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)

The benefits of parenteral feeding need no longer be emphasised. However, qualitative and quantitative food supplements raise a certain number of difficulties which should be better known. Infection is the most frequent complication. It may be avoided by strict aseptic precautions throughout parenteral feeding. Hypoglycemia is a major risk owing to the possible consequence. Hyperglycemia and its consequence of osmotic polyuria is more frequent and should be controlled to avoid loss of water and salt. Complications due to the use of lipid emulsions are exceptional when soya oil is used. Hypophosphoremia should be corrected by increasing phosphate intake. Hypocalcemia is common; it is often associated with hypoproteinemia and sometime a low calcium intake, vitamin D deficiency or a sudden increase in phosphate intake. Vitamin deficiencies, hypomagnesemia, and oligo-element deficiencies should be correcty by appropriate supplements.
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PMID:[Parenteral feeding. Prevention of complications in adults during exclusive mid-term parenteral feeding]. 19 99

A model in Wistar rats (n = 30, 279-345 g) was developed to study circulatory, respiratory, metabolic, and lethal effects of an intravenous infusion (30 min; 1.25, 1.5, 1.75, and 2.0 mg/kg) of rattlesnake (Crotalus viridis helleri) venom. Venom produced perfusion failure with lactacidemia, hemoconcentration, hypoproteinemia, and death. The severity of poisoning was proportional to the quantity of venom given and to the elevation in lactic acid and hematocrit. Hemorrhages in the diaphragm, intercostal muscles, and intestine were observed at necropsy. In a separate test, rats (n = 12, 311-355 g) received an infusion of 1.5 mg/kg of venom or physiological salt solution. Blood volume was measured 30 min after the end of infusion in both groups with radioiodinated (125I) human serum albumin (RIHSA) and 51Cr-labeled rat red cells. Venom produced a significant reduction in total blood volume index (35%, P less than 0.001), plasma volume index (46%, P less than 0.001), and red cell mass indec (22% P less than 0.005). The slope of the RIHSA-disappearance curve of animals that received venom was more than twice that of the control group. We conclude that perfusion failure following rattlesnake envenomation is associated with hypovolemia due to increases in vascular permeabiltiy and hemorrhage.
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PMID:Rattlesnake venom shock in the rat: development of a method. 121

Animal studies have indicated that volume resuscitation is successful with salt-containing crystalloid solutions as well as colloid solutions. Hyperosmolar salt solutions appear to have benefits over isosmolar solutions. Both, however, produce hypoproteinemia, which can lead to edema formation due to changes in the transcapillary oncotic gradient and possibly by changing the interstitial matrix. The lung appears to be much more resistant to edema formation than the soft tissues. Except for the dog, the lung does not appear to be significantly altered from shock with no substantial increase in protein permeability being evident in most studies. Colloid therapy, either proteins or dextran, effectively restores cardiovascular stability after hypovolemia and also prevents the increased transcapillary fluid flux seen in the lung and soft tissues, the former not appearing to be of much clinical significance, while the latter may lead to significant tissue edema. Blood replacement is necessary to restore adequate oxygen delivery to the tissues. The ideal hematocrit appears to be around 30-35.
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PMID:Animal research on hypovolemic shock and resuscitation: an update. 618 28

This paper is a study of 117 patients with endstage renal failure, treated by continuous ambulatory peritoneal dialysis (CAPD) over periods of 1-56 months. The study has shown CAPD to be an effective form of dialysis with a number of advantages over intermittent peritoneal dialysis and hemodialysis (better control of salt and water status, hypertension and anemia, steady state biochemistry and greater ease of self-dialysis). Peritoneal clearance and ultrafiltration have remained adequate in all but a few patients. Hypoproteinemia, poor nutrition, obesity and abdominal herniae have been problems in a small percentage of patients. Hyperlipidemia has developed in half the patients but improved with diet. Peritonitis remains the major barrier to the more widespread use of CAPD, although its incidence can be considerably reduced by use of better connectors, bacterial filters and choice of patients.
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PMID:Continuous ambulatory peritoneal dialysis (CAPD): an established treatment for endstage renal failure. 636 Jan 16

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

We present a 72-year-old man who had episodes of severe, acute renal failure during severe attacks of diarrhea caused by Vibrio cholerae. Patterns of acute tubular necrosis and tubulointerstitial nephritis developed following hypotension and decrease in renal blood flow, causing secondary renal ischemia. There was severe dehydration with profound hypovolemia and infection. The clinical picture included fever, weakness, arthralgia, pedal edema, mild bilateral pleural effusions, anemia, leukocytosis, azotemia with a maximum of 330 mg/dl of urea, creatine to a maximum of 9.8 mg/dl, hypoproteinemia, severe metabolic acidosis, marked increase in lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), microscopic hematuria, sterile leukocyturia, normoglycemic glucosuria and phosphaturia with diminished tubular reabsorption of phosphorus. A short oliguric phase was followed by a polyuric phase lasting about 10 days, and glomerular and tubular function became normal after about 3 weeks. Treatment was by intensive infusions of fluids, electrolytes, sodium bicarbonate, salt-free albumin and antibiotics. To the best of our knowledge, this renal complication of cholera has not yet been described in Israel.
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PMID:[Acute renal failure as a complication of cholera]. 868 55

