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Evaluation of semen variables, sperm chromosomal abnormalities and reproductive endocrine profile in patients with chronic hepatitis C
Author(s) -
Safarinejad Mohammad Reza,
Kolahi Ali Asghar,
Iravani Shahrokh
Publication year - 2010
Publication title -
bju international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 1464-4096
DOI - 10.1111/j.1464-410x.2009.08720.x
Subject(s) - endocrinology , medicine , luteinizing hormone , testosterone (patch) , semen quality , follicle stimulating hormone , semen , endocrine system , hormone , biology , andrology
Study Type – Aetiology (case series)
Level of Evidence 4 OBJECTIVE To evaluate reproductive endocrine profile, sperm chromosomal abnormalities, and semen quality in patients with chronic hepatitis C. PATIENTS, SUBJECTS AND METHODS In all, 82 patients with chronic hepatitis C, aged 18–60 years, were recruited for the study; 76 age‐matched healthy male volunteers served as controls. All participants provided a medical history and had a complete physical examination and routine semen analysis. Two blood samples were drawn from each participant at 15‐min intervals to determine the resting levels of luteinizing‐hormone (LH), follicle‐stimulating hormone (FSH), prolactin, testosterone, oestradiol, and sex hormone‐binding globulin. The hypothalamus‐pituitary‐testis axis was assessed using the gonadotrophin‐releasing hormone (GnRH) test. All participants also received an injection of human chorionic gonadotrophin (hCG) and serum testosterone was determined before the hCG injection and on the third day afterwards. Conventional karyotype analysis and triple‐colour fluorescence in situ hybridization for chromosomes X, Y and 18 were conducted in all patients and controls. RESULTS The mean basal serum levels for LH, FSH, and testosterone in patients with hepatitis C was significantly lower than the mean for normal controls ( P = 0.01). The injection of GnRH analogue did not yield significantly higher FSH and LH levels in the patients than in normal controls ( P = 0.001). In patients with chronic hepatitis C, the mean total sperm count, motility and normal morphology was significantly lower than in controls ( P = 0.001). There was a significantly greater frequency of disomy in men with chronic hepatitis C than controls for chromosomes 18, X, and Y ( P = 0.01). CONCLUSIONS Patients with chronic hepatitis C are at risk of showing sperm chromosomal abnormalities, the incidence of which is higher in patients with more advanced disease. Hypogonadotrophic hypogonadism is caused by the selective loss of pituitary gonadotrophin function. Further studies are needed to replicate our results.