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Biomedical subjects

F Y Murphy

Publications and source records attributed to F Y Murphy.

5 recordsLinked to original sources
PubMed1987

Persistent adrenal insufficiency secondary to low-dose ketoconazole therapy.

Persistent adrenal insufficiency secondary to ketoconazole therapy has not previously been documented. A case of adrenocortical insufficiency secondary to low-dose (400 mg per day) ketoconazole therapy for blastomycosis is described. Symptomatic adrenal insufficiency was documented on endocrine testing, required physiologic replacement doses of glucocorticoids, and has not been reversible in two years of follow-up. Thus, adrenal insufficiency may be caused by low-dose ketoconazole therapy, and such adrenal insufficiency may have a prolonged course.

Adrenal Insufficiency↗
PubMed1987

Giant invasive prolactinomas.

Two of the largest prolactinomas ever documented that have been followed for nine and 10 years, respectively, demonstrate how aggressive prolactinomas may become and how difficult invasive prolactinomas are to treat. One of these prolactinomas invaded both internal auditory canals and simultaneously grew inferiorly, reducing the bony support of the skull and necessitating the patient to utilize both hands to hold his head up. The second patient's prolactinoma invaded the sphenoidal, ethmoidal, and cavernous sinuses. Both of these patients had neurosurgical debulking of their tumors followed by radiation therapy. Neither patient's prolactin levels decreased significantly during their first five years post-surgically, at which time bromocriptine was added. Since then, there has been a gradual lowering of serum prolactin levels and a decrease in the size of these tumors. These cases demonstrate that prolonged treatment and very large doses of bromocriptine may be necessary for tumor reduction in patients with invasive prolactinomas.

Adult↗
PubMed1987

Milk-alkali syndrome with a serum calcium level of 22 mg/dl and J waves on the ECG.

A man with severe hypercalcemia (22 mg/dl) secondary to ingestion of a calcium carbonate antacid (Tums) was admitted with obtundation and hyperreflexia, which disappeared with treatment. Laboratory values, which were consistent with milk-alkali syndrome, included low-normal serum chloride (96 mEq/L), normal phosphorus of 2.7 mg/dl (phosphorus is usually normal to increased in this syndrome), increased blood urea nitrogen (39 mg/dl), and increased serum creatinine (2.4 mg/dl). A normal C-terminal parathormone level helped distinguish this patient from patients with severe hypercalcemia due to primary hyperthyroidism. The ECG revealed a widened rather than a shortened QT interval, as well as a J wave, a broadened T wave, and a U wave with this marked hypercalcemia, all of which reverted to normal with correction of the hypercalcemia.

Aged↗
PubMed1987

Facial flushing secondary to hypoglycemia.

Facial flushing is usually not associated with hypoglycemia. Diabetics treated with chlorpropamide can have an antabuse-like flushing with ingestion of alcohol, but flushing secondary to hypoglycemia per se has not been reported. The first case demonstrating that facial flushing can occur in insulin-induced hypoglycemia is described. This patient had marked erythematous facial flushing that was repeatable with each instance of hypoglycemia. Endocrine evaluation revealed no evidence of carcinoid or a pheochromocytoma in this patient and the facial flushing was unrelated to alcohol. Without insulin-induced hypoglycemia, this diabetic patient has had no further facial flushing in one year follow-up.

Aged↗