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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension is one of the most important accelerating factors for progression of nephropathies. Its prevalence is about 35% in patients with nephropathies, even in minor or medium severe functional impairment. This is evidence that it is essential to select an optimal therapeutic regimen as soon as possible. A group of 38 patients (14 hypertensive patients) with a minor or medium severe functional impairment were included in a controlled trial. The patients were served a low-protein diet--0.6-0.7 g/kg/day and 2-10mg enalapril/day divided into two doses. The amount of enalapril depended on the blood pressure and enalapril was given also to normotensive patients. The investigation lasted 8 months. In the course of 8 months the authors did not reveal progression of the renal disease, as apparent from results of assessment of the creatinine level and clearance, assessment of uric acid and urea. The authors did not find deterioration of metabolic acidosis, nor of nephrogenic anaemia. Hypertensive patients had a tendency to deteriorating of insulin sensitivity while in normotensive patients a decline of triacylglycerols, VLDL and rise of HDL was recorded. The total cholesterol and LDL cholesterol level did not change. The authors conclude that the combination of a low-protein diet with ACEI in hypertensive and normotensive patients with mild to medium severe functional disorders inhibits the progression of nephropathies, but in hypertensive patients it does not prevent deterioration of insulin sensitivity.
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PMID:[A protein-restricted diet combined with ACE inhibitors does not improve insulin sensitivity in renal hypertension]. 868 2

In Saudi Arabia, pediatricians compared data on infants of 52 mothers who received insulin therapy during pregnancy (group A) with data on infants of 81 mothers who either did not receive insulin therapy during pregnancy or prenatal care (group B) to evaluate the outcome in infants of diabetic mothers (IDMs) managed at Qatif Central Hospital. These 133 IDMs comprised 1.14% of the 11,677 deliveries at this hospital during 1988-92. 19.7% of all mothers had gestational diabetes mellitus. Mothers in group A were younger than those in group B (31.5 vs. 35.1 years; p 0.01). They were less likely than those in group B to suffer fetal loss (23.1% vs. 53.1%; p 0.001 and [mean fetal loss] 0.62 vs. 1.33; p 0.05). All six stillbirths (2 in group A and 4 in group B) were large for gestational age (LGA) (4.543 vs. 3.753 kg for overall birth weight; p 0.001). One stillbirth was macerated and had multiple congenital anomalies including Down's syndrome. Two liveborn IDMs also had Down's syndrome. There were no early neonatal deaths. The perinatal mortality rate (PMR) was not significantly different between the groups, but the PMR for both groups was higher than it was for the same period for the hospital overall (45.1 vs. 16.6/1000; p 0.02). 57.9% of IDMs from both groups were LGA. 38.6% of all IDMs had a blood glucose level less than 30 mg/dl. Other problems identified in IDMs included bacterial infections, birth trauma, preterm delivery, respiratory distress, polycythemia, and anemia. These findings suggest that poor maternal diabetic control contributed to the high perinatal morbidity and mortality in IDMs. Health education and improved care of diabetic pregnant women are seriously needed.
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PMID:Perinatal morbidity and mortality in offspring of diabetic mothers in Qatif, Saudi Arabia. 873 Jun 18

The effects of recombinant human erythropoietin (rHuEPO) on the glucose metabolism were evaluated by intravenous glucose tolerance test in 20 maintenance hemodialysis patients. In 8 cases the glucose tolerance tests were performed before and after a single intravenous injection of 50 IU/kg of rHuEPO and in 12 cases before and after 3 months of rHuEPO therapy at doses of 50 IU/kg three times/week and 2 weeks after rHuEPO withdrawal. For each test glucose, immunoreactive insulin (IRI) and C peptide (C-p) plasma values were measured, and glucose constant decay, whole IRI (area IRI) and C-p area C-p) production, insulinogenic index, and insulin resistance index were calculated. After 3 months of rHuEPO therapy, the glucose constant decay increased significantly, area IRI, area C-p, and insulin resistance index decreased significantly, and the insulinogenic index did not change. No correlations were found between changes in hemoglobin values and changes in glucose metabolism parameters. Acute rHuEPO administration and rHuEPO withdrawal had no effect on glucose metabolism, despite significant changes in plasma erythropoietin levels. Long-term rHuEPO therapy improves glucose metabolism in maintenance hemodialysis patients significantly, mainly by reduction of insulin resistance. Neither anemia correction nor a direct effect of rHuEPO on some metabolic steps seem to be responsible of these effects.
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PMID:Early and late effects of erythropoietin on glucose metabolism in maintenance hemodialysis patients. 873 83

