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)

Alcohol-related disturbances are seen against the three blood cell systems. They appear after important alcohol consumption within few days and are independent from the existence of liver cirrhosis with splenomegaly. They are promptly and completely reversible after interruption of alcohol supply. Disturbances in erythropoiesis are manifested in bone marrow with megaloblasts, ring sideroblasts, and vacuoles in cytoplasma and nucleus of nucleated red cells. They are caused by folate deficiency and by perturbations of iron utilization, which is perhaps connected with impaired heme synthesis following pyridoxal phosphate deficiency. Serum iron generally increases during alcohol consumption and decreases in the following alcohol-free period. The anemia may be macrocytic and normochromic or dimorphic with hypochromic microcytes. Anemias of hard alcohol drinkers are observed also as consequence of bleeding or hemolysis of different causes. The lability against infections of drinkers is associated with changes in granulopoiesis. The most important findings are granulocytopenia, vacuoles in the immature marrow cells, perturbations in granulopoietic maturation, and decrease of marrow response. Frequently, alcohol drinkers demonstrate thrombocytopenia which is caused by ineffective thrombopoiesis and by shortened life span of platelets as direct effect of ethanol. Functional impairments of thrombocytes have been published, too.
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PMID:[Alcohol-related disturbances in haematopoiesis (author's transl)]. 64 97

Effects of dietary vitamin B6 at levels ranging from deficiency to megadoses on the development of herpes simplex virus type 2-transformed (H238) cell-induced tumors and on in vitro responses relating to cell-mediated immunity were examined. Male BALB/cByJ mice (n = 260), 5 weeks of age, were fed 20% casein diets containing pyridoxine (PN) at 0.2, 1.2 for the control diet, 7.7, or 74.3 mg/kg diet for 4-11 weeks. After 4 weeks of dietary treatment, 120 of the mice received an injection of H238 cells; mice without H238 injection served as controls. At 4, 8, and 11 weeks, animals from each group were euthanized and blood and spleen samples obtained. Mice fed 0.2 mg PN developed mild deficiency symptoms and gained significantly less weight than those fed 1.2-, 7.7-, and 74.3-mg PN diets. Thirteen to 16 days after tumor cell injection, primary tumor incidence was lowest in mice fed 74.3 mg PN; later, incidence among groups was similar. Mice fed 1.2 mg PN had the largest primary tumor volume, the highest incidence of lung metastases, and the greatest number of metastatic nodules per animal at 7 weeks post injection. Overall, lower tumor volumes were found in animals fed 7.7 and 74.3 mg PN (14 and 32% less than the tumor volume for those fed 1.2 mg PN, respectively); mice fed 0.2 mg PN had the lowest tumor volume. Blood and spleen lymphoproliferative response to stimulation by phytohemagglutinin or concanavalin A generally tended to be higher in mice fed 7.7 and 74.3 mg PN as compared to that in animals fed either 0.2 or 1.2 mg PN. However, decreased mitogen-stimulated responsiveness was observed in all animals with progressive tumor growth. Tumor growth also resulted in splenomegaly and increased thymic atrophy. Significant negative relationships between tumor volume and tumor pyridoxal 5-phosphate (PLP) concentrations were observed for 1.2-, 7.7-, and 74.3-mg PN diet groups. These data suggest that high dietary intake of vitamin B6 may have suppressed tumor development by either immune enhancement or PLP growth regulation of this tumor.
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PMID:Suppression of tumor growth and enhancement of immune status with high levels of dietary vitamin B6 in BALB/c mice. 347 3