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A E Ruiz

Publications and source records attributed to A E Ruiz.

6 recordsLinked to original sources

A giant prolactinoma and the effect of chronic bromocriptine therapy on basal and TRH-stimulated serum prolactin levels.

The role of bromocriptine as primary therapy for prolactin-producing tumors is currently well accepted in the literature. Bromocriptine decreases the concentration of serum prolactin and this decrease precludes tumor shrinkage, despite the lack of correlation between amount of decrease in tumor size and baseline serum prolactin. We submit the case of a patient on chronic bromocriptine therapy followed by measuring baseline and thyrotropin-releasing hormone (TRH)-stimulated serum prolactins. Bromocriptine affects both release and storage of prolactin. The literature has suggested that the effects of bromocriptine on storage and synthesis may be responsible for its effects on tumor size. It was felt that TRH stimulation would more accurately reflect storage and synthesis, and thus correlate better with tumor size. The pituitary was initially debulked via a right frontal approach; then the patient was placed on bromocriptine therapy and postoperatively followed with baseline and TRH-stimulated serum prolactins. The size of the pituitary was measured by computed tomography. Baseline serum prolactin levels rapidly decreased, but despite the slow decrease in TRH-stimulated prolactins no change was noted in tumor size. Because of the time difference between the baseline and TRH-stimulated prolactin levels, we conclude that clinically bromocriptine affects primarily secretion of prolactin and secondarily storage and synthesis. We also show that TRH-stimulated prolactin does not correlate with size of prolactin-secreting pituitary tumors and therefore tumor size should be independently measured. The literature has shown that prolactinomas do not respond well to TRH stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Bromocriptine

Interpreting EKGs.

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Electrocardiography

Primary adrenal hyperplasia: a new subset of primary hyperaldosteronism.

The existence of a new subset of primary hyperaldosteronism that combines the morphology of bilateral hyperplasia with the biochemical and therapeutic responses typical of adenoma recently was suggested. The following is the first detailed case report of that subset. The patient had severe hypokalemia and hypertension responsive to spironolactone, and elevated supine plasma aldosterone and 18-hydroxycorticosterone values that did not increase after ambulation. Surgical removal of 75% of both adrenal glands decreased mineralocorticoid levels into the low normal range and allowed the return of normal renin-angiotensin function, although plasma aldosterone was still unresponsive to postural change. Glucocorticoid reserve remained normal. Histology showed bilateral cortical hyperplasia. The results support the existence of a new subset of adrenal hyperplasia, termed primary adrenal hyperplasia, in which biochemical parameters and response to surgery mimic those of adrenal adenomas. The existence of such a subset indicates that morphological categorization alone is insufficient to rule out a possible therapeutic response to surgery in patients with aldosterone-secreting adrenal hyperplasia.

Adenoma

Panhypopituitarism and anemia secondary to traumatic fracture of the sella turcica.

A case of a 27 year old man who developed anemia after fracture of the sella turcica is reported. The diagnosis of anterior pituitary insufficiency was made by a combined provocative test with TRH, LHRH, and insulin. The anemia was characterized by a hypocellular bone marrow which appeared to be functioning only in the thoracic-lumbar vertebrae, an absence of measurable erythropoietic activity, and by the return to normal of the hematological findings after hormonal replacement therapy. This patient had the highly unusual combination of proven panhypopituitarism and significant anemia resulting from a distinct fracture of the sella turcica.

Adult