UMLS:C0028754 - FACTA Search

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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this work was to determine the prevalence of obesity, defined as BMI >95th percentile, in children treated with glucocorticoids for steroid-sensitive nephrotic syndrome (SSNS), and to identify risk factors for the development for glucocorticoid-induced obesity. The experimental design involved a cross-sectional study of 96 individuals (4 to 21 yrs) treated with glucocorticoids for SSNS and 186 healthy reference subjects. Logistic regression was used to generate odds ratios for obesity. Glucocorticoid exposure was classified as recent in the 54 subjects treated with glucocorticoids in the prior six months, and remote in the remaining 42 subjects. Recent exposure was associated with significantly increased odds of obesity [odds ratio (95% CI): 26.14 (7.54, 90.66)] in non-blacks only. Each one-unit increase in maternal BMI was associated with a 35% increase in the odds of obesity in recent SSNS subjects (p=0.003). The effect of maternal BMI on the odds of obesity was significantly greater in recent SSNS subjects than in reference subjects (test for interaction p=0.038). The odds of obesity were also significantly increased [odds ratio 5.22 (1.77, 15.41), p=0.003] in all subjects with remote glucocorticoid exposure (black and non-black). These results indicate that non-black race and increased maternal BMI are risk factors for glucocorticoid-induced obesity in subjects with recent exposure.
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PMID:Risk factors for glucocorticoid-induced obesity in children with steroid-sensitive nephrotic syndrome. 1715 75

A retrospective study was performed in 68 patients diagnosed as having idiopathic nephrotic syndrome with steroid-dependent, steroid-resistant or frequent relapse subtypes at the Department of Pediatrics, Siriraj Hospital during Jan 1996-Dec 2004. Male to female ratio was 3.3:1 and mean age (+/- SD) was 8.4 +/- 3.5 years. Mean follow up time (+/- SD) was 47.4 +/- 30.5 months. Renal biopsy was done in 60 patients, showing IgM nephropathy in 73.3%. Fifty-four patients (79.4%) received cyclophosphamide at a dose (+/- SD) of 2.2 +/- 0.5 mg/kg/d for 11.6 +/- 3.4 weeks. Negative proteinuria at 1 year was found in 70% and prednisolone was discontinued in 52%. Leucopenia was found in 9.2%. At last follow up, 34% of the patients were still in remission. Enalapril was prescribed in 50 patients for 12.4 +/- 10.0 months. Thirty-six patients also received cyclophosphamide. Remission at 1 year was achieved in 66% and prednisolone discontinued in 28%. Twelve patients (24%) were still in remission at last follow up. The results of 3 regimens: cyclophosphamide, enalapril, and cyclophosphamide plus enalapril were compared using chi-square test. Remission was significantly better in cyclophosphamide group (p = 0.014). Dipyridamole was prescribed in 14 patients due to thrombocytosis. Only 2 of 14 patients achieved remission although 11 patients received cyclophosphamide plus enalapril, and another 2 patients received only cyclophosphamide. Complications included hypertension (44%), cataract (40%), glaucoma (15%), short stature (17.6%), and obesity (5.9%). Recurrent infection was found in 69%, including dental caries (16.29%), urinary tract infection (14.7%), intestinal parasitic infestration (10.3%), respiratory tract infection (8.8%), and skin infection (7.4%). Chronic renal failure was found in 3 patients and portal vein thrombosis was found in 1 patient. We suggest that cyclophosphamide should be used as first line drug in difficult-to-treat nephrotic syndrome patients. Enalapril may be beneficial in some patients. Thrombocytosis may be associated with poor response to both medications. Difficult-to-treat patients also need long-term follow up and surveillance for complications due to disease and/or treatment.
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PMID:Difficult-to-treat nephrotic syndrome: management and outcome. 1685 34

