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 hematologic, biochemical, and light and scanning electron microscopic features of eperythrozoonosis in four llamas are described. One female and three male yearling llamas were presented for evaluation of chronic weight loss. Three of four llamas had historical evidence of chronic inflammatory conditions. On examination, multiple clinical problems were apparent, including poorly to non-regenerative anemia, inflammatory disease, and hypoproteinemia. Coccoid- and ring-shaped basophilic organisms were present on the erythrocytes of all the llamas. On scanning electron microscopy, individual, pairs, and clusters of coccoid-shaped organisms were present on the erythrocytes. The organisms measured 0.4 to 0.6 micron in diameter and caused no marked deformation of the erythrocyte membrane. A rare organism could be found that produced a slight indentation into the erythrocyte membrane. The light and scanning electron microscopic morphologic features suggested that the organism was an Eperythrozoon. Serial evaluation of serum iron concentrations of the llamas showed a decrease serum iron in all animals, with a concurrent decrease in the total iron binding capacity and percent transferrin saturation in two of the llamas. Common abnormalities seen on serum electrophoresis included a decrease in albumin and beta serum fraction in all llamas and a decrease in the gamma globulin fraction of two individuals.
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PMID:The clinicopathologic, light, and scanning electron microscopic features of eperythrozoonosis in four naturally infected llamas. 227 30

Hematologic features were characterized in 12 dogs with iron deficiency anemia attributable to chronic external blood loss. Consistent abnormalities in hemograms included moderate to marked reticulocytosis, decreased mean corpuscular volume, and decreased mean corpuscular hemoglobin concentration. Hypoproteinemia occurred in only four of 12 dogs. Consistent blood film findings included hypochromic cells, leptocytosis, and erythrocyte fragmentation. These dogs had significantly decreased serum iron values (p less than 0.001) and percent transferrin saturation values (p less than 0.001) compared with 33 clinically healthy adult dogs. The total iron binding capacity values of these dogs were not significantly different (p greater than 0.5) than those of the healthy dogs. Using erythrocyte volume distribution curves, the percentages of microcytic cells (less than or equal to 45 fl) were determined to range from 20% to 82%. Sequential changes in erythrocyte subpopulations were evaluated in four dogs which received iron therapy. The hematologic response consisted of fairly rapid restoration of packed cell volume by production of normocytes followed by a more gradual replacement of residual microcytes by new normocytes.
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PMID:Erythrocyte volume distribution analysis and hematologic changes in dogs with iron deficiency anemia. 683 79

The purpose of this study was to evaluate the sensitivity and specificity of laboratory methods in the diagnosis of posterythropoietin-era, iron-deficient, chronic renal failure patients. The patient population comprised 25 anemic (hemoglobin < 11 g/dL) patients with creatinine greater than 3 mg/dL; 20 were dialysis patients, two were transplant patients, and three patients had renal failure from other causes. Criteria for study inclusion were as follows: bone marrow iron was the reference standard and was graded 0 to +4, ranging from absent to diffuse homogeneous iron staining; serum ferritin concentration and serum transferrin saturation were tested in terms of sensitivity and specificity. The reference standard indicated that iron deficiency existed in 40% of patients. Neither serum ferritin nor transferrin saturation were completely adequate diagnostic tools. Serum ferritin levels less than 200 ng/dL were 100% specific for the diagnosis but only 41% sensitive. Transferrin saturation of less than 20% was 88% sensitive, but only 63% specific. By excluding patients with hypoproteinemia (transferrin values of < 150 mg/dL), the sensitivity of the test increased to 100% and the specificity to 80%. We conclude that transferrin saturation is an adequate screening tool in anemic chronic renal failure patients, provided that hypoproteinemia is not present. By determining both the serum ferritin concentration and the transferrin saturation, a high sensitivity and specificity can be achieved, even in patients with hypoproteinemia. Furthermore, we believe that on this basis, iron therapy in patients with renal insufficiency can be improved.
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PMID:Diagnosis of iron deficiency anemia in renal failure patients during the post-erythropoietin era. 862 43

