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)

Combination of isolated blood ultrafiltration (IBUF) and hemosorption (HS) produced subcompensation of severe congestive heart failure (CHF) in 10 of 14 patients refractory of IBUF alone and to drug therapy. HS included in the therapy complex was the only way to correct secondary hyperaldosteronism, to reduce antidiuretic hormone blood level, to increase diuresis and natriuresis and to reduce kaliuresis as well as to normalize blood electrolyte level. The withdrawal of excessive water with IBUF and bilirubin and creatinine with HS as well as direct detoxication effect on the liver with HS reduced in most patients hyperbilirubinemia, hypoproteinemia and azotemia--aggravating factors in patients with CHF.
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PMID:[Combined use of hemosorption and isolated ultrafiltration of the blood in patients with refractory heart failure]. 274 68

Renal responses to atrial natriuretic peptide were examined in conscious dogs with congestive heart failure (tricuspid insufficiency) and in conscious rats with nephrotic syndrome (adriamycin). Heart-failure dogs displayed elevated atrial pressure and heart weights, blunted natriuresis to a saline load, and ascites. Nephrotic rats displayed proteinuria, hypoproteinemia, sodium retention, and ascites. In control animals, atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion. Although atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion in conscious heart-failure dogs and nephrotic rats, the responses were markedly blunted. In heart-failure dogs, infusion of atrial natriuretic peptide increased plasma concentrations of norepinephrine and epinephrine. In nephrotic rats, renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide. Mean arterial pressure, glomerular filtration rate, and p-aminohippurate clearance were affected similarly by atrial natriuretic peptide in heart-failure dogs or nephrotic rats vs. control animals. Conscious congestive heart-failure dogs and conscious nephrotic rats have blunted diuretic and natriuretic responses to atrial natriuretic peptide.
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PMID:Blunted natriuresis to atrial natriuretic peptide in chronic sodium-retaining disorders. 295 52

Oedema fluid was collected from the leg through a sterile 21 gauge needle inserted into the subcutaneous space in 12 patients with protein energy malnutrition, 12 with nephrosis, 5 with Indian childhood cirrhosis, 4 with acute nephritis, 4 with epidemic dropsy and 3 with congestive heart failure. The concentrations of protein, free amino acids and electrolytes were measured in plasma and oedema fluid. The plasma/oedema fluid ratios were 36:1, 49:1, 32:1 and 52:1 in protein energy malnutrition, nephrosis, Indian childhood cirrhosis and congestive heart failure. These ratios were significantly smaller in epidemic dropsy (4:1) and acute nephritis (21:1). The free alpha amino nitrogen concentrations in these two compartments were almost in equilibrium. This was also found for essential and non-essential amino acid distributions in protein energy malnutrition and nephrosis, whereas differences in amino acid patterns were found in nephritis and epidemic dropsy. Sodium and potassium concentrations varied substantially between diseases where the underlying cause was gross hypoproteinemia compared to non-hypoproteinemic conditions.
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PMID:Oedema fluid composition in childhood disorders. 641 20

Gallbladder wall thickening (3 mm or greater) has been described as a sign of acute or chronic inflammatory disease of the gallbladder. However, gallbladder wall thickening is a nonspecific finding in contracted, postprandial gallbladders and in cases of hypoproteinemia, elevated portal venous pressure, congestive heart failure, multiple myeloma, and hepatitis. This report describes the case of a patient who had a markedly thickened gallbladder wall secondary to focal obstruction of gallbladder lymphatic drainage by malignant lymphoma in the portal lymph nodes.
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PMID:Gallbladder wall thickening secondary to focal lymphatic obstruction. 684 62

