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At least 19 recordsLinked to original sources
PubMed1976

A rabbit reticulocyte model for the role of hemin-controlled repressor in hypochromic anemias.

Hemin allows maximal protein synthesis in intact rabbit reticulocytes and their cell-free lysate preparations by retarding the formation of a translational repressor (HCR) found in the postribosomal supernate. In order to evaluate the role of HCR in the pathogenesis of hypochromic anemias, HCR was isolated and partially purified from intact rabbit reticulocytes incubated in vitro with either 0.1 mM alpha,alpha-dipyridyl (an iron-chelating agent) or 0.1 M ethanol. Both of these agents inhibit reticulocyte protein synthesis. Hemin (50 muM) protects against the inhibition by both agents. A ferrous iron-transferrin mixture, however, protects only against alpha,alpha-dipyridyl. Both alpha,alpha-dipyridyl and ethanol inhibit heme synthesis before the time that protein synthesis is affected, while neither lowers either ATP or GSH levels. These results indicate that while both agents inhibit heme synthesis, alpha,alpha-dipyridyl does so by inducing iron deficiency while ethanol works at a non-iron-requiring step. When HCR was isolated from intact cells and assayed in the reticulocyte cell-free systems, plus and minus hemin, premature appearance of HCR was found in cells incubated in vitro with alpha,alpha-dipyridyl or ethanol. When hemin was present in the intact cell incubation, the appearance of HCR was retarded. The HCR from alpha,alpha-dipyridyl ethanol-treated cells was partially purified and eluted at the same location on a Sephadex G-200 column (molecular weight approximately 3 x 10(5)) as that from postribosomal supernates incubated minus hemin. In addition rabbits with phenylhydrazine-induced hemolytic anemia were given intravenous ethanol in vivo at a dose of 0.4 ml/kg. This concentration of alcohol resulted in an inhibition of the rate of heme synthesis and protein synthesis as well as an acceleration of HCR formation in reticulocytes. The HCR from these in vivo treated rabbits was isolated, partially purified, and assayed in an identical fashion as the in vitro experiments. These in vivo experiments further support the physiological and pathophysiological role of HCR in reticulocytes. On the basis of these results a model for a role of HCR in some of the hypochromic anemias is proposed. In iron deficiency or chronic disease (where iron is not available to the erythroblast for heme synthesis) HCR appears prematurely and inhibits protein synthesis. When heme synthesis is inhibited by ethanol but there is sufficient intracellular iron, HCR appears prematurely and inhibits protein synthesis, iron accumulates in the erythroblast, and the end result is sideroblastic anemia.

2,2'-Dipyridyl↗
PubMedDate not supplied

[Haematologic disorders in Crohn's disease (author's transl)].

Anemia is the most commonly haematologic disorder observed in Crohn's disease. Secondary megaloblastic anemia related to a nutritional deficiency of vitamin B 12 and/or folic acid is a rare condition as well as auto-immune haemolytic anemia. Iron lack microcytic hypochromic anemia is far more frequent. It is probably due to several causes as microscopic or macroscopic haemorrhages, inflammatory syndrome, disturbance of iron absorption. Hyperleucocytis, hypereosinophilia, hypoprothrombinemia related to the inflammatory syndrome and/or lesions of the bowels are frequently observed in such patients. Anyhow, heamatologic disorders seem markedly correlated with the activity of the disease and should be useful in the follow up patients with Crohn's disease.

Anemia↗
PubMed1978

Blood effects of permanent normoxic hypercapnia in conventional rats.

Rats were exposed 24 hours a day to carbon dioxide, 8 +/- 1%, during 2 and 4 weeks under normoxic conditions (21% oxygen). On the last day, blood was taken from the abdominal aorta under anesthesia. Leukocyte and erythrocyte counts, hemoglobin concentration, and mean cell volume were electronically measured. Hematocit and Wintrobe indexes were calculated. Leukocyte differential counts and peroxidase activity were determined on blood smears. After 4 weeks of hypercapnia, a slight decrease of neutrophilic granulocytes was observed. In mature polymorphs, peroxidase activity (cytochemically demonstrated) simultaneously decreased. Erythrocyte counts and mean cell volume remained unchanged. The most important hematological disturbance was an hemoglobin concentration drop. Consequently, it was concluded that an hypochromic anemia characterized the permanent normoxic hypercapnia in rats.

Anemia, Hypochromic↗
PubMed1977

Clinical, morphologic, and clinicopathologic findings in Beagles treated for two years with melengestrol acetate.

Melengestrol acetate (MGA) was administered orally to groups of 10 female and 3 male Beagles at doses of 0, 1, 2, or 8 microgram/kg of body weight/day for 2 years. Treatment was continuous at the same dose rate in the first 3 groups, but in the 4th group, the dose for bitches was reduced to 4 microgram of MGA/kg/day during the 2nd year. Matings were made within MGA-dosage groups and among 10 additional bitches treated at 1 microgram of MGA/kg/day and the dogs treated at 8 microgram/kg/day. Doses of 8 and 4 microgram of MGS/kg caused progestational effects on the uterus resulting in expected histopathologic changes, dystocia, and pyometritis. Leukocytosis, normocytic, hypochromic anemia, and increased alkaline phosphatase values were the results of systemic and uterine effects consistent with the indirect and expected pharmacologic action of progestational agents in the bitch. Doses of 1 and 2 microgram of MGA/kg in dogs and bitches and 8 microgram/kg in dogs produced no significant differences in clinical observations, hematologic findings, blood chemical analysis, urinalysis, organ weights, or gross and microscopic observations at necropsy.