Quantitative study of serum protein loss into the alimentary tract from the tumor of gastric cancer using 111Indium-transferrin (111In-Tf) was performed. Gamma counting of 111In-Tf excreted in feces and 111In-Tf scintigram were performed in 24 patients with gastric cancer and 10 controls. Transferrin was labelled by incubating 111MBq (3mCi) of 111In chloride with approximately 13ml of patient plasma in vitro. After intravenous injection of 111In-Tf, an aliquot was weighed and its radioactivity was measured in a gamma-counter. Feces were collected every 24hrs up to 72hrs. Then 111In in the feces was calculated as a percentage of the injection dose. 111In excreted in the feces within 72hrs in patients with gastric cancer was 3.71 +/- 3.87% (mean +/- SD), which was significantly higher than the 0.48 +/- 0.26% in 10 controls. 111In in feces correlated the area of the tumor in the stomach (p < 0.001). In 18 patients positive scan was recognized and was localized the protein loss in the cavity of the stomach within 10 minutes. Positive scan was found to move along the intestine successively. 111In-Tf can be useful in assessing of hypoproteinemia of gastric cancer.
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PMID:[Quantitative study of serum protein loss into the alimentary tract in patients with gastric cancer]. 793 36

The present study was performed to clarify the possibility of IGF-I as an early indicator of malnutrition in patients with end-stage renal disease. Thirty-two patients (19 males, 13 females; mean age 49.6 +/- 10.0 years) undergoing dialysis were enrolled in the study. Body weight, skinfold thickness, and midarm muscle circumferences (MAMCs) were measured for anthropometric nutritional indices. Blood samples were collected to measure the following endocrinological, biochemical and hematological indices: IGF-I, growth hormone, (GH), total protein, prealbumin, albumin, transferrin, hematocrit, and lymphocyte count. Nutritional indices were measured again 1 month later to calculate the percent difference among them. Moreover, 2 patients who showed a decrease in IGF-I and suffered from malnutritional complications, such as hypoproteinemia and emaciation, which could not be successfully treated by conventional therapies were selected in order to confirm the nutritional role of IGF-I mediated by recombinant human GH (r-hGH). The serum IGF-I concentration distribution ranged from 22 to 225 ng/ml. In 15 patients (10 males, 5 females), it fell from 22 to 82 ng/ml below the normal range. Partial correlation coefficient analysis demonstrated that baseline IGF-I and the percent difference of each the body weight, MAMC, prealbumin and albumin were highly significantly correlated (r = 0.431, 0.641, 0.624 and 0.348, respectively; p = 0.014, 0.001, 0.001 and 0.028, respectively). The percent difference of IGF-I did not correlate significantly with that of any other nutritional index during the 1-month observation without administration of r-hGH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:IGF-I as an early indicator of malnutrition in patients with end-stage renal disease. 805 72

From a clinical aspect, there are still a number of unsolved problems in patients with end-stage renal disease, for instance intractable malnutrition. The present study was undertaken to establish the therapeutic effect of recombinant human growth hormone (r-hGH) on the nutritional state and clarify the usefulness of the insulin-like growth factor-I (IGF-I) insulin-like growth factor binding protein-1 (IGFBP-1) ratio as nutritional indices for prediction of the clinical response in uremic patients on hemodialysis. Thirty hemodialysis patients (13 females and 17 males, mean age 56.7 +/- 15.2 years) were studied who were suffering from malnutrition and could not be treated by any of the usual nutritional therapies; they were subjected to 0.5 IU/kg/week of r-hGH subcutaneously after hemodialysis for 2 weeks. Blood samples were collected for measurement of the following plasma biochemical and hematological indices: serum IGF-I, IGFBP-1, growth hormone, total protein (TP), prealbumin, transferrin, albumin, serum urea nitrogen (SUN), creatinine, hematocrit, and amino acids. Immediately after r-hGH administration, SUN, essential amino acid and nonessential amino acid changed from 67.7 +/- 12.3 to 56.5 +/- 10.5 mg/dl (p < 0.05), from 798 +/- 84 to 1,115 +/- 208 microM/l (p < 0.05 vs. baseline), and from 2,185 +/- 221 to 2,814 +/- 621 microM/l (p < 0.05), respectively. Serum IGF-I increased markedly from 193 +/- 49 to 321 +/- 81 ng/ml, whereas serum IGFBP-1 decreased from 139 +/- 13 to 81 +/- 19 micrograms/l (p < 0.05). Four weeks after r-hGH administration, serum TP and albumin increased from 5.5 +/- 0.2 to 6.0 +/- 0.3 g/dl (p < 0.05) and from 3.2 +/- 0.2 to 3.6 +/- 0.3 g/dl (p < 0.05), respectively. Serum IGF-I/IGFBP-1 ratio was significantly higher in patients with an increase of 0.5 g/dl or more in serum albumin than in other patients with poor response and the control group before r-hGH administration. Patients with marked improvement in serum albumin showed an IGF-I/IGFBP-1 ratio of 2 or less. On the other hand, patients without favorable improvement in serum albumin had a higher ratio of 4 or more. We conclude that r-hGH and IGF-I improve the malnutritional state by alleviating hypoproteinemia and abnormality of serum amino acid profile in uremic patients on hemodialysis. In addition, the serum IGF-I/IGFBP-1 ratio is useful not only as a nutritional parameter but also as a predicting index of responsiveness to r-hGH.
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PMID:IGF-I/IGFBP-1 as an index for discrimination between responder and nonresponder to recombinant human growth hormone in malnourished uremic patients on hemodialysis. 938 Feb 35