Characteristic alterations in the serum and urine biochemical profiles of Doberman Pinschers with congestive heart failure (CHF) resulting from idiopathic dilated cardiomyopathy were determined. We compared these alterations with those observed in 2 other models of CHF: rate overload induced by rapid ventricular pacing in dogs, and biventricular hypertrophy and dilatation induced in turkey poults by furazolidone toxicosis. Serum and urine biochemical changes in both models of CHF in dogs were mild to moderate in degree, and were moderately consistent. They could be attributed to secondary neurohumoral, hepatic, and renal effects of heart failure. The most marked and consistent changes observed were mildly decreased anion gap that developed, in part, because of decreased serum sodium concentration, moderately increased catecholamine concentrations, moderate lactaciduria, hyposthenuria, and mildly increased urea concentrations and liver enzyme activities. In birds with furazolidone cardiomyopathy, we observed mild increases in serum urate concentration, liver and muscle enzyme activities, but moderately increased sodium concentration with decreased chloride concentration. In the pacing and furazolidone models, in which CHF was rapidly induced, moderate to marked hypoproteinemia was attributable to decreases in albumin and globulin concentrations. Using the avian model we found that the hypoproteinemia could be largely attributed to blood volume expansion, and to a lesser extent, inanition. Development of hypoalbuminemia during rapid ventricular pacing and furazolidone treatment may contribute to the effects of rate overload or drug toxicity in the pathogenesis of CHF, because hypoalbuminemia may contribute to altered hemodynamics and neuroendocrine system activation. Our data indicate that clinical biochemical analysis of serum and urine may be useful for assessing progression of CHF.
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PMID:Clinical pathologic profiles of dogs and turkeys with congestive heart failure, either noninduced or induced by rapid ventricular pacing, and turkeys with furazolidone toxicosis. 842 73

A 76-year-old female patient who had been taking vitamin D2 100,000 U/day for more than 14 years due to hypoparathyroidism following total throidectomy was admitted because of protracted hypercalcemia. On admission, the levels of serum vitamin D2 (99.8 ng/ml) and 25-OHD2 (356 ng/ml) were very high, and 1,25-(OH)2D2 was low (4.0-18.7 pg/ml). Serum D3' 25-OHD3 and 1,25-(OH)2D3 were below the normal range. Despite intensive hydration with saline, intravenous hyperalimentation with phosphate- and calcium-free nutrients, and administration of glucocorticoid and calcitonin, the hypercalcemia persisted, accompanied by hypoproteinemia, edema, pleural effusion and congestive heart failure. The serum D2 and 25-OHD2 concentrations remained high and were accompanied by a gradual increase in 1,25-(OH)2D2 (121 pg/ml), which further increased after the administration of bisphosphonate (pamidronate) to 183 pg/ml. Seventeen months later, serum calcium and 1,25-(OH)2D2 were normalized but serum D2 and 25-OHD2 remained high. The serum 24,25-(OH)2D2/25-OHD2 ratio was relatively constant throughout her clinical course, whereas the low serum 1,25-(OH)2D2/25-OHD2 ratio at admission gradually increased during admission, suggesting that the increase in serum 1,25-(OH)2D2 is due to increased production rather than decreased degradation. The administration of pamidronate further increased serum 1,25-(OH)2D2. These features of the clinical course demonstrate that the 1,25-dihydroxyvitamin D concentration in hypercalcemic patients with protracted vitamin D intoxication may be decreased, normal or increased. Possible factors responsible for a protracted increase in serum 1,25-(OH)2D2 are body weight loss, hypoproteinemia, and phosphate depletion. In addition, some bisphosphonates would certainly promote PTH-independent production of 1,25-(OH)2D2.
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PMID:Progressively increased serum 1,25-dihydroxyvitamin D2 concentration in a hypoparathyroid patient with protracted hypercalcemia due to vitamin D2 intoxication. 852 47

