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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mild to moderate hypertriglyceridemia is not associated with specific signs or symptoms in either IDDM or NIDDM. However, symptoms of the "chylomicronemia syndrome," including abdominal pain and acute pancreatitis, can occur when poorly controlled diabetes is present in a patient with a familial form of hyperlipidemia. The low-carbohydrate, high-fat diet that was commonly recommended for diabetics during past years may have contributed to the elevated plasma LDL levels in some individuals. Such "diabetic diets" may also have played a role in the predisposition of diabetics toward atherosclerotic complications.
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PMID:Hyperlipidemia: forestalling complications in older diabetics. 388 43

Profound hypothermia (core temperature of less than 28 degrees C) is a life threatening state and a medical emergency associated with a high mortality rate. The prognosis depends on underlying diseases, advanced or very early age, the duration prior to treatment, the degree of hemodynamic deterioration, and especially, the methods of treatment, including active external or internal rewarming. This is a case study of an 80-year-old female patient with severe accidental hypothermia (core temperature 27 degrees C). She was found in her home lying immobile on the cold floor after a fall. The patient was in a profound coma with cardiocirculatory collapse, and the medical staff treating her was inclined to pronounce her deceased. On her arrival at the hospital, she was resuscitated, put on a respirator and actively warmed. Very severe metabolic disorders were found, including a marked metabolic acidosis composed of diabetic ketoacidosis (she had suffered from insulin treated type 2 diabetes mellitus) and lactic acidosis with a very high anion gap (42) and a hyperosmotic state (blood glucose 1202 mg/dl). There were pathognomonic electrocardiographic abnormalities, J-wave of Osborn and prolonged repolarization. Slow atrial fibrillation with a ventricular response of 30 bpm followed by a nodal rhythm of 12 bpm and reversible cardiac arrest were recorded. The pulse and blood pressure were unobtainable. Despite the successful resuscitation and hemodynamic and cognitive improvement, rhabdomyolysis (CKP 6580 u/L), renal failure and hepatic damage developed. She was extubated and treated with intravenous fluids containing dopamine, bicarbonate, insulin and antibiotics. Her medical condition gradually improved, and she was discharged clear minded, functioning very well and independent. Renal and liver tests returned eventually to normal limits. Progressive bradycardia, hypotension and death due to ventricular fibrillation or asystole commonly occur during severe hypothermia. Respiratory and metabolic, sometimes lactic, acidosis, lethargy and coma, hypercoagulopathy, hyperosmolar state, acute pancreatitis and renal and hepatic failure are frequent complications of hypothermia. Underlying predisposing causes of hypothermia are diabetic ketoacidosis, cerebrovascular disease, mental retardation, hypothyroidism, pituitary and adrenal insufficiency, malnutrition, acute alcoholism, liver damage, hypoglycemia, sepsis, hypothalamic dysfunction, sepsis and polypharmacy, and especially, the use of sedative and narcotic drugs. Our case demonstrates once again that CPR once begun should continue until the successful rewarming because "no one is dead until warm and dead".
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PMID:[Severe accidental hypothermia in an elderly woman]. 1175 73

We report tamoxifen-induced hypertriglyceridemia and asymptomatic acute pancreatitis in a 51 year-old women with type 2 diabetes mellitus and stage III-b infiltrative ductal carcinoma, admitted to the hospital with weakness, oliguria and glucose dysregulation. On admission, there was no fever, abdominal or back pain, rebound tenderness, nausea, or vomiting. Following 1 year of tamoxifen treatment, triglycerides increased from 400 to 1344 mg/dl (blood urea nitrogen 52 mg/dl, creatinine 2.0 mg/dl, glucose 341 mg/dl). Hypertriglyceridemia was considered to be due to either diabetic dyslipidemia and/or tamoxifen. On computerized tomography, pancreatic enlargement, heterogenity, hypodensity and a pancreatic pseudocyst (5 x 7.5 cm diameter) were found. Acute pancreatitis was suspected, and serum amylase level was found to be increased (273 IU/L). Tamoxifen was discontinued and gemfibrozil was started. Triglycerides decreased to 301 mg/dl and amylase decreased to 66 IU/L a week later and remained normal thereafter. This case indicates that tamoxifen-induced hypertriglyceridemia may cause acute pancreatitis without classical symptoms which might be due to autonomic neuropathy in diabetic patients. Effects on lipid metabolism should be considered and triglycerides should be closely followed in patients on tamoxifen.
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PMID:Asymptomatic acute pancreatitis due to tamoxifen-induced severe hypertriglyceridemia in a patient with diabetes mellitus and breast cancer. 1212 Aug 88