Protein losing enteropathy (PLE) is a gastrointestinal disorder that is associated with excessive loss of plasma protein into the gut resulting from abnormal mucosal permeability. The disease is usually caused by inflammation. The loss of protein in PLE is a nonselective process affecting albumin, globulin and transferrin. Abdominal scintigraphy with human serum albumin marked by Tc99m seems to be an easy and sensitive method for diagnosing PLE. An 4-year-old girl was presented to an outside Pediatric Department due to hypoproteinemia and recurrent pneumonia which had caused several prior hospitalizations. The laboratory tests revealed hypoproteinemia, hypoalbuminemia, low level of IgG, sideropenia, and a decreased level of T lymphocytes. The loss of protein into the gut was confirmed by fecal clearance of alfa-1 antitrypsin. Only nonspecific inflammation was detected by biopsy of the small intestine. These clinical and laboratory findings, quickly decreasing IgG and albumin levels in spite of i.v. supplementation and the lack of proteinuria permitted PLE diagnosis. The abdominal scintigraphy was planned to assess and localise protein losing through GIT and for strategy of possible surgical treatment. Abdominal dynamic scintigraphy was performed immediately after the injection of 300 MBq Tc99m human albumin. 90 images were taken within 180 minutes. Delayed abdominal images were obtained 6 and 24 hours after the tracer injection. Anterior abdominal scintigraphy showed pathological activity of Tc99m-albumin in small bowel in the upper left segment of the abdomen in the 40th minute after injection. Extensive accumulation of albumin was seen in the 160th minute. Delayed images, after 3 and 6 hours, revealed translocation of the tracer into the lower right abdominal segment. The further passage and tracer concentration was detected in ascendant and transverse colon. Based on the laboratory tests and scintigraphic images the girl was suspected to have segmental lymphangiectasia of small intestine and was qualified for laparatomy and, possibly, for surgical resection of the pathologically changed bowel. However, diffuse pathological changes revealed in the guts during the operation, rendered the operation impossible. Tc99m-labelled human serum albumin scintigraphy may be considered the method-of-choice in the diagnosis of protein-losing enteropathy. However, in this test the assessment of the enteropathy dimension is difficult and surgical treatment should be planned with caution.
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PMID:[Protein losing enteropathy (PLE) detected by Tc99m-labelled human serum albumin abdominal scintigraphy--case report]. 1506 43

