Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have evaluated the incidence, long term evolution and pathogenesis of posttransplant hyperlipidaemia (HL) in 88 transplanted patients without nephrotic syndrome followed for 2 to 13 years by the same staff. Incidence of HL decreased strikingly over the years from 51% at 2 years to 25% at 10 years. This fall was due solely to the return to normal of the lipid profile in 13 patients between 2 and 8 years after transplantation. This progressive decrease should be taken into account when the frequency of posttransplantation dyslipaemia is assessed. The incidence of hyperlipidaemia increases with age. Above 40 years, hyperlipidaemia is more frequent in females than in males. Obesity and reduced renal function are both associated with a higher incidence of dyslipaemia. No relationship was found between lipid disorders and either steroid dosage or fasting blood glucose levels. Dyslipaemia appears thus to be due to the interplay of several factors. Normalisation of the lipid profile occurred in 13 patients without significant decrease in bodyweight, serum creatinine or prednisone dosage. At 8 years atheromatous lesions were not more frequent in dyslipaemic than in normolipaemic subjects.
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PMID:The evolution of hyperlipidaemia late after renal transplantation. 39 4

A study of 3451 cholesterol determinations in different diseases was carried out. The mean cholesterol levels for male and female adults and children with different diseases were compared with values for their healthy counterparts. Sickle cell anemia, leukemia, liver cirrhosis, hepatosplenomegaly, tuberculosis, and diabetic, nutritional, ataxic, and tropical neuropathies in male and female adults were associated with reduced cholesterol level while in children malnutrition and anemia were the main causes of low cholesterol levels. Obesity and hypertension caused an elevated level but the mean values were within the range for adult Nigerians in the high income group. Only nephrotic syndrome in both adult and children was associated with a markedly increased cholesterol level in Nigerians of low income status.
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PMID:Serum cholesterol and diseases in Nigerians. 50 76

The morphologic features observed in the renal biopsy specimens from three patients with massive obesity complicated by the nephrotic syndrome are described. In the two patients with active disease, the majority of the glomeruli showed focal to extensive fibrin deposition both within and adjacent to capillary loops, associated with adhesions to Bowman's capsule, with a variable endocapillary proliferative response. In the patient with inactive disease, the majority of the glomeruli appeared normal. However, fibrin-like material, similar to that seen in the active phase, was infrequently found ultrastructurally in the subendothelial portion of the capillary loops. Subendothelial vacuolated material was also observed. Although intravascular coagulation was suggested in this disorder, only minor coagulation abnormalities were discovered. In two of the patients, the massive proteinuria has resolved with weight reduction.
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PMID:The nephrotic syndrome in massive obesity: a study by light, immunofluorescence, and electron microscopy. 58 Aug 86

In children, too, treatment with glucocorticoids may occasionally be necessary. On the one hand, replacement treatment in children with the adrenogenital syndrome, on the other pharmacotherapy in a number of diseases may be required. The latter include the genuine nephrotic syndrome, autoimmunological diseases, hypsarrhythmia, and, in the field of neonatology and neonatological intensive care, the treatment of the respiratory distress syndrome and bronchopulmonary dysplasia. Side effects of pharmacotherapy include suppression of the adrenal cortical function and growth disorders, together with truncal obesity, formation of striae of distension or osteoporosis.
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PMID:[Glucocorticoid therapy in childhood]. 191 78

Although hypoalbuminemia is a fundamental characteristic of nephrotic syndrome (NS), there are many patients with massive proteinuria that do not develop hypoalbuminemia. We have studied the clinical and biochemical characteristics of 19 patients with persistent massive proteinuria (greater than 5 g/d) and normal serum albumin (group I) in comparison with 16 patients with similar proteinuria excretion, but persistent hypoalbuminemia (group II). Most of group I patients had diagnoses suggesting glomerular hyperfiltration (focal glomerulosclerosis [FGS] associated with vesicoureteral reflux [VUR], reduction of renal mass, proteinuria associated with obesity, sclerotic phase of idiopathic crescentic glomerulonephritis [GN] in contrast with those of group II, in which membranous GN was the most frequent diagnosis. We prospectively investigated differences in the antiproteinuric effect of captopril, an antiotensin-converting enzyme inhibitor (ACEI); after 6 months of treatment, proteinuria decreased clearly in group I (7.1 +/- 1.7 to 3.7 +/- 1.7 g/d; P less than 0.001), whereas no significant changes were observed in group II (8.1 +/- 2.4 to 8.8 +/- 4 g/d). Serum creatinine (Scr) remained stable during captopril treatment in group I, whereas three patients in group II showed a worsening of renal function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nephrotic proteinuria without hypoalbuminemia: clinical characteristics and response to angiotensin-converting enzyme inhibition. 199 78

An obese patient with nephrotic syndrome was admitted to the hospital because of increasing edema in the legs. With 25 kg weight loss, proteinuria decreased from 15 g to 5 g/day. Renal biopsy revealed mesangial glomerulopathy. The serum IgE level was highly elevated, and the radioallergosorbent test (RAST) was strongly positive for many kinds of allergens. No significant change in proteinuria, compared with the highly right atrial pressure period, was observed after normalization in the right atrial pressure. In spite of a decrease in body weight (27 kg) (113 to 86 kg) in 140 days, no significant change in proteinuria was observed. After additional therapy with an anti-allergic drug, proteinuria was completely abolished. These results suggest that a combination of weight loss and treatment with an anti-allergic drug is very important therapy for massive obesity with nephrotic syndrome. Since RAST was strongly positive for many kinds of allergens, the pathophysiology in this nephrotic syndrome may be, at least partially, related to the immunologic abnormalities.
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PMID:Improvement of nephrotic syndrome in a massively obese patient after weight loss and treatment with an anti-allergic drug. 209 99

