Androgens and Erythropoiesis

Shahidi, Nasrollah T.

doi:10.1056/nejm197307122890205

Cited by 279 publications

(140 citation statements)

References 87 publications

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“…Received for publication 24 June 1975 and in revised form 18 August 1975. steroids and other steroids with a 5f-H configuration increase red cell production both in vivo and in vitro by direct and indirect mechanisms (4). Androgenic steroids appear to stimulate granulopoiesis as well (5,6).…”

Section: Introductionmentioning

confidence: 99%

“…The degree of augmentation at maximal stimulating levels of erythropoietin was comparable to the results obtained with murine tissues. DISCUSSION Although the 5,8-H steroids are known stimulators of red cell production (4,17), the relationship of glucocorticosteroids to erythropoiesis is uncertain. Addison's disease in man is associated with normocytic, normochromic anemia (18), and a congenital erythroid hy- poplasia of children (Diamond-Blackfan syndrome) is frequently responsive to low doses of glucocorticoids (19).…”

Section: Introductionmentioning

confidence: 99%

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Potentiation of erythropoiesis in vitro by dexamethasone.

Golde¹,

Bersch²,

Cline³

1976

J. Clin. Invest.

141

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A B S T R A C T The effect of dexamethasone on erythropoiesis was examined in vitro. Hematopoietic cells from 13-day mouse fetal livers were cultured for 48 h in the presence or absence of erythropoietin and erythroid colonies enumerated. Colony formation occurring in cultures containing no added erythropoietin was inhibited by the incorporation of antierythropoietin antibody, suggesting that these colonies formed in response to endogenous hepatic erythropoietin. Maximal colony formation was observed with 0.5 U/ml of sheep erythropoietin. Dexamethasone increased erythroid colony formation with peak stimulation at 10-M. Dexamethasone potentiation was most marked in cultures containing less than maximally stimulating concentrations of erythropoietin. The cells required only a brief exposure to glucocorticosteroid to exhibit the augmented cloning capacity, and dexamethasone stimulation was inhibited by progesterone (10 M). A comparable response to dexamethasone was observed in cultures of adult murine and human bone marrow erythroid progenitors, implying that the phenomenon is not peculiar to fetal cells and is not dependent on the presence of fetal hepatocytes. These data suggest that erythroid progenitor cells possess a glucocorticoid receptor mechanism that can modulate the response to erythropoietin in vitro.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Potentiation of erythropoiesis in vitro by dexamethasone.

Golde¹,

Bersch²,

Cline³

1976

J. Clin. Invest.

141

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“…Testosterone is known to exert a stimulatory effect on erythropoiesis in the bone marrow (3). Inflammation, on the other hand, is known to suppress erythropoiesis, partly through its direct action on erythropoiesis and partly through its suppression of erythropoietin secretion (4 -7).…”

mentioning

confidence: 99%

Low Testosterone and High C-Reactive Protein Concentrations Predict Low Hematocrit in Type 2 Diabetes

