Loss of Pulsatile Luteinising Hormone Secretion in Men With Chronic Renal Failure

Rodger, R. S. C.; Morrison, L.; Dewar, J.; Wilkinson, Robert W.; Ward, M. K.; Kerr, David

doi:10.1016/s0022-5347(17)45262-1

Cited by 12 publications

(18 citation statements)

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“…The endocrinology is not yet clear but there is clearly hypothalamic±pituitary involvement since prolactin and LH concentrations are both elevated and the pattern of LH secretion is changed with fewer peaks. 86,87 These effects are reversed by transplantation.…”

Section: Chronic Renal Failure and Hepatic Cirrhosismentioning

confidence: 99%

Endocrinology of gynaecomastia

Ismail¹,

Barth²

2001

Ann Clin Biochem

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Gynaecomastia is the most common disorder of the male breast. It can occur at any age, and for this reason laboratory investigations may be requested by clinicians from many specialties. Gynaecomastia may occur transiently in neonates. It may also occur transiently during puberty, when it is common and generally benign. It must, however, be regarded as unusual in prepubertal children and all young and middle-aged men. Although iatrogenic and benign gynaecomastia are common in the elderly, further investigations may still be justi®ed since breast cancer or other neoplasm must be ruled out. Biochemical investigations, when warranted, are aimed at establishing an underlying cause. Endocrine investigations might include serum oestradiol (or oestrone if available), testosterone, luteinizing hormone, sex-hormone-binding globulin, human chorionic gonadotrophin, prolactin and thyroid function tests. In this review, the source and role of oestrogens in men, the androgen±oestrogen dynamics, the causes and clinical entities of gynaecomastia, and interpretation of laboratory tests are described.

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Section: Chronic Renal Failure and Hepatic Cirrhosismentioning

confidence: 99%

Endocrinology of gynaecomastia

Ismail¹,

Barth²

2001

Ann Clin Biochem

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Section: Introductionmentioning

confidence: 99%

“…Little is known of LH pulsatility in uraemia but two recent studies on I-LH pulsatility have indicated that it is reduced [10] or absent [11]. After renal transplantation l-LH pulsatility returned to normal [11]. Following these reports of abnor mal pulsatility of l-LH and of increased basal levels of B-LH we have now investigated the mode of secretion of B-LH and l-LH in patients with end-stage renal failure treated by dialysis and in patients having undergone successful renal transplantation.…”

Section: Introductionmentioning

confidence: 99%

Pulsatile Bioactive Luteinizing Hormone Secretion in Men with Chronic Renal Failure and following Renal Transplantation

Talbot

Rodger

Robertson

1990

Nephron

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We have measured plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (To) by radioimmunoassay (RIA) and bioactive LH (B-LH) by in vitro bioassay at 10-min intervals over 6 h in men treated by haemodialysis for renal failure and in men after renal transplantation. Eleven normal male volunteers acted as controls. Immunoreactive LH (I-LH) and FSH levels were elevated (p < 0.03) in uraemia (mean ± SE; 10.0 ± 1.0 and 4.6 ± 0.7 IU/l for LH and FSH, respectively) and following renal transplantation (8.1 ± 1.2 and 5.3 ± 0.5 IU/l) compared to controls (C) (4.9 ± 0.5 and 2.7 ± 0.4 IU/l) whereas B-LH [17.3 ± 2.5, 14.8 ± 1.8 and 12.9 ± 1.3 IU/l in dialysis (D), transplant (T) and C groups, respectively] levels were normal. Prolactin levels were elevated (p < 0.03) in the D group (median 348, range 162–1,780 mU/l) compared to the T group (161, 91–206 mU/l) and controls (163, 124–312 mU/l) whereas total To levels (mean ± SE; 17.3 ± 4.8,15.5 ± 1.3 and 19.6 ± 2.1 nmol/l in the D, T and C groups, respectively) were similar as was the free To index. B-LH (median frequency, 2 and range 1–3 pulses/6 h) and I-LH (median frequency, 2 and range 1–2 pulses/6 h) was pulsatile in all the C group but B- and I-LH pulses were absent in 2 of the 5 subjects treated by dialysis. Following renal transplantation B-LH pulses were detected in all subjects, whilst I-LH pulses were absent in 1 subject. I-LH pulse frequency (median 1, range 0–1 pulse/6 h) was reduced (p < 0.03) in the D and T groups. B-LH pulse frequency was normal in the D group (median 1, range 0–2 pulses/6 h) but reduced in the T group (1,1–2 pulses/6 h). B :I LH ratios were decreased (p < 0.03) in the D and T groups (median and range; 1.7,1.27–2.46 and 2.05,1.52–2.88, respectively, compared to normal controls – (2.49, 2.04–3.49). The mean B:I LH ratio was correlated with mean To levels in the D group only (r = 0.93, p < 0.01). In conclusion, LH pulsatility is abnormal in uraemia and renal transplantation only partially reverses this condition.

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“…LH and FSH levels are virtually always elevated in uraemic men (Holdsworth et al, 1977). A primarily hypothalmo-pituitary problem has been advocated -after finding abnormal LH pulsatility in patients with renal failure compared to normal controls and to renal transplant patients (Rodger et al, 1985). Elevated oestradiol levels were found in the dialysis group, and it has been suggested that increased oestradiol, hyperprolactinaemia, chronic disease or malnutrition may have a role in producing an abnormality of the LH pulse generator.…”

Section: Renal Diseasementioning

confidence: 99%