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)

On the basis of recent pathophysiological data and clinical observations in three patients, this paper draws attention to the commonly neglected importance of postoperative hypoproteinemia as the cause of an edema of the intestinal wall with a consequent "interstitial" paralytic ileus. The characteristic features of this syndrome are its onset between the third and the eighth postoperative day; the absence of other known causes of intestinal hypomotility; the benign, but protracted course without treatment; and the therapeutic success achieved by the correction of a hypoproteinemic fluid overload with concentrated albumin and a diuretic. In addition, parenteral hyperalimentation and Rheomacrodex-Sorbit may be indicated, but the hypoproteinemia should at any rate be corrected.
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PMID:[Hypoproteinemia causing postoperative "interstitial" paralytic ileus]. 58 62

Patient characteristics, clinical outcomes, and proposed pathophysiologic mechanisms are reviewed in 138 patients reported in the literature to have had ascites associated with end-stage renal disease. Contributing mechanisms may include fluid overload, peritoneal membrane changes (not necessarily related to peritoneal dialysis), hypoproteinemia, and lymphatic drainage disturbances. In 15% of cases, extensive evaluations may reveal an underlying disease. The most effective therapy may be kidney transplantation.
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PMID:Ascites associated with end-stage renal disease. 330 Feb 89

Techniques of jejunostomy were established in surgical practice by the turn of the century. They were mainly used to administer normal food for the palliation of advanced gastric cancer. Standard postoperative intravenous fluid therapy did not begin in earnest until the late 1930's and did not become routine until the late 1940's because of pyrogens, fear of fluid overload, and commercial nonavailability. For most gastric procedures performed from 1900 until 1940, postoperative treatment consisted of nutrient and saline enemas and subcutaneous infusion of fluid. Jejunal feedings had their greatest use between 1930 and 1950. Gastrectomy was widely applied for cancer and ulcers in dehydrated, malnourished patients. The importance of hypoproteinemia and malnutrition on postoperative morbidity and mortality was established, and the inability of subcutaneous infusions and nutrient enemas to counteract malnutrition and dehydration was recognized. Jejunostomy or nasojejunal tubes were recommended for routine use after gastric operations. During this period, the major advances in jejunal diets and methods of feeding were accomplished. Attention was paid to assuring adequate amounts of nutrients, minerals, and vitamins, and finding diets that were easily tolerated by the jejunum. Important in these developments was the collaboration of surgeons with physiologists, gastroenterologists, pharmacologists, and members of industry. Several factors combined to reduce the use of jejunostomy after 1950. Intravenous therapy became familiar to the surgical profession, widely available, and safe. The number of gastric resections performed has decreased. Earlier referral for operation has resulted in patients with less preoperative debility and malnutrition. By 1970, total parenteral nutrition was available, and fewer jejunostomies were perceived as necessary. During the same interval, however, the increasing incidence of patients with pancreatic, esophageal, and hepatobiliary disease who faced major operations and catabolic postoperative courses presented a new challenge to the surgical community. A resurgence of concern for nutritional support, in part generated by the availability of total parenteral nutrition, prompted a renewed interest in using the gut for feeding the postoperative patient. This renewed interest, an understanding of the techniques of parenteral nutrition, the rediscovery of the gut as an absorptive surface in the postoperative patient, and the ready availability of a variety of defined formula diets have combined to rekindle the enthusiasm of many surgeons for complementary or adjuvant feeding jejunostomy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Intrajejunal feeding: development and current status. 642 23

Nephrogenic ascites is a clinical diagnosis defined as persistent ascites in an uremic patient without evidence for a causative (specific) underlying disease. The incidence is not known. Contributing mechanisms may include peritoneal membrane changes, fluid overload, hyperparathyroidism, reduced lymphatic drainage, heart failure and hypoproteinemia. Rigid fluid control, intensive hemodialysis, high-protein diet, intravenous albumin infusion, intraperitoneal steroid injections and paracenteses as well as implantation of a peritoneatrial pump have all been found ineffective as treatment. Peritoneal dialysis has been shown to resolve ascites, however, the only effective treatment is so far renal transplantation. The development of nephrogenic ascites is associated with a poor prognosis. Thus, one year after the development of nephrogenic ascites 1/3 had died.
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PMID:Nephrogenic ascites. Case report and review of the literature. 781 79

Nephrogenic ascites is a clinical diagnosis defined as persistent ascites in a uraemic patient without evidence of a causative specific underlying disease. Contributing mechanisms may include peritoneal membrane changes, fluid overload, hyperparathyroidism, reduced lymphatic drainage, heart failure and hypoproteinemia. A specific treatment has not yet been found. Rigid fluid control, intensive haemodialysis, high-protein diet, intravenous albumin infusion, intraperitoneal steroid injections and paracenteses as well as implantation of a peritoneoatrial pump were all found to be ineffective. Use of peritoneal dialysis has been shown to resolve ascites, but the only effective treatment is renal transplantation, as demonstrated in the case-report.
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PMID:[Nephrogenic ascites]. 831 65

