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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper describes a case of acute pancreatitis occurring in a patient immediately after delivery and in primigravida. The patient had a family case history of dyslipidemia (Type IV). The pregnancy had been complicated by preeclampsia treated at home with nifedipine tablets (one tablet three times a day) with good results on pressure values; lipidic values were high despite dietary measures taken. The baby at birth weighed 3830 g after physiologic labour and a natural delivery. Acute pancreatitis was diagnosed after observation of epigastralgia with irradiation on the left shoulder, vomiting, symptoms of acute abdomen such as sweating, increased pulse rate, hypotension, abdominal pain on palpation, and absence of peristalsis. An analysis of the blood showed high levels of amylase and hyperglycemia, an increase in XDP, and leucocytosis. Instrumental tests such as pancreatic echography revealed an increase in pancreatic volume, uneven structure of the parenchyma and higher levels of liquid in the peritoneum. The patient was moved to intensive-care, a nasal gastric probe inserted, hydroelectrolytic treatment was begun, vital functions monitored, pain kept under control by medical therapy, and antibiotics administered. Subsequent tests showed an improvement in the parameters of pancreatic functions (amylase, lipase, calcium hematic) and their gradual return to normal values. The computerized tomography of abdomen additionally revealed the presence of pancreatic pseudo-cysts and effusion of peritoneal liquid near the right kidney. The patient was discharged after two weeks in the surgical ward. There are many caused of acute abdomen during and immediately after pregnancy, and one of these is acute pancreatitis, though rare (occurring between 1:3800 and 11.467 according to Rabkin).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute pancreatitis in pregnancy]. 835 Oct 66

The authors base their experience on 12 women affected by endometrial carcinoma. Problems have been diagnosed in the post-menopausal and climacterium period, considering the clinical, hormonal and lipidic profile and some tumoral markers. The most risk factors for the endometrial adenocarcinoma have been collected in the adiposity with hypertension and hyperglycemia, above all in nullipara women with late menopause and dyslipidemia.
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PMID:[Risk factors of endometrial carcinoma]. 841 44

In older type II diabetics, complications progress more rapidly than in younger diabetics for any given degree of hyperglycemia. Therefore, it is important to closely monitor blood glucose levels. When their sugars are controlled, older diabetics will have less nocturia and polyuria; fewer infections; better wound healing; a decrease in the rate of progression of cataracts, diabetic retinopathy, and nerve and renal disease; and better control of dyslipidemia. To learn some useful tips for managing older patients with type II diabetes, GERIATRICS reader David B Jack, MD, interviewed Nancy J.V. Bohannon, MD, for this "Ask the Expert" article.
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PMID:Type II diabetes: tips for managing your older patients. 864 90

Fructose (FR) feeding in rats provides a model of dietary-induced insulin resistance that has been used to examine interactions among the cluster of metabolic disorders including insulin resistance, hyperinsulinemia, hypertension, and dyslipidemia known as Syndrome X. In animals with reduced beta-cell mass, however, insulin resistance may not have similar associated disorders. Therefore this study examined the consequences of FR feeding in rats with a reduced beta-cell mass. Formerly diabetic islet-transplanted (TX) or shamoperated (SHAM) male Wistar Furth rats were fed a purified control (CNTL) diet or a diet containing either 40 or 70% (wt/wt) FR for 3-5 wk. FR feeding in SHAM animals resulted in elevated triglyceride levels but did not affect fed or fasting glucose and insulin concentrations, blood pressure, glucose tolerance, and the acute insulin response to a glucose bolus compared with CNTL-fed animals. Among TX animals, hypertriglyceridemia and fasting hyperglycemia were observed only in those fed FR. Thus the effects of diet-induced insulin resistance are limited to dyslipidemia, if insulin secretory capacity is adequate, but are detrimental to both glucose and lipid metabolism in combination with a reduced beta-cell mass.
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PMID:Consequences of high dietary fructose in the islet-transplanted rat with suboptimal beta-cell mass. 877 51