Metformin is a biguanide commonly used in type 2 diabetes and considered to be a safe drug with minimal side effects. Approximately 2% of cases of acute pancreatitis may be caused by drugs, but it is not a known complication of metformin therapy. To date only one case of pancreatitis has been reported in association with metformin, but that was secondary to metformin poisoning (overdose). This is the first reported case of pancreatitis caused by a therapeutic dose of metformin (although in this case renal failure precipitated the metformin toxicity). Severe lactic acidosis is a rare but life threatening complication of metformin, which occurs particularly in patients with renal failure.
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PMID:Metformin induced acute pancreatitis precipitated by renal failure. 1508 49

Xanthoma and xanthelasma are typical symptoms of lipid and lipoprotein metabolism impairment. On the basis of their incidence and morphology, it is even possible to specify the impairment type. Hypercholesterolemia or certain liver dysfunctions are characterized by slow development of surface xanthelasmas usually located on mechanically stressed regions (e.g. eyelids). Tuberous and tendinous xanthomas are typical for familiar hypercholesterolemia and are common symptoms of homozygous familiar hypercholesterolemia. Small and quickly developing eruptive xanthomas are typical for mixed hyperlipoproteinemia (secondary hyperlipoproteinemia is typical for diabetes). Mechanism of accumulation of lipids in skin morphs is similar to the development of atheroma, especially when talking about the role of modified LDL and the way of accumulation of lipids in macrophages. The following factors are very important for etiopathogenesis of skin xanthomas development: mechanical stress of tissues, increased permeability of skin capillaries and reaction of proteoglycans in sparse connective tissue. Xanthomas and xanthelasmas are typical indicators of other complicating diseases as e.g. development of acute pancreatitis during hyperlipoproteinemic crisis, aggravation of insulin resistance, and decompensation of type 2 diabetes mellitus. The therapy focuses on adjustment of dietary regime (elimination of dietary fat and concentrated saccharides); no food and sufficient hydration via infusion of crystalloid solutions is indicated in cases of serious hyperlipoproteinemic crisis. In vital indication, it is possible to perform repeated plasmapheresis (or better continual plasmapheresis) that can correct even serious hyperlipoproteinemic crises within several hours. And what is more, continual plasmapheresis can significantly reduce the period when hyperlipoproteinemic crisis might induce acute necrotizing pancreatitis. In the long run, we require that patients strictly observe their dietary regime based on the type of hyperlipoproteinemia. As for medicamentous therapy, fibrates and atorvastatin (from statin family) are the preparations of choice. It is very important not to focus on symptoms, i.e. xanthoma or xanthelasma, but fully compensate lipid metabolism impairment or the disease that underlies hyperlipoproteinemia (e.g. type 2 diabetes mellitus or metabolic syndrome). Unfortunately, it still can be seen that dermatologists, ophthalmologists or plastic surgeons remove extensive xanthelasmas, while the underlying cause is not approached diagnostically and therapeutically at all.
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PMID:[Internist's view on skin manifestations of hyperlipidemia in diabetic patients]. 1677 Oct 91

Elevated triglycerides are now considered an independent risk factor for coronary heart disease and continue to be a major risk for acute pancreatitis, especially when levels exceed 1000 mg/dL (SOR: B). Elevated triglycerides are a component of atherogenic dyslipidemia and often signal the presence of other conditions (eg, metabolic syndrome, type 2 diabetes mellitus) associated with an increased cardiovascular risk (SOR: A). When evaluating a patient with elevated triglycerides, it is important to be cognizant of all atherogenic lipoproteins to more accurately determine the risk of coronary heart disease (SOR: C). Patients with hypertriglyceridemia should first achieve their low-density lipoprotein cholesterol goal, followed by their non-high-density lipoprotein cholesterol goal (SOR: C). Fibrates, niacin, and omega-3 acid ethyl esters are highly effective at reducing triglycerides, while statins are considered moderately efficacious (SOR: A).
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PMID:Hypertriglyceridemia: management of atherogenic dyslipidemia. 1682 43

