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

In iron deficiency anaemia basic red cell content of ferritin is appreciably reduced. This variable was determined in 62 patients with rheumatoid arthritis to evaluate conventional laboratory indices for iron deficiency in the anaemia of rheumatoid arthritis. For 23 patients with rheumatoid arthritis and normocytic anaemia irrespective of plasma ferritin concentration, red cell ferritin content did not differ significantly from that for non-anaemic patients with rheumatoid arthritis. For 27 patients with rheumatoid arthritis and microcytic anaemia, the mean red cell ferritin content for patients with a plasma ferritin concentration in the 13-110 micrograms/l range was appreciably reduced. It was indistinguishable from that for patients with rheumatoid arthritis and classical iron deficiency anaemia, indicated by plasma ferritin concentrations of less than 12 micrograms/l. In contrast, the mean red cell ferritin content for patients with rheumatoid arthritis, microcytic anaemia, and plasma ferritin concentrations above 110 micrograms/l did not differ from that for patients with rheumatoid arthritis and normocytic anaemia. Oral treatment with iron in patients with rheumatoid arthritis, microcytic anaemia, and appreciably reduced red cell ferritin concentrations was accompanied by significant increases in haemoglobin concentration (p less than 0.01), mean corpuscular volume (p less than 0.01), and red cell ferritin contents (p less than 0.05). This treatment, however, did not produce any appreciable change in haemoglobin concentration in patients with rheumatoid arthritis, normocytic anaemia, and normal red cell ferritin contents. These findings suggest that the indices for iron deficiency in patients with rheumatoid arthritis and anaemia should include peripheral blood microcytosis together with a plasma ferritin concentration of less than 110 micrograms/l.
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PMID:Red cell ferritin content: a re-evaluation of indices for iron deficiency in the anaemia of rheumatoid arthritis. 643 23

Dialysis patients exposed to high aluminum (Al) dialysate develop a microcytic anemia which is reversed by deionization (DI) of the dialysate. Because DI removes substances in addition to Al which are known to cause anemia, these experiments were undertaken to determine if Al causes anemia and if the anemia of uremia can be enhanced by Al. Four groups of rats were studied: sham control (A) N = 6; uremic control (B) N = 6; Al-loaded non-uremic (C) N = 7; and Al-loaded uremic (D) N = 5. Aluminum treatment was 1 mg Al intraperitoneally daily for 6 weeks. Uremic rats (B+D) were 1 5/6 nephrectomized; non-uremic (A+C) were sham-operated. Blood samples (200 microliter) were obtained prior to (C1) and weekly during treatment (T1 to T6) and analyzed by Coulter Counter. No significant difference in hemoglobin (Hb), hematocrit (Hct), or mean cell volume (MCV) was noted at C1 X At T3, MCV of Al-treated rats (C+D) was significantly less than sham control (A) (55.1 +/- 0.5 and 53.0 +/- 0.8 vs. 60.8 +/- 1.5 mu3, P less than 0.05). At T6, MCV, Hb, and Hct of Al-loaded uremic rats (D) (49 +/- 0.5 mu3; 11.8 +/- 0.5 g/dl; 25.1 +/- 2%) were significantly less than both A (58.6 +/- 1.3 mu3; 16.1 +/- 0.4 g/dl; 44.8 +/- 0.3%) and B (58.7 +/- 1.4 mu3; 13.8 +/- 0.4 g/dl; 33.6 +/- 0.5%) (P less than 0.05) and MCV, Hb, and Hct of Al-loaded non-uremic rats (C) (51.7 +/- 1.7 mu3; 12.6 +/- 0.3 g/dl; 29.4 +/- 1.5%) was significantly less than A (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microcytic anemia secondary to intraperitoneal aluminum in normal and uremic rats. 651 72

One hundred and fifty randomly selected individuals aged 65 years and over voluntarily participated in haematological studies which formed part of a comprehensive survey of the psychiatric and physical health of elderly Coloured persons in Cape Town. Complete haematological information was available for 139 of the respondents and showed that values for a standard profile of screening tests did not differ from those in groups of White subjects living in Cape Town or Western Europe or from those in subjects from the same ethnic group but aged between 20 and 60 years. In 16 cases (11,5%) the initial haematological studies showed some abnormality. In 7 subjects (5%) the total white cell counts were raised, in 4 they returned to normal and in 3 remained elevated with normal differential distributions of the cells; no explanation for this has been found. Three respondents (2%) had a raised mean cell volume attributable to alcoholism. Eight (6%) had hypochromic microcytic anaemia due to iron loss resulting from occult gastro-intestinal tract bleeding. In 1 case this was due to a hiatal hernia and in the remaining 7 to carcinoma. The study shows that in this population nutrition is generally satisfactory and emphasizes the importance of investigation to determine the cause of anaemia in the elderly.
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PMID:The coloured elderly in Cape Town--a psychosocial, psychiatric and medical community survey. Part IV. Haematological values. 669 41

