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)

Five years following jejunoileal intestinal bypass surgery for obesity, a patient developed debilitating weakness and muscle pain. Osteomalacia was suspected clinically by radiographic and laboratory abnormalities and confirmed by bone biopsy. Malabsorption was documented as well as secondary hyperparathyroidism. Successful treatment of this syndrome with vitamin D and calcium identified a medically reversible disorder which obviated the need for surgical reanastomosis.
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PMID:Osteomalacia and weakness complicating jejunoileal bypass. 43 11

A 26-year-old woman, who had undergone jejunoileal bypass surgery six years previously for obesity, had symptoms of intermittent fever, myalgia, polyarthralgia, and aseptic joint swelling. These symptoms commenced one year after her surgery and gradually grew in intensity and frequency of occurrence. The patient, observed to have moderately decreased renal function, hyperoxaluria, and circulating cryoglobulins, underwent liver and renal biopsies. Both organ specimens demonstrated granulomatous involvement, but the kidneys exhibited no evidence of oxalate deposition. The findings of circulating cryoglobulins and suppression of symptoms with doxycycline, taken collectively with the circumstances surrounding this case, suggest that the observed granulomatous disease may be due to systematically adsorbed bacterial antigen(s).
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PMID:Jejunoileal bypass surgery and granulomatous disease of the kidney and liver. 63 46

An association between the ingestion tryptophan and a syndrome characterized by scleroderma-like skin abnormalities, fasciitis, and eosinophilia has recently been recognized in the United States. We report the clinical and histopathological findings in nine patients and the results of biochemical analyses of tryptophan metabolism in seven patients with this syndrome. Edema of the extremities, frequently accompanied by pruritus, paresthesia, and myalgia, developed in the nine patients (six women and three men; age range, 30 to 66 years) 1 to 18 months after the start of therapy with tryptophan (1.5 to 3.0 g daily) for insomnia, depression, or obesity. Five patients were taking drugs (benzodiazepines) known to inhibit hypothalamic-pituitary-adrenal function, and one had adrenal insufficiency. All had blood eosinophilia in the acute phase of their illness (mean eosinophil count [+/- SD], 3.62 +/- 2.87 X 10(9) cells per liter). All had histopathological changes in the dermis and subcutaneous tissue typical of scleroderma, and seven patients had eosinophils. The fascia was inflamed and fibrotic, and adjacent skeletal muscle often showed perifascicular inflammation. Tryptophan was discontinued in all patients, and eight received prednisone. The cutaneous symptoms improved, but only two patients had complete resolution of their illness. The patients had plasma levels of tryptophan before and after an oral dose of tryptophan that were similar to those in normal subjects. Plasma levels of L-kynurenine and quinolinic acid, which are metabolites of tryptophan, were significantly higher in four patients with active disease than in three patients studied after eosinophilia had resolved or in five normal subjects (P less than 0.001)--findings consistent with the activation of the enzyme indoleamine-2,3-dioxygenase. This illness resembles eosinophilic fasciitis and probably represents one aspect of the recently reported eosinophilia-myalgia syndrome. The development of the syndrome may result from a confluence of several factors, including the ingestion of tryptophan, exposure to agents that activate indoleamine-2,3-dioxygenase, and possibly, impaired function of the hypothalamic-pituitary-adrenal axis.
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PMID:Scleroderma, fasciitis, and eosinophilia associated with the ingestion of tryptophan. 231 25

Long-term treatment with high doses of corticosteroids leads to the development of truncal obesity and focal fatty deposition. These deposits characteristically are located on the face, the nuchal and truncal areas, and episternally, as well as in the mediastinum and epicardium. We studied a patient with juxta-articular adiposis dolorosa who had L-tryptophan-associated eosinophilia-myalgia syndrome and was treated with high doses of prednisone. This is the first reported case of adiposis dolorosa occurring as a complication of corticosteroid treatment. Alterations of fat metabolism induced by corticosteroid excess may have played a role in the development of this unusual painful syndrome.
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PMID:Corticosteroid-induced juxta-articular adiposis dolorosa. 199 Sep 89