Six patients with severe and complicated falciparum malaria (6.7 +/- 2.7 WHO criteria) were admitted to our Intensive Care Unit. All patients acquired the disease while travelling in tropical Africa without appropriate chemoprophylaxis. The clinical manifestations included hyperpyrexia (all patients), chills (4), sweating (2), asthenia (3), anorexia (2), headache (1), arthralgias (1), vomiting (4), diarrhoea or abdominal discomfort (3), jaundice (2) and disturbances of consciousness (4). All patients had anemia, thrombocytopenia, hyponatremia, hypoproteinemia, hypoalbuminemia, hypocalcemia and acute renal failure, in one case associated with anuria. A low grade parasitemia was observed in two patients and a high grade parasitemia (20%-58% of erythrocytes) in four. Exchange transfusion was performed only in high parasitemic patients and all of them survived. All patients were treated with quinine, a sulfonamide and pyrimethamine. Additionally, five patients received oxytetracycline, doxycycline or clindamycin. Three patients required hemodyalisis. Five patients had delirium, coma or seizures. All patients had at least one sign of hepatic impairment: liver enlargement, jaundice or increased bilirubin or aminotransferase levels. Two patients had spleen enlargement. Laboratory findings suggested disseminated intravascular coagulation in four patients. Four patients developed pulmonary changes and three of them required mechanical ventilation. A Swan-Ganz catheter was placed in four patients. In three of them (two with pulmonary edema) the pulmonary capillary wedge pressure was initially increased, which suggested a cardiogenic or hypervolemia mechanism, but soon returned to normal level. One patient with low grade parasitemia died because of adult respiratory distress syndrome after 18 days. In our series, the degree of parasitemia was not related to the severity of the disease.
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PMID:[Severe and complicated malaria. Report of six cases]. 977 80

Based on observations in 110 children with nephrotic syndrome (NS) and data from the literature, existing concepts on the pathogenesis of edema formation in the NS have been modified. The data suggest that the basic abnormality is a primary disturbance in renal sodium excretion. Depending on the stage in the development of the NS, the rate of progression in the development of hypoproteinemia, and the absolute levels of plasma oncotic pressure, functional hypovolemia may develop, resulting in stimulation of hemostatic mechanisms and secondary sodium retention. This applies as much to patients with minimal change NS as to patients with histological lesions. Alterations in kidney function (glomerular filtration rate, renal plasma flow, filtration fraction) in the NS cannot be explained by hypo- or hypervolemia, but reflect variations in plasma oncotic pressure and glomerular basement membrane permeability. These abnormalities will also influence sodium excretion. Evaluation of the presence of functional hypovolemia will have therapeutic consequences. A quick diagnosis can be made by assessment of FENa+ and UK+/ (UK+ + UNa+) Sodium retention associated with increased distal Na/K exchange indicates functional hypovolemia, and may be treated by albumin infusion if clinically required.
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PMID:Pathogenesis of edema formation in the nephrotic syndrome. 1132 79

Capillary leakage Syndrome (CLS) is a rare clinical syndrome, that was first described in 1960, characterized by acute episodes of generalized edema, hemoconcentration, hypoproteinemia and monoclonal gammopathy, in the vast majority of cases. We describe a 39-year-old man with anasarca, bilateral pleural and pericardial effusions, ascites and diffuse alveolo-intersticial edema. Clinical and laboratory findings were consistent with an acute episode of CLS. Treatment with prednisone, furosemide and aminophylline was started, which lead to a gradual improvement in 48 hours. Pathophysiologically there is an increase in capillary permeability with the extravasation of fluid and plasmatic proteins to the extravascular space that can lead to hypovolaemic shock. In the second phase there is a reentry of the fluid overload leading to pulmonary edema. The etiology of this hyperpermeability still remains unclear. The role of cytokines has become central in the comprehension of pathophysiology of CLS. Adhesion molecules are probably also involved in the genesis of capillary leakage. CLS treatment remains empirical. However, at present it seems that the association of steroids with furosemide, aminophylline and terbutaline are capable of controlling the clinical manifestation of the acute episodes in most cases. To our knowledge no prophylatic therapy has clearly proven its efficacy. There are only a few series analyzing the long-term evolution of patients with CLS. Further studies are necessary with the objective to collect enough patients with CLS to observe natural history of the disease and evaluate the efficacy of empiric treatments.
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PMID:Capillary leakage syndrome: a case report and a review. 1257 19