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)

A retrospective review of the cases of congestive heart failure admitted to Holberton Hospital in Antigua in 1995 and 1996 was undertaken. Two hundred and ninety-three (293) patients were identified by International Statistical Classification of Diseases, 10th revision (ICD-10) coding as having congestive cardiac failure in the period but only 138 charts were either available or fitted the definition of congestive cardiac failure and these provided the basis for this analysis. The average age of patients admitted for congestive cardiac failure was 69 years (range: 5 months to 99 years), and 63% were female. the aetiology of congestive cardiac failure was hypertension (41%), ischaemia (33%), valvular (12%), alcohol related (2%), idiopathic (5%) and mixed (7%). Treatment included diuretics (95%), angiotensin converting enzyme inhibitors (78%), digoxin (75%), nitrates (34%), calcium channel blockers (25%), other vasodilators (7%) and antiarrhythmics (5%). Of those with congestive heart failure, diabetes was present in 38%, atrial fibrillation in 19%, renal insufficiency in 17%, elevated cholesterol in 11%, obesity in 9% and tobacco use in 7%. The in-hospital mortality in the 2-year period was 17.4% (females 15%, males 22%, 11% < 65 years, 20% > 65 years, 14% for those with 1 to 3 admissions and 83% for those with > 3 admissions, 19% for those with atrial fibrillation and 16% for those without). The prevalence of congestive cardiac failure utilizing the data analysed in this study (138 patients) was 0.21% of the population of the island state but based on the discharge diagnosis using ICD-10 coding it was 0.5%; it was 1% in the 40 to 65-year-age group and 4% in those > 65 years of age. The patients in this study represented only those with New York Heart Association (NYHA) classes III and IV, hence the true prevalence would be higher than recorded here. Congestive cardiac failure is emerging as a significant health problem in Antigua and Barbuda.
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PMID:The prevalence, aetiology and treatment of congestive cardiac failure in Antigua and Barbuda. 1055 60

Focal and segmental glomerulosclerosis (FSGS) is a common, non-specific renal lesion. Although it is often secondary to other disorders, including HIV infection, obesity, hypertension and diabetes, FSGS also appears as an isolated, idiopathic condition. FSGS is characterized by increased urinary protein excretion and decreasing kidney function. Often, renal insufficiency in affected patients progresses to end-stage renal failure, a highly morbid state requiring either dialysis therapy or kidney transplantation. Here we present evidence implicating mutations in the gene encoding alpha-actinin-4 (ACTN4; ref. 2), an actin-filament crosslinking protein, as the cause of disease in three families with an autosomal dominant form of FSGS. In vitro, mutant alpha-actinin-4 binds filamentous actin (F-actin) more strongly than does wild-type alpha-actinin-4. Regulation of the actin cytoskeleton of glomerular podocytes may be altered in this group of patients. Our results have implications for understanding the role of the cytoskeleton in the pathophysiology of kidney disease and may lead to a better understanding of the genetic basis of susceptibility to kidney damage.
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PMID:Mutations in ACTN4, encoding alpha-actinin-4, cause familial focal segmental glomerulosclerosis. 1070 Jan 77

Previous observations raised the possibility that circulating GH-binding protein (GHBP) may serve as a useful index for tissue GH receptor (GHR) responsiveness in humans. Indeed, there are many examples to indicate that across a wide scope of comparative studies, ontogenic data, experimental systems, physiological conditions, nutritional states, and diseases there is a close relationship between the concentration of GHR and the level of serum GHBP. In the present review, we discuss various aspects that might affect differentially cellular GHR and circulating GHBP, based on species and tissue divergence, regulation of cell-surface GHR turnover, GHR cleavage mechanism, GHR mRNA splicing, and GH insensitivity (GHI) syndrome patients with normal or high serum GHBP levels. Most previous experimental data were collected through comparative analysis of human GHBP against GHR and GHBP determinations in animal models. Yet, GHBPs possess species-specific properties, and the mechanism for their generation and regulation display evolutionary divergence. Another important aspect is tissue divergence, in terms of GHR regulation and its cleavage to GHBP. Although GHBP is generated mainly from the liver GHR, many other tissues express GHRs and probably also contribute to the total GHBP level. Human GHBP is generated by proteolytic cleavage of GHR at the cell-surface and, thus, occupancy or modulation of GHR turnover/internalization would impact the level of cell-surface GHR that are available for proteolysis. An additional degree of complexity arises from recent reports, implicating a protein kinase C-regulated metalloprotease activity in GHBP generation. This suggests that the proteolytic system, which controls the specific cleavage mechanism and switch between GHR proteolysis and GHBP shedding, is a regulated process. Finally, differential splicing regulation to the full-length, active human GHR (hGHR) and the inactive truncated hGHRtr isoform messenger RNA transcripts might regulate both the production of GHBP and GHR bioactivity, as hGHRtr generates large amounts of GHBP but has a dominant negative effect on GH signaling. Several clinical GH-resistant conditions, such as liver cirrhosis, renal insufficiency, insulin-dependent diabetes mellitus, hypothyroidism, malnutrition, or critical illness are associated with reduced GHBP levels. However, this is not universally true, as in other conditions (e.g. early childhood, acromegaly) decreased GHBP levels are not associated with GHI. Divergence between serum GHBP and insulin-like growth factor I, such as which occur during puberty or obesity, also questions whether GHBP levels reflect GHR function. Even in patients with GHI syndrome, serum GHBP cannot be relied on to detect all GHR mutations. The correct assessment of GHR expression and GH functionality in an individual patient will require, in parallel to measurements of serum GHBP, additional detailed diagnostic screening of the entire GH-insulin-like growth factor I axis.
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PMID:Clinical review 112: Does serum growth hormone (GH) binding protein reflect human GH receptor function? 1072 17