Flow cytometry allows a rapid and accurate analysis of the cells in serous fluids. The aim of this study was to evaluate the use of flow cytometric analysis in malignant pleural effusions. 26 patients (13 females, 13 males; mean age 52 +/- 19 years; range 16-82) were included in the study. 15 had malignant pleural effusions (7 adenocarcinoma, 2 lymphoma, 2 chronic myeloid leukemia, 1 ovarian carcinoma, 1 small cell lung carcinoma, 1 squamous cell lung carcinoma and empyema, and 1 malignant mesothelioma) with positive cytology. 2 had benign effusions associated with malignancy (1 squamous cell lung carcinoma and congestive heart failure, and 1 neuroblastoma and hypoproteinemia). 9 had benign effusions (3 tuberculosis, 1 congestive heart failure, 3 parapneumonic pleural effusion, 1 benign mesothelioma, and 1 pulmonary embolism). Flow cytometric analysis of pleural effusions revealed an increased DNA index in malignant effusions: 1.32 +/- 0.44 versus 0.88 +/- 0.23 in benign effusions (p < 0.04). The cell cycle distribution of cells such as G1/G0 and S in malignant effusions did not differ from that of benign pleural effusions; however G2+M increased significantly in malignant effusions (p < 0.03). Using analysis of mononuclear immunophenotyping, CD3+, CD4+, and CD8+ cells did not show any significant difference between the two groups. The lymphocyte activation marker CD38 was positive in 57.6 +/- 11.5% of malignant fluid cells and 38.5 +/- 6.2% of benign fluid cells (p < 0.04). The mean carcinoembryonic antigen levels in malignant and benign pleural effusions were 98.7 +/- 157.3 and 0.9 +/- 1.2 ng/ml, respectively (p < 0.03). In conclusion, the results of our study indicate that finding cells with an abnormal DNA content strongly supports the diagnosis of malignant pleural effusions. Additionally, mononuclear cell phenotypes have to be taken into consideration for malignant pleural effusions, particularly activated T cells. We recommend that flow cytometry should be performed if the cytology is equivocal.
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PMID:Analysis of pleural effusions using flow cytometry. 883 88

A 77-year-old woman complaining of anorexia and nausea was referred to the hospital with a diagnosis of advanced gastric cancer. The patient also had congestive heart failure with atrial fibrillation and severe hypoproteinemia. Proteinuria, hypoproteinemia and other laboratory data suggested that she had nephrotic syndrome. Total protein level was 4.6 g/dl and albumin level was 1.6 g/dl. In order to avoid postoperative complications such as wound dehiscence, anastomotic leakage and so on, careful pre- and post-operative management of nephrotic syndrome is necessary. Administration of albumin and fresh frozen plasma regimen was continued after the operation. Urinary protein level started to decrease after subtotal gastrectomy. Histological examination revealed moderately differentiated tubular adenocarcinoma with nodal metastases. Her post-operative course was uneventful. Although the signs and symptoms of nephrotic syndrome did not improve immediately, twelve months after operation she has become well and has no symptoms of ascites and hypoproteinemia.
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PMID:A case of gastric cancer with nephrotic syndrome. 978

A 71-year-old man who had a history of open chest surgery was admitted due to anasarca and bilateral pleural effusions. Although imaging modalities could not demonstrate any pericardial abnormalities, right-sided cardiac catheterization revealed 'dip and plateau' in diastolic pressure waveform. He was admitted frequently because of the episodic right-sided congestive heart failure and hypoproteinemia due to protein-losing enteropathy. The peripheral lymphocyte count and serum gamma-globulin concentration were gradually decreased, and finally showed lymphocytopenia and hypoglobulinemia. On the last admission, the patient showed extensive cellulitis on both legs, and he developed septicemia, and finally died due to septic shock. Post-mortem examination showed that both visceral and parietal layers of the pericardium adhered tightly with mediastinal fibrosis. This case report suggested that constrictive pericarditis should be considered even if there is a lack of typical abnormal pericardial imaging findings when patients have a history of open chest surgery and recurrent right-sided congestive heart failure. In addition, we should be aware of a serious outcome due to immune compromised conditions such as lymphocytopenia and dysglobulinemia in this disorder.
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PMID:Post-operative constrictive pericarditis complicated with lymphocytopenia and hypoglobulinemia. 1549 16

Protein-losing enteropathy (PLE) with hypoproteinemia is an uncommon but serious complication of congestive heart failure. Reports of patients with PLE resulting from severe tricuspid regurgitation (TR) caused by trauma are rare. A 66-year-old male diabetic patient had a chest contusion as a result of a road traffic accident, and one year later suffered from progressively generalized edema. Examination revealed severe TR with a high central venous pressure and PLE with serum protein deficiency. Treatment with albumin administration and diuretic therapy proved ineffective, and consequently the TR was corrected by valve replacement. Postoperatively, the serum protein level gradually returned to normal. Surgical intervention successfully improved this patient with severe TR and PLE resistant to medical treatment.
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PMID:Traumatic tricuspid regurgitation resulting in protein-losing enteropathy: a case report. 1635 69


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