Investigations into the probable role of haemolysins in the causation of hookworm anaemia have been undertaken in living infected dogs. Secondly, the effects of living hookworms and various worm products on erythrocytes in vitro have been assessed. In dogs infected with varying numbers of A. ceylanicum, severe microcytic anaemia developed in the most heavily infected animals six weeks after infection. Erythrocytes from the latter animals showed significantly greater autohaemolysis in the presence of added glucose. When serum bilirubin and methaemalbumin, plasma haemoglobin, urinary urobilinogin and osmotic fragility of their red cells were measured, however, no evidence of haemolysis was detected. Erythrocytes from these animals appeared normal under scanning electron microscopy. In in vitro studies varying concentrations of adult worm extract had no effect on the haemolysis of either dog or human erythrocytes in the presence or absence of glucose nor on their mechanical fragility. There was no increase in 51Cr release from dog or human labelled red cells when incubated with either adult worm extract or excretory/secretory products of worms. Living adult worms caused an increase in 51Cr release from human but not dog labelled erythrocytes. Thus, the role of haemolysins in the genesis of hookworm anaemia is minimal.
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PMID:Investigation of the haemolytic effects of Ancylostoma ceylanicum: observations on infected dogs in vivo and human and dog blood in vitro. 674 Mar 75

Hematologic abnormalities in childhood lead poisoning may be due, in part, to the presence of other disorders, such as iron deficiency or thalassemia minor. In order to reassess increased lead burden as a cause of microcytic anemia, we studied 58 children with class III or IV lead poisoning, normal iron stores, and no inherited hemoglobinopathy. Anemia occurred in 12% and microcytosis in 21% of these children. The combination of anemia and microcytosis was found in only one of 58 patients (2%). When only children with class IV lead poisoning were studied, the occurrence of microcytosis increased to 46%. However, the combination of microcytosis and anemia was found in only one of these 13 more severely affected patients. Microcytic anemia was similarly uncommon in children with either blood lead concentration greater than or equal to 50 microgram/100 ml. These data indicate that microcytosis and anemia occur much less commonly than previously reported in childhood lead poisoning uncomplicated by other hematologic disorders.
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PMID:Reassessment of the microcytic anemia of lead poisoning. 723 54

An 11-year-old boy was noted to have microcytic anemia, growth retardation, polyclonal hypergammaglobulinemia, and abnormal platelet function. An angiomatous lymphoid hamartoma was removed from the retroperitoneal space. Postoperatively the child exhibited a dramatic growth spurt and complete resolution of the abnormal laboratory measurements. Studies were performed before and after tumor removal to investigate the nature of the associated anemia, growth retardation, and altered hemostasis. There was no evidence of iron deficiency, thalassemia, or an antierythropoietin factor. Prolonged bleeding time and impaired ristocetin-induced platelet aggregation normalized following tumor resection. Serum obtained before surgery inhibited lymphocyte proliferation in mixed lymphocyte culture as well as fibroblast growth in vitro. Detailed study of growth regulatory hormones failed to reveal significant alterations except for significantly reduced somatomedin which normalized after surgery. The factor(s) which inhibit in vitro cellular growth and lower in vivo plasma somatomedin concentration remain unknown.
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PMID:Angiomatous lymphoid hamartoma: inhibitory effects on erythropoiesis, growth, and primary hemostasis. 726 91

In a review of 17 adolescents and children (excluding newborns) with definite clinical signs, symptoms, and laboratory findings of hypothyroidism, 11 patients (65%) had anemia. The mean corpuscular volume (MCV) of the red blood cells was either macrocytic or normocytic. The hemoglobin did not correlate with the serum thyroxine level. Anemia occurred only in those patients with heights below the third percentile, but there was no similar correlation with weights. Of the 10 patients who had radiographs for bone age, all showed severe delay (47 to 103 months) and had heights below the third percentile. Nine of these patients were anemic, but the severity of the anemia did not correlate with the delay in bone age. Neither microcytic anemia nor pernicious anemia, noted in many adult hypothyroid patients, was found in the children and adolescents with hypothyroidism studied here. The "uncomplicated" anemia secondary to hypothyroidism responded to thyroid replacement therapy alone. Anemia can be the most prominent feature of hypothyroidism. In patients with mild to moderate anemia of unknown origin, especially those with fall-off in linear growth and increased MCV, hypothyroidism should be considered in the differential diagnosis of the anemia.
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PMID:Anemia in children and adolescents with hypothyroidism. 729 10