The patient was a 50-year-old house wife. There were complicated consanguineous marriages in the family tree. Since 30 years of age, she had suffered from progressive limb muscle weakness, but without myalgia and myasthenia. At present, she was wheelchair-bound. Physical examinations showed obesity, congenital livedo racemosa, epicanthus palpebrae and left renal defect. Neurologically, facial, anterior cervical, and iliopsoas muscles were well preserved, but others were severely involved. Laboratory examinations revealed mildly elevated myogenic serum enzymes, and myogenic changes on needle EMG. In her muscle biopsy from the left rectus femoris muscle, there were no inflammatory changes, but marked variations of the fiber size as well as adipose tissue replacement were recognized. Strickingly, basophilic masses located in the center of the sarcoplasm were present in about 10% of the fibers. Histochemically, the masses were present in both type 1 and 2 fibers, and exhibited almost similar stained patterns to the tubular aggregates, but were dystrophin-, GRP78- and clathrin-positive. Under electron microscopy, the masses consisted of aggregates of the vesiculotubular structure, measuring approximately from 60 nm to more than 6 microns in diameter, which were continuous with T system/sarcoplasmic reticulum and were clearly segregated from myofilaments. This is a chronic progressive muscular disorder of adult onset with the peculiar pathological finding of vesiculotubular structure.
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PMID:[Clinico-pathological analysis of vesiculotubular myopathy of adult onset]. 1020 72

Recently, 5-hydroxy-L-tryptophan (5-OHTrp) has been promoted as an alternative to banned L-tryptophan as a dietary supplement. It has been claimed to help alleviate obesity, insomnia, depression, and headaches. However, eosinophilia-myalgia syndrome (EMS)-like symptoms have also been associated with ingestion or exposure to 5-OHTrp. HPLC-UV analysis of EMS-implicated 5-OHTrp revealed the presence of peak X, described as case-implicated. We show that peak X is actually a family of contaminants with the same molecular weight (234 Da) and similar HPLC retention times. We also demonstrate that all eight samples of commercially available 5-OHTrp analyzed by HPLC-MS contained three or more contaminants of the peak X family. The significance of these findings is discussed.
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PMID:Eosinophilia-myalgia syndrome case-associated contaminants in commercially available 5-hydroxytryptophan. 1072 Oct 89

Hyperlipidaemia is a pivotal risk factor for the development of atherosclerotic disease. A large number of studies have demonstrated that the treatment of abnormalities in lipoprotein levels reduces the risk for myocardial infarction, peripheral vascular disease, carotid artery disease, stroke, and cardiovascular mortality. Despite the development of multiple drug classes to treat dyslipidaemias and the promulgation of clearly defined guidelines for the management of lipid disorders, dyslipidaemia tends to be undertreated in the majority of patients at risk for cardiovascular disease. A part of the reluctance to treat different lipoprotein fractions to goal levels is attributable to physician- and patient-related concerns over the increasing toxicity of available therapies, as their dosages are increased. The risks of hepatotoxicity, myalgia, and rhabdomyolysis are fairly well characterised in patients receiving statins, fibrates and niacin. Another issue affecting treatment success rates is the fact that many patients with complex dyslipidaemias are inadequately responsive to single-agent therapy. As the epidemics of obesity, metabolic syndrome and diabetes mellitus continue to worsen, physicians will encounter severe, mixed dyslipidaemias more frequently. Many of these patients will require combinations of drugs to address the various metabolic derangements causing changes in multiple lipoprotein fractions. Although the need for combination therapy is well-established in the management of disorders, such as hypertension and diabetes, it is less often used for the treatment of dyslipidaemias. The development of safe, cost-effective, and efficacious combination dyslipidaemic therapy is an important goal in cardiovascular medicine. Simvastatin plus ezetimibe has recently been combined as a fixed dose therapy, which offers clinicians the opportunity to simultaneously inhibit two key pathways in cholesterol metabolism: hepatic cholesterol biosynthesis and the absorption of cholesterol at the level of the proximal jejunum. This dual mechanism of inhibition substantially increases the capacity to decrease serum levels of atherogenic low-density lipoproteins and increase high-density lipoprotein, compared with that observed when either drug is used alone. This combination increases the likelihood of therapeutic success in patients with dyslipidaemia.
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PMID:Simvastatin plus ezetimibe: combination therapy for the management of dyslipidaemia. 1570 90

