Twenty-four-hour urinary free cortisol in patients with acquired immunodeficiency syndrome.

Many patients with acquired immune deficiency syndrome (AIDS) have symptoms consistent with adrenal insufficiency, but only a small subset of these patients meet criteria for adrenal insufficiency during a short corticotropin (ACTH) stimulation test. We hypothesized that patients with AIDS and symptoms of adrenal insufficiency who produce normal amounts of cortisol in response to administration of 0.25 mg cosyntropin may nevertheless produce lower amounts of cortisol in a course of 24 hours than comparably sick AIDS patients without symptoms of adrenal insufficiency or comparably sick patients without AIDS. We studied four groups of male patients: AIDS patients with symptoms suggestive of adrenal insufficiency but with a normal response to cosyntropin (group I), AIDS patients without symptoms suggestive of adrenal insufficiency (group II), human immunodeficiency virus (HIV)-negative patients with serious acute or chronic illness (group III), and healthy subjects (group IV). The following variables were examined: age, CD4 cell count, Acute Physiologic and Chronic Health Evaluation (APACHE) score, serum cortisol and plasma ACTH at baseline; serum cortisol at 30 and 60 minutes after intravenous administration of 0.25 mg cosyntropin; and 24-hour urinary free cortisol. The four groups had a similar mean age and baseline plasma ACTH and serum cortisol levels. However, a change in cortisol from baseline to 30 and 60 minutes after administration of cosyntropin was significantly smaller in both groups of AIDS patients than in the sick patients without AIDS and normal subjects. There were also differences noted between the two groups of AIDS patients: both baseline and stimulated levels of cortisol tended to correlate directly with ACTH levels in patients without symptoms of adrenal insufficiency, while this relationship appeared to be inverse in patients with symptoms suggestive of adrenal insufficiency (r = -.57 to -.7, P < .05 to .14). The 24-hour urinary free cortisol levels were similar among all groups, but correlated strongly with baseline and stimulated serum cortisol levels only in patients with AIDS and symptoms of adrenal insufficiency (r = .8 to .9, P < .002 to .015). We conclude that (1) AIDS patients with and without symptoms of adrenal insufficiency may have either normal adrenal function or somewhat suboptimal adrenal reserve as demonstrated by a blunted cortisol response during the short ACTH stimulation test in comparison to HIV-negative comparably sick patients or healthy subjects; and (2) 24-hour urinary free cortisol is not a useful test for detection of subtle abnormalities of adrenal function in patients with AIDS.

Coexistence of diabetes and phosphofructokinase deficiency.

OBJECTIVE: To report the first case of coexisting diabetes mellitus and phosphofructokinase deficiency. METHODS: We describe a 50-year-old woman who had a history of diabetes mellitus, muscle weakness, and mild hemolysis. Phosphofructokinase deficiency was diagnosed with use of the ischemic forearm exercise test and magnetic resonance spectroscopy during exercise. RESULTS: The presence of phosphofructokinase deficiency affected the methods of follow-up and choices of diabetes therapy. Insulin therapy was avoided because insulin may exacerbate muscle weakness by suppressing production of free fatty acids. Strenuous exercise had to be avoided as well because it may induce myoglobinuria in patients with phosphofructokinase deficiency. Glycosylated hemoglobin measurements could not be used because they were falsely low (from hemolysis), and other indicators of long-term glycemic control were utilized instead. CONCLUSION: Diabetes mellitus and phosphofructokinase deficiency can coexist. In such cases, choices of diabetes therapy and methods of monitoring of glycemic control must be adjusted to account for the presence of phosphofructokinase deficiency.

Kikuchi's disease associated with Hashimoto's thyroiditis.

We describe a unique association of histiocytic necrotizing lymphadenitis (Kikuchi's disease) and chronic lymphocytic (Hashimoto's) thyroiditis in a patient who presented with significant cervical lymphadenopathy and a goiter. This case illustrates the value of lymph node biopsy combined with the fine needle aspiration of the thyroid in determining the nature of the relationship between the goiter and lymphadenopathy.