Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-arteriosclerotic, virgin and arteriosclerotic, breeder rats were treated with aniline to suppress adrenal steroidogenic capacity and responsiveness to the stress of acute myocardial infarction. After two weeks of aniline treatment, some of the non-arteriosclerotic and arteriosclerotic animals were given two injections of isoproterenol, spaced 24 h apart, to induce massive myocardial infraction. On the 3 rd day, when myocardial necrosis reaches its zenith, the animals were sacrificed. Aniline-induced adrenal insufficiency caused increased mortality, absence of congestive heart failure, cardiac and adrenal enlargement but no evidence of the characteristic intense catabolism and increased corticoid production which attends acute myocardial infarction. Serum enzymes, e.g., SGOT, SGPT and LDH, triglycerides, but not glucose, free fatty acids and cholesterol, became acutely elevated in animals treated with aniline and isoproterenol. Animals developed a fatty liver, beta cell degranulation, post hypophy-sectomy-like changes in their adrenal cortices, unusually severe infarction, marked distention of intermuscular spaces, frequent foci of dystrophic calcification and cartilaginous metaplasia of the papillary muscles. It is believed that aniline-induced adrenal suppression altered the usual pathophysiologic response to acute myocardial infarction.
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PMID:Adrenocortical suppression and myocardial infarction in non-arteriosclerotic (virgin) and arteriosclerotic (breeder) rats. 126 59

Male and female, normotensive, Sprague-Dawley (S-D) rats, and spontaneously hypertensive rats (SHR) were subjected to acute and massive myocardial infarction with isoproterenol. Some of the animals were pre-treated (7 days) with the prolactin-lowering drug, bromocryptine. SHR survived in greater numbers than S-D but developed massive congestive heart failure of late onset. The adrenal glands and hearts became greatly hypertrophied in parallel with severely involuted thymus glands. ECG tracings demonstrated intense tachycardia and myocardial ischaemia. Bromocryptine reduction of prolactin (PRL) showed no effect on ECG tracings but reduced triglyceride, free fatty acid, total cholesterol and glucose levels. Isoproterenol caused dynamic increase in glucose, free fatty acids and triglycerides. CPK levels demonstrated greater cardiac damage in S-D vs SHR; greatly elevated SGOT and SGPT levels confirmed the presence of fatty liver in S-D and SHR. Myocardial infarction caused marked increase in circulating PRL in females only and sustained increases in aldosterone and corticosterone. SHR survivors had a high incidence of atrial and ventricular thrombi, left ventricular aneurysms, and intense fibroplasia and cartilaginous metaplasia in areas adjacent to damaged myocardium. It is suggested that adrenal steroidogenesis during an acute myocardial infarct favours survival and more complete myocardial repair in females vs males, and preexisting hypertension in SHR is associated with hormonal and metabolic response patterns different from normotensive S-D rats.
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PMID:Hormonal and metabolic changes during acute myocardial infarction in normotensive vs hypertensive rats. 684 10

We report a case of maternal mortality in a 34-year-old multipara who presented at the 35th week of gestation with severe hypoglycaemia. She had no history of diabetes mellitus. This episode was a prelude to catastrophic and refractory congestive cardiac failure due to previously undiagnosed severe mitral stenosis. The rapid cardiovascular deterioration initially appeared to be consistent with amniotic fluid embolism. She also developed deranged liver function with disseminated intravascular coagulation, which mimicked acute fatty liver of pregnancy. The problems of diagnosis and management are discussed. Unfortunately the patient died before mitral valvular commissurotomy could be effected.
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PMID:Severe mitral stenosis in a parturient with congestive cardiac failure and hypoglycaemia. 1532 Dec 12

Epidemiological studies indicate that obesity, insulin resistance, and diabetes are important comorbidities of patients with ischemic heart disease and increase mortality and development of congestive heart failure after myocardial infarction. Although ob/ob and db/db mice are commonly used to study obesity with insulin resistance or diabetes, mutations in the leptin gene or its receptor are rarely the cause of obesity in humans, which is, instead, primarily a consequence of dietary and lifestyle factors. Therefore, we used a murine model of diet-induced obesity to examine the physiological effects of obesity and the inflammatory and healing response of diet-induced obese (DIO) mice after myocardial ischemia-reperfusion injury. DIO mice developed hyperinsulinemia and insulin resistance and hepatic steatosis, with significant ectopic lipid deposition in the heart and cardiac hypertrophy in the absence of significant changes in blood pressure. The mRNA levels of chemokines at 24 h and cytokines at 24 and 72 h of reperfusion were higher in DIO than in lean mice. In granulation tissue at 72 h of reperfusion, macrophage density was significantly increased, whereas neutrophil density was reduced, in DIO mice compared with lean mice. At 7 days of reperfusion, collagen deposition in the scar was significantly reduced and left ventricular (LV) dilation and cardiac hypertrophy were increased, indicative of adverse LV remodeling, in infarcted DIO mice. Characterization of a murine diet-induced model of obesity and insulin resistance that satisfies many aspects commonly observed in human obesity allows detailed examination of the adverse cardiovascular effects of diet-induced obesity at the molecular level.
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PMID:Effects of diet-induced obesity on inflammation and remodeling after myocardial infarction. 1673 44

