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 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

Hookworms are among the most widespread of human parasites and occur all over the tropics and subtropics. They are bloodsucking roundworms that inhabit the duodenum and jejunum. Usually the infection is mild (hookworm carrier state), but sometimes the infection is heavy and results in anaemia and/or hypoproteinemia (hookworm disease). Hookworms are occasionally imported to Norway by immigrants. This paper describes two cases of severe and life-threatening hookworm disease treated in our hospital. The first patient was a Pakistani woman born in 1929 who on admission was hypovolemic with severe hypochromic anaemia (haemoglobin 3.6 g/100 ml). The second patient was a Bolivian refugee born in 1946 with a similar clinical picture (haemoglobin 3.3 g/100 ml). Both patients were treated with blood transfusions followed by mebendazol and iron substitution. The article also reviews the current literature on the epidemiology, pathogenesis and therapy of hookworm infection.
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PMID:[Hookworm disease. A differential diagnosis in iron deficiency anemia]. 785 38

Serum ferritin concentration correlates with tissue iron stores in humans, horses, calves, dogs, and pigs but not in rats. Because serum iron and total iron-binding capacity can be affected by disorders unrelated to iron adequacy (such as hypoproteinemia, chronic infection, hemolytic anemia, hypothyroidism, and renal disease), serum ferritin is probably the most reliable indicator of total body iron stores in larger species. To test the hypothesis that serum ferritin might be correlated with tissue iron levels in cats, we developed a quantitative enzyme-linked immunosorbent assay that uses two monoclonal antibodies in a sandwich arrangement to measure feline serum ferritin. The recovery of purified ferritin added to feline sera ranged from 94% to 104%; the within-assay coefficient of variability was 8.4%, and the assay-to-assay variability was 13.2%. Mean serum ferritin from 40 apparently healthy cats was 76 ng/ml (SD = 24 ng/ml). Serum ferritin concentration was significantly correlated (P < 0.001, n = 101, r = 0.365) with the nonheme iron in the liver and spleen (expressed as milligrams of iron per kilogram of body weight), as determined by Pearson product-moment correlation analysis. Because serum iron can decrease in diseases other than iron deficiency, the combination of serum iron and serum ferritin should provide sufficient evidence to differentiate anemia of chronic inflammation from anemia of iron deficiency in the cat.
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PMID:Enzyme-linked immunosorbent assay to measure serum ferritin and the relationship between serum ferritin and nonheme iron stores in cats. 786 83

The presence of anaemia and serum protein alteration frequently makes the treatment of pressure ulcers more difficult. Several haemato-chemical parameters were observed in 40 patients with sacral pressure ulcers in order to determine the pathogenesis of these complications. All of the patients showed mild-moderate anaemia with low serum iron and normal or increased ferritin and hypoproteinemia with hypoalbuminemia. Our results suggest that both anaemia and serum protein alteration depend on the chronic inflammatory state due to the presence of pressure ulcers. Both anaemia and hypoproteinemia disappeared after pressure ulcer healing. A correct diagnosis is important for the treatment. Iron therapy is useless and potentially dangerous (iatrogenic haemochromatosis) since anaemia is the result of the inability to use iron stores and not iron deficiency. The treatment of serum protein alterations should be based on a dietary therapy rich in protein and calories; the administration of albumin should be reduced, since albumin is low in essential amino-acids and too expensive; albumin administration should be limited to cases with severe hypoproteinemia and oedema.
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PMID:Anaemia and serum protein alteration in patients with pressure ulcers. 902 23

To evaluate the health and nutritional status of children with two different nutritional habits, the authors examined 26 vegetarians (lacto- and lacto-ovo; an average period of vegetarianism 2.8 years) and 32 individuals on mixed diet (omnivores) in the age range 11-14 years. Vegetarian children had significantly lower erythrocyte number as well as reduced levels of haemoglobin and iron compared to omnivores. The average level of iron did not reach the lower limit of the physiological range and hyposiderinemia was found in 58% of vegetarians vs 9% of omnivores. Reduced iron levels were observed in spite of increased intake of vegetable iron sources and vitamin C (which facilitates the conversion to ferro-form). This reduction can be attributed to the absence of animal iron sources with high utilizability and to lower iron utilization in the presence of phytic acid (higher intake of grains compared to omnivores). The incidence of hypoalbuminemia and hypoproteinemia in vegetarian children was 38 and 12%, respectively, compared to 0% in omnivores. The protein mixture from milk, eggs and vegetable sources is complete, but vegetarian children had significantly reduced intake of milk and dairy products. Favourable lipid and antioxidant parameters in vegetarian children reflect the optimal nutrition composition with respect to the prevention of free radical diseases. Such a nutrition results in significantly lower levels of cholesterol and LDL-cholesterol compared to omnivores and significantly higher and over threshold values of essential antioxidants--vitamin C, vitamin E/cholesterol (more effective protection against LDL oxidation), beta-carotene, vitamin A.
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PMID:Influence of vegetarian and mixed nutrition on selected haematological and biochemical parameters in children. 939 58