The object of this review is to provide the definitions and criteria for diabetic ketoacidosis (DKA) and the hyperglycemic hyperosmolar state (HHS), and convey current knowledge of the causes of permanent disability or mortality from complications of these conditions, of the risk factors for DKA and HHS, and of early indicators and contemporary treatment of suspected cerebral edema. The frequency of DKA at onset of type 1 diabetes mellitus (DM1) varies from 10-70%, depending on availability of health care and frequency of diabetes. At the onset of type 2 diabetes (DM2), DKA occurs in 5-52%. One study reported HHS in approximately 4% of new patients with DM2. Recurrent DKA rates are equally dependent on variability in medical services and socio-economic circumstances, and are estimated to be eight episodes per 100 patient years, with 20% of patients accounting for 80% of the episodes. Mortality for each episode of DKA internationally varies from 0.15-0.31%, with idiopathic cerebral edema accounting for two-thirds or more of this mortality. Other causes of death or disability include untreated DKA or HHS, hypokalemia, hypophosphatemia, hypoglycemia, other intracerebral complications, peripheral venous thrombosis, mucormycosis, rhabdomyolysis, acute pancreatitis, acute renal failure, sepsis, aspiration pneumonia, and other pulmonary complications. Population-based studies from the UK, Australia, the USA, and Canada report cerebral edema incidence in DKA of 0.5-2.0%. Published information does not support the notion that treatment factors are causal in cerebral edema. Younger age, greater severity of acidosis, degree of hypocapnia, and severity of dehydration have been suggested as risk factors in several studies. Bimodal distribution of the time of onset of cerebral edema and wide variation in brain imaging findings suggest the variability and likely multiple causation of the clinical picture. Functional brain scanning has indicated that DKA is accompanied by increased cerebral blood flow suggesting that the predominant mechanism of edema formation is a vasogenic process. A method of monitoring for diagnostic and major and minor signs of cerebral edema has been proposed and tested which indicates that intervention will be required in five individuals to provide early intervention for a single case of cerebral edema. The preferred intervention of mannitol infusion has typically been accompanied by intubation and hyperventilation, but recent evidence indicates outcome is adversely affected by aggressive hyperventilation. The prevention of DKA and HHS at the onset of diabetes mellitus requires a high degree of awareness and suspicion by primary care providers; prevention of recurrent DKA necessitates a diligent team effort.
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PMID:Hyperglycemic crises and their complications in children. 1731 23

Elevated plasma triglyceride concentration is a common biochemical finding, but the evidence for the benefit of treating this lipid disturbance remains less robust than that for treating elevated low-density lipoprotein-cholesterol. Part of the difficulty in the provision of specific recommendations has been the frequent coexistence of elevated triglycerides with other conditions that affect cardiovascular disease risk, such as depressed high-density lipoprotein-cholesterol, obesity, metabolic syndrome, proinflammatory and prothrombotic biomarkers, and type 2 diabetes. Recent investigations of outcomes of cardiovascular disease when medications are used to reduce triglyceride levels suggest that, although a net benefit probably exists, both relative and absolute risk reductions seem underwhelming when compared with the benefit of reducing low-density lipoprotein-cholesterol levels with treatment. However, the totality of evidence suggests that elevated triglyceride levels likely contribute independently to increased risk of cardiovascular disease, although there is no consensus about appropriate target levels. Furthermore, severe hypertriglyceridemia is associated with an increased risk of acute pancreatitis, irrespective of its effect on risk of cardiovascular disease. We review the causes and classification of elevated triglyceride levels, the clinical manifestations of primary hypertriglyceridemia and the management of patients with elevated triglyceride levels.
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PMID:Hypertriglyceridemia: its etiology, effects and treatment. 1784 46

Acute pancreatitis and eruptive xanthomas are the only recognised direct complications of severe hypertriglyceridaemia. We present the case of a 33-years old male patient in whom the onset of a type 2 diabetes, added to an unknown familial hyperlipidemia, precipitated a dramatic raise of serum triglyceride levels, that cause in turn an acute pancreatitis and the appearance of dermic eruptive xanthomas. TRANSLATION: This article is translated from Spanish, originally published in Archivos de Medicina. The original work is at doi:10.3823/001.
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PMID:Eruptive xanthomas and acute pancreatitis in a patient with hypertriglyceridemia. 1847 88

We have previously described a duodenojejunal bypass (DJB) surgical model in healthy C57BL/6 mice. However, our pilot study showed that the same surgical technique caused a high mortality rate in obese mice. In this study, to significantly improve animal survival rate following bariatric surgery and thereby providing a stable surgical model for the study of glucose homeostasis in obese mice, we have used modified techniques and developed the end-to-side gastrojejunal bypass (GJB) surgery in obese C57BL/6 with impaired glucose tolerance. The modification consisted of using the distal part of the jejunum for biliopancreatic diversion including: 1) ligation of the distal stomach at the level of the pylorus; 2) connection the jejunum to the anterior wall of stomach in an end-to-side fashion; and 3) diverting the biliopancreatic secretions through the blind limb into the distal jejunum through an end-to-side anastomosis. We found that by modifying the proximal end-to-end duodenojejunal anastomosis, described in our original model, to an end-to-side gastrojejunal anastomosis in these obese mice, we were able to significantly improve the postoperative mortality in this study. We have also demonstrated that performing the GJB surgery in obese mice resulted in significant weight loss, normalized blood glucose levels, and prevented acute pancreatitis. This newly developed GJB surgery in the obese mice offers a unique advantage to study the mechanisms of gastrointestinal surgery as treatment for type 2 diabetes.
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PMID:Development of techniques for gastrojejunal bypass surgery in obese mice. 2004 16


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