Insulin-induced cardiac failure.

Self-limited edema is a well-recognized complication of insulin therapy. However, progression to overt cardiac failure has only recently been reported in one patient with pre-existing heart disease. This report describes the first case of insulin-induced cardiac failure in a patient without underlying heart disease. Current trends toward intensive insulin therapy for rapid near-normalization of blood glucose levels will increase the recognition of this entity. Careful follow-up of so-called "self-limited" insulin edema is encouraged, and the early institution of diuretic therapy is advocated in elderly patients to prevent the development of overt cardiac failure.

Lack of demonstrable tumor growth in progressive hyperprolactinemia.

Prolactin has been regarded as an excellent tumor marker for patients harboring prolactinomas, and a significant rise in the basal prolactin level is generally regarded as being commensurate with tumor growth. This report describes a case in which the basal serum prolactin level rose from 250 ng/ml to 1,528 ng/ml over a 10-year follow-up period in the absence of definitive therapy. Three sequential contrast-enhanced direct coronal computed tomographic scans obtained over a four-year period failed to demonstrate any evidence of growth of the 5 mm microprolactinoma. Progressive hyperprolactinemia may not be synonymous with tumor growth in patients with microprolactinomas.

The natural history of untreated microprolactinomas.

The development of radioimmunoassay (RIA) for prolactin (PRL) and sensitive high-resolution computed tomography (HRCT) has resulted in documentation of large numbers of microprolactinomas (microPRL). To try to define the rate and prevalence of tumor growth, the authors performed serial HRCT scans in 38 untreated patients, an average of 31.7 months apart. In no patient, including two patients with exuberant rises in PRL, was there any evidence of subtle tumor growth. The authors conclude that the majority of patients with microPRL have a benign course, with tumor growth occurring, if at all, over a period of years.

Chronic neutropenia following gold therapy.

We describe the first case of chronic neutropenia of 17 years' duration following gold therapy in a 53-year-old woman given a 1-g course of gold therapy in 1965 for treatment of seropositive rheumatoid arthritis. Although she had a good response to the gold therapy, her originally normal leukocyte count fell to 1.2 x 10(9)/L. Over the subsequent 17 years, she required multiple hospitalizations for recurrent skin, mouth, and respiratory tract infections. Serial leukocyte counts failed to show a cyclical nature to the chronic neutropenia. Normal results of a technetium Tc 99m spleen scan and lack of increased bone marrow leukocyte precursors rendered a diagnosis of Felty's syndrome unlikely. A bone marrow biopsy specimen revealed an isolated reduction in the number of myeloid precursors, which is consistent with gold-induced bone marrow toxicity. This patient's relative freedom from serious life-threatening infections remains enigmatic, but is undoubtedly related to her ability to augment another phagocytic cell line, and the remarkable phagocytic activity of her monocytes appears to have well compensated for her neutropenia. This activity was most likely responsible for her long-term survival.