Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 7 patients with end stage renal failure, anterior pituitary function was tested by simultaneous application of maximally effective doses of the hypothalamic releasing peptides, corticotropin-releasing hormone, growth hormone-releasing hormone, thyrotropin-releasing hormone and gonadotropin-releasing hormone, and compared to 8 normal controls. In addition to the pituitary hormones, plasma cortisol, thyroxine and testosterone concentrations were measured. To test for possible effects of treatment with recombinant human erythropoietin (rhu-EPO), all patients with chronic renal failure were studied again after partial correction of anemia by treatment with erythropoietin. Before initiation of rhu-EPO treatment, plasma concentrations of follicle-stimulating hormone were significantly elevated and the thyroid-stimulating hormone and prolactin responses to thyrotropin-releasing hormone blunted when compared to normal controls. Treatment with rhu-EPO induced a significant increase in plasma ACTH and follicle-stimulating hormone concentrations. All other pituitary functions remained unchanged. Thus, the general improvement in well-being, working capacity and sexual activity cannot be attributed to hormonal changes.
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PMID:Effect of recombinant human erythropoietin on anterior pituitary function in patients on chronic hemodialysis. 166 42

In five hemodialyzed patients the influence of erythropoietin (EPO) treatment for 3 months on function of the pituitary-adrenal feedback and STH secretion was studied. Results were compared with those obtained in 6 hemodialyzed patients (No-EPO group) showing a comparable Hb concentration and Hct value as patients in the EPO group post-treatment and in 15 healthy subjects. EPO treatment was followed by a significant (ACTH and STH) or moderate (cortisol) suppression of basal plasma levels of ACTH, STH and cortisol respectively, and by a significant reduction of the response of plasma concentrations of these hormones to insulin-induced hypoglycemia. As the response of plasma levels of ACTH, STH and cortisol respectively in patients of the EPO group post-treatment differed markedly from that of the No-EPO group with similar Hb and Hct values, it seems that the EPO-induced endocrine alterations are not, at least not exclusively, a consequence of the improvement of anemia. Results presented in this study suggest that EPO treatment influences directly or indirectly the function of endocrine organs.
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PMID:Influence of erythropoietin treatment on function of the pituitary-adrenal axis and somatotropin secretion in hemodialyzed patients. 216 62

The anaemia, leucopenia, thrombocytopenia and impaired DNA and RNA synthesis in the bone marrow of hypophysectomized rats could be restored by syngeneic pituitary grafts placed under the kidney capsule, or by treatments with ovine or bovine prolactin or growth hormone. Treatment with ACTH, FSH, LH and TSH had no effect in this respect. These results indicate that bone marrow function is regulated by the pituitary gland.
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PMID:Pituitary dependence of bone marrow function. 246 58

Data presented in this study suggest existence of hyperendorphinism in uraemic patients. This hyperendorphinism may be regarded both as a primary beneficial compensatory mechanism counteracting disturbances of the internal environment, while causing secondary harmful side effects, which contribute to the uraemic state. Erythropoietin treatment of uraemic, haemodialyzed patients is followed by marked endocrine alterations (suppression of plasma levels of STH, ACTH, prolactin, glucagon, aldosterone, cortisol and plasma renin activity, elevation of plasma insulin and atrial natriuretic levels, lack of influence on plasma PTH, CT and AVP). It remains to be clarified whether the erythropoietin induced endocrine alterations are due to correction of the existing anaemia or reflect a specific effect of this hormone.
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PMID:Endocrine abnormalities in patients with endstage renal failure. 256 Mar 46