The high prevalence of obesity and its well documented association with the cardiovascular risk factors diabetes mellitus, dyslipidemia and hypertension represents a major problem for the general health status of industrialized societies. Although numerous studies have shown that genetic factors have a major influence on the regulation of energy homeostasis and the susceptibility to obesity, the genes and predisposing mutations involved are insufficiently understood. Among several known rodent models of obesity due to single gene mutations, mice homozygous for the obese (ob) gene exhibit massive early-onset obesity, hyperphagia, non-insulin-dependent diabetes mellitus, defective thermoregulation and infertility. Recently the ob gene was identified by positional cloning and shown to be mutated in ob/ob mice. Leptin, the product of the ob gene, is a 167-amino acid secreted protein that is synthesized exclusively in adipose tissue. With the exception of ob/ob mice, circulating plasma leptin is elevated in obesity. Administration of recombinant leptin to ob/ob mice reduces fat mass, food intake, hyperglycemia and hyperinsulinemia. The various effects of the hormone are mediated by leptin receptors expressed at high levels in the hypothalamus, but also in several other non-neuronal tissues. A mutation in the leptin receptor gene is responsible for the obese phenotype of db/db mice. Plasma leptin in humans is positively correlated with body fat mass, suggesting that leptin resistance rather than leptin deficiency is a common feature of human obesity. This review briefly summarizes the current status of the rapidly growing evidence that leptin plays an important role in the regulation of body weight and fat deposition.
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PMID:Regulation of energy balance by leptin. 888 45

Insulin resistance is a major component of non-insulin-dependent diabetes mellitus (NIDDM). While a genetic contribution is likely, as yet none of several proposed candidate genes have been incriminated in the typically obese patient with NIDDM to explain their insulin resistance. Accordingly, this review focuses on some recent advances in understanding three acquired factors contributing to insulin resistance: visceral obesity, glucotoxicity and lipotoxicity. Newer computerized tomography scans allow quantitation of fat accumulating in visceral organs including the mesentery and omentum. This visceral fat relates much more to the insulin resistance syndrome than does subcutaneous fat. Moreover, exercise, as performed by active Sumo wrestlers, is associated with low visceral fat, absent hyperglycemia and absent dyslipidemia despite massive subcutaneous obesity. It remains to be seen whether exercise programs more moderate than Sumo wrestling will also mobilize visceral fat. A new metabolic pathway has recently been described whereby hexosamines are formed by an increased flux of glucose into fat and muscle. These hexosamine products appear to explain how glucotoxicity results in insulin resistance. They act as a negative feedback system to limit further glucose transport by insulin target tissue during hyperglycemia. Lipotoxicity has previously been implicated in insulin resistance by its inhibitory effect on glucose uptake by muscle because of the Randle-fatty acid cycle. Recently the role of elevated fatty acids in producing "hepatic" resistance to insulin in NIDDM has also been documented, but the site of insulin resistance may be the fat cell rather than the hepatocyte. Therapy consists mainly of hygienic measures, including caloric restriction and exercise, which can reverse all three of these acquired forms of insulin resistance. In addition, pharmacologic measures to reduce hyperglycemia can reduce the glucotoxicity and lipotoxicity. The use of insulin-sparing antihyperglycemia drugs may be particularly useful in the insulin-resistant patient to avoid weight gain while correcting the hyperglycemia.
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PMID:Reversible insulin resistance in non-insulin-dependent diabetes mellitus. 891 80

Secondary prevention of arteriosclerosis tries to inhibit progression of the atherosclerotic process. Therapeutic measures focus on modification of cardiovascular risk factors and antithrombotic treatment. Hypercholesterolemia is the main risk factor for coronary artery disease. The risk of a coronary event is correlated to the plasma cholesterol level. Lowering plasma cholesterol results in reduction of vascular morbidity and mortality. Cigarette smoking is the predominant risk factor for peripheral arterial occlusive disease (PAOD). Smoking cessation reduces progression of PAOD and lowers cardiovascular morbidity and mortality. The preventive effect of antihypertensive therapy in hypertensive patients is most pronounced for cerebrovascular events. Antihypertensive measures improve prognosis after stroke and myocardial infarction. The increased cardiovascular risk in diabetics is in part explained by hyperglycemia and hyperinsulinemia, but also depends on coexisting dyslipidemia and hypertension. Intensive treatment of elevated blood glucose levels, dyslipidemia and hypertension are important preventive measures. Aspirin is highly effective in secondary prevention of vascular events. For the coronary arteries, low-dose aspirin is well established. Whether low-dose aspirin is equally effective for reducing progression of arteriosclerosis in the cerebrovascular and in the peripheral vessels is questionable. Ticlopidine serves as an alternative to aspirin; however, neutropenia may occur, which requires supervision of the patient.
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PMID:[Secondary prevention of arteriosclerosis]. 892 4

