was compared with activities of nucleotide pyrophosphohydrolase, alkaline and neutral phosphatases, and adenosine deaminase, in the same samples. Higher levels of 5NT activity occurred in synovial fluid from osteoarthritic joints than from joints of patients with gout, pseudogout, or rheumatoid arthritis.

Differential deoxyadenosine toxicity to immature rabbit cartilage in vitro. A model for the chondro-osseous dysplasia of adenosine deaminase deficiency.

Deoxyadenosine metabolism was investigated in rabbit growth plate and articular cartilage to elucidate the biochemical basis for the chondro-osseous dysplasia observed in adenosine deaminase (ADA) deficiency. Models of ADA deficiency, the combination of deoxy-adenosine and either of 2 ADA inhibitors, were selectively toxic to immature cartilage, supporting the hypothesis that the chondro-osseous dysplasia of ADA deficiency is the consequence of the enzyme deficiency. Depletion of ATP may play a role in the altered chondrocyte viability and function observed in this model.

Myoadenylate deaminase deficiency and forearm ischemic exercise testing.

Myoadenylate deaminase (MADA) deficiency has been associated with symptoms of postexertional aches, cramps, weakness, and skeletal muscle dysfunction. Measurement of plasma lactate and ammonia concentrations after forearm ischemic exercise has been suggested as a screening test for this disorder. We performed forearm ischemic tests on 3 patients with histochemically defined MADA deficiency and 13 healthy control subjects, in a standardized fashion.

Myoadenylate deaminase deficiency: diagnosis by forearm ischemic exercise testing.

These results indicate that measuring venous ammonia concentrations after forearm ischemic exercise is an effective means of screening for MADA deficiency but that submaximal exercise performance, whether due to weakness, pain or poor effort, can provide false positive results. Measurements of purine compounds released after exercise may increase the specificity of forearm ischemic exercise testing for MADA deficiency. The low level of purines released after exercise in MADA-deficient subjects supports the hypothesis that disordered purine metabolisms occurs when MADA activity is absent.

Adenosine deaminase deficiency and chondro-osseous dysplasia.

An in vitro model of ADA deficiency is selectively toxic to cartilage from immature rabbits with a greater effect on growth plate than articular cartilage. The selective toxicity observed appears to be the consequence of ATP depletion. These results support the hypothesis that the chondro-osseous dysplasia observed in patients with ADA deficiency is caused by the disordered metabolism that results from the enzyme deficiency.