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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We analyzed the serum anion gap (AG = sodium plus potassium minus chloride plus bicarbonate, N = 11-21 mEq/l), serum uric acid and urea concentrations in hyponatremia of various origins. We found that characteristic chemical patterns emerged in association with different hypotonic states: Low uric acid concentration was typically observed in the SIADH and in hyponatremia related to hypopituitarism. The same observation was also frequently noted in hyponatremia secondary to diuretics or to polydypsia. In the SIADH, we observed a decrease in the AG but to a greater extent (-26%) than one would expect from the simple dilutional effect (-16%). Fifty percent of the patients presented an AG lower than 11 mEq/l. In patients with diuretic-related hyponatremia, one group presented an hypouricemia and a low AG as in SIADH (reflecting volume expansion), in the other group the AG was normal or increased as was uric acid concentration (reflecting volume depletion). In adrenocorticotropin deficiency, hyponatremia was typically associated with a low bicarbonate concentration, a normal AG and hypouricemia. In polydypsic patients with hyponatremia, the AG was usually normal or increased despite sometimes very low sodium levels. Uric acid levels were highly variable, most often decreased. We also noted in these patients that the serum urea levels were correlated with urine osmolality (R = +0.8; p < 0.001), and in 40% of them we observed very low blood urea concentration (0.5-2 mmol/l) at the admission time. In hyponatremia related to cardiac failure or cirrhosis, the AG was usually normal despite mild hypoproteinemia.
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PMID:Uric acid, anion gap and urea concentration in the diagnostic approach to hyponatremia. 852 2

Nephrogenic ascites is a clinical diagnosis defined as persistent ascites in a uraemic patient without evidence of a causative specific underlying disease. Contributing mechanisms may include peritoneal membrane changes, fluid overload, hyperparathyroidism, reduced lymphatic drainage, heart failure and hypoproteinemia. A specific treatment has not yet been found. Rigid fluid control, intensive haemodialysis, high-protein diet, intravenous albumin infusion, intraperitoneal steroid injections and paracenteses as well as implantation of a peritoneoatrial pump were all found to be ineffective. Use of peritoneal dialysis has been shown to resolve ascites, but the only effective treatment is renal transplantation, as demonstrated in the case-report.
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PMID:[Nephrogenic ascites]. 831 65

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

In order to examine the clinical characteristics and genetic background of secondary amyloidosis associated with rheumatoid arthritis, we analyzed clinical features and HLA typing of 85 patients in a multicenter study. Eighty-five patients with secondary amyloidosis associated RA were studied. The diagnosis of secondary amyloidosis were made on histological findings by biopsy or autopsy. The most common biopsy site was gastrointestinal tract (79.5%). Clinical symptom and the frequency at the time of diagnosis were; diarrhea (35 cases), abdominal pain (22 cases) and vomiting and nausea (16 cases). Abnormalities and the frequency in a laboratory test included proteinuria (49 cases), increased serum creatinine (32 cases), anemia (30 cases) and hematuria (15 cases). Twenty-eight patients were dead and 57 patients were alive at the time of the study. The average duration between diagnosis of amyloidosis and death was 19.4 +/- 18.5 (SD) months among the dead patients. The average duration after diagnosis of amyloidosis was 24.2 +/- 19.5 (SD) months in surviving patients. The causes of death were renal failure complicated with heart failure (6 patients), heart failure alone (3 patients) and renal failure alone (2 patients). Fifty-nine patients in the control group who were negative to amyloid deposition on biopsies at more than one site in the gastrointestinal tract, were clinically compared with patients in the amyloidosis group. No difference were noted in the age of RA occurrence and the stage between the two groups. As to the class, however, the number of patients with severe functional disorder (class 3 or severe) was larger in the amyloidosis group. There were no significant difference between the two groups in Lansbury's activity index. On hematology, biochemistry and urinalysis, the incidences of increased white blood cell count, anemia, increased platelet count, increased serum creatinine, hypoproteinemia, hypoalbuminemia, increased IgA, and increased urine and blood BMG were statistically significantly higher in the amyloidosis group than in the control group. HLA-A, -B, -C, and DR-locus antigens were compared in the 53 patients in the amyloidosis group and in the 59 subjects in the control group. There were no significant differences in frequency of HLA-A, and -B antigens between two groups. Frequency of CW7 antigen was significantly decreased in the amyloidosis group (13.2%) than in the control group (39.0%). Frequency of DR1 antigen was decreased in the amyloidosis group (3.8%) than in the control group (22.0%), although the difference was not significant. These findings suggest the possible involvement of genetic factors in the occurrence of amyloidosis. It is suggested that the occurrence of amyloidosis is suppressed by some genes which are linked with CW7 antigen.
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PMID:[Clinical characteristics and genetic background of secondary amyloidosis associated with rheumatoid arthritis in Japanese]. 871 35

