Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anemia developing during the course of chronic renal disease is a frequent complication often necessitating periodic transfusion therapy. A number of etiologic factors have been implicated, including decreased production of erythropoietin; decreased erythrocyte life span secondary to uremia and splenomegaly; increased bleeding tendency due to platelet dysfunction; and acquired lack of folic acid and iron. This paper concerns the problem of acquired hypochromic, microcytic anemia secondary to heavy urinary loss of iron and transferrin in a child with the nephrotic syndrome. The patient had microcytic, hypochromic anemia with serum iron, 12 mug. per dl. and a serum iron-binding capacity of 12 mug. per dl. There was no evidence of major bleeding resulting in a chronic hemorrhagic anemia. Urinary iron was 64 mug. per dl., with a urinary iron-binding capacity of 366 mug. per dl. Renal biopsy showed mesangio-proliferative glomerulonephritis. Evaluation of any patient with the nephrotic syndrome should include careful analysis of the various serum and urinary proteins and determination of serum and urinary iron and iron-binding capacity. This information would offer a more precise evaluation of the underlying cause of anemia in the nephrotic patient who may develop urinary loss of iron and transferrin and subsequent hypochromic, microcytic anemia.
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PMID:Transferrin loss into the urine with hypochromic, microcytic anemia. 124 90

Eighty-eight patients with Hemoglobin (Hb) H diagnosed in our hospital in the past decade were reviewed. Among them, 37 were males and 51 were females, and their age ranged from 10 to 77 years. In physical examination, 43.3% of them showed to have jaundice, 47% had splenomegaly, 14% had hepatomegaly and 19.3% had gall stone. Hb electrophoresis revealed the presence of Hb H (1.4-40%), Hb F (23/88, range: 0.5-7.5%) and decreased Hb A2 (mean = 1.23 +/- 1.2%). The study of iron status showed increased serum ferritin concentration (mean = 421.4 +/- 343.7 ug/dl) and transferrin saturation ratio (53.9% +/- 20.5%). Hemosiderosis was found in three out of four patients received liver biopsy. Although most patients did not receive blood transfusion frequently, iron overload was not uncommon in the patients with Hb H disease. Further study would be needed to explore the true relationship between iron overload and Hb H disease.
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PMID:Hemoglobin H disease--ten years' experience. 216 37

We examined the iron status of 23 adult patients with hemoglobin H (Hb H) disease. None of them had received multiple blood transfusions or prolonged iron therapy. Studies included serum iron and ferritin concentrations, transferrin saturation, a desferrioxamine test, computed tomography (CT) scan of the liver, and liver biopsy. Iron overload was found in 17 patients (73.9%), especially in males and in patients with splenomegaly (92.9% and 100%, respectively). Four patients with excessive alcohol consumption had clinical manifestations of severe iron overload. Idiopathic hemochromatosis associated HLA antigens, i.e., HLA-A3, -B7, or -B14, were not found in any of the 15 patients tested. These findings indicate that iron overload is common in adult patients with Hb H disease; such patients should abstain from alcohol and be considered for treatment with an iron chelating agent before irreversible organ damage occurs.
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PMID:Iron overload in Chinese patients with hemoglobin H disease. 236 95

A method was established for estimation of plasma volume and splenic plasma pool by quantitative scanning using 113mIn labelled transferrin (TF). The method was used in 12 patients with various haematological disorders and degrees of splenomegaly. 113mIn-TF consistently gave about 6% over-estimation of plasma volume by comparison with the standard 125I HSA method. The splenic plasma pool ranged from 1.2% to 11.4% of the total plasma volume. By concurrent measurement of splenic red cell pool the splenic haematocrit (SHct) was obtained: mean 0.51, SD 0.08; the SHct/PCV ratio was 1.21 (SD 0.31) and the SHct/body Hct ratio was 1.30 (SD 0.30). SHct was independent of PCV and body Hct but there was a trend to a lower SHct in cases where splenomegaly was more marked. Direct measurement of splenic plasma pool may help to elucidate the cause of increased total plasma volume in such patients.
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PMID:Splenic haematocrit and the splenic plasma pool. 359 58

During an experimental chronic infection of inbred mice with Trypanosoma congolense several physiological parameters become altered. Splenomegaly followed later by hepatomegaly are predominant. Lactate dehydrogenase and aminotransferase activities of the plasma are elevated, the number of erythrocytes and thrombocytes decreases, whereas monocytic cells are detected in higher concentrations. Gamma-Globulins and transferrin become elevated. Some of the pathobiochemical alterations depend directly on the parasitaemia and are reversed to normal values after chemotherapy with diminazene aceturate (Berenil). The curative effect of this drug depends largely on when it is administered. In acute T. congolense infections, leading to the death of the animals in 3-4 days, pathobiochemical alterations are found only shortly before the exitus.
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PMID:Pathobiochemical alterations in experimental chronic and acute trypanosomal infection in mice. 369 25