In hyponatremia related to syndrome of inappropriate antidiuretic hormone (SIADH), hypouricemia is explained primarily by the high uric acid clearance rate that results from the decrease in tubular uric acid reabsorption. This modification of tubular handling of uric acid is considered to be induced by the increase in the "effective vascular volume". This study was designed to determine if V1-receptor stimulation participates in the development of a high uric acid clearance rate as in SIADH, in which the antidiuretic hormone acts on V1 and V2 receptors. Therefore, the urate clearance rate was measured in seven volunteers with 1-desamino-8-D-arginine vasopressin (dDAVP)-induced hyponatremia, with dDVAP stimulating exclusively the V2 receptors (Group I), and in six patients with SIADH (Group II) during both normo- and hyponatremia. As expected, in both groups, the serum uric acid concentration decreased during hyponatremia, but did so to a larger extent in the patients with SIADH (-53% versus -29%, P < 0.02). Despite similar levels of hyponatremia (126 +/- 5 mmol/L and 125 +/- 5.5 mmol/L), of hypoproteinemia (64 +/- 5 g/L and 63 +/- 5 g/L) and of salt excretion (FENa, 0.66 +/- 0.28% and 0.73 +/- 0.25%), the urate clearance (8.3 +/- 3.3 mL/min) and the fractional excretion of filtered uric acid (5.7 +/- 2%) in Group I were not significantly different during hyponatremia than during normonatremia (6.4 +/- 1.5 mL/min and 5.4 +/- 0.9%). On the other hand, in Group II, both parameters were increased (17.8 +/- 2.9 mL/min and 19.6 +/- 5.3%; P < 0.001) and both values were higher than in the dDAVP-induced hyponatremia (P < 0.01). Additionally, the administration of a potent V1-receptor agonist (triglycyl-lysine-vasopressin) in a patient with central diabetes insipidus with preexisting dDAVP-induced hyponatremia produced a rapid increase of urate clearance. Because dDAVP acts only on the V2 receptors, these data suggest that the higher urate clearance observed during hyponatremia related to SIADH is not only the consequence of an increased "effective vascular volume," but that V1-receptor stimulation also contributes to it, by a mechanism that remains to be determined.
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PMID:Evidence in hyponatremia related to inappropriate secretion of ADH that V1 receptor stimulation contributes to the increase in renal uric acid clearance. 873 18

Eighty-two children with the toxic dystrophic syndrome coursing in the presence of acute enteric infection were examined. A number of pathogenetically significant disorders were revealed: salt-deficient exsicosis, exsication, hypopotassemia, anemia, hypoproteinemia, stable metabolic acidosis, protein and energy insufficiency. Among the causes of protein and energy insufficiency associated with progressive weight loss the principal were impaired cavitary digestion, decrease of the absorption capacity of the intestine for proteins, fats, and carbohydrates, and long inadequate nutrition because of protracted diarrhea. Newly developed three-staged intensive care protocol with correction of homeostasis, provision with energy and nutrients, and repair of cavitary digestion and absorption capacity of the intestine helped reduce the mortality in this patient population from 13.4 to 4.8%.
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PMID:[Pathogenesis and intensive care of infants with toxic-dystrophic syndrome]. 904 71

It has been shown that children with nephrotic syndrome due to minimal change disease (MCD) can present with avid salt retention and stimulated vasoactive hormones, as well as with stable edema. The present study examines these conditions in children with nephrotic syndrome not due to MCD (non-MCD). In six children with hypovolemic symptoms (congenital nephrotic syndrome in four), strong sodium retention (fractional sodium excretion, FE(Na), 0.2 +/- 0.2%) was found. Lithium clearance (FE(Li)) and maximal water excretion (Vmax) were suppressed, suggesting avid sodium reabsorption throughout the nephron. Aldosterone, renin, and norepinephrine were elevated. Sixteen other children with non-MCD had stable edema. FE(Na) was 1.8 +/- 1.1%, whereas FE(Li), Vmax, and hormones were normal, and not different from data in 35 nonproteinuric children. In children with MCD, 12 presented with hypovolemic symptoms and strong sodium retention (FE(Na) 0.3 +/- 0.3%), whereas 15 were stable (FE(Na) 1.1 +/- 0.7%). Regarding tubular sodium handling and hormones, the same distinction could be made as for the children with non-MCD. However, hypoproteinemia differed. In the children with non-MCD lesions, plasma colloid osmotic pressure was significantly lower in the hypovolemic types (4.2 +/- 0.4 mmHg) than in those with stable edema (13.0 +/- 3.8 mmHg; P < 0.05); in MCD, no such difference existed (respectively, 8.1 +/- 3.0 and 9.9 +/- 2.2 mmHg). In summary, children with nephrotic syndrome may present with pathophysiologic pictures of decreased effective circulating volume or of stable edema, regardless of whether they have non-MCD or MCD. The pathogenesis of the hypovolemic picture seems to be different, since it is associated with extreme hypoproteinemia only in the children with non-MCD.
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PMID:Pathophysiology of edema formation in children with nephrotic syndrome not due to minimal change disease. 1021 32

Acute hemorrhage is a main cause of reduction of blood oxygen capacity. The main aim of correction of sequels of acute hemorrhage is to maintain effective gas exchange by restoring central circulation and microcirculation, the rate of diuresis, by normalizing water-salt exchange, to eliminate anemia, hypoproteinemia, and acute blood coagulability disorders. The values of oxygen budget with calculated oxygen delivery and consumption and those of hemoglobin and hematocrit which are of great value only after recovery of circulating blood volume are considered to be major indications for hemotransfusion. A relationship is established between the extraction and uptake of oxygen and its delivery. The concept of the critical level of oxygen delivery is considered, ways of correcting oxygen indebtedness are presented. Alternatives to the use of hemotransfusions by employing the solutions of modified hemoglobulin and perfluorocarbon-containing emulsions are under consideration. A possible algorithm of aid rendering in acute hemorrhage is given.
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PMID:[Acute hemorrhage. View on the problem]. 1261 Nov 47


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