Coronary artery disease (CAD) is a major cause of morbidity and mortality in SLE, including the Hopkins Lupus Cohort. Currently, 9% of the cohort have had clinical evidence (angina or myocardial infarction) of CAD. In our initial prospective study we found that duration of prednisone, hypertension, hyperlipidemia and obesity were risk factors for later CAD. We can now extend that list to include age, male sex, elevated homocysteine, renal insufficiency and antiphospholipid antibodies. Many of the risk factors are amenable to intervention, but the timing of intervention, and the effectiveness of intervention, must be determined.
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PMID:Detection of coronary artery disease and the role of traditional risk factors in the Hopkins Lupus Cohort. 1080 83

Renal artery stenosis may be a cause of hypertension and a potential contributor to progressive renal insufficiency. However, the prevalence of renal artery disease in a general population is poorly defined. The purposes of this study were to evaluate the prevalence of angiographically-determined renal artery narrowing in a patient population undergoing routine cardiac catheterization, and to identify the risk factors for renal artery stenosis. After left ventriculography, abdominal aortography was performed to screen for the presence of renal artery stenosis. A total of 427 patients (274 males, 153 females) were studied and the mean age was 59 years. Renal artery narrowing was identified in 10.5% of patients. Significant (> or = 50% diameter narrowing) renal artery stenosis was found in 24 patients (5.6%) and insignificant stenosis was found in 21 patients (4.9%). Significant unilateral stenosis was present in 4.2% of patients and bilateral stenosis was present in 1.4%. The stem of the renal artery was a more common site of stenosis in 62.2% of patients than in the ostium (37.8%), but the severity of stenosis was not significantly different according to the site of stenosis. By univariate and multivariate logistic regression analysis, the association of clinical variables with renal artery stenosis was assessed. Multivariable predictors included age, hypertension and peripheral vascular disease (p < 0.05). The variables such as sex, smoking history, hyperlipidemia, renal insufficiency, as well as the presence of obesity, severity of coronary heart disease and D.M., were not associated. In conclusion, the prevalence of angiographically-determined renal artery narrowing in a patient population undergoing cardiac catheterization is 10.5%. Old age, hypertension and evidence of peripheral vascular disease represent the predictors of renal artery stenosis.
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PMID:The prevalence and associated risk factors of renal artery stenosis in patients undergoing cardiac catheterization. 1081 23

Renal transplantation has been a usual medical practice in developed countries for several decades. A large number of studies report the excellent results obtained with such a practice. The survival of the graft, although able to be improved, is excellent and gives a great deal of hope to patients with renal insufficiency. The high level of investigation into immunosuppressor drugs offers, almost continuously, more efficient and better tolerated products. Paradoxically, the usual problems of patients with a renal transplant are not immunological but cardiovascular. Elevated serum cholesterol levels, obesity, diabetes and other cardiovascular risk factors (CVRFs) are usual in these patients, arterial hypertension (AHT) being the most frequent. Nephrologists are increasingly using ambulatory blood pressure monitoring (ABPM) on a daily basis. In the last 10 years, we have obtained highly valuable and interesting results with this technique which have allowed us to study and understand with greater precision the relationship of AHT to the kidney. Here we analyse and review the most relevant aspects of ABPM in the different stages of kidney disease, with special emphasis on renal transplantation.
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PMID:Ambulatory blood pressure after renal transplantation. 1136 36

