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.
Key words
testosterone - oestrogen - primary hypoadrenalism