High doses of oestradiol (150 micrograms/kg) or an oestradiol/progesterone combination (150 micrograms/kg oestradiol plus 6.25 mg/kg progesterone) were administered subcutaneously on alternate days to immature ovariectomised and mature intact female Beagle dogs for 13 weeks. The effects of hormonal treatment on different parameters were studied. The results revealed severe anaemia (mainly at week 3) and the blood films showed morphological indication of blood loss and abnormal erythrogenesis. Neutrophil leucocytosis and non-progressive thrombocytopenia were also observed. Treatment with oestradiol alone induced changes in the endometrial stroma and myometrium, whereas treatment with the oestradiol/progesterone combination induced cystic endometrial hyperplasia. The pituitary glands of the dogs treated with oestradiol alone had a slight increase in the number of ACTH cells. These cells and STH cells showed cytological changes indicative of accelerated secretory activity; the PRL and gonadotropin-producing cells were not affected significantly. The oestradiol/progesterone combination increased the number of ACTH and PRL cells. These cells as well as STH cells exhibited several cytological criteria typical of a pituitary cell with accelerated activity; the gondadotropin-producing cells showed involutionary changes. The mammary glands of oestradiol-treated dogs showed stromal and ductal cell proliferation; whereas the oestradiol/progesterone combination induced secretory epithelial cell proliferation in addition to stromal and ductal cell proliferation.
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PMID:Thirteen-weeks subcutaneous treatment with oestradiol or an oestradiol/progesterone combination in beagle bitches. 279 8

A male patient with corticotropin-releasing factor (CRF) and adrenocorticotropin (ACTH)-producing syndrome is described. Soon after being referred to us the patient developed pneumonia, anaemia, oedema and respiratory distress, and died on the 24th day after admission. Autopsy and histology revealed that he had a rare type of multiple endocrine neoplasia (type 1 + paraganglioma) with a mediastinal paraganglioma, parathyroidal hyperplasia, pancreatic islet cell adenoma, duodenal multiple carcinoid tumours and adrenocortical nodular hyperplasia. It was not possible to examine the pituitary. The paraganglioma contained a large amount of immunoreactive (IR)-CRF (606 ng/g wet weight), IR-ACTH (59.4 ng/g wet weight), IR-human proopiomelanocortin n-terminal (1-76) peptide (hNT, 156.8 ng/g wet weight) and IR-beta-lipotropin (beta-LPH, 146.9 ng/g wet weight). The major IR-ACTH, beta-LPH and IR-hNT were eluted at ACTH-(1-39), beta-LPH and hNT marker positions, respectively. Big ACTH was not detected. IR-CRF eluted at the human CRF marker position on Sephadex G-75 chromatography and high performance liquid chromatography (HPLC). The IR-CRF fraction from the HPLC showed CRF bioactivity which paralleled that of synthetic human CRF in monolayer cultured rat anterior pituitary cells. Our results suggest that not only ACTH but CRF produced by the paraganglioma was responsible for the patient's Cushing's syndrome.
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PMID:Multiple endocrine neoplasia with Cushing's syndrome due to paraganglioma producing corticotropin-releasing factor and adrenocorticotropin. 287 33

The most common cause of hypoadrenocorticism in dogs is idiopathic immune-mediated destruction of the adrenal cortex. Other causes include anterior pituitary insufficiency, pituitary or adrenal neoplasia, acute withdrawal of exogenous corticosteroids, and mitotane toxicity. Females are affected more often than males; only 1 feline case has been documented. Animals 2-5 years old are most commonly affected. Clinical signs include lethargy, weakness, weight loss, anorexia, vomiting, diarrhea and bradycardia. Hematologic and biochemical changes can include eosinophilia, lymphocytosis, anemia, hyperkalemia, hyponatremia and hypercalcemia. Diagnosis is by finding negligible resting levels of plasma cortisol and no response to ACTH administration, and a serum Na:K ratio of 20:1 or less. Treatment involves restoring fluid volume, correcting acidosis, and supplementing salt and glucocorticoids. Daily oral use of prednisone at 0.05 mg/kg can safely maintain most affected dogs. Some dogs only require glucocorticoids in stressful situations. Iatrogenic secondary adrenocortical insufficiency (iatrogenic Cushing's disease) may result from a single injection of long-acting glucocorticoids or from long-term use. Clinical signs are the same as for natural hyperadrenocorticism, but endogenous cortisol release is suppressed. Treatment is gradual withdrawal of the offending glucocorticoid and elimination of the cause that initially prompted glucocorticoid therapy.
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PMID:Diseases of the adrenal cortex of dogs and cats. 674 17

