Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We assessed the clinical characteristics of newly-diagnosed diabetic patients presenting to the Mulago Hospital Diabetic Clinic for the first time between 1 January 1993 and 10 August 1994. There were 252 patients: 117 men and 135 women. Mean age at onset of diabetes was 45 years (range 2-87 years) and peak incidence was at 40-49 years. Body mass index (BMI) was available in only 71 patients, of whom 53.5% (33.8% female, 19.7% male) were overweight (BMI > 25 in women, in > 27 men) and 11.3% (8.5% men, 2.8% women) were underweight (BMI < 20). Obesity was more marked in young women. Almost all patients presented with the classical symptoms of diabetes, and the majority were severely hyperglycaemic. A family history of diabetes was identified in 16%. Concurrent illnesses at diagnosis of diabetes were unusual. Sepsis was commonest (11.9%), followed by malaria (7.8%), tuberculosis (1.2%), AIDS (1.2%) and pancreatitis (0.8%). Peripheral neuropathy was present in 46.4% of patients, hypertension (BP > 150/100) in 27.3%, impotence in 22.2% of the men, proteinuria in 17.1%, ischaemic heart disease in 4.8%, foot ulcers in 4.0% and cataracts in 3.2%. Insulin was the most commonly prescribed treatment (52.8%); 31% of patients received oral hypoglycaemic agents, only 15.1% were managed on diet only, and 1.2% opted for herbal medicine.
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PMID:The presentation of newly-diagnosed diabetic patients in Uganda. 891 47

Hyperlipidemia is recognized as one of the major risk factors for the development of coronary artery disease and progression of atherosclerotic lesions. Dietary therapy together with hypolipidemic drugs are central to the management of hyperlipidemia, which aims to prevent atherosclerotic plaque progression, induce regression, and so decrease the risk of acute coronary events in patients with pre-existing coronary or peripheral vascular disease. In patients at high risk of coronary artery disease but without evidence of atherosclerosis, treatment is designed to prevent the premature development of coronary artery disease, whereas in those with hypertriglyceridemia, treatment aims to prevent the development of hepatomegaly, splenomegaly, and pancreatitis. The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, are the most potent lipid-lowering agents currently available, and their use in the treatment of hyperlipidemia provides the focus for this review. Particular emphasis is given to cerivastatin, a new HMG-CoA reductase inhibitor that combines potent cholesterol-lowering properties with significant triglyceride-reducing effects. Recently completed primary and secondary intervention trials have shown that the significant reductions in low-density lipoprotein (LDL) cholesterol achieved with statins result in significant reductions in morbidity and mortality associated with coronary artery disease as well as reductions in the incidence of stroke and total mortality. Such benefits occur early in the course of statin therapy and have led to suggestions that these drugs may possess antiatherogenic effects over and above their capacity to lower atherogenic lipids and lipoproteins. Experimental studies have also shown statin-induced improvements in endothelial function, decreased platelet thrombus formation, improvements in fibrinolytic activity, and reductions in the frequency of transient myocardial ischemia.
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PMID:Current and future treatment of hyperlipidemia: the role of statins. 973 40

A 71-year-old man presented with left upper quadrant abdominal pain. Serial electrocardiograms (ECGs) demonstrated an evolving left bundle branch block, a sign of acute myocardial infarction (AMI). However, a coronary angiogram demonstrated minimal coronary artery disease, and serum troponin T was undetectable in serial serum measurements. Later, serum pancreatic enzyme levels were elevated and a computed tomography scan of the abdomen was consistent with pancreatitis. In patients presenting with acute pancreatitis and ECG changes suggesting AMI, measurement of serum troponin T concentrations can aid in differentiating ECG changes driven by acute pancreatitis from those of true myocardial ischemia or infarction.
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