Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Management of major blood loss utilizing protein-free fluids for volume replacement frequently results in plasma protein depletion and plasma volume expansion. These factors can increase pulmonary transvascular fluid filtration which may lead to life-threatening pulmonary edema. We studied the combined effects of plasma protein depletion and plasma volume expansion on lung lymph flow (QL) in awake sheep prepared with chronic lung lymph fistulae. Animals were first chronically protein-depleted by batch plasmapheresis and then infused for 2 hr with either lactated Ringer's (Hypo/LR; n = 7) or 6% hydroxyethyl starch (Hespan) (Hypo/HES; n = 6). Control normoproteinemic animals (Norm/LR; n = 13) only received lactated Ringer's. Hypoproteinemia alone resulted in an average 2-fold increase in QL over normoproteinemic baseline levels (P less than or equal to 0.05). Infusion of LR into hypoproteinemic animals caused a 7.9-fold increase in QL (P less than or equal to 0.05). By comparison, HES infusion under similar hypoproteinemic conditions limited the increase in QL to 3.2-fold over baseline. We attributed this reduced rise in QL to Hespan's high oncotic pressure, which dramatically widened (by 4-5 mm Hg) the pulmonary-to-lymph oncotic pressure gradient. We did not observe this with LR infusion, or in previous studies employing intravenous infusion of plasma protein. Thus, the oncotic pressure of Hespan appears to significantly limit pulmonary fluid filtration during hypoproteinemia compared to LR. We do not believe that these effects are the results of any changes in microvascular porosity.
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PMID:Pulmonary transvascular fluid filtration response to hypoproteinemia and Hespan infusion. 169 7

An eosinophilic myeloproliferative disorder resulted in edema and hemorrhagic diathesis in a 10-month-old Standardbred colt. Laboratory abnormalities included severe thrombocytopenia, anemia, mild hypoproteinemia, and marked eosinophilia. Circulating eosinophils were immature or atypical with variation in granule size, disproportionate nuclear to cytoplasmic maturation, and abnormal nuclear size and shape. Bone marrow aspirate had mainly atypical eosinophil precursors, few erythroid precursors, and no megakaryocytes. A blood transfusion and dexamethasone therapy resulted in some improvement; however, the horse was euthanatized due to poor prognosis. Postmortem examination showed gastrointestinal parasitism; histologically the spleen was infiltrated by atypical eosinophils and there were sites of eosinophilopoiesis. The disease was broadly similar to idiopathic hypereosinophilic syndrome in people, but typical cardiac and neurologic involvement of hypereosinophilic syndrome were absent. Progressive myelophthesis and marked eosinophil atypia suggested malignancy.
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PMID:Eosinophilic myeloproliferative disorder in a horse. 651 43