Nephrotic syndrome has been reported in obesity; its precise incidence in obese patients without diabetes mellitus and/or arterial hypertension is however unknown. Thirty-two obese subjects without complications were therefore assessed before and after weight loss, together with 18 healthy control subjects. Overnight albumin excretion rate (AER) was assessed using a RIA method (H. Albumin-Kit, Sclavo). Glomerular filtration rate (GFR) was also evaluated in 10 obese subjects using Cr51 before and after weight loss. AER was found to be higher, although the difference was not statistically significant, in obese subjects compared to controls, but was significantly reduced after weight loss (p = 0.05). GFR also showed a non-significant tendency to decrease following loss of weight. Systolic and diastolic blood pressures were significantly decreased following weight loss (p less than 0.01 and p less than 0.025 respectively). In conclusion, although it is not possible to confirm the presence of true nephropathy in uncomplicated obesity, the latter can facilitate the onset of hemodynamic-type mechanisms which, in the presence of diabetes mellitus or arterial hypertension, may lead to the appearance of the nephrotic syndrome.
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PMID:[Possible correlations between protein-loosing nephropathy and obesity]. 209 54

Deep venous thrombosis and its complication pulmonary embolism are responsible for more than 50,000 deaths annually in the US, 2/3 of which occur postoperatively. Nearly 75% of such deaths could be avoided by adequate prophylaxis. All forms of surgery entail some risk of deep venous thrombosis, ranging from 10% after endoscopic prostate resection to over 50% for total hip replacement. 1.6 of thromboses will embolize and 1/4 of pulmonary emboli are fatal. The goal of prevention is to decrease the incidence of fatal pulmonary emboli while limiting the risks related to prevention. A secondary goal is to reduce the frequency of postthrombotic syndrome, a late complication of deep venous thrombosis which frequently causes invalidism. A preoperative evaluation of risks of deep venous thrombosis and of the likelihood of bleeding problems should be followed by selection of appropriate preventive measures. The evaluation should be repeated postoperatively, taking into account such factors as the duration of the intervention, the diagnosis, and the predicted duration of bed rest. Evaluation of the risk of deep venous thrombosis requires knowledge of its etiopathogenesis. Deep venous thrombosis results from a multifactorial process involving venous stasis, lesion of the vascular wall, and anomalies of blood composition. All the clinical risk factors for deep venous thrombosis are related to 1 or more of these elements. Risk factors related to stasis include immobilization, postoperative or postpartum status, pregnancy, and Cockett's syndrome. Risk factors related to lesions of the vascular wall include hip surgery, trauma, age, sepsis, varices and obesity, and postthrombotic syndrome. Risk factors related to blood anomaly include postoperative status, pregnancy, oral contraceptive use, cancer, nephrotic syndrome, hypercoagulability, trauma, and heredity. The most common clinical risk factors for deep venous thrombosis are age, surgical intervention, trauma, burns, cancer, pregnancy and delivery, oral contraceptive use, varices, obesity, and postthrombotic syndrome. The relative risk of deep venous thrombosis among OC users is 4.0 overall and higher for those with type A blood. The pathogenic mechanisms are similar to those of pregnancy except that the fibrinolytic capacity is not change. The principal mechanism is perhaps the declining level of antithrombin III, observed with estrogens and some progestins. Among methods of prevention are different forms of compression, use of heparin alone or in combination with other drugs, and oral anticoagulants.
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PMID:[Epidemiology and etiopathogenesis of deep venous thrombosis of the lower limbs]. 224 Apr 6

A prospective study was performed to evaluate the effect of long-term small-dose prednisone therapy in frequently relapsing nephrotic syndrome (NS); 37 patients were included, with a relapse rate 4.6/patient/year (range, 3-8) (mean age, 6.7 years; range, 2-15 years). Prednisone was started 2 mg/kg/day once remission was induced. Prednisone was progressively reduced over weeks until 10 mg/day was reached, and then the daily dose was changed to 10 mg on alternate days. On follow-up (mean, 25.4 months; range, 10-58 months), only five had subsequent relapses and their relapse rate decreased significantly to 1.2/patient/year (p less than 0.05). Forty-six episodes of infection were associated with exacerbation of NS; 41 of these excerbations remitted spontaneously without an increase in the dose of prednisone. Serial height and weight measurements revealed evidence of improved height velocity and obesity persisted in only two of 13 initially obese children.
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PMID:Long-term, small dose prednisone therapy in frequently relapsing nephrotic syndrome of childhood. Effect on remission, statural growth, obesity, and infection rate. 313 74

The severity and persistence of corticosteroid-induced obesity were evaluated retrospectively in 23 children aged 1-14 yrs requiring more than 60 days of therapy with prednisone for idiopathic nephrotic syndrome. Mean relative weight (after clearing of proteinuria) at initiation of therapy was 107 +/- 10 percent. Peak relative weight on therapy was 119 +/- 15 percent following a mean total of 31 months of cumulative steroid therapy. The most recent available relative weight in remission at least 6 months following cessation of therapy was 107 +/- 18 percent. The number of children whose relative weight exceeded 120 percent at initiation of, during and following therapy was 3, 10, and 4, respectively. In those with normal initial relative weight (less than 110%) there was no persistent obesity. Two of three initially obese patients (relative weight greater than 120%) remained obese. All patients with persistent obesity following therapy had initial relative weight of at least 110 percent and peak relative weight of more than 130 percent. The risk of persistent obesity as a result of chronic corticosteroid therapy in initially normal weight children who do not exceed 130 percent relative weight during therapy appears to be small.
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PMID:Corticosteroid therapy-induced obesity in children. 394 57


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