A syndrome of chronic diarrhea, vomiting, and failure to thrive was described 35 years ago. The syndrome was caused by damage in the jejunum after ingestion of cow's milk. Symptoms appeared in young infants shortly after introduction of cow's milk formula. Patients had moderate steatorrhea, decreased absorption of D-xylose, and, often, iron-deficiency anemia and hypoproteinemia. They had strong IgA and IgG antibodies to cow's milk. IgE antibodies to cow's milk were negative, as a rule. Indicators of cell-mediated immune reaction to cow's milk proteins were often positive. Patients were tolerant to cow's milk by the age of 3 years. Malabsorption was due to damage to the jejunal mucosa: Varying villus atrophy was associated with inflammation in surface epithelium and lamina propria. The epithelial cell renewal rate increased. Surface epithelial cells decreased in height, with short, furry microvilli and large aggregates of lysozymes. The number of intraepithelial lymphocytes was markedly increased, but normalized during cow's milk elimination. Most of these lymphocytes had alpha/beta T-cell receptors, and many were cytotoxic. Some specimens had an increase in gamma/delta T-cell receptor-bearing cells. In the lamina propria, CD4+ cells predominated, and some of them were activated. IgA- and IgM-containing cells were markedly increased during cow's milk exposure, but IgE cells were not abnormal. The density of eosinophils was moderately increased. Secretion of interferon-gamma by cells isolated from patients' intestines was markedly increased. Morphologic and immunologic findings suggest that T-cell-mediated reaction to proteins in cow's milk is present in the small intestines of patients with this syndrome and causes this enteropathy.
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PMID:Food-induced malabsorption syndromes. 1063 1

The results of 361 plastic operations in 296 patients with morbid obesity late after horizontal gastroplasty were analyzed. Plastic and corrective operations aimed at removal of redundant lipocutaneous "aprons" at the anterior abdominal wall, thighs, thoracic wall, gluteal region and the arms, represent a final stage of surgical treatment of patients with morbid obesity. The indications, technique and the results of plastic operations performed from 1985 to 1998, are thoroughly elucidated. The analysis of early postoperative complications has established, that it a reasonable to perform such operations 1-3 years after gastroplasty when body weight stabilizes and there are no vitamin deficiency, iron deficient anemia, hypoproteinemia, hydroionic disturbances or other complications of the later period. Complex prophylactic measures for prevention of pyoseptic and thromboembolic complications in patients with obesity late after gastroplasty permits to avoid severe complications and lethal outcomes in patients after plastic operations.
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PMID:[Plastic surgery in patients with obesity late after horizontal banded gastroplasty]. 1071 Sep 14

METHODS: Evaluated are surgical difficulties, management problems and weight loss in patients with distal gastric bypass as a revisionary procedure. Eighty patients were followed up to 3 years; four were lost to follow-up. Mean age was 43; mean prebariatric surgery weight 134 kg; height 1.65 meters; body mass index 40.1; ideal body weight 62.7 kg; excess weight 70.5 kg; per cent excess weight 214%. A 250 cm stomach-to-ileocecal valve segment of small bowel was used, and the biliopancreatic secretions were brought into the terminal ileum 100 6 in from the ileocecal valve. Mean pouch size was 63 cc; length of hospital stay 5 days; operative blood loss 616 cc; operative time 130 min. RESULTS: Intraoperative complications included three splenic injuries (without splenectomy). Early complications included one deep vein thrombosis, two marginal ulcers, one GI hemorrhage, one wound dehiscence, one pouch outlet obstruction and one pancreatitis. Late complications included: one death from protein malnutrition/ ARDS; 21 hypoproteinemia; six protein malnutrition, and of these, three had hyperalimentation; three cholecystitis; 27 anemia; 22 incisional hernia; two staple-line disruption (reoperated); 26 low serum iron; 11 prolonged (>6 months) diarrhea; three prolonged frequent vomiting; and two unrelated deaths (chronic myelogenous leukemia and amyotrophic lateral sclerosis). Mean excess weight loss was 83% at 12 months; 89% at 24 months; and 94% at 36 months. CONCLUSION: The distal gastric bypass is fraught with the operative and immediate post-operative complications experienced in any revisionary bariatric surgery. Distal gastric bypass is very effective in producing long-term weight loss. Nutritional problems are common but usually easily corrected. The most serious nutritional complication is protein malnutrition, which must be identified and corrected early. Success of this procedure is dependent upon patient compliance with proper nutrition and supplements, and regular office follow-up with monitoring of laboratory data. Patients who are noncompliant are at significant risk for complications.
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PMID:The Gastric Bypass for Failed Bariatric Surgical Procedures. 1072 55