We report the case of a 35-year-old patient who presented with acute adrenal insufficiency, then developed fever, hypoalbuminuria, anasarca, thrombocytopaenia and anaemia. Lymphadenopathy appeared later with microscopic features typical of Castleman's disease. Clinical remission followed treatment with intravenous immunoglobulin. Circulating interleukin-6 levels were elevated initially but were normal after immunoglobulin therapy. We surmise that high circulating levels of interleukin-6 (and ACTH) may have induced haemorrhagic necrosis of the adrenal glands and accounted for the constitutional symptoms.
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PMID:Acute adrenal insufficiency: a new presentation of Castleman's disease. 760 51

Endocrine abnormalities in chronic hemodialysis patients are in part corrected by control of anemia with recombinant human erythropoietin (rHu-EPO). We further examined the role of rHu-EPO in select hormonal abnormalities thought to be anemia related as well as the GH-insulin-like growth factor 1 (GH-IGF-1) axis that is abnormal in hemodialysis patients. We studied responses to the administration of two hypothalamic hormones, GHRH and ovine corticotropin-releasing hormone (CRH), in five anemic male patients on chronic hemodialysis before and after correction of the anemia with rHu-EPO. For comparison, five age-matched normal male volunteers were tested once. Anemic patients on chronic hemodialysis had high basal GH concentrations, an exaggerated GH response to exogenous GHRH, increased levels of IGF-1, and elevated levels of IGF-1 binding protein-3 in comparison to controls. ACTH response to CRH was comparable in dialysis patients and normal controls, but the cortisol response to endogenous ACTH release was prolonged. The cortisol binding globulin was similar to the controls. After correction of anemia, the basal elevation of GH was no longer present, but the exaggerated response of GH to exogenous GHRH persisted. IGF-1 and IGF-1 binding protein-3 levels remained elevated. The ACTH response to CRH, which was normal before correction of the anemia, became exaggerated in terms of elevated levels. Nevertheless, the prolonged cortisol response persisted. It appears that correction of the anemia in hemodialysis patients with rHu-EPO can partly correct perturbations in the GH secretory axis but may lead to new abnormalities in the CRH-ACTH axis.
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PMID:The effects of corticotropin and growth hormone releasing hormones on their respective secretory axes in chronic hemodialysis patients before and after correction of anemia with recombinant human erythropoietin. 828 16

A 64-year-old female referred to our hospital because of severe anemia. Peripheral blood examination showed macrocytic anemia; red blood cell count was 1.49 x 10(6)/microliters, hemoglobin concentration was 5.6 g/dl, hematocrit was 16.1% and MCV was 108 fl. Serum VB 12 level was significantly low as 58 pg/ml. Upper gastrointestinal examination disclosed chronic atrophic gastritis. Anti-intrinsic factor and anti-parietal cell antibodies were detected in the serum and Schilling's test was positive. Thus a diagnosis of pernicious anemia was made. Though the serum free T 3 and free T 4 levels were in normal ranges, the elevated serum TSH and positive tests for anti-microsome and anti-thyroglobulin antibodies indicated that the patient had chronic thyroiditis. Then other endocrinological examinations were performed. Low level of urinary 17-OHCS and a hypo-reactive pattern of rapid ACTH test led to a diagnosis of latent adrenal insufficiency. This case could be categorized into polyglandular autoimmune syndrome.
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PMID:[Pernicious anemia associated with chronic thyroiditis and suspected latent adrenal insufficiency]. 939 8


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