Early Report“Buffalo hump” in men with HIV-1 infection
Introduction
The accumulation of adipose tissue in the dorsocervical region, commonly referred to as “buffalo hump, is a typical finding in patients with glucocorticoid excess. Although benign, this disorder can lead to substantial disfigurement and so compromise quality of life. Recently, anecdotal reports of HIV-1-infected patients who developed a buffalo hump have appeared on the Internet (“Crix list”: http://crix.pinkpage.com/; accessed on March 9, 1998) and in the medical literature.1, 2 The observation that enlargement of the dorsocervical fat pad occurred after initiation of combination antiretroviral therapy that included a protease inhibitor has led to the suggestion that the enlargement could be a consequence of protease-inhibitor therapy.
We report the results of studies done in eight HIV-1-positive men referred for investigation of a buffalo hump, four of whom were on triple antiretroviral regimens that included a protease inhibitor. Measurement of urinary free cortisol excretion and an overnight low-dose dexamethasone suppression test were done to screen for Cushing's syndrome. In addition, total and regional body-composition analysis and measurements of lipids, glucose, and cortisol in these men were compared with those obtained in a control population of HIV-1-infected men without buffalo hump.
Section snippets
Patients
We studied eight consecutive HIV-1-positive men referred to the Division of Endocrinology, San Francisco General Hospital, for investigation of dorsocervical-fat-pad enlargement between June, 1995, and October, 1997. 15 HIV-1-positive men without dorsocervical-fat-pad enlargement were selected as controls during the same period from a natural history cohort study conducted by our group. The controls were selected to be within the range of the age, body-mass index (BMI), and CD4-lymphocyte count
Results
The clinical characteristics of the eight men with buffalo hump are shown in table 1. The mean time from diagnosis of HIV-1 infection was 9·6 (SD 3·7; range 5–15) years. All eight patients were on stable nucleoside-analogue therapy; four of these (patients 5–8) had started treatment with a protease inhibitor 2–18 months (median 7·5) before development of a buffalo hump. Patients 1–6 reported stable bodyweights. Patient 7 reported 7 kg weight loss due to colitis 4 months before the development
Discussion
We have excluded Cushing's syndrome as the cause of dorsocervical-fat-pad enlargement in the eight HIV-1-positive men reported here. All patients had a normal response to a low dose of dexamethasone, with suppression of plasma cortisol values to less than 83 nmol/L. These findings exclude Cushing's syndrome with more than 95% certainty.6, 7, 8 24 h urinary free cortisol excretion, which is higher than normal in more than 90% of patients with Cushing's syndrome,9, 10, 11 was within the normal
References (23)
- et al.
Benign symmetric lipomatosis associated with protease inhibitors
Lancet
(1997) - et al.
Dual-energy x-ray absorptiometry for total-body and regional bone-mineral and softtissue composition
Am J Clin Nutr
(1990) - et al.
Overnight (1 mg) dexamethasone suppression testing reliably distinguishes non-cushingoid obesity from Cushing's syndrome
Steroids
(1991) Cushing's syndrome: a review of diagnostic tests
Metabolism
(1979)- et al.
Biochemical and radiologic diagnosis of Cushing's syndrome
Endocrinol Metab Clin North Am
(1994) - et al.
Glucocorticoid action and the clinical features of Cushing's syndrome
Endocrinol Metab Clin North Am
(1994) - et al.
Does central obesity reflect “Cushing's disease of the omentum”?
Lancet
(1997) Fat cells
Endocrinol Metab Clin North Am
(1996)- et al.
Contribution of intraabdominal fat accumulation to the impairment of glucose and lipid metabolism in human obesity
Metabolism
(1987) - Ruane PJ. Atypical accumulation of fatty tissue [abstr]. 37th Interscience Conference on Antimicrobial Agents and...