We report two cases of hyperthyroidism clinically associated to edema, in which no usual causes for the latter were found. Correction of the hyperthyroidism state was associated with complete resolution of edema. The fact that one of the cases consisted of a farmacologically induced hyperthyroidism points to a direct effect of the thyroid hormone itself as the origin of this complication. The de novo occurrence of edema can be due to thyroid hyperfunction as the only underlying cause, the presence of other associated factors such as heart failure, hypoproteinemia or dermopathy not being necessary for its development.
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PMID:[Edema as clinical manifestation of hyperthyroidism. Report of 2 cases]. 894 19

A nine-year old girl with T cell acute lymphoblastic leukemia (ALL) had acute severe neurologic complications at the end of the remission-induction chemotherapy course. Thirty-six hours following triple intrathecal (IT) therapy and intravenous (IV) administration of L-asparaginase (L-asp), tetraplegia developed and she became unconscious. She had bouts of hypertension and persistent tachycardia unresponsive to digitalis therapy. Magnetic resonance imaging (MRI) showed multiple brain white matter hyperintensities and filling defects in the saggital sinus, suggesting thrombosis. Over the 40 days, in addition to her neurologic compromise she also had transient diabetes mellitus, severe hyperlipidemia, hypoproteinemia and edema, liver and heart failure and staphylococcus aureus sepsis with prolonged bone marrow depression. Despite, coexistence of all these chemotherapy related complications, her neurologic functions and multiple organ failure improved gradually. After a 70 days' period of interruption, chemotherapy was resumed and continued without any further complications. Although, the etiology of her extensive sensitivity to some drugs remains unclear, we believe that it is important to document these unusual events in this child.
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PMID:Coexistence of life threatening chemotherapy related leukoencephalopathy, saggital sinus thrombosis and multiple organ failure in a child with acute lymphoblastic leukemia: an unusual case with clinical recovery. 932 1

Although an increasing incidence of upper extremity venous thrombosis (U/E-DVT) has been reported, a relative paucity of information regarding the etiologic categories, precipitating causes, and proper management for this disorder is available. To settle on a strategy for the management of U/E-DVT, retrospective analyses were performed using records from the authors' hospital. In 12 patients (seven men, five women), 61 (mean) years of age, diagnosed as having symptomatic venography-proved U/E-DVT and followed up for 41 (mean) months, etiologic factors, precipitating causes, treatments, and outcomes were retrospectively analyzed. As etiologic factors, five of the patients had neoplastic disease, one had hemodialysis, and two had transvenous pacemaker implantations. Among various precipitating causes of U/E-DVT, hypoproteinemia was most frequently noted (67%). Various types of therapeutic management were selected: from thrombolysis with urokinase in six, balloon angioplasty in two, thrombectomy in two, and venous bypass surgery in one patient. Pulmonary embolism did not occur in any of the patients and only three of them complained of mild intermittent arm swelling during the follow-up period. Four patients died of neoplastic disease or heart failure (three within the first 6 months). This study, though limited, suggests that the rate of mortality depends on multiple underlying medical problems in U/E-DVT patients. Low incidences of late postthrombotic sequelae and pulmonary embolism were noted in this series. Symptomatic U/E-DVT patients could be managed conservatively with a revised supplementary therapy for their precipitating causes of U/E-DVT.
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PMID:Upper extremity vein thrombosis: etiologic categories, precipitating causes, and management. 1043 94