We report a case of adult T-cell leukemia (ATL) accompanied by polycythemia vera (PV) in which rapid development of myelofibrosis and clinical features of hemophagocytic syndrome (HPS) were observed at the terminal stage. The patient, a 53-year-old man who was born in Oita Prefecture, Japan, was diagnosed as having PV in 1996. He had undergone venesection but had not received any chemotherapy. In June 1997, he showed systemic lymphadenopathy with positivity for serum HTLV-1 antibody (x 10,240). Pathological findings and Southern blotting analysis for detection of monoclonal integration of HTLV-1 provirus DNA in a lymph node biopsy sample revealed that he also had acute-type ATL. Although several courses of chemotherapy were transiently effective, high fever, pancytopenia, increased serum LDH, hypoproteinemia and hyperferritinemia appeared, all of which were compatible with the clinical features of HPS. In addition, cytomegalovirus infection became evident. He died of multiple organ failure with rapid progression of myelofibrosis in May 1998. Detection of both increased CD68-positive histiocytes by immunohistochemistry and iron-stained phagocytic cells in marrow biopsy specimens appeared to be helpful for diagnosis of HPS in this patient, whose marrow showed myelofibrosis with hypocellularity.
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PMID:[Rapidly progressive fibrosis and increased CD68-positive cells in the bone marrow at the terminal stage of adult T-cell leukemia accompanied by polycythemia vera]. 1120 Nov 50

Intravascular precipitates, comprised at least in part of iron, formed regularly in rabbits given one or more injections of a saccharated iron oxide preparation intravenously, and these lodged in numerous capillaries throughout the body, particularly those of the lungs and kidneys. Large numbers of the brownish precipitates remained in the capillaries of the renal glomeruli during the first few days following injection of the iron, but most of them disappeared after 5 to 7 days, with only moderate amounts of brown pigment remaining in the endothelial cells of the renal glomeruli. Signs of acute injury of the glomerular tufts-namely) pyknosis of some of the endothelial cells, margination of leukocytes within the glomerular capillaries, and slight proliferation of the epithelial cells-also developed some 5 to 7 days following injection of the iron, along with marked proteinuria, which proved transitory if no further injections were given. When the iron preparation was given repeatedly over prolonged intervals, however, the proteinuria persisted and became extreme, and hypoproteinemia developed, often with hypercholesterolemia and transitory edema as well. Histological studies of the kidneys of rabbits manifesting the nephrotic syndrome, as just described, disclosed that virtually all the renal glomeruli were greatly altered, mainly owing to proliferation of the epithelial cells, together with some fibrosis and atrophy. Some of the rabbits having marked proteinuria and other functional changes eventually developed azotemia following repeated injections of the iron, and several of them lost weight and died; the renal glomeruli of these animals showed changes like those just described, but the alterations were more extensive. Considered together, the findings provide evidence that the intravascular precipitates first occluded the glomerular capillaries for a period of several days following injection of the iron and then largely disappeared from them just prior to the development of morphologic signs of glomerular injury and proteinuria. Hence the possibility was considered that the intracapillary precipitates might have produced acute injury to the walls of the glomerular capllaries through the agency of anoxia. But it is plain that the findings of the present study do not disclose the essential nature of the anatomical change responsible for the proteinuria, or the means whereby this was produced. The findings as a whole were briefly considered in relation to the pathogenesis of the nephrotic syndrome as it occurs naturally in human beings.
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PMID:Glomerular lesions and the nephrotic syndrome in rabbits given saccharated iron oxide intravenously; with special reference to the part played by intracapillary precipitates in the pathogenesis of the lesions. 1327 60


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