Horm Metab Res 2014; 46(10): 691-696
DOI: 10.1055/s-0034-1374589
Endocrine Care
© Georg Thieme Verlag KG Stuttgart · New York

Male and Female Hypogonadism are Highly Prevalent in South Africans with Addison’s Disease

I. L. Ross
1   Division of Endocrinology, Department of Medicine, University of Cape Town, Cape Town, South Africa
,
N. S. Levitt
1   Division of Endocrinology, Department of Medicine, University of Cape Town, Cape Town, South Africa
,
D. J. Blom
2   Division of Lipidology, Department of Medicine, University of Cape Town, Cape Town, South Africa
,
D. Haarburger
3   Ampath Laboratories, Pomona, Gauteng Province, South Africa
› Author Affiliations
Further Information

Publication History

received 03 January 2014

accepted 26 March 2014

Publication Date:
05 May 2014 (online)

Abstract

Hypogonadism may complicate Addison’s disease (primary hypoadrenalism), but prevalence and metabolic sequelae of hypogonadism in Addison’s disease are poorly described. We recruited patients from the South African Addison’s disease national registry who received stable replacement doses of hydrocortisone and had no acute illness. Male biochemical testosterone deficiency was defined as an early morning basal testosterone<9.9 nmol/l and premature ovarian failure (POF) when menopause occurred before 40 years of age. Cardiometabolic risk variables were measured in males only. Male hypogonadism prevalence was 33% (14/42), and 10 patients had newly diagnosed hypogonadism. Two untreated patients had elevated FSH or LH (>10 or 12 IU/l). Testosterone deficiency did not correlate with age, disease duration or hydrocortisone dose. Untreated male hypogonadal subjects had a higher (mean±standard deviation) BMI compared to eugonadal subjects 29.2±4.9 kg/m2 vs. 24.7±3.4 kg/m2 (p=0.01) and a higher median (interquartile range) high-sensitive-CRP 6.4 (2.5–14.0) mg/l vs. 1.45 (0.6–2.8) mg/l (p=0.002). There were no differences between the 2 groups in lipids, lipoproteins and fasting glucose. The median (interquartile range) DHEAS was lower in the hypogonadal 0.31 (0.27–0.37) μmol/l, compared with the eugonadal group 0.75 (0.50–1.51) μmol/l (p=0.005). POF was documented in 11% of female patients. Male testosterone deficiency was highly prevalent in this cohort and was primarily due to secondary hypogonadism. Only BMI and hs-CRP were increased in untreated male hypogonadal subjects. Male and female hypogonadism appears to be a common complication of Addison’s disease and may contribute to its morbidity.

 
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