TY - JOUR
T1 - Obesity, acanthosis nigricans, insulin resistance, and hyperandrogenemia
T2 - Pediatric perspective and natural history
AU - Richards, Gail E.
AU - Cavallo, Anita
AU - Meyer, Walter J.
AU - Prince, Melvin J.
AU - Peters, Edward J.
AU - Stuart, Charles A.
AU - Smith, Edward R.
N1 - Funding Information:
From the Departments of Pediatrics, Medicine, and Obstetrics and Gynecology, The University of Texas Medical Branch. Presented in part at the Annual Meeting of the American Pediatric Society-Society for Pediatric Research, San Francisco, May 1984. Supported by Clinical Research Center Grant MOI RR-73, Division of Research Resources, by Grant AM 26644 from the National Institutes of Health and by grants from National Medical Enterprises and the Kempner Foundation. Submitted for publication Jan. 8, 1985; accepted June 12, 1985. Reprint requests: Gall E. Richards, M.D., Department of Pediatrics, C-63, University of Texas Medical Branch, Galveston, TX 77550.
PY - 1985/12
Y1 - 1985/12
N2 - We studied the syndrome of acanthosis nigricans, obesity, insulin resistance, and hyperandrogenemia in 22 patients. Although isolated case reports in adolescents have appeared, this syndrome has not received full recognition as a pediatric entity. Our patients (17 girls, five boys) had a mean weight 5.7 SD above the mean for age, although mean height was only 0.5 SD above the mean for age. All patients had acanthosis nigricans. Their insulin resistance was significantly greater than that in a control group with comparable obesity. Fasting insulin concentration was 5.25 μU/ml in lean controls, 19.6 μU/ml in obese controls, and 49.8 μU/ml in study patients (P<0.002). Mean glucose disappearance rate during an insulin tolerance test was 6.7%/min in lean controls, 5.19%/min in obese controls, and 2.35%/min in study patients (P<0.02). After menarche, mean plasma testosterone concentration was 106 ng/dl, compared with <50 ng/dl in all lean and obese control patients. Data derived from our series of patients lead us to conclude that (1) this is a genetic syndrome, although the exact mode of inheritance is unclear; (2) the natural history of the syndrome invariably begins with the onset of obesity, followed by acanthosis nigricans that worsens with progressive weight gain; (3) acanthosis nigricans is thus a marker for hyperinsulinemia, which occurs before hyperandrogenemia; (4) hyperandrogenemia occurs only after menarche. Identification of this syndrome should permit monitoring for the development of hyperandrogenemia during puberty and determination of other affected family members.
AB - We studied the syndrome of acanthosis nigricans, obesity, insulin resistance, and hyperandrogenemia in 22 patients. Although isolated case reports in adolescents have appeared, this syndrome has not received full recognition as a pediatric entity. Our patients (17 girls, five boys) had a mean weight 5.7 SD above the mean for age, although mean height was only 0.5 SD above the mean for age. All patients had acanthosis nigricans. Their insulin resistance was significantly greater than that in a control group with comparable obesity. Fasting insulin concentration was 5.25 μU/ml in lean controls, 19.6 μU/ml in obese controls, and 49.8 μU/ml in study patients (P<0.002). Mean glucose disappearance rate during an insulin tolerance test was 6.7%/min in lean controls, 5.19%/min in obese controls, and 2.35%/min in study patients (P<0.02). After menarche, mean plasma testosterone concentration was 106 ng/dl, compared with <50 ng/dl in all lean and obese control patients. Data derived from our series of patients lead us to conclude that (1) this is a genetic syndrome, although the exact mode of inheritance is unclear; (2) the natural history of the syndrome invariably begins with the onset of obesity, followed by acanthosis nigricans that worsens with progressive weight gain; (3) acanthosis nigricans is thus a marker for hyperinsulinemia, which occurs before hyperandrogenemia; (4) hyperandrogenemia occurs only after menarche. Identification of this syndrome should permit monitoring for the development of hyperandrogenemia during puberty and determination of other affected family members.
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U2 - 10.1016/S0022-3476(85)80182-7
DO - 10.1016/S0022-3476(85)80182-7
M3 - Article
C2 - 2933497
AN - SCOPUS:0022386164
SN - 0022-3476
VL - 107
SP - 893
EP - 897
JO - The Journal of Pediatrics
JF - The Journal of Pediatrics
IS - 6
ER -