Alkaline Phosphatase↗
PubMed1978

[Iron deficiency anemia caused by occult intestinal bleeding due to milk allergy (author's transl)].

With the passive hemagglutination method the authors proved antibodies against milkprotein fractions in three of nine patients with hypochrome anemia aged 7, 12 and 17 months. In these children the X-ray examination showed an intestinal allergy, presumably the reason for occult intestinal bleeding which inturn caused hypochrome anemia. After milk was eliminated from the diet iron therapy restored a normal haemoglobin content. Iron therapy alone only improved the anemia, since continuing intestinal bleeding prevented fullrecovery.

Anemia, Hypochromic↗
PubMed1979

Ferrochelatase deficiency in an infant with anemia and growth delay.

A 5-month-old infant with hypochromic anemia and iron overload secondary to ferrochelatase (heme synthetase) deficiency is described. Decreased activity of iron-containing enzymes in the absence of any other proven cause is suggested as the main cause of the associated growth retardation.

Anemia, Hypochromic↗
PubMed1978

[The treatment of anemia due to iron-deficiency with iron combined with vitamins (author's transl)].

The effect of combined iron-vitamin therapy and iron therapy only was studied in 14 respectively 14 children with hypochromic anemia. Pyridoxalphosphate in serum, activity of red cell glutamic oxaloacetic transaminase and excretion of 4-pyridoxic acid were measured as indices of vitamin B6 nutriture before therapy was started, four and seven days under therapy once more. Erythrocytes, reticulocytes, concentration of hemoglobin were simultaneously counted, whereas serum iron and transferrin have been measured before and after therapy. A group of 22 hematologically healthy children was studied as controls. After iron therapy a decrease of vitamin B6 body pool came off as a consequence of increased requirement of pyridoxalphosphate for heme synthesis. Additional dosage of vitamins compensated the biochemical B6 deficit and had an accelerating effect on heme synthesis.

Anemia, Hypochromic↗
PubMed1978

beta-Thalassemia arising as a new mutation in an American child.

A 6-year-old child of northern European ancestry was found to have microcytic, hypochromic anemia with an elevated level of hemoglobin A2 and an unbalanced pattern of globin chain synthesis characteristic of beta-thalassemia trait. Hematologic and globin synthesis studies of both parents yielded entirely normal results. Identification of the mother and father as the biological parents was established with a high order of reliability by determination of erythrocyte, serum, and HLA genetic markers. These findings suggest that the picture of beta-thalassemia observed in this child represents a new mutation.

Child↗
PubMed1979

Large basophilic cells in the bone marrow in iron deficiency anemia.

Many large cells with a strongly basophilic cytoplasm and large nuclei with a delicate chromatin pattern and large nucleoli were studied in 1 mu sections of core biopsies in 8 patients with iron deficiency anemia and in 5 patients with pernicious anemia. In 2 normal controls these cells were rare. Possible features of granulocytic differentiation were assessed with the Giemsa stain and with the naphtol-ASD-chloroacetate esterase reaction which is indicative of early granule formation: the large cells were constantly negative. In thin sections the morphological appearances of the large basophilic cells are rather similar in such different haematological disorders as pernicious anemia or iron deficiency anemia. A clear difference can be demonstrated by karyometry, which shows that the large basophilic cells in pernicious anemia are significantly larger than those in iron deficiency anemia or in the normal control.

Anemia, Hypochromic↗
PubMed1979

Bile gastritis without prior gastric surgery: contributing role of cholecystectomy.

This study reports on ten patients with typical bile gastritis who had no prior gastric surgery. Clinical symptoms included burning epigastric pain unrelieved by food or antacid, episodic nausea, and vomiting of bile. In all patients the symptoms appeared after cholecystectomy, with (four patients) or without (six patients) transduodenal sphincterotomy; the symptoms were often initially attributed to chronic pancreatitis. Six patients had hypochromic, microcytic anemia. Eight patients had basal achlorhydria; stimulated acid secretion was low or absent in seven patients. Gastroscopic examination revealed gastritis, most prominent in the prepyloric antrum, and abundant bile lakes. Mucosal biopsy disclosed chronic gastritis. Although medical therapy failed, seven of eight patients treated by vagotomy, hemigastrectomy, and long Roux-en-Y gastrojejunostomy had immediate and sustained relief. Cholecystectomy appears to be a critical factor in the pathogenesis of bile gastritis in patients who have not had prior gastric surgery. Without the reservoir function of the gallbladder, the unregulated flow of bile into the duodenum probably promotes the access of bile to the unprotected gastric mucosa.

Achlorhydria↗