Thiazolidinediones (TZDs) or glitazones are agents that are widely used for the treatment of type 2 diabetes mellitus. These drugs have a multitude of therapeutic effects including reduction in insulin resistance and hyperglycaemia, anti-inflammatory effects and amelioration of hypertension, microalbuminuria and hepatic steatosis. The TZD molecular target, peroxisome proliferator-activated receptor gamma (PPARgamma), a nuclear transcription factor, is expressed diffusely in humans, including many tissues comprising the cardiovascular and renal systems. This suggests a potential for TZDs to elicit perturbing effects on these systems, which are independent of their effects on glucose and lipid metabolism. One of the most common adverse effects of TZDs is fluid retention, which can result in, or exacerbate, oedema and congestive heart failure (CHF). The frequency of peripheral oedema is approximately 5% when TZDs are used in mono- or combination oral therapy, and about 15% when used with insulin. Patients with type 2 diabetes are at high risk of myriad morbid complications, including CHF. The development of CHF, particularly in the elderly, is a harbinger of premature mortality. TZD-induced oedema is largely peripheral, may have its origins in changes in haemodynamics, with some contribution from molecules, which regulate cell and tissue permeability (e.g. vascular endothelial growth factor and protein kinase Cbeta), and remains the preponderant manifestation of TZD-induced fluid retention even in those with existing heart failure. Preclinical and pilot clinical data attest to the fact that at least part of the fluid retention derives from a direct effect of TZDs on sodium reabsorption via the renal medullary collecting duct, a mechanism that is sensitive to diuretic agents that have this nephron segment as their site of action, in whole or in part (spironolactone, amiloride and hydrochlorothiazide). Our review suggests various potential clinical strategies by which TZD-induced fluid retention might be effectively monitored and addressed.
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PMID:Thiazolidinediones and their fluid-related adverse effects: facts, fiction and putative management strategies. 1772 67

Thiazolidinediones (TZDs) are relatively new agents for the treatment of type 2 diabetes. They act as agonists at the PPAR-gamma nuclear receptor and their therapeutic effects include decreased insulin resistance and hyperglycaemia, an improved plasma lipid, inflammation and pro-coagulant profile, and amelioration of hypertension, microalbuminuria and hepatic steatosis. The most common side effects of TZDs include weight gain and oedema, with occasional reports of congestive heart failure (CHF). This review discusses the benefit-risk profile of TZDs in treating patients with type 2 diabetes, with particular reference to the heart. To provide context, we explore briefly the epidemiology and pathophysiology of heart failure in patients with type 2 diabetes, touch on the association of heart disease and cardiovascular mortality with antihyperglycaemic treatment modalities other than TZDs, and then focus on the effects of TZDs on the heart, cardiovascular risk factors and outcomes. We describe the cluster of host factors, which seems to predispose patients with type 2 diabetes to TZD-induced or TZD-exacerbated oedema and CHF and then provide an overview of the putative mechanisms of these TZD-related side effects. We also propose that certain diuretics (amiloride and spironolactone), by targeting the distal nephron that expresses PPARgamma in collecting duct cells, might be of benefit in ameliorating the fluid retention and oedema associated with TZDs.
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PMID:Thiazolidinedione insulin sensitizers and the heart: a tale of two organs? 1833 90

Gamma-glutamyl transferase (GGT) is a second-generation enzymatic liver function test available for several decades, initially used as a sensitive indicator of alcohol ingestion, hepatic inflammation, fatty liver disease, and hepatitis. Longitudinal and cross-sectional investigational studies since 1990 have associated GGT with an increase in all-cause mortality, as well as chronic heart disease events such as congestive heart failure and components of the metabolic syndrome (abnormal body mass index and levels of high-density lipoprotein cholesterol, glucose, triglycerides, and systolic and diastolic blood pressure). In the upper reference range, GGT was found to be an independent biomarker of the metabolic syndrome, with a 20% per GGT quartile trend rise. Additionally, GGT was positively correlated with an 18% per quartile risk of cardiovascular events and a 26% per quartile increased risk of all-cause mortality. Furthermore, it may be considered a biomarker for "oxidative stress" associated with glutathione metabolism and possibly a "proatherogenic" marker because of its indirect relationship in the biochemical steps to low-density lipoprotein cholesterol oxidation. GGT is becoming an important addition to the multimarker approach to cardiovascular risk evaluation. It should be considered a valuable adjunct in stratifying patient risk and in assessing the aggressiveness of appropriate treatment, with hopes of preventing unnecessary cardiac events and deaths in future years.
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PMID:Gamma-glutamyl transferase: a novel cardiovascular risk biomarker. 2002 25