The acute phase response to tissue injury is art of the wound healing process after surgery. The aim of study was to determine levels of acute phase proteins and levels of thrombocytes in patients with laparoscopic surgery (intraabdominal preperitoneal repair) and in patients with open surgery (tension free repair). Exclusion criteria in both groups of patients: malignity, diabetes mellitus, obesity (BMI > 30), infection, hypoproteinemia, hepatic or renal insufficiency and hypertension. Type of anaesthesia: general. Perioperative preventive antithrombotic medication: LMWH 5 days after surgery. The observed parameters were estimated before, one hour, 2nd and 7th days after surgery. Statistical test: ANOVA, statistical by significant difference p < 0.05. The results of the study demonstrate an increase of acute phase proteins CRP, OROSO and Fb in both groups of patients in comparison to their levels before surgery. In this respect we did not find a difference between the two types of operation. In patients with laparoscopic surgery the observed peak of FBG increase (+69%) was on the 2nd day after surgery followed by a slight drop of values in comparison to the results of open surgery patients with a FBG increase on the 2nd day (+42%) and with continuation on the 7th (%) postoperative day. The peak of CRP values was on the 2nd day in both groups. OROSO values increased even on the 7th day. The same situation occurred with Plt levels (p < 0.05). We suggested, that laparoscopic and open surgery of inguinal hernia repair are both followed by an acute phase response related to the tissue injury and this response perists even 1 week after surgery. But the recovery time of some parameters of the acute phase response (e.g. orosomucoid and fibrinogen levels) to the basical preoperative state is longer in patients with open type of surgery. We do not confirm differences in the degree of risk of postoperative thrombophilia in both types of surgery and suggest, that the prevention of thromboembolic complications is indicated in both types of surgery.
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PMID:[The acute phase reaction in laparoscopic and open surgery of inguinal hernias]. 1139 49

Standard medical treatment for patients with acute venous thrombosis is antithrombotic therapy. Following a historical overview of the evolution of heparin therapy to include low-molecular weight heparin (LMWH), the pharmacokinetic properties of enoxaparin are described. Therapeutic advantages of LMWH over unfractionated heparin (UFH) are also discussed, including once- or twice-daily subcutaneous dosing, reduced hospital stays, elimination of therapeutic monitoring for most patients, and possibly less bone density loss. Studies have demonstrated that enoxaparin is at least equivalent to UFH with regard to efficacy and safety. Opportunities for future study include evaluation of enoxaparin's efficacy for the prevention of deep vein thrombosis within high-risk groups and for the treatment of thrombosis in such conditions as pregnancy, cancer, obesity, and renal insufficiency, and in children.
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PMID:Overview of enoxaparin in the treatment of deep vein thrombosis. 1148 2

We examined whether the age at onset, gender, arthritic manifestations, and tophus formation in familial gout are different from those in nonfamilial gout, and we also examined the contributory effect of genetic association to the concurrence of hypertriglyceridemia, hypercholesterolemia, type 2 diabetes mellitus (DM), hypertension, obesity, and renal insufficiency with gout in Taiwan. A total of 21,373 gout patients' data from Ho-Ping Gout database were analyzed in this study retrospectively. The clinical and laboratory data were compared between familial and nonfamilial gout. Mean age at onset of gout in familial subjects was significantly 7.5 years lower than that of nonfamilial subjects (40.9 +/- 13.4 v 48.4 +/- 14.2 years, P =.0001), while gender, arthritic severity, and tophus formation were not significantly different between these 2 groups. Familial gout had lower serum triglyceride (TG), total cholesterol (TC), and percentage of hypertension than nonfamilial gout (182.4 +/- 125.3 v 195.9 +/- 135.8 mg/dL, P =.0001; 207.5 +/- 42.5 v 210.4 +/- 48.8 mg/dL, P =.0003; and 19.57% v 22.56%, P <.0001, respectively). Their serum creatinine, body mass index (BMI), and percentage of type 2 DM were not significantly different. Our results demonstrate that familial gout is associated with precocious onset. Furthermore, the contributory effect of genetic association to the concurrence of hyperlipidemia and hypertension with gout is less than that of environmental factors, while the effect of genetic association to the concurrence of obesity, type 2 DM, and renal insufficiency with gout is equivalent to that of environmental factors.
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PMID:Clinical features of familial gout and effects of probable genetic association between gout and its related disorders. 1158 94

In recent years several multicentric prospective studies have demonstrated the efficacy of some therapeutic measures to slow the progression of renal diseases. Inhibition of renin-angiotensin system (RAS) both by ACE inhibitors (ACEI) and angiotensin II receptor antagonists (ARA) is probably the strongest therapeutic alternative: The antiproteinuric effect of these drugs is an excellent surrogate marker and a predictor of the beneficial influences on the progression of renal failure. The type of renal disease, an inadequate control of blood pressure, and the presence of obesity may counteract the beneficial influences of RAS inhibition, whereas early treatment of all patients with significant proteinuria before the appearance of renal insufficiency and combined therapy with an ACEI and an ARA may augment it. Dietary protein restriction is a classic treatment of chronic renal insufficiency whose effectiveness has been validated by multicentric studies. However, a poor compliance of the patient and the risk of malnutrition with very strict protein restriction could limit the benefits of this treatment. Treatment of hyperlipidemia, prevention of obesity, avoidance of smoking, and regular physical exercise are interventions whose therapeutic potential is progressively recognized, particularly in type 2 diabetic nephropathy. Early correction of anemia may contribute to the slowing of renal disease progression. Although further studies are required, the accumulated evidence and the likelihood of additive beneficial effect of these therapeutic measures advise their combined implementation in patients with chronic renal diseases.
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PMID:Slowing the progression of renal failure. 1198 7


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