The prognosis of a fetus with hydrothorax at mid-trimester is extremely poor. We encountered a fetus who developed bilateral chylothoraxes at 23 weeks of gestation. Bilateral pleuroamniotic shunts with double-basket catheters were successfully installed at 25 weeks of gestation. Hydrothorax did not recur in this fetus. After the shunting, however, polyhydroamnios, fetal hypoproteinemia, and placental edema developed, and the hydrops worsened. The drainage of the fetal pleural effusion into the amniotic cavity was believed to have contributed to these complications. The infant, born at 29 weeks of gestation, died of cardiac failure and pulmonary hypoplasia. Thus, the shunts did not ameliorate the adverse conditions in this patient.
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PMID:Severe hypoproteinemia in a fetus after pleuro-amniotic shunts with double-basket catheters for treatment of chylothorax. 1114 26

Nonimmune hydrops fetalis (NIHF) is used to describe fetuses and newborns with generalized edema and cavity effusions. It is helpful to alert physicians about the presence of anemia, heart failure, and/or hypoproteinemia, but this diagnosis is frequently overlooked. We reviewed the autopsy files from 1990 to 2000, selected all cases with NIHF including clinical information (with maternal laboratory tests and ultrasound), and classified patients by etiology. Among 840 stillborn autopsies during the 11-year period, we found 51 with NIHF (6.07%). The clinical summary had mentioned hydrops in 14 patients and the etiology in another 7 by fetal ultrasonography, but without addressing the possibility of hydrops. In the remaining 30 cases neither hydrops nor an etiology was mentioned. Other pertinent diagnoses were maternal diabetes mellitus (4), congenital heart disease (3), and cystic hygroma (2). The following diagnoses were made in one instance each: cardiac tumor, twin transfusion syndrome, congenital adenomatoid malformation, syphilis, Turner syndrome, and cerebral arteriovenous malformation. Postmortem and placental examination confirmed the following etiologies: congenital infections (17); placental pathology significant enough to explain NIHF (10); cardiovascular diseases (8) (further classified as congenital heart disease [3], rhabdomyoma [1], and vascular malformations [4]); chromosomal abnormalities (6); uncontrolled maternal diabetes (4); intrathoracic lesions (2); prune-belly syndrome (2); and idiopathic NIHF (2). Only 3.9% of the cases studied had no identifiable etiology. The cause of hydrops was confirmed by autopsy in 47 fetuses (92%), which further supports the importance of performing an autopsy. Thirty-two cases (62.74%) had placental abnormalities helpful to the etiology (parvovirus, syphilis, Turner's syndrome, etc.). In 20 instances, the clinical summary had no mention of either hydrops or any of the diseases leading to it. The autopsy in conjunction with placental examination and fetal ultrasound represent the best combination to determine the etiology of NIHF among stillborn fetuses.
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PMID:Value of autopsy in nonimmune hydrops fetalis: series of 51 stillborn fetuses. 1201 30

Famine edema was produced experimentally in 34 normal men who lost a quarter of their body weight while subsisting for 6 months on a European type of semi-starvation diet. The ratio of extracellular water to cellular tissue was roughly doubled. Their clinical state closely resembled that seen in Europe in 1945. There were no signs of renal or cardiac failure. The plasma protein concentration fell only slightly and the A/G ratio remained within normal limits. The venous pressure was roughly 50 per cent below normal. Data from the field lend support to these indications that famine edema is not simply a result of hypoproteinemia or of renal or cardiac failure. It is concluded that there is a dynamic nonequilibrium state of the capillary wall and, accordingly, calculations from equilibrium equations are inadmissible.
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PMID:Famine Edema and the Mechanism of Its Formation. 1775 25


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