Beta-thalassemia trait is a frequent cause of microcytic anemia in Mediterranean children. Because striking age-related changes occur in hemoglobin and mean corpuscular volume during childhood, we assessed developmental hematologic characteristics of 132 patients less than or equal to 18 years of age with beta-thalassemia trait. Thirty-nine kindred were studied to examine intrafamilial correlations of hematologic abnormalities. Patients with beta-thalassemia trait demonstrated Hgb values about 2 gm/dl below normal standards, with a progressive rise with age paralleling normal trends. Thalassemic MCV values showed a far greater deviation from normal than Hgb levels. In contrast to normal developmental trends which show a sharp increase in the first five years of life, the MCV in thalassemia trait showed no age-related increase prior to adolescence. No age-related changes in hemoglobin A2 levels were noted. Kindred studies demonstrate a correlation of the degree of anemia, microcytosis, and elevated hemoglobin A2 levels in affected family members (r = 0.318 P < 0.004, r = 0.525 P < 0.001, r = 0.416 P < 0.0015, respectively). Our findings support the use of electronically determined MCV values as an initial screening procedure for children with beta-thalassemia trait. Values of < 70 fl prior to adolescence and < 75 fl during adolescence were present in nearly all thalassemic subjects. Intrafamilial correlations of Hgb, MCV, and hemoglobin A2 levels suggest that these characteristics are genetically determined.
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PMID:Hematology of beta-thalassemia trait--age-related developmental aspects and intrafamilial correlations. 744 18

In a 24-year old man presenting with hypochromic microcytic anaemia, low reticulocyte count, increased serum iron and bone marrow erythroid hyperplasia with numerous ringed sideroblasts, the diagnosis of sideroblastic anaemia was confirmed by radioisotope study and bone marrow electron microscopy. The hereditary nature of the disease was demonstrated by the presence of microcytosis and increased serum iron in the mother and two sisters of the patient. One of the two sisters also had anaemia and abnormal ringed sideroblasts in her bone marrow. Her haemoglobin values and those of the propositus returned to normal under pyridoxine treatment, but hypochromia and abnormal sideroblasts persisted. This case of familial pyridoxine-responsive sideroblastic anaemia is consisted with X-chromosome-mediated transmission. The incomplete effect of pyridoxine suggests a congenital deficiency of some pyridoxine metabolism enzyme or another, as yet unidentified mechanism.
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PMID:[Familial pyridoxine-responsive sideroblastic anaemia. One case (author's transl)]. 744 86

A 77-year-old male having multiple small nevi over the lips, face, mucous membrane of mouth, tongue, neck and thorax was admitted to our hospital because of severe anemia. He has been diagnosed as Rendu-Osler-Weber disease (Osler's disease) since his 42 years of age. Although the stools were positive for occult blood, hematologic examination disclosed no abnormalities except for severe hypochromic and microcytic anemia. Gastrointestinal examination showed multiple stigmata in the esophagus, stomach, duodenum, and several tumors in the colon. Histological findings of biopsy specimens obtained from these tumors revealed adenocarcinomas and tubular adenomas. Surgical resection was carried out. Resected specimens showed two tumors (one is in ascending colon appeared to be 2 type carcinoma, 1.9 x 2.3 cm in size, another is in caecum, 3 type, 7.0 x 5.0 cm in size) and three Yamada-II approximately III type polyps. Pathohistologically, the tumor in ascending colon showed moderately differentiated adenocarcinoma, another one in caecum showed mucinous carcinoma, and polyps showed tubular adenomas, respectively. Unfortunately, the anemia of this case was regarded as stemming from Osler's disease, so the precise gastrointestinal examination was not performed for a long time. It should be emphasized to be faithful to the fundamentals of medical diagnosis.
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PMID:[A case of Rendu-Osler-Weber disease associated with simultaneous, multiple advanced cancers in the colon]. 770 55


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