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Recent work shows a high prevalence of low testosterone and inappropriately low LH and FSH concentrations in type 2 diabetes. This syndrome of hypogonadotrophic hypogonadism (HH) is associated with obesity, and other features of the metabolic syndrome (obesity and overweight, hypertension and hyperlipidemia) in patients with type 2 diabetes. However, the duration of diabetes or HbA1c were not related to HH. Furthermore, recent data show that HH is also observed frequently in patients with the metabolic syndrome without diabetes but is not associated with type 1 diabetes. Thus, HH appears be related to the two major conditions associated with insulin resistance: type 2 diabetes and the metabolic syndrome. CRP concentrations have been shown to be elevated in patients with HH and are inversely related to plasma testosterone concentrations. This inverse relationship between plasma free testosterone and CRP concentrations in patients with type 2 diabetes suggests that inflammation may play an important role in the pathogenesis of this syndrome. This is of interest since inflammatory mechanisms may have a cardinal role in the pathogenesis of insulin resistance. It is relevant that in the mouse, deletion of the insulin receptor in neurons leads to HH in addition to a state of systemic insulin resistance. It has also been shown that insulin facilitates the secretion of gonadotrophin releasing hormone (GnRH) from neuronal cell cultures. Thus, HH may be the result of insulin resistance at the level of the GnRH secreting neuron. Low testosterone concentrations in type 2 diabetic men have also been related to a significantly lower hematocrit and thus to an increased frequency of mild anemia. Low testosterone concentrations are also related to an increase in total and regional adiposity, and to lower bone density. This review discusses these issues and attempts to make the syndrome relevant as a clinical entity. Clinical trials are required to determine whether testosterone replacement alleviates symptoms related to sexual dysfunction, and features of the metabolic syndrome, insulin resistance and inflammation.
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PMID:Hypogonadotrophic hypogonadism in type 2 diabetes, obesity and the metabolic syndrome. 1907 78

Endocrine dysfunction in Thalassaemia major (TM) is a common and disturbing complication, which requires prompt recognition and treatment. The contribution of the underlying molecular defect in TM to the development of endocrinopathies is significant because the patients with the more severe genetic defects have a greater rate of iron loading through higher red cell consumption. TM patients frequently present delay of growth and puberty with reduction of final height. The pathogenesis of growth failure is multifactorial and is mainly due to chronic anemia and hypoxia, chronic liver disease, zinc and folic acid deficiency, iron overload, intensive use of chelating agents, emotional factors, and endocrinopathies (hypogonadism, delayed puberty, hypothyroidism) and GH-IGF-1 axis dysregulation. Although appropriate iron chelation therapy can improve growth and development, TM children and adolescents treated intensively with desferrioxamine remain short as well, showing body disproportion between the upper and lower body segment. Body disproportion is independent of pubertal or prepubertal period of greater height gain. Treatment with recombinant GH (rhGH) is recommended when GH deficiency is established, and even so, the therapeutic response is often non satisfactory. Growth acceleration is mostly promoted with sex steroids in children with associated pubertal delay. Sexual complications in TM, which include Delayed Puberty, Arrested Puberty and Hypogonadism, present the commonest endocrine complication. Iron deposition on gonadotroph cells of the pituitary leads to disruption of gonadotrophin production which is proven by the poor response of FSH and LH to GnRH stimulation. In the majority of patients gonadal function is normal as most women with Amenorrhea are capable of achieving pregnancy with hormonal treatment and similarly men with azoospermia become fathers. Secondary Hypogonadism appears later in life, and is manifested in women as Secondary Amenorrhea and in men as decline in sexual drive and azzoospermia. The damage to the hypothalamus and pituitary is progressive, even when intensive chelating therapy is given and the appearance of Hypogonadism in both sexes is often unavoidable. Close follow up and proper management is crucial for every patient with TM. Early recognition of growth disturbance and prevention of hypogonadism by early and judicious chelation therapy is mandatory for the improvement of their quality of life. Patients with TM can now live a better life due to modern advances in their medical care and our better understanding in the pathogenesis, manifestation and prevention of endocrine complications.
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PMID:Thalassaemia and aberrations of growth and puberty. 2141 85

Studies over the last few years have clearly established that at least 25% of men with type 2 diabetes have subnormal free testosterone concentrations in association with inappropriately low LH and FSH concentrations. Another 4% have subnormal testosterone concentrations with elevated LH and FSH concentrations. The Endocrine Society, therefore, now recommends the measurement of testosterone in patients with type 2 diabetes on a routine basis. The subnormal testosterone concentrations are not related to glycosylated hemoglobin or duration of diabetes, but are associated with obesity, very high C-reactive protein concentrations, and mild anemia. In addition, subnormal testosterone concentrations in these men are associated with a two to three times elevated risk of cardiovascular events and death in two early studies. Short-term studies of testosterone therapy in hypogonadal men with type 2 diabetes have demonstrated an increase in insulin sensitivity and a decrease in waist circumference. However, the data on the effect of testosterone replacement on glycemic control and cardiovascular risk factors such as cholesterol and C-reactive protein concentrations are inconsistent. As far as sexual function is concerned, testosterone treatment increases libido but does not improve erectile dysfunction and thus, phosphodiesterase inhibitors may be required. Trials of a longer duration are clearly required to definitively establish the benefits and risks of testosterone replacement in patients with type 2 diabetes and low testosterone.
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PMID:Update: Hypogonadotropic hypogonadism in type 2 diabetes and obesity. 2189 95

Hypogonadism may affect as much as 70% of the patients with chronic renal failure (CRF) in comparison with general population. Physiopathologically, it is a hypergonadotropic hypogonadism, with alterations in the pulsatile production of GnRH, FSH, LH and testicular testosterone, that is a general disorder of the hypothalamic-hypophysis-testicular axis. This disorder may determine important consequences in this population of patients, with varied sexual dysfunction, trophic and functional muscular and fatty tissue disorders, bone demineralization, anemia and increase of cardiovascular disease associated mortality.Treatment in these patients must be focused from a general point of view, increasing their clinical condition, the systemic complications associated with CRF, complementing in this way with exogenous testosterone replacement therapy. If possible, it seems that the most efficacious therapy will be renal transplantation.
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PMID:[Testosterone deficit syndrome in the chronic renal failure patient]. 2404 30


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