Dyslipoproteinemia is common in lupus patients. In this study, we investigated the pattern of dyslipoproteinemia in the course of active systemic lupus erythematosus (SLE) in possible association with anti-double-stranded DNA (anti-dsDNA) antibodies. Forty-six lupus patients under 45 years old who fulfilled the American College of Rheumatology revised criteria for the classification of SLE were selected. The exclusion criteria were renal failure, nephrotic syndrome, thyroid or liver disease, diabetes mellitus, obesity, pregnancy and taking drugs that induce dyslipidemia. Disease activity was measured by Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Comparison of the lipid profiles, between active and inactive groups determined high levels of serum TG and VLDL and low levels of serum HDL in active group in comparison with inactive group (P < 0.05). The results indicated that the levels of TG and VLDL were significantly elevated in the patients with positive anti-dsDNA (P < 0.05). Although, the mean of serum HDL levels was also lower in patients with positive anti-dsDNA, the difference was not significant. This pattern of dyslipoproteinemia in active SLE may be associated with the autoimmune mechanisms especially in relation to the presence of anti-dsDNA antibodies.
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PMID:Dyslipoproteinemia during the active course of systemic lupus erythematosus in association with anti-double-stranded DNA (anti-dsDNA) antibodies. 1694 55

A retrospective study was done in 66 children (0.21% of all admitted children) below the age of 18 years with persistent hypertension diagnosed at the Department of Pediatrics, Faculty of Medicine Siriraj Hospital from Jan 1999 to Dec 2003. Male to female ratio was 1.4:1 with 54.5% aged between 6-12 years old and 9.1% aged less than 1 year. Hypertension was found to be severe (BP more than the 99th percentile for age, sex and height) in 79.1% but most (78.6%) of the patients did not have symptoms related to hypertension. Chronic headaches were found in 10%, hypertensive encephalopathy in 8.6%, epistaxis in 1.4% and visual disturbance in 1.4%. The most common cause of hypertension was renal parenchymal diseases (62.7%) mainly lupus nephritis (26.9%), idiopathic nephrotic syndrome (16.4%) and chronic renal failure (16.4%). Other causes of hypertension included renovascular diseases (7.5%), drug-induced (7.5%), essential (7.5%), tumors (4.5%), coarctation of aorta (3.0%), bronchopulmonary dysplasia (3.0%), and pheochromocytoma (1.5%). Obesity and overweight (body mass index, BMI more than 25) was found in only 10 patients (15.1%). The proportion of children with BMI more than 25 was not different between essential and secondary hypertension (p = 0.15). Left ventricular hypertrophy was noted in 7.5%, hypertensive retinopathy in 3.0%, and hypertensive encephalopathy in 9.0%. One-third of the patients had normal BP within 1 month and another 47.0% had normal BP within 6 months of diagnosis. One-fifth of the patients also needed surgical intervention for specific underlying diseases. The authors suggest that since a large number of children with hypertension have secondary hypertension, intensive investigation and prompt management should be done in all. Obesity and overweight is not reliable in the differentiation between primary and secondary hypertension. Short term outcome of hypertension is good with medications and surgery in selected cases but long term outcome is still unknown.
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PMID:Persistent hypertension in Thai children: etiologies and outcome. 1704 51

Clinical practice in paediatric nephrology is continuously evolving to mirror the research output of the 21st century. The management of antenatally diagnosed renal anomalies, urinary tract infections, nephrotic syndrome and hypertension is becoming more evidence based. Obesity and related hypertension is being targeted at primary and secondary care. The evolving field of molecular and cytogenetics is discovering genes that are facilitating clinicians and families with prenatal diagnoses and understanding of disease processes. The progression of chronic kidney disease in childhood to end-stage renal failure (ESRF) can be delayed using medical treatment to reduce proteinuria and treat hypertension. Pre-emptive living-related renal transplantation has become the treatment of choice for children with ESRF, thereby reducing the morbidity and mortality associated with peritoneal and haemodialysis. Although peritoneal dialysis, which is performed in the patient's home, is the preferred modality for children for whom there is no living or deceased donor for transplantation, home nocturnal haemodialysis is becoming a feasible option. Imaging modalities with the use of magnetic resonance and computerised tomography are continuously improving. As mortality for renal and vasculitic diseases improves, the gauntlet is now thrown down to reduce morbidity with secondary prevention of longer-term complications such as atherosclerosis and hyperlipidaemia. Clinical and drug trials in the fields of hypertension, nephrotic syndrome, systemic lupus erythematosus, vasculitis and transplantation are producing more effective treatments, thereby reducing the morbidity resulting from the disease processes and the side effects of drugs.
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PMID:How have the past 5 years of research changed clinical practice in paediatric nephrology? 1737 45

