Mitral valve replacement and repair. Report of 5 patients with systemic lupus erythematosus.

Severe mitral valve regurgitation due to systemic lupus erythematosus is a rare cause of valvular heart disease, necessitating valve surgery. Currently, there are 36 case reports in the world medical literature of mitral valve replacement or repair in patients who have lupus. The current trend in mitral valve surgery is toward anatomic valve repair. In patients who have systemic lupus erythematosus, however, valve repair often leads to repeat surgery and valve replacement. We report the cases of 5 patients with lupus and severe mitral valve regurgitation who underwent mitral valve surgery. In 3 of these patients, replacement with a mechanical prosthetic mitral valve was performed with good long-term results. In the other 2 patients, mitral valve repair was performed, but only 1 of the repairs was successful. The 2nd patient required subsequent replacement with a mechanical valve. To our knowledge, this report of 5 patients is the largest series of mitral valve surgery in patients with lupus. These results, along with a review of the literature, suggest the superiority of mechanical prosthetic valve replacement to repair in patients who have systemic lupus erythematosus.

Absence of p53 point mutations in parathyroid adenoma and carcinoma.

Primary hyperparathyroidism is a common disorder characterized by aberrant growth and function of solitary or multiple parathyroid glands. Many, if not all, parathyroid adenomas are examples of benign clonal neoplastic growth. The molecular events associated with the development of parathyroid neoplasia have not been well characterized. We examined benign and malignant parathyroid tissues for structural abnormalities of the p53 tumor suppressor gene. To screen for mutations in the p53 gene, we analyzed polymerase chain reaction-amplified DNA by denaturing gradient gel electrophoresis. DNA was isolated from 26 benign parathyroid adenomas and 3 parathyroid carcinomas, and polymerase chain reaction was used to amplify DNA fragments corresponding to the 4 evolutionarily conserved domains within exons 5, 7, and 8 of the p53 gene in which the majority of point mutations have been identified. Amplified DNA fragments were electrophoresed through polyacrylamide gels with linearly increasing gradients of the denaturants urea and formamide. After electrophoresis, the gels were examined for the presence of abnormally migrating bands, which represent DNA with altered melting points due to nucleotide sequence changes. Amplified fragments were of the expected size in DNA from 26 parathyroid adenomas and 3 parathyroid carcinomas. Denaturing gradient gel electrophoresis studies failed to disclose evidence of mutations in exons 5, 7, and 8 of the p53 gene in these neoplasms. We conclude that p53 point mutations do not appear to be a primary event responsible for neoplastic growth in parathyroid tissue.