Chronic diseases are major killers in the modern era. Physical inactivity is a primary cause of most chronic diseases. The initial third of the article considers: activity and prevention definitions; historical evidence showing physical inactivity is detrimental to health and normal organ functional capacities; cause versus treatment; physical activity and inactivity mechanisms differ; gene-environment interaction (including aerobic training adaptations, personalized medicine, and co-twin physical activity); and specificity of adaptations to type of training. Next, physical activity/exercise is examined as primary prevention against 35 chronic conditions [accelerated biological aging/premature death, low cardiorespiratory fitness (VO2max), sarcopenia, metabolic syndrome, obesity, insulin resistance, prediabetes, type 2 diabetes, nonalcoholic fatty liver disease, coronary heart disease, peripheral artery disease, hypertension, stroke, congestive heart failure, endothelial dysfunction, arterial dyslipidemia, hemostasis, deep vein thrombosis, cognitive dysfunction, depression and anxiety, osteoporosis, osteoarthritis, balance, bone fracture/falls, rheumatoid arthritis, colon cancer, breast cancer, endometrial cancer, gestational diabetes, pre-eclampsia, polycystic ovary syndrome, erectile dysfunction, pain, diverticulitis, constipation, and gallbladder diseases]. The article ends with consideration of deterioration of risk factors in longer-term sedentary groups; clinical consequences of inactive childhood/adolescence; and public policy. In summary, the body rapidly maladapts to insufficient physical activity, and if continued, results in substantial decreases in both total and quality years of life. Taken together, conclusive evidence exists that physical inactivity is one important cause of most chronic diseases. In addition, physical activity primarily prevents, or delays, chronic diseases, implying that chronic disease need not be an inevitable outcome during life.
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PMID:Lack of exercise is a major cause of chronic diseases. 2379 98

A 54-year-old Caucasian male had a witnessed collapse on the street. He was transported to the emergency department and subsequently pronounced dead. An unlimited autopsy examination was conducted under authorization of the coroner. Medical record review later revealed that the decedent had a history of alcohol abuse, chronic obstructive pulmonary disease, congestive heart failure, and chronic osteomyelitis treated by minocycline 100 mg twice daily. Autopsy revealed the cause of death to be ruptured gastroesophageal varices with nearly one liter of recent hemorrhage in the stomach and gastrointestinal tract. Other findings compatible with a history of alcoholism included hepatosplenomegaly, hepatic steatosis, and early bridging fibrosis. The decedent's thyroid was multinodular and enlarged at 50 gm. The thyroid gland, in its entirety, is shown below with serial sections made longitudinally through the gland capsule to reveal the underlying parenchyma.
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PMID:Pathology Image of the Month: Black Thyroid. 2507 33

Background. Emerging evidence suggests that nonalcoholic fatty liver disease (NAFLD) is associated with coronary artery diseases and arrhythmias. The FibroScan (Echosens, France), a widely available, noninvasive device, is able to detect liver fibrosis and steatosis within this patient population. However, the FibroScan is currently contraindicated in patients with cardiac pacemakers (PM) or implantable cardioverter-defibrillators (ICD). Objective. To determine the safety profile of FibroScan testing in patients with PM or ICD. Methods. Consecutive outpatients undergoing routine device interrogations at a tertiary level teaching hospital underwent simultaneous liver stiffness measurements. PM or ICD performance data, device types, patient demographics, medical history, and previous laboratory and conventional liver imaging results were collected. Results. Analysis of 107 subjects with 33 different types of implanted cardiac devices, from 5 different companies (Medtronic, Sorin, ELA Medical, Boston Scientific, and St. Jude), did not demonstrate any adverse events as defined by abnormal device sensing/pacing or ICD firing. This population included high risk subjects undergoing active pacing (n = 53) and with right pectoral PM placement (n = 1). None of the subjects had any clinical signs of decompensated congestive heart failure or cirrhosis during the exam. Conclusion. TE with FibroScan can be safely performed in patients with PM or ICD.
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PMID:Safety Profile of Liver FibroScan in Patients with Cardiac Pacemakers or Implantable Cardioverter-Defibrillators. 2834 45


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