A rare case of severe acute hepatitis A complicated by pure red cell aplasia (PRCA) is reported. A 60-year-old man with jaundice and hepatomegaly was diagnosed as having acute hepatitis A by positive IgM anti-hepatitis A antibody (anti-HAV). Severe anemia rapidly developed 3 weeks after admission, and the patient was diagnosed with PRCA by both bone marrow smears and erythrocyte survival study. The anemia was transient and bone marrow recovered within 1 week. However, concomitant with bone marrow recovery, the hepatitis worsened. He became drowsy and disoriented and severe jaundice, ascites, prolonged prothrombin time, increased transaminase levels, and abnormal electroencephalogram (EEG) were exhibited. Plasma exchange transfusion and glucagon-insulin (GI) therapy improved the consciousness level, but bilirubin, transaminase levels, and IgM anti-HAV titer remained high. Intravenous administration of lipophilized prostaglandin E1 (lipo-PGE1) was added to the GI therapy. Bilirubin and transaminase levels were normalized in the 8th week after the initiation of this combination therapy (17 weeks after admission). The combined use of lipo-PGE1 with plasma exchange and GI therapy appeared to be useful for the prolonged severe hepatitis in this patient.
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PMID:Severe acute hepatitis A associated with acute pure red cell aplasia. 884 89

Malignant otitis externa is a necrotising infection of the external ear canal which may spread to include the mastoid and petrous parts of the temporal bone, leading to skull base osteomyelitis. It is almost exclusively caused by infection with Pseudomonas aeruginosa, and usually occurs in elderly non-insulin-dependent diabetic patients. However isolated cases have been reported in a small number of non-diabetic patients, particularly in children who are immunocompromised due to malignancy, malnutrition and severe anaemia. In 1984 a case of malignant otitis externa was reported in a child with an acquired immunodeficiency syndrome (AIDS)-like illness, prior to identification of the human immunodeficiency virus (HIV). Since that time further sporadic cases of this invasive infection have been reported in HIV and AIDS. We present two further cases and also a review of the current literature.
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PMID:Malignant otitis externa in HIV and AIDS. 886 14

The thiazolidinediones improve insulin sensitivity in animal models and have promise as potent oral antidiabetic agents. Their clinical use has been limited because of the resulting anemia and cardiac hypertrophy. Some compounds of this class have been reported to induce bone marrow fat accumulation in animals, and this effect could account for the observed anemia. We examined the biological mechanism contributing to this phenomenon. The thiazolidinediones BRL49653 and pioglitazone induced adipocyte differentiation in the BMS2 bone marrow stromal cell line in a dose- and time-dependent manner. These actions were further enhanced by the presence of glucocorticoids and other adipogenic agonists. The thiazolidinediones increased the mRNA levels of adipocyte-specific genes, including that of their receptor, the peroxisome proliferator-activated receptor-gamma (PPAR gamma). In contrast, mRNA levels of genes encoding other PPAR family members (PPAR alpha, PPAR delta, or NUC-1) were unchanged or decreased. Thiazolidinedione treatment of primary bone marrow stromal cells elicited a comparable dose-dependent response. Using a polyclonal antibody, PPAR gamma was detected in protein lysates from adipose-rich bone marrow. Thus, thiazolidinedione directly regulates bone marrow stromal cell differentiation; induced PPAR gamma expression may play a key regulatory role in this process.
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PMID:Peroxisome proliferator-activated receptor-gamma activation by thiazolidinediones induces adipogenesis in bone marrow stromal cells. 891 39

Ten patients (18 +/- 1 yr) on chronic hemodialysis (HD) with anemia were studied before and after treatment with erythropoietin (EPO) for 9 mo. Six patients had evidence of iron overload (serum ferritin over 300 ng/ml; group I) and the other four patients (serum ferritin below 300 ng/ml; group II) did not. Before treatment, both groups of patients were glucose tolerant but insulin resistant and hyperinsulinemic. There was equal correction of anemia but no significant changes in serum biochemistry (apart from iron studies) or anthropometric measurements in both groups. With amelioration of anemia and iron overload in group I, insulin sensitivity increased by 53% to within normal values. Insulin secretion also normalized. With amelioration of anemia but no change in iron status in group II, insulin sensitivity (increased by 60%) and insulin secretion also normalized. Thus correction of anemia by EPO reversed insulin resistance and hyperinsulinemia in HD patients with or without iron overload. The effects of correction of anemia rather than iron overload may be more important in the pathogenesis of insulin abnormalities in end-stage renal disease.
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PMID:Correction of anemia by erythropoietin reverses insulin resistance and hyperinsulinemia in uremia. 892 46

We describe a 56-year-old woman suspected of Fanconi anemia on the basis of the following clinical findings: microcephaly, short stature, congenital deafness, and the clinical findings in her deceased brother. Hematologic or other signs of malignancy were absent. The diagnosis was confirmed by demonstrating hypersensitivity of her lymphocytes to mitomycin C (MMC). Cell fusion experiments indicated that the patient belongs to complementation group A. The patient's brother died at the age of 50 of heart and renal failure, and anemia. He had clinical findings similar to those of his sister, and a horseshoe kidney. From 31 years on he had thrombocytopenia and leucopenia. Both patients had insulin-dependent diabetes mellitus. A chromosomal breakage test carried out elsewhere before his death failed to demonstrate MMC hypersensitivity of his lymphocytes, which led to the investigation of his sister. To our knowledge these two cases are the oldest Fanconi anemia patients reported thus far.
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PMID:An atypical case of Fanconi anemia in elderly sibs. 902 73

