A non-ACTH aldosterone-stimulating factor(s) has been implicated in the pathogenesis of idiopathic hyperaldosteronism (IHA). Although this factor has not been fully characterized, some evidence suggests that it may be related to a pro-ymelanotropin (pro-'y-MSH), derived from the NH2-terminal region of pro-opiomelanocortin. In the present study, plasma immunoreactive (IR-) -y-MSH levels at 0800 h in patients with IHA were evaluated (90±17 fmol/ml; range: 13-173 fmol/ml) and found to be significantly higher (P < 0.05) than those in subjects with aldosterone-producing adenomas (33±8 fmol/ ml), essential hypertension (33±6 fmol/ml), and normotensive controls (19±2 fmol/ml). Seven of nine IHA subjects had circulating IR--y-MSH levels above the normal range (>35 fmol/ml). In plasmas sampled at 1200 h, IR-y-MSH was significantly higher in patients with IHA (95±26 fmol/ml) and adenomas (63±23 fmol/ml), as compared with essential hypertensives (31±6 fmol/ml) and normotensives (19±3 fmol/ml). Mean plasma IR-ACIH, plasma cortisol, and urinary cortisol levels did not differ significantly between any of these groups. In order to evaluate the effect of a pro-'y-MSH in vitro, adrenal adenoma tissue was obtained from two patients, one with elevated IR-'y-MSH (61 fmol/ml) and a second with low IR-

A 49-year-old diabetic woman developed polymicrobial anaerobic meningitis secondary to a meningorectal fistula one year after receiving neutron beam therapy for a rectal adenocarcinoma. The meningitis was refractory to chloramphenicol and penicillin but responded to oral metronidazole. Sustained eradication of meningitis was achieved with continued metronidazole for 51/2 months, despite persistence of the fistula. Metronidazole may be a superior antimicrobial agent for polymicrobial anaerobic meningitis, especially when caused by a large or continuing bacterial inoculum. This meningorectal fistula is the first of its kind to our knowledge to be demonstrated by microbiologic, radiologic, and pathologic studies.

Excessive production of an as yet unidentified aldosterone-stimulating factor may cause idiopathic hyperaldosteronism (IHA). This putative factor may be related to proopiomelanocortin-derived peptides, some of which have aldosterone-stimulating properties. The present study evaluated plasma beta-endorphin, ACTH, cortisol, and aldosterone levels in patients with IHA (n = 10), aldosterone-producing adenomas (n = 4), essential hypertension (n = 11), and normal subjects (n = 10). Plasma and urinary hormone measurements were obtained at timed intervals during an isocaloric, fixed electrolyte intake (Na+, 128 meq/day; K+, 80 meq/day) in a metabolic unit. Plasma for beta-endorphin assay was preincubated with sepharose-bound anti-beta-lipotropin to remove beta-lipotropin that cross-reacted with the beta-endorphin RIA. Mean +/- SE plasma beta-endorphin levels at 0800 h were elevated in IHA patients (47 +/- 13 fmol/ml) compared to those in aldosterone-producing adenoma (25 +/- 9), essential hypertension (16 +/- 1), and normal control (20 +/- 2; P less than 0.05) subjects. Plasma ACTH, plasma cortisol, and urinary cortisol levels were not different in these four groups. These data support the hypothesis that excess production of either beta-endorphin or related proopiomelanocortin-derived peptides may function as aldosterone secretogogue(s) in IHA.

Objective: To report a massive increase in subcutaneous insulin requirements following spinal cord injury in a type 1 diabetic and how it was managed over a 22-month period with pramlintide. Methods: A case report and brief literature review is presented. Results: The patient is a 43-year-old male who was diagnosed with type 1 diabetes mellitus at age 18. He remained relatively well-controlled without end-organ complications until age 37, when he developed a spinal epidural abscess following a methicillin-resistant Staphylococcus aureus cellulitis of the foot. The patient became ventilator-dependent and tetraplegic. He remained in rehabilitation for 18 months and returned home with a total daily dose of subcutaneous insulin of 600 U (4 U/kg); a 500 U increase over his prespinal cord injury requirements. Total daily intravenous insulin requirement was determined to be 259 U (1.96 U/kg). The patient was started on pramlintide. Twenty-two months after the onset of pramlintide treatment his total daily dose of subcutaneous insulin was decreased to 150 U (1.3 U/kg). Conclusion: Maintenance of glycemic control and obesity in type 1 diabetics with spinal cord injury may be complicated by autonomic dysregulation and the inability to induce activity-related lifestyle changes. Our patient exhibited clinical evidence of impaired subcutaneous insulin absorption that was not ameliorated by site changes, leading to massive insulin requirements which greatly reduced his quality of life. Following treatment with pramlintide, he decreased the volume of his insulin injections and lost 19 kg (41 pounds). Uncovering the precise mechanisms by which pramlintide benefited our patient requires further studies.