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The presence of both toxoplasmic myocarditis and myositis in the same individual has been reported only at autopsy. We report the first case of biopsy-proven toxoplasmic myocarditis and polymyositis simultaneously occurring in the same individual that was diagnosed during life. Results of her toxoplasmic serology were consistent with acute toxoplasmosis. She subsequently developed visual symptoms consistent with toxoplasmic chorioretinitis. She had a positive clinical response to therapeutic agents specific against Toxoplasma gondii. Her toxoplasmic serological profile established the diagnosis of acute toxoplasmosis. A toxoplasmic serological profile should be obtained for patients with myocarditis and/or polymyositis of unclear etiology. Endomyocardial or skeletal muscle tissue biopsies may establish the definitive diagnosis of toxoplasmic myocarditis or polymyositis, respectively. Examination of blood by polymerase chain reaction analysis before antitoxoplasmic treatment and early in the course of primary infection with T. gondii may prove useful.

To determine the usefulness of commercially available somatomedin C levels in the evaluation of the treatment of acromegaly, 15 patients were tested at 0.25-15.4 yr after onset of therapy. Clinical response, as determined by a numerical scoring system, was compared with RIA of GH and somatomedin C. Symptomatic response was poorly correlated with somatomedin C (r = 0.033) as well as with GH (r = 0.24). The correlation of GH and somatomedin C was also poor (r = 0.46, P greater than 0.05). Eighty-three percent of patients with clinical improvement had GH less than or equal to 10 ng/ml, 50% had GH less than or equal to 5 ng/ml, while 42% had somatomedin C less than or equal to 3.0 U/ml. All patients who were evaluated at 1 yr or less after therapy had elevated somatomedin C levels with normal or near normal GH values. In contrast only 2 of 11 patients evaluated at more than 1 yr after therapy had a mild persistence of somatomedin C elevation with normal GH levels. Determination of somatomedin c costs more than GH determinations and appears to offer no apparent advantage over GH in following patients treated for acromegaly.

Pituitary abscess is an unusual cause of sella turcica enlargement. Because its presentation closely mimics that of a pituitary tumor, the condition is seldom recognized preoperatively. Most cases have been of bacterial etiology; however, a single patient with a primary mycotic pituitary abscess secondary to Aspergillus species has been reported. That patient died of diffuse Aspergillus meningoencephalitis following a transfrontal craniotomy. In the present case, a woman with primary pituitary aspergillosis survived her infection with virtually intact pituitary function following a transsphenoidal approach which avoided contamination of cerebrospinal fluid. Postoperative amphotericin-B and 5-fluorocytosine therapy probably contributed greatly to her survival. Factors that should alert the clinician to the presence of a pituitary abscess in a patient with sella turcica enlargement are prior episodes of meningitis, sinusitis, or cerebrospinal fluid abnormalities, including pleocytosis, depressed glucose, and elevated protein.

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