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)

We determined the effect of a body burn on pulmonary function. Full-thickness burns varying in size from 25 to 70% of total body surface (TBS), were produced in sheep. Resuscitation was performed with lactated Ringer's. We noted an increase in lung transvascular fluid flux as measured by lymph flow, Q1, during the resuscitation period, varying from one- to threefold over baseline with the degree of increase directly proportional to the burn size. The increase in QL could be totally explained by the degree of hypoproteinemia which was also proportional to burn size. Transient pulmonary hypertension 20 +/- 4 to 26 +/- 5 mm Hg and a decrease in PaO2 from 90 +/- 5 to 83 +/- 6 torr occurred in the 50 and 70% burns as well as a significant decrease in lung compliance. These alterations were not due to pulmonary edema as there was no increase in measured lung water. Also, the increase in QL could be prevented by using a combination of Dextran and protein for resuscitation but this had no effect on the hypertension or hypoxia. Burn lymph and venous plasma thromboxane levels were increased during this period of lung dysfunction. Ibuprofen 12.5 mg/kg preburn and 12.5 mg/kg every 2 hours postburn decreased the degree of dysfunction suggesting a cause and effect relationship.
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PMID:Early lung dysfunction after major burns: role of edema and vasoactive mediators. 241 27

Peripheral edema, hypoproteinemia, and increased fluid requirements are characteristically seen with sepsis. Our purpose was to determine whether the soft tissue edema is caused by a direct vascular injury from sepsis or is secondary to hypoproteinemia. We determined the effect of endotoxin on peripheral (soft tissue) microvascular integrity using lymph flow (QL) and lymph/plasma (L/P) protein ratio to reflect fluid flux and increased permeability. Response was compared with that seen in the lung. Fourteen unanesthetized sheep were given intravenous E. coli endotoxin 2 micrograms/kg. Vascular pressures and cardiac output (CO) were maintained constant with the necessary fluid infusion. Lung QL increased two- to fourfold in all animals with lymph being protein-rich, indicating increased permeability. Peripheral QL increased transiently in response to an initial increase in vascular pressure returning rapidly to baseline except in those animals (N = 5) demonstrating hypoproteinemia where QL remained increased by 50 to 75%. The increased QL was totally explained by the degree of protein depletion, with no evidence of increased permeability. To assure an adequate endotoxin exposure to the peripheral microvessels, endotoxin (2 micrograms/kg) was also directly injected into the tissue drained by the soft tissue lymphatic. We noted a characteristic endotoxin pulmonary hypertension phase but, again, no increase in peripheral microvascular permeability was found. We conclude that endotoxemia does not alter peripheral microvascular permeability if tissue perfusion is maintained, while the lung is clearly a target organ. Hypoproteinemia may be responsible for the early edema in soft tissues with sepsis.
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PMID:Effect of endotoxin on the integrity of the peripheral (soft tissue) microcirculation. 637 Apr 90

We compared the use of hypertonic salt solution (300 mEq Na/liter) with Ringer's lactate as an initial resuscitation fluid for the treatment of hemorrhagic shock. We monitored vascular pressures and cardiac output as well as microvascular function using chronic lymph fistulae in the lung and soft tissues to reflect transvascular fluid and protein flux. Seven unanesthetized sheep were bled to an aortic pressure of 50 mm Hg (2 hours) on two occasions 4-5 days apart, and were resuscitated initially with either lactated Ringer's (LR) or hypertonic saline (HS) to restore left atrial pressure to baseline. This was followed later by the blood return. We found that cardiac output with HS was significantly increased over that with LR, 8.9 +/- 1.8, compared with 6.0 +/- 1.1, in the immediate postresuscitation period with comparable volumes in both groups. Urine output was increased twofold with HS over LR. The initial pulmonary hypertension seen with LR was eliminated with HS. Lymph flow in lung and soft tissue increased to a comparable degree in both groups, the increase being explained by the degree of plasma hypoproteinemia which was present. We conclude that HS increases cardiac output with less net fluid, decreases pulmonary vascular resistance, and does not result in more edema formation when compared with lactated Ringer's as an initial fluid for treatment of hemorrhagic shock.
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PMID:Resuscitation from hemorrhagic shock with hypertonic saline or lactated Ringer's (effect on the pulmonary and systemic microcirculations). 683 27

A case of tricuspid regurgitation (TR) complicated by severe hypoproteinemia is presented herein. A 68-year-old man who had undergone coronary artery bypass grafting (CABG) for postinfarction angina suffered repeated inferior myocardial infarction due to obstruction of the proximal right coronary artery, 3 years after which he developed systemic edema. Investigations revealed TR associated with hypoproteinemia; however, treatment consisting of aggressive diuretic therapy and albumin administration proved ineffective. The hypoproteinemia manifested as protein-losing enteropathy clinically, and the tricuspid valve was replaced to eliminate high venous pressure. The serum protein levels became normalized after the operation. Although TR is generally well tolerated in the absence of pulmonary hypertension, surgical management is recommended for patients with severe protein deficiency resistant to medical treatment.
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PMID:Hypoproteinemia caused by tricuspid regurgitation: report of a case. 987 51

A 62-year-old man with well-controlled diabetes mellitus developed numbness of the bilateral feet and hands, followed by subacutely progressive weakness and amyotrophy of extremities. He became bed-ridden state, and dyspnea also appeared, so he was referred to our hospital. Physical examination revealed a lean man, with dark-reddish skin pigmentation, crabbed fingers, bilateral pretibial pitting edema, and bristles in extremities. Thoracoabdominal paradoxical respiration was observed and pulmonary vesicular sounds was decreased markedly in the both lungs. Laboratory data revealed hypoproteinemia, abnormalities of endocrine system, but M-protein was not detected. Serum vascular endothelial growth factor level was quite high. Chest radiography revealed elevation of the bilateral diaphragm, the % vital capacity (%VC) was 24%, and arterial blood gas analysis showed marked hypoxia with hypercapnia. These findings suggested that his respiratory failure was induced by bilateral diaphragmatic paralysis caused by bilateral phrenic nerve palsy due to Crow-Fukase syndrome. He became somnolent because of hypercapnic narcosis, so non-invasive positive pressure ventilation (NIPPV) was started. We treated him with intravenous immunoglobulin and oral corticosteroids therapies, and after these therapies, his symptoms were remarkably recovered and NIPPV became unnecessary soon. The most frequent causes of respiratory failure in Crow-Fukase syndrome are pleural effusion and pulmonary hypertension, and only two cases of this syndrome with respiratory failure caused by bilateral diaphragmatic paralysis were reported until now. When the patients with Crow-Fukase syndrome complain of dyspnea, we should take the diaphragmatic paralysis into consideration, which may be improved by appropriate therapies.
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PMID:[A case of Crow-Fukase syndrome with respiratory failure due to bilateral diaphragmatic paralysis]. 1266 Nov 11