The ICR-derived glomerulonephritis (ICGN) mouse, a new inbred mouse strain with a hereditary nephrotic syndrome, is considered to be a good model of human idiopathic nephrotic syndrome and notably exhibits proteinuria and hypoproteinemia from the neonatal stage. In chronic renal disorder (CRD), anemia is a major subsequent symptom (renal anemia). The precise cause of renal anemia remains unclear, primarily owing to the lack of appropriate spontaneous animal models for CRD. To establish adequate animal models for anemia with CRD, we examined the hematological-biochemical properties and histopathological characteristics. With the deterioration of renal function, ICGN mice developed a normochromic and normocytic anemia, and exhibited normochromic and microcytic at the terminal stage. The expression of erythropoietin (EPO) mRNA both in the kidneys and liver and the EPO leak into the urine were observed in ICGN mice, indicating a disrupted metabolism of EPO in ICGN mice. In addition, a lack of iron induced by the hemolysis in the spleen and the leak of transferrin into urine as proteinuria aggravated the anemic condition. In conclusion, the ICGN mouse is a good model for anemia with CRD.
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PMID:Anemia with chronic renal disorder and disrupted metabolism of erythropoietin in ICR-derived glomerulonephritis (ICGN) mice. 1513 73

We present two siblings with a previously undescribed congenital disorder of glycosylation (CDG). The first child died in utero with severe hydrops fetalis and the second presented following preterm delivery with respiratory insufficiency, generalised edema and a protein-losing enteropathy. Both had a similar pattern of facial dysmorphism and joint contractures. The diagnosis of CDG-I was made following the birth of the second child based on the serum transferrin isoform pattern. CDG-Ia and -Ib were excluded by specific enzyme analysis. Joint contractures are a relatively uncommon finding in CDG, although fetal hydrops (CDG-Ia) and protein-losing enteropathy (CDG-Ib) are well recognized. CDG must be considered in the differential diagnosis of hydrops fetalis, congenital hypoproteinemia and death in early infancy, particularly when associated with dysmorphic features.
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PMID:A previously undescribed form of congenital disorder of glycosylation with variable presentation in siblings: early fetal loss with hydrops fetalis, and infant death with hypoproteinemia. 1766 80

The nephrotic syndrome is characterized by the loss of many proteins, via the urinary system. It exceeds the bodies compensatory abilities and results in abnormalities in blood clotting system, particularly due to antithrombin deficiency. It significantly increases the risk of thromboembolic complications. A loss of erythropoietin and transferrin leads to anemia. Polycythemia is a rarely reported phenomenon. The case describes a 20-years old patient with massive nephrotic syndrome and polycythemia, complicated by a pulmonary embolism. The patient had a steroid-dependent submicroscopic glomerulonephritis with a severe episode of nephrotic syndrome associated with centralization of circulation, proteinuria 40.9 g/day, deep hypoproteinemia (albumin=1.2 g/dl), hyperlipidemia, hypercoagulable state (antithrombin activity 29%), polycythemia (Hb=21.1 g/dl, HTC=60%). Kidney function parameters were normal. We started the immunosupression (glycocorticosteroids i.v., continuated p.o. and cyclosporine A) and intensive symptomatic treatment. To reverse hypovolemia and polycythemia, 20% albumin solutions, intravenous infusions and diuretics were used. There was no effect. Due to intensive polycythemia the erythroapheresis procedure was performed. It resulted in normalization of the red blood cell count (Hb=13.4 g/dl, HCT=37%) and the improvement of blood circulation. To prevent the patient from thromboembolism, the prophylactic dose of low molecular weight heparin (LMWH) was administered (dalteparin 5000 IU subcutaneously, once a day). Despite the prophylaxis, an episode of dyspnea with tachycardia occured. It was connected with elevated Ddimer and troponin levels and a right ventricle overload in echocardiographic imaging. The pulmonary embolism was suspected. Perfusion lung scintigraphy confirmed this diagnosis. We supposed that the heparin was ineffective due to an antithrombin deficiency. Therefore, apart from a therapeutic dose of LMWH, intravenous antithrombin concentrate was given to the patient (1500 IU twice). The dyspnea resolving was observed. The D-dimer and troponin level reversion to normal was noticed. Heparin injections, connected with antithrombin infusion, was an effective treatment of the pulmonary embolism. Due to the lack of antithrombin in nephrotic syndrome, using only heparin may be insufficient. The erythroapheresis is an effective treatment of polycythemia.
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PMID:[Above-standard proceeding in nephrotic syndrome - case report]. 2708 3


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