Liver allograft recipients are at increased risk of death from cerebrovascular and cardiovascular disease. We propose the following strategy of risk-reduction, based on currently available literature. Lifestyle: standard advice should be given (avoidance of smoking, excess alcohol and obesity, adequate exercise, reduction of excess sodium intake). Hypertension: target blood pressure should be 140/90 mmHg or lower, but for those with diabetes or renal disease, 130/80 mmHg or lower. For patients without proteinuria, antihypertensive therapy should be initiated with a calcium channel blocker and for those with proteinuria, an angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker. If monotherapy fails to achieve adequate response, calcium channel blockers and ACE-inhibitors or angiotensin II receptor blockers should be combined. If hypertension remains uncontrolled, an alpha-blocker may be added. Consideration should be given to changing immunosuppression and avoiding use of calcineurin inhibitors. Diabetes: recipients should be regularly screened for diabetes. For patients with new-onset diabetes after transplant, stepwise therapy should be guided by HbA1c concentrations, as with type II diabetes mellitus. Hyperlipidemia: annual screening of lipid profile should be undertaken, with treatment thresholds and targets based on those advocated for the high risk general population. Dietary intervention is appropriate for all patients. A statin should be considered as the first line treatment to achieve specified targets. In patients receiving a calcineurin inhibitor, Pravastatin should be commenced at a dose of 10 mg/day. In patients receiving other forms of immunosuppression, pravastatin may be commenced at a dose of 20 mg/day. Liver tests should be monitored and patients warned to report myalgia. If monotherapy is inadequate, ezetimibe or a fibrate may be added. Consideration may be given to change in immunosuppression if combination lipid-lowering therapy proves inadequate.
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PMID:Reducing the risks of cardiovascular disease in liver allograft recipients. 1749 26

Rhabdomyolysis is an acute skeletal muscle disorder characterized by altered integrity of the cell membranes of muscle fiber cells. It can be related to a variety of factors: muscular trauma, muscle enzyme deficiencies, infections, drugs, toxins, alcohol ingestion, endocrinopathies and electrolyte imbalances such as hypokalemia. We report the case of a 46-year-old woman admitted to the Emergency Department for frequent episodes of vomiting associated with food intake in the last two weeks, general muscular weakness and myalgia. Physical examination on admission was unremarkable, except for a symmetrical and dominantly proximal muscular weakness of all four extremities. Blood pressure was 116/70 mmHg with a sinus bradycardia (53 beats/min) on the electrocardiogram. Laboratory tests showed a metabolic alkalosis with marked hypokalemia (K+= 1.9 mEq/l) and elevation of muscular enzymes (myglobin= 993 ng/ml, troponin T= 0,10 ng/ml e CK= 1113 U/l). No symptoms of recurrent rhabdomyolysis were reported, patient denied alcohol consumption and there was not clinical evidence of hyperthyroidism. A iatrogenic etiology could not be excluded for certain because patient was in therapy with lansoprazole (Naranjo algorithm 3/13) but, revealing medical history that she underwent a laparoscopic adjustable gastric banding for the treatment of a severe obesity, we focused our attention on hypokalemia, due to persistent vomiting. Fasting, administration of metoclopramide and infusion of potassium chloride resulted in steady improvement of clinical conditions and normalization of electrolyte imbalance. At the clinical follow-up of three months, after partial deflation of the gastric banding, the patient was asymptomatic with muscular enzymes and potassium levels in the normal range. Authors discuss the pathophysiologic mechanisms of these alterations.
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PMID:Hypokalemic rhabdomyolysis in a patient with a laparoscopic adjustable gastric banding. 1859 46

Recently, the World Health Organization declared a pandemic mediated by the novel A H1N1 influenza virus. Soon after the first report from Mexico, the disease arrived in Chile, where it spread quickly from south to north, mimicking cold weather progression through the country. Between May and September 2009, 366,624 cases of H1N1 were reported; 12,248 were confirmed by real-time reverse-transcription polymerase chain reaction and 1562 were hospitalized. One hundred thirty-two deaths were attributable to the infection, creating a death rate of 0.78 per 100,000 inhabitants. Common comorbidities were present in 59%, including obesity, chronic obstructive pulmonary disease, hypertension, type II diabetes, and congestive heart failure. Nine percent were pregnant. Severe disease developed early; the median time to admittance was 5 days, and the most common clinical manifestations were cough, fever, dyspnea, and myalgia. Mean acute physiology and chronic health evaluation II and sequential organ failure assessment scores were 14 and 5, respectively. Highlighted laboratory data were lactate dehydrogenase and creatine kinase elevation, leukocytosis in 50%, elevated creatinine in a 25%, and thrombocytopenia in 20%. Severe respiratory failure requiring high-frequency oscillatory ventilation and extracorporeal membrane oxygenation as sophisticated modes of respiratory support was seen in 17%. Acute renal failure occurred in 25% of the intensive care unit patients, with death rates near 50%. Health systems reinforced outpatient guards with extra staff and extension of the duty schedules. Antivirals were supplied free for medically diagnosed cases. Admissions for severe cases were prioritized, reconverting hospital beds into advanced care ones; a central coordination station rationed their assignment. Recommendations for small hospitals include adding ventilators, using videoconferences, providing tutorial activity from experts, developing guidelines for disease management, and outlining criteria for transport.
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PMID:Influenza A pandemics: clinical and organizational aspects: the experience in Chile. 1993 12


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