The influence of gender on the prevalence of rheumatoid arthritis (RA) is well known. We examined 40 female patients with RA to show the possible influence of androgen hormones on inflammation and immune system. We measured blood count, blood sedimentation rate, C-reactive protein routinely and free and bound testosterone, dehydroepiandrosterone-sulfate (DHEA-S), prolactin, insulin like growth factor-1 (IGF), IgA-rheumatoid factor (IgA-RF) and the monocyte marker CD 14 of radioimmunoassays and enzymeimmunoassays. The female patients with RA had lower androgen levels correlating with higher inflammatory markers which are not rising significantly with higher age. The significantly raised IgA-RF with abnormal low testosterone levels points out a poor prognosis for developing joint erosions. The simultaneously reduced levels of prolactin may be rather caused by cytokines and could have additional connections to the anemia in RA. Somatomedin correlated inversely to the degree of inflammation, measured by BSR, CRP and CD 14, a fact which could indicate a reduced, Somatomedin-induced, synthesis in matrix and collagen of cartilage in "active" RA. The results point to the existence of a reciprocal connection of the endocrine system with the immune system.
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PMID:[Possible effect of hormones on immune and inflammatory processes in female patients with chronic polyarthritis]. 903 22

Interferon-gamma (IFN-gamma) has been shown to inhibit proliferation and differentiation of erythroid progenitor cells and to produce apoptosis of erythroid cells, but IFN-gamma receptors are not present on red cells and have never been demonstrated on erythroid progenitor cells. We obtained highly purified day 6 erythroid colony-forming cells (ECFCs) from human blood in sufficient quantity and purity to measure binding of radioiodinated recombinant human IFN-gamma ([125I]rhIFN-gamma). When [125I]rhIFN-gamma was incubated with day 6 ECFC, 77% of the binding was inhibited by excess unlabeled rhIFN-gamma, but no inhibition occurred with a variety of growth factors and glycoproteins. Specific binding was directly proportional to the cell concentration with a straight line passing through the origin, and equilibrium was reached at 0 degree C by 24-48 hours. Saturation of specific binding occurred at a [125I]rhIFN-gamma concentration of 1.0 nM and internalization was demonstrated with further incubation at 37 degrees C. Scatchard analysis showed a single class of binding sites and at a high ECFC cell purity of 80-89%, 1910-2070 binding sites per ECFC were present with a Kd of 0.01-0.02 nM. As day 5 ECFC developed into more mature day 7-day 12 cells, with incubation at 37 degrees C in vitro, specific binding for [125I]IFN-gamma greatly decreased. These experiments delineate specific binding sites for IFN-gamma on human erythroid progenitor cells and indicate that the enhanced sensitivity to rhIFN-gamma inhibition of mature day 3-day 6 burst-forming units-erythroid may be a result of enhanced specific binding. Human IFN-gamma is a multifunctional lymphokine, secreted by activated T lymphocytes and NK cells, which exerts antiviral, antiproliferative, and immunomodulatory activities on a wide variety of cells [1,2]. With regard to hematopoietic cells, IFN-gamma has been reported to inhibit the growth of granulocyte-macrophage colony-forming units, burst-forming units-erythroid (BFU-E) and colony-forming units-erythroid (CFU-E) in vitro [3-7]. Most recently, mature day 3 to day 6 BFU-E have been shown to be most sensitive to the inhibitory effect of recombinant human (rh) IFN-gamma, while primitive day 1 to day 2 cells and later day 7 cells were less affected [7]. Incubation of rhIFN-gamma with mature BFU-E inhibits hemoglobin accumulation and produces apoptosis of the maturing erythroid cells [7]. Moreover, since blood IFN-gamma levels are elevated and vary directly with the degree of the anemia, in patients with hematologic malignancies [8] and HIV-seropositivity [9], IFN-gamma appears to have a prominent role in producing the anemia associated with chronic disease [10,11]. Although characterization of human IFN-gamma receptors has been extensively performed for a variety of human cells including fibroblasts, lymphocytes, monocytes, granulocytes, eosinophiles, platelets, and many tumor cells [12-17], IFN-gamma receptors have not been identified on red cells [12] and the presence plus the extent of IFN-gamma receptors on progenitor cells, including human erythroid progenitor cells, remains unknown. A method has been reported from our laboratory by which human erythroid colony-forming cells (ECFC) can be highly purified, starting with peripheral blood BFU-E, in a sufficient amount for analysis of cytokine binding [18-20]. In this paper, we report the results of [125I]rhIFN-gamma binding to day 6 ECFC in vitro and demonstrate the presence of specific binding that is saturable at 1.0 nM. Scatchard analysis reveals that there are 1910-2070 rhIFN-gamma binding sites per ECFC with a Kd of 0.01-0.02 nM and, as with erythropoietin (EP) and insulin-line growth factor I (IGF-I) receptors, specific binding is highest with the earliest BFU-E studied and declines progressively as the erythroid progenitors mature.
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PMID:Specific binding of interferon-gamma to high affinity receptors on human erythroid colony-forming cells. 909 Dec 93


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