et al. 2006

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OBJECTIVE -After the demonstration that one-third of male patients with type 2 diabetes have hypogonadotrophic hypogonadism, we have shown that patients with hypogonadotrophic hypogonadism also have markedly elevated C-reactive protein (CRP) concentrations. We have now hypothesized that type 2 diabetic subjects with hypogonadotrophic hypogonadism may have a lower hematocrit because testosterone stimulates, whereas chronic inflammation suppresses, erythropoiesis.RESEARCH DESIGN AND METHODS -Seventy patients with type 2 diabetes at a tertiary referral center were included in this study.RESULTS -The mean hematocrit in patients with hypogonadotrophic hypogonadism (n ϭ 37), defined as calculated free testosterone (cFT) of Ͻ6.5 ng/dl, was 40.6 Ϯ 1.1%, whereas that in eugonadal patients (n ϭ 33) was 43.3 Ϯ 0.7% (P ϭ 0.011). The hematocrit was related to cFT concentration (r ϭ 0.46; P Ͻ 0.0001); it was inversely related to plasma CRP concentration (r ϭ 0.41; P Ͻ 0.0004). Patients with CRP Ͻ3 mg/l had a higher hematocrit (42.7 Ϯ 0.7%) than those with CRP Ͼ3 mg/l (39.9 Ϯ 1.1%; P Ͻ 0.05). The prevalence of normocytic normochromic anemia (hemoglobin Ͻ13 g/dl) was 23% in the entire group, whereas it was 37.8% in the men with hypogonadotrophic hypogonadism and 3% in the eugonadal men (P Ͻ 0.01). Erythropoietin concentration was elevated or high normal in all 11 patients with anemia in whom it was tested.CONCLUSIONS -We conclude that hypogonadotrophic hypogonadism in male type 2 diabetic subjects is associated with a lower hematocrit and a frequent occurrence of mild normocytic normochromic anemia with normal or high erythropoietin concentrations. In these patients, hematocrit is also inversely related to CRP concentration. Thus, low testosterone and chronic inflammatory mechanisms may contribute to mild anemia. Such patients may also have a high risk of atherosclerotic cardiovascular events in view of their markedly elevated CRP concentrations. Diabetes Care 29:2289 -2294, 2006A fter our previous observations that one-third of patients with type 2 diabetes have hypogonadotrophic hypogonadism (1), that type 1 diabetic subjects do not suffer from this condition (2), and that the patients with hypogonadotrophic hypogonadism have markedly elevated plasma C-reactive protein (CRP) concentrations (V.B., R.T., S.D., A. Chandel, A.C., H.G., P.D., unpublished observ a t i o n s ) , a n i n d e x o f s y s t e m i c inflammation, we have now studied whether patients with hypogonadotrophic hypogonadism have lower hemoglobin concentrations. Testosterone is known to exert a stimulatory effect on erythropoiesis in the bone marrow (3). Inflammation, on the other hand, is known to suppress erythropoiesis, partly through its direct action on erythropoiesis and partly through its suppression of erythropoietin secretion (4 -7). Thus, we hypothesized that hematocrit in patients with type 2 diabetes is lower in patients with hypogonadotrophic hypogonadism who also have an elevated CRP concentration, an index of systemic inflammation. RESEARCH DESI...

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“…This physiologic augmentation of red blood cells is not universal, but has been reported in 2-44% of men receiving TRT, depending on the dosage and route of administration [15]. The underlying etiology of erythrocytosis is the anabolic ability of testosterone to target erythroblast in bone marrow [16], as well as its physiologic potentiation of erythropoietin [17]. The ability of testosterone to induce erythropoietin has also been reported in anephric patients, demonstrating an extrarenal capability [18].…”

Section: Erythrocytosismentioning

confidence: 92%

Therapeutic Dilemmas for Androgen Deficiency in Aging Males

Salazar¹,

Tan

2005

Aging Health

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Androgen decline with aging typically occurs after 50 years, although the fall in testosterone levels can begin as early as 30 years of age. The patient may or may not be symptomatic. Symptoms can range from fatigue to sexual dysfunction. Long-term effects of lowered testosterone can be seen in organ systems including the brain, muscle, adipose tissue, hair, bone, and the cardiovascular system. There is no consensus for androgen replacement as prevention, but there is consensus in the treatment and reversal of symptoms associated with hypogonadism. However, treatment must be carefully monitored. While there are significant benefits in the improvement of symptoms, there are also possible side effects that will be discussed in detail in this article. A careful risk–benefit analysis has to be carried out and treatment must be individualized.

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Androgens and Erythropoiesis

Cited by 279 publications

References 87 publications

Potentiation of erythropoiesis in vitro by dexamethasone.

Potentiation of erythropoiesis in vitro by dexamethasone.

Low Testosterone and High C-Reactive Protein Concentrations Predict Low Hematocrit in Type 2 Diabetes

Therapeutic Dilemmas for Androgen Deficiency in Aging Males

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