Fertility and sterility · 1996
Hypogonadism in Rhodesian sleeping sickness: evidence for acute and chronic dysfunction of the hypothalamic-pituitary-gonadal axis.
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Petzke F, Heppner C, Mbulamberi D, Winkelmann W, Chrousos G P, Allolio B, Reincke M
Аннотация
OBJECTIVE: To investigate acute and long-term effects of Rhodesian sleeping sickness on the function of the hypothalamic-pituitary-gonadal (HPG) axis in men.
DESIGN: An observational, cross-sectional study.
SETTING: Primary health care centers under care of the National Sleeping Sickness Control Program in southeast Uganda.
PARTICIPANTS: Fifty-two male patients with sleeping sickness at different stages of treatment and 11 clinically healthy male volunteers recruited from health care personnel.
INTERVENTIONS: Patients and controls were questioned about loss of libido and impotence. All received 100 micrograms GnRH i.v. Blood was drawn before and 30 minutes after GnRH administration.
MAIN OUTCOME MEASURES: Frequency of loss of libido and impotence. Baseline T and sex hormone-binding globulin baseline and GnRH- stimulated serum LH and FSH concentrations.
RESULTS: Loss of libido and/or impotence were present in 39% of men with active disease before therapy, whereas 84% were biochemically hypogonadal. After cure, 45% of men still were symptomatic and 45% were biochemically hypogonadal. Compared with controls (806 +/- 59 pg/mL [conversion factor to SI unit, 0.03467]; mean +/- SEM), T concentrations were decreased substantially in patients before (249 +/- 48 ng/dL), during treatment (429 +/- 56 ng/dL), and after cure (431 +/- 58 ng/dL). Corresponding baseline LH concentrations were inappropriately low and the relative LH response to GnRH was reduced both before and during treatment (794% +/- 131% versus 322% +/- 68%). Follicle-stimulating hormone concentrations increased gradually up to 8.0 +/- 1.3 mIU/mL (conversion factor to SI unit, 1.00) at the end of treatment, returning to 4.2 +/- 0.6 mIU/mL after cure.
CONCLUSIONS: Rhodesian sleeping sickness causes acute and chronic HPG axis dysfunction. The clinical and biochemical picture suggest a combined central and peripheral hypogonadism. This is only in part reversible after cure and most likely due to direct parasitic infiltration and/or secondary inflammation causing necrosis and/or fibrosis at the pituitary and gonadal levels.
DESIGN: An observational, cross-sectional study.
SETTING: Primary health care centers under care of the National Sleeping Sickness Control Program in southeast Uganda.
PARTICIPANTS: Fifty-two male patients with sleeping sickness at different stages of treatment and 11 clinically healthy male volunteers recruited from health care personnel.
INTERVENTIONS: Patients and controls were questioned about loss of libido and impotence. All received 100 micrograms GnRH i.v. Blood was drawn before and 30 minutes after GnRH administration.
MAIN OUTCOME MEASURES: Frequency of loss of libido and impotence. Baseline T and sex hormone-binding globulin baseline and GnRH- stimulated serum LH and FSH concentrations.
RESULTS: Loss of libido and/or impotence were present in 39% of men with active disease before therapy, whereas 84% were biochemically hypogonadal. After cure, 45% of men still were symptomatic and 45% were biochemically hypogonadal. Compared with controls (806 +/- 59 pg/mL [conversion factor to SI unit, 0.03467]; mean +/- SEM), T concentrations were decreased substantially in patients before (249 +/- 48 ng/dL), during treatment (429 +/- 56 ng/dL), and after cure (431 +/- 58 ng/dL). Corresponding baseline LH concentrations were inappropriately low and the relative LH response to GnRH was reduced both before and during treatment (794% +/- 131% versus 322% +/- 68%). Follicle-stimulating hormone concentrations increased gradually up to 8.0 +/- 1.3 mIU/mL (conversion factor to SI unit, 1.00) at the end of treatment, returning to 4.2 +/- 0.6 mIU/mL after cure.
CONCLUSIONS: Rhodesian sleeping sickness causes acute and chronic HPG axis dysfunction. The clinical and biochemical picture suggest a combined central and peripheral hypogonadism. This is only in part reversible after cure and most likely due to direct parasitic infiltration and/or secondary inflammation causing necrosis and/or fibrosis at the pituitary and gonadal levels.