Various haematological parameters were followed in a group of 47 Kenyan patients with visceral leishmaniasis during treatment and follow up. The WBC and platelet numbers were normal by the time of cure, the Hb level took longer to become normal. Red cells were microcytic and hypochromic. MCV and MCH increased during follow up but microcytosis persisted up to a year after cure. Low serum iron and transferrin concentration, low total iron binding capacity and normal to high serum ferritin levels were found in 10 patients and are consistent with 'anaemia of chronic inflammation'. Bone marrows of 15 patients before treatment were normo- to hypercellular with increased erythropoietic activity. Low haemosiderin content of the bone marrow was consistent with iron deficiency, but normalization of Hb without iron suppletion would argue against a major role of iron deficiency. Coagulation studies did not indicate diffuse intravascular coagulation. Splenomegaly seems the most important factor in the causation of the pancytopenia. Further studies of contributing factors and of the cause and mechanism of 'hypersplenism' are needed.
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PMID:Haematological investigations in visceral leishmaniasis. 381 Aug 41

This study reports the case of a patient who presented with evidence for a diagnosis of chronic myelogenous leukemia, as shown by blood and bone marrow analysis, and with generalized lymphadenopathy and splenomegaly. A lymph node biopsy revealed that the majority of the cells had plasmacytoid features but were consistently negative for surface or cytoplasmic immunoglobulin products, myelomonocytic surface markers, and peroxidase. Rather, lymph node plasmacytoid cells expressed T-cell markers (T 4/Leu 3+, T 10+), transferrin receptors (T 9+), and a proportion of them was also positive for sheep erythrocyte receptors (T 11/Leu 5+). This case is strikingly similar to a case reported by Lennert's group with respect to morphology, surface phenotypic features of the malignant plasmacytoid cells, and the association between a lymphoproliferative and a myeloproliferative disorder. This association suggests that plasmacytoid T-cells might exert a regulatory role on proliferation of myeloid cells.
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PMID:Plasmacytoid T-cell lymphoma associated with chronic myeloproliferative disorder. 387 6

Enlarged spleen, fever, increased susceptibility to infections, and thrombocytosis, are manifestations of iron deficiency which are relatively specific of pediatric patients. Iron deficiency anemia is part of everyday pediatrics. Patients are referred to the hematologist in the following situations: 1) Therapy is ineffective for one of the following reasons: the hypochromic anemia is not caused by iron deficiency (hemoglobinopathies); iron is less efficiently used because of transferrin deficiency or infectious, inflammatory or cancerous disease; iron therapy is inadequate either because of insufficient dosage or of suboptimal duration. 2) A relapse occurs in spite of adequate therapy. Before investigating the digestive tract, abnormal hemostasis. Osler-Weber-Rendu syndrome and pulmonary hemosiderosis should be considered. 3) Iron deficiency anemia is less common in adolescents. This condition, known as chlorosis, results mainly from increased needs, unbalanced diet, and onset of menses. In some cases no explanation is found but iron therapy leads to recovery. 4) Difficult problems arise in patients with complex anemias: iron deficiency with folic acid or vitamin B12 deficiency; hyposideremia complicating one of the hemoglobinopathies.
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PMID:[Iron-deficiency anemia. Hematologist's viewpoint]. 629 49

Red cell kinetics and albumin metabolism were studied in calves infected with either 100 or 200 Schistosoma bovis cercariae per kg body weight, by the use of 59Fe-labelled transferrin, 51Cr-labelled erythrocytes and 125I-labelled albumin; a third group of worm-free animals acted as controls. The anaemia which developed in the infected calves was shown to be due basically to an accelerated rate of red cell loss from the circulation, and became evident around the seventh week of infection, increased in severity during the following two months, and subsequently subsided. In view of its close similarity to the pattern of faecal egg excretion, it was concluded that haemorrhage into the intestine caused by the exit of eggs was the principal aetiological factor: haemolysis was excluded by the absence of both splenomegaly and hyperferraemia . Erythropoiesis was also accelerated in infected animals, but could not keep pace with the rate of red cell breakdown to which the animals were concurrently subjected. Haemodilution was involved, but not to a significant extent. The hypoalbuminaemia associated with infection was caused by an increased rate of albumin catabolism, and a plasma volume expansion, and was accompanied by marked depletion of all albumin pools, but particularly the extravascular pool. The pattern of albumin catabolism closely followed that of red cell loss, suggesting that passage of plasma as whole blood into the intestine was the basic cause of hypoalbuminaemia. Red cell losses and albumin hypercatabolism were more severe in the more heavily infected group, and although both subsided as egg counts fell, they remained evident even 1 year after infection. This may partly explain the failure of infected animals to regain the weight lost during earlier stages of disease.
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PMID:Erythrokinetics and albumin metabolism in primary experimental Schistosoma bovis infections in Zebu calves. 673 11

Full blood counts and some serum biochemistry were carried out on 349 male and 22 female apparently healthy Papua New Guinea subjects, most of whom were highlanders. In males, RBC, Hb, PCV, MCH, MCHC, serum albumin, ferritin, iron, per cent transferrin saturation and folate means were significantly lower than the Australian normal means; WBC and MCV means were similar to Australian values; and eosinophil and reticulocyte counts and serum transferrin and vitamin B12 means were higher than Australian means. In females, WBC, RBC, Hb, PCV, MCV, MHC, MCHC and serum ferritin means were lower than Australian means; eosinophil counts, serum iron, per cent transferrin saturation, and folate means were similar to Australian means; and serum transferrin and B12 means were higher than the Australian means. Hepatomegaly and mild splenomegaly were common. beta-Thalassemia was present in three subjects two of whom were from Simbu Province.
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PMID:Some haematological and physical characteristics of a group of Papua New Guinea highlanders. 694 72


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