Recently, the number of diabetic patients in Japan has increased and reached 6 millions, and it was estimated that 1.5 million diabetic patients were suffering from diabetic complications of microangiopathy (neuropathy, retinopathy and nephropathy) and macroangiopathy. According to the study for the causes of death among Japanese diabetic patients during 10 years from 1981 to 1990, mean longevity of diabetic patients was shorter of 9.4 years in men and 13.5 years in women than those of non-diabetics. Forty percent of diabetic patients died from the vascular diseases (ischemic heart disease 14.6%, cerebrovascular disease 13.5% and renal disease 11.2%). The frequency of death due to ischemic heart disease was almost double in diabetic patients in comparison to non-diabetics in Japan. From the data obtained from the study of Japanese-American, more than 50% of them showed abnormal glucose tolerance and the frequency of ischemic heart disease was higher twice than that of Japanese. Diabetes has been recognized as one of the important risk factors for atherosclerosis, and so many factors, such as hyperglycemia, glycation, dyslipidemia, hyperinsulinemia, insulin resistance, hypertension and obesity in diabetes, are related to atherosclerosis. The relation of these factors will be introduced. Clinically, it is very important to make a check list of these factors and make an effort to diminish them for prevention of atherosclerosis of diabetic patients.
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PMID:[Diabetes and atherosclerosis]. 895 31

The aim of the present investigation was to study normal rats fed a sucrose-rich diet (SRD) for a prolonged period (up to 30 weeks) (1) to obtain additional data on the hormonal and metabolic patterns induced by this treatment and (2) to provide information on changes taking place in the pancreatic islet cell populations. We found that long-term feeding with a SRD resulted in a steady state of hypertriglyceridemia and hyperglycemia in which insulin levels remained unchanged and unable to compensate for the increased demands of the developing metabolic changes. The endocrine pancreas showed a significant increase of both islet number and B-cell area, as well as changes in the profile of islet cell distribution. However, these changes were not accompanied by an increase in the pancreatic content of immunoreactive insulin (IRI). It may therefore be postulated that the newly emerged B-cell mass has some sort of derangement with the increased insulin demand resulting from insulin resistance induced by the long-term SRD feeding. Thus, feeding a SRD to normal rats may prove to be an attractive animal model for studying the role of environmental nutritional factors in the unsettled issue of the relationship between insulin resistance and relative insulin deficiency. The model might provide key information for understanding the pathophysiology of human diseases such as type II diabetes, dyslipidemia, and a number of entities included in so-called syndrome X.
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PMID:Long-term administration of a sucrose-rich diet to normal rats: relationship between metabolic and hormonal profiles and morphological changes in the endocrine pancreas. 896 87

We examined the association between psychosocial stress-related variables and insulin resistance syndrome (IRS) risk-factor clustering. In 90 middle-aged male volunteers, psychosocial stress-related variables, defined as feelings of excessive tiredness and as personality and behavioral factors reflecting a stress-inducing life-style (type A behavior, hostility, and anger), were significantly correlated with the hyperinsulinemia, hyperglycemia, dyslipidemia, hypertension, increased abdominal obesity, and increased plasminogen activator inhibitor-1 (PAI-1) antigen comprising the IRS. The correlations remained significant after adjusting for body mass index (BMI), age, educational level, smoking status, alcohol consumption, and physical activity. However, the different stress-related factors reflected different risk-factor clustering profiles. Type A behavior was associated with normotension and a normal metabolic profile (canonical r = .50, chi2(36) = 59.1, P = .008). Hostility was related to elevated systolic blood pressure (SBP) and elevated triglycerides (TGs) (canonical r = .38, chi2(14) = 23.2, P = .052), whereas feelings of excessive tiredness were related to abdominal obesity, augmented glycemic responses to glucose ingestion, dyslipidemia, and increased PAI-1 antigen (canonical r = .39, chi2(24) = 36.8, P = .046). Although hostility and feelings of excessive tiredness have partly overlapping but clearly different clinical and metabolic correlates, their combination represents a full-blown IRS. Thus, even though insulin resistance is presumably to some extent genetically determined, these results suggest that considering psychosocial stress may be beneficial in understanding IRS risk-factor clustering.
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PMID:Psychosocial stress and the insulin resistance syndrome. 896 88


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