Primary focal segmental glomerulosclerosis (FSGS) is a major cause of nephrotic syndrome and eventual end-stage renal disease. It is known to be due to an abnormality of the visceral epithelial cells (podocytes) of the glomerulus. The morphological hallmark of primary FSGS is diffuse effacement of podocyte foot processes. The etiology of the podocyte damage is not been clearly established. FSGS can also be a secondary process due to underlying conditions including obesity and heroin use. In the secondary processes, the mechanism appears to be a decreased ratio of podocytes to the glomerular filtration surface area. Familial forms of FSGS also exist due to alterations of several different podocyte proteins. Primary FSGS is an increasing cause of end-stage renal disease. Recurrence of severe FSGS in renal allograft recipients presents a major challenge to transplant physicians. The incidence of recurrence is generally accepted to be between 20% and 30%. Risk factors for and characteristics of recurrence include a rapid progression of the primary disease to end-stage renal failure, early onset of nephrotic range proteinuria after allografting, frequent loss of the allograft, a high frequency of recurrence in subsequent allografts, and children less than 15 years of age. Some investigators have identified a circulating factor called the FSGS factor that appears to be associated with recurrence after transplantation. This factor has been shown to be a protein between 30 and 50 kd molecular weight. Logically, the possibility of a circulating factor associated with recurrence of FSGS led investigators to treat patients with plasmapheresis. Several studies have been reported with varying success. The response of patients to plasmapheresis seems to be completely individual. Other studies have added cyclophosphamide and/or mycophenolate mofetil to the plasmapheresis protocol. Again success in these studies has been variable. However, because some patients show complete recovery with plasmapheresis, individuals who develop recurrent FSGS after transplantation usually are given a trial of plasmapheresis therapy.
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PMID:Focal segmental glomerulosclerosis and renal transplantation. 1744 86

A 13-year-old girl with obesity and hyperinsulinism developed steroid-resistant nephrotic syndrome due to collapsing glomerulopathy with dominant C1q-containing mesangial immune deposits (CG/C1qN). She became overtly diabetic while receiving alternate-day prednisone and tacrolimus, requiring insulin injections. Despite the addition of mycophenolate mofetil to the treatment regimen, renal function subsequently declined. Rituximab (four weekly doses of 375 mg/m2) was tried 6 months after initial presentation and 3 months after weaning all glucocorticoids. Glomerular filtration rate (GFR) and proteinuria improved. Unexpectedly, blood sugar control normalized 6 weeks after antibody infusion. Rituximab was readministered 20 months after the first course because of deteriorating renal function, but the effect on GFR and proteinuria was modest. A retrospective analysis revealed that tubulointerstitial infiltrates present in the biopsies prior to treatment with rituximab contained numerous CD20+ and CD3+ (CD4 > CD8) lymphocyte aggregates. Rebiopsy 10 weeks after repeat rituximab therapy demonstrated the elimination of B-cell infiltrates and the apparent decrease of interstitial T-cell infiltrates, yet persistent, advanced global glomerulosclerosis, interstitial fibrosis and tubular atrophy. In conclusion, CG/C1qN was associated with B- and T-cell-rich tubulointerstitial infiltrates. B-cell-directed therapy delayed clinical progression during early disease but failed to prevent or ameliorate chronic changes, despite effective tissue B-cell clearance. The incidental resolution of diabetes was noted after rituximab treatment.
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PMID:Rituximab treatment of collapsing C1q glomerulopathy: clinical and histopathological evolution. 1835 94

Idiopathic nodular glomerulosclerosis is an enigmatic condition closely resembling diabetic nodular glomerulosclerosis without evidence of diabetic mellitus or other specific disease. Idiopathic nodular glomerulosclerosis remains a rare disease entity with an unclear pathogenesis. Clinicopathologic features of 15 patients with idiopathic nodular glomerulosclerosis were evaluated in a retrospective review of renal biopsies between 1998 and 2007. Our study cohort consisted predominantly of older (mean age, 64.2 years) white (73%) women (67%). Fourteen patients (93%) had a history of hypertension, and 10 (67%) were active smokers at the time of biopsy. Nine patients (60%) were obese (body mass index, >30 kg/m(2)) and 4 (27%) were overweight (body mass index, 25-29.9 kg/m(2)). Fourteen patients (93%) presented with renal insufficiency with mean serum creatinine level of 2.8 mg/dL. All 15 patients presented with proteinuria (mean urinary protein excretion, 5.6 g/24 h). Eleven patients (73%) presented with nephrotic-range proteinuria and 8 (53%) with nephrotic syndrome. Histopathologic findings showed nodular glomerulosclerosis (100%), moderate to severe arterio-arteriolosclerosis (100%), and glomerular basement membrane thickening (100%). Immunofluorescence and electron microscopy studies had no other specific findings. Our results confirm previous studies of a close association of hypertension and smoking with idiopathic nodular glomerulosclerosis. A significantly higher incidence of obesity and overweight in patients with idiopathic nodular glomerulosclerosis suggests that increased body mass index may also contribute to the development and progression of idiopathic nodular glomerulosclerosis.
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PMID:Idiopathic nodular glomerulosclerosis: a clinicopathologic study of 15 cases. 1870 Nov 35

A proportion of patients with refractory nephrotic syndrome (NS) due to focal segmental glomerulosclerosis (FSGS) often require long-term hospitalization, which results in the loss of quality of life (QOL) of the patients. An-11-year-old girl was brought to a regional hospital with an 8-day history of generalized edema. Laboratory studies revealed massive proteinuria without hematuria and marked hypoalbuminemia associated with hyperlipidemia. A percutaneous renal biopsy revealed lesions characteristic of FSGS. Although methylprednisolone pulse therapy was administered followed by oral prednisolone combined with cyclosporine A, heavy proteinuria persisted for the next 4 months. The patient was referred subsequenthy to our hospital for further examinations. High-dose intermittent mizoribine pulse therapy, LDL-apheresis, cyclosporine A, tacrolimus and intravenous cyclophosphamide pulse therapy proved to be partially effective. As a result, long-term hospitalization and intravenous administration of albumin, diuretics and immunoglobulin was required for this patient. Also, she developed severe steroid toxicity such as obesity, cataract and osteoporosis. A third renal biopsy revealed an advanced stage of FSGS lesions, suggesting subsequent development of end-stage renal disease (ESRD). Since the patient suffered from long-term hospitalization over 3 years and significant loss of QOL, we therefore proposed early initiation of peritoneal dialysis (PD), as in cases of congenital NS, in order to preserve the patient's general condition without intravenous drug administrations and for the preparation of a future renal transplantation. After obtaining informed consent from the patient and her family, the initiation of PD was performed at the age of 15 years before the ESRD state(serum creatinine level 2.0 mg/dL). The patient was successfully free from intravenous drug administrations and hospitalization, and the QOL was significantly improved thereafter. We, therefore, suggest that early initiation of PD might be a treatment of choice for elected patients with severe refractory nephrotic syndrome such as this presented case.
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PMID:[Early initiation of peritoneal dialysis for the treatment of a patient with refractory nephrotic syndrome]. 1923 11

Familial hypertriglyceridaemia is inherited in an autosomal dominant manner. The responsible genetic abnormality is unknown but recently, a novel gene encoding apolipoprotein AV has been linked to familial hypertriglyceridaemia. All patients develop the same phenotype with elevated levels of very low density lipoproteins (VLDL) in plasma. The main disorder of this dyslipidaemia is decreased intestinal absorption of biliary acids, leading to a compensatory increase of VLDL production. In familial hypertriglyceridaemia, a marked increase in plasma triglyceride (TG) levels can cause acute pancreatitis. Moreover, patients with other genetic factors, like familial chylomicronaemia, familial combined hyperlipidaemia, familial dysbetalipoproteinaemia and other rare disorders (e.g. Tangier disease and fish eye disease) may present increase of TG levels or cholesterol levels or both. Secondary hypertriglyceridaemias include hypothyroidism, kidney abnormalities (e.g. nephrotic syndrome or chronic kidney failure), diabetes mellitus, heavy alcohol consumption and obesity. In men and postmenopausal women, it seems that estrogen deficiency is responsible for higher TG levels compared with premenopausal women postprandially. In every state -fasting or postprandial-, women demonstrate lower plasma TG levels compared with men. This fact is due not only to increased muscular TG uptake and storage but also to higher TG clearance. Many studies demonstrated an age impact on plasma TG increase and larger variation of fasting TG levels caused by age. Also, hypertriglyceridaemia (TG >150 mg/dl; 1.7 mmol/l) is one of the diagnostic criteria of metabolic syndrome. Finally, several drugs may increase TG levels (e.g. chlorthalidone or beta-blockers).
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PMID:Primary and secondary hypertriglyceridaemia. 1935 54

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