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 purpose of this investigation was to determine the effect of nephrotic syndrome (NS) on the pharmacodynamics of a barbiturate. NS was induced in male rats by puromycin aminonucleoside; it caused hypoproteinemia, increased liver and kidney weight and elevated serum creatinine and urea nitrogen concentrations. Serum albumin concentration decreased from 3.5% in controls to 0.90% in NS animals. The rats were infused i.v. with heptabarbital, 1 mg/min, until they lost their righting reflex. The total dose (mean +/- S.D.) required by rats with NS, 40.2 +/- 4.2 mg/kg, was substantially lower than that required by normal animals (68.6 +/- 6.2 mg/kg, P less than .001). Serum protein binding of heptabarbital was reduced from 49% in controls to 26% in NS rats. However, the drug concentration in cerebrospinal fluid (CSF) at the pharmacologic endpoint was not significantly different in controls and NS rats (18.9 +/- 1.5 vs. 18.3 +/- 1.4 mg/l). Serum, CSF and the brain contained appreciable concentrations of a metabolite of heptabarbital. To determine if the metabolite contributes to the pharmacologic effect of the parent drug, rats received an i.v. injection of 46, 60 or 100 mg/kg of heptabarbital. Concentrations of heptabarbital in CSF at return of righting reflex (which occurred after 15, 25 and 50 min, respectively) were independent of dose whereas metabolite concentrations increased with increasing dose. Thus, the metabolite of heptabarbital in male rats is pharmacologically inactive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kinetics of drug action in disease states. XXIX. Effect of experimental nephrotic syndrome on the pharmacodynamics of heptabarbital: implications of severe hypoalbuminemia. 256 85

The nephrotic syndrome is characterized by increased urinary excretion of albumin and other serum proteins, accompanied by hypoproteinemia and edema formation. Nephrotic patients have lower serum albumin concentrations than do patients undergoing continuous ambulatory peritoneal dialysis when albumin and protein losses are the same in both groups, suggesting that nephrotic patients may not maximally adapt to loss of protein. The fractional rate of albumin catabolism is increased in nephrotic patients, possibly as a result of increased albumin catabolism by the kidney, but the absolute albumin catabolic rate is decreased in nephrotic patients. The rate of albumin synthesis may be increased, but not sufficiently to maintain normal serum albumin concentration or albumin pools. Augmentation of dietary protein in nephrotic rats directly stimulates albumin synthesis by increasing albumin mRNA content in the liver, but also causes an increase in glomerular permeability to macromolecules so that much if not all of the excess albumin synthesized is lost in the urine. When dietary protein is restricted, the rate of albumin synthesis is not increased either in nephrotic patients or in rats, despite severe hypoalbuminemia. Although dietary protein supplementation may lead to positive nitrogen balance, dietary protein supplementation alone does not cause an increase in serum albumin concentration or body albumin pools, and may instead cause further albumin pool depletion because of changes induced in glomerular permselectivity. The use of angiotensin-converting enzyme inhibitors may blunt the increased albuminuria caused by dietary protein supplementation and allow albumin stores to be increased.
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PMID:Albumin metabolism in the nephrotic syndrome: the effect of dietary protein intake. 305 80

Hypoproteinemia by itself produces a metabolic alkalosis. It is not clear whether a respiratory compensation (hypercapnia) develops with this alkalosis; patients with liver cirrhosis, most of them with hypoproteinemia, are known to hyperventilate. We studied 23 clinically stable patients with hypoproteinemia, with very low albumin-to-globulin ratios (range 0.4 to 1.1), who had either liver cirrhosis (n = 12) or other medical conditions (n = 11). In both groups, there was marked hypocapnia, accompanied by alkalemia (PaCO2 values (mean +/- SD) 31 +/- 2 and 32 +/- 3 torr; pH (mean +/- SD) 7.45 +/- 0.03 and 7.47 +/- 0.03, for the patients with cirrhosis and those without, respectively). Hypoxemia was not the stimulus provoking hyperventilation. The lowering of PaCO2 was proportional to the reduction of serum albumin and total protein concentrations; no detectable difference was seen between the patients with cirrhosis and those without cirrhosis in this apparent dependence of PaCO2 on the concentration of serum proteins. Many of these clinically stable patients with hypoproteinemia, with or without liver cirrhosis, had appreciable concentrations of unidentified anions in plasma (inappropriately high anion gap). Whatever the nonrespiratory acid-base status of the patients with hypoproteinemia, their pulmonary ventilation (hypocapnia) appeared excessive when compared with subjects (presumably) without proteinemia who had similar nonrespiratory acid-base states. The mechanism responsible for the hyperventilation in hypoproteinemia and the nature of the unidentified anions in this condition are obscure.
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PMID:Hyperventilation with hypoproteinemia. 318 88

We compared the effect of crystalloid to colloid fluid infusion on extravascular lung water (EVLW) in hypoproteinemic dogs. Plasmapheresis was used to decrease plasma colloid osmotic pressure (COP) to less than 40% of its base-line level. Five animals were then infused with 0.9% sodium chloride (saline), five with 5% human serum albumin (albumin), and five with 6% hydroxyethyl starch (hetastarch) to increase the pulmonary arterial occlusive pressure by 10 Torr in comparison to the postplasmapheresis level for a 5-h study interval. On completion of the procedure, the lungs were harvested and EVLW measured by the blood-free gravimetric technique. Three to six times the volume of saline compared with albumin or hetastarch (P less than 0.001) was infused. In the saline animals, COP was decreased to 3.3 +/- 1.3 Torr, whereas COP was increased to 18.1 +/- 1.4 Torr in albumin animals (P less than 0.001) and 20.1 +/- 1.6 Torr in the hetastarch group (P less than 0.001). The saline-treated dogs developed gross signs of systemic edema. The EVLW was 8.1 +/- 0.9 ml/kg in saline animals compared with 5.3 +/- 2.1 ml/kg in the albumin (P less than 0.05) and 4.1 +/- 1.4 ml/kg in the hetastarch (P less than 0.01) groups. These data indicate that crystalloid fluid infusion during hypoproteinemia is associated with the development of both systemic and pulmonary edema.
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PMID:Effects of crystalloid and colloid fluids on extravascular lung water in hypoproteinemic dogs. 361 Sep 36

Hypocalcemia was found in 122 (1.6%) of the patients attending a large oncological center. In 10% of the cases, hypocalcemia was caused by hypoparathyroidism and/or uremia, in 12% it was related to a major infection. Osteoblastic metastases were responsible in 4% of the cases and in 74% hypocalcemia accompanied an impairment of the general condition due to the malignancy or its treatment, usually in the terminal stage of the disease. The most common cause of hypocalcemia in this group of patients seemed to be hypoproteinemia. Correction of serum calcium for variations in serum albumin concentration, however, indicated that a small proportion had a decreased ionized calcium value as well, the mechanism of which remained obscure. The hypocalcemia was usually relatively mild, especially after correction for albumin variations. Tetanic symptoms were not seen. Hypocalcemia thus seems to be a fairly common complication of malignant disease, the clinical relevance of which, however, appears to be relatively small in most cases.
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PMID:A hospital survey of hypocalcemia in patients with malignant disease. 377 91

Sheep were rendered hypocupraemic using parenteral ammonium tetrathiomolybdate (ATM). Fifteen thousand third stage larvae of Trichostrongylus axei and T. colubriformis in the ratio 1:1 were administered three times per week for six weeks, starting four weeks after cessation of ATM treatment. The changes in liver and plasma copper (Cu), caeruloplasmin activity, serum proteins, faecal nematode egg counts and total nematode counts were measured in the sheep for 10 weeks after infection. Decreases in liver Cu, plasma Cu and caeruloplasmin activities were detected soon after infection. There was a significant (P less than 0.05) interaction of the effects of Cu deficiency and nematode infection on these changes. Hypoproteinaemia, attributed to serum albumin loss, was demonstrated seven weeks after infection, but this was not associated with the interaction of Cu deficiency and nematode infection. No changes in serum globulins were detected. Although the results support the contention that gastro-intestinal nematodiasis can significantly exacerbate an existing Cu deficiency in sheep, there was no evidence that hypocuprosis would predispose sheep to higher nematode burdens.
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PMID:Effects of concurrent copper deficiency and gastro-intestinal nematodiasis on circulating copper and protein levels, liver copper and bodyweight in sheep. 396 64

The circulatory, respiratory, metabolic, lethal and tissue permeability effects of an i.v. infusion (30 min; 1.5, 2.0, 2.5 and 3.0 mg/kg) of puff adder (Bitis arietans) venom were studied in Sprague-Dawley rats (n = 35, 275-325 g). Venom (2.5 mg/kg) produced circulatory failure with arterial hypotension, hemodilution, hypoproteinemia, lactacidemia and marked hyperventilation by +4 hr. In a separate test (n = 20, 282-325 g) blood volume was measured at end venom (2.5 mg/kg) infusion (0 time) and at +3 hr with radioiodinated (125I) human serum albumin and 51Cr-labeled rat red blood cells. Venom produced a significant reduction in total blood volume index (9%, P less than .05), plasma volume index (12%, P less than .01) and red cell mass index (6%, P = N.S.) as compared to the control group at 0 time. Critically low levels of these indices were observed (43, 42 and 46%, respectively) at +3 hr. At both intervals the transvascular escape rate of radioiodinated human serum albumin but not 51Cr-labeled rat red blood cells was significantly increased in comparison to the control group. Tissue permeability index to 51Cr-labeled rat red blood cells and radioiodinated human serum albumin was increased primarily in the stomach and small intestine. These data suggest that increased vascular permeability to protein and red cells, primarily in the splanchnic region, leads to hypovolemic shock and death after a lethal dose of i.v. Bitis venom in rats.
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PMID:Puff adder venom shock: a model of increased vascular permeability. 399 22

Intestinal lymphangiectasia is a disease characterized by hypoproteinemia and edema resulting from protein-losing gastroenteropathy secondary to abnormal intestinal lymphatics. Immunologic abnormalities associated with this disease include hypogammaglobulinemia, lymphocytopenia, skin anergy, and impaired allograft rejection. In the present study, the in vitro blastogenic transformation of lymphocytes from 12 patients with intestinal lymphangiectasia was assessed in order to gain insight into the mechanism of the cellular immune defect in this disease. Peripheral blood lymphocytes from patients with intestinal lymphagiectasia showed impaired in vitro transformation to nonspecific mitogens, specific antigens, and allogeneic cells when compared to equal numbers of cells from normal individuals. Patients with the most deficient in vitro reactivity tended to have the lowest serum albumin concentration and the lowest absolute lymphocyte count. Lymphocytes obtained from chylous effusions in each of the four patients studied transformed more vigorously than peripheral blood cells from the same patients. These results may be explained by the loss of recirculating, long-lived lymphocytes into the gastrointestinal tract, resulting in a relative depletion of the population of lymphocytes necessary for in vitro blast transformation. This disease thus represents a clinical analogue of animals with experimental thoracic duct drainage, and provides evidence for the existence, in man, of two functionally distinct lymphocyte populations. In addition, these findings establish a new mechanism of impaired delayed hypersensitivity and defective in vitro lymphocyte transformation, i.e. the gastrointestinal loss and consequent depletion of the long-lived, recirculating population of lymphocytes from the peripheral lymphocyte pool.
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PMID:Impaired lymphocyte transformation in intestinal lymphangiectasia: evidence for at least two functionally distinct lymphocyte populations in man. 455 85

Low anion gap occurs in a variety of disorders including hypoproteinemia. We evaluated anion gap in 28 children - 18 boys and 10 girls with minimal change nephrotic syndrome during 55 separate episodes of exacerbations. To assess the contribution of serum total proteins, albumin, cholesterol and immunoglobulin levels to low anion gap, a coefficient of correlation was calculated. Anion gap was significantly low (p less than 0.01) during exacerbations in nephrotic. The low anion gap correlated with low serum total proteins (less than 4 g/dl) and serum albumin levels (less than 1.5 g/dl) but not to serum cholesterol or immunoglobulin levels. Low total serum protein at patients blood pH, contributed fewer negative charges to anion gap thereby lowering the anion gap. The major cause of low anion gap in nephrotic syndrome is hypoproteinemia especially hypoalbuminemia.
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PMID:Anion gap in nephrotic syndrome. 649 Mar 22

We wished to determine whether subtotal replacement of protein in plasma removed at plasma exchange would be adequate to prevent hypovolemia and hypoproteinemia. Seven well nourished outpatients with chronic progressive multiple sclerosis underwent 60 plasma exchanges in which two liters of plasma were replaced with 750 ml saline followed by 1250 ml of a 5% albumin solution (62.5% albumin replacement). Total serum protein, protein electrophoresis, and immunoglobulin levels were measured before and after each exchange. Clinically, the exchanges were well tolerated. Total serum protein dropped by a mean of only 18% during the study and mean preexchange serum albumin levels were unchanged, even though immunoglobulins decreased by 57-72%. We conclude that in well nourished patients, partial albumin replacement of this magnitude is an adequate substitute for plasma removed in a plasma exchange.
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PMID:Partial plasma protein replacement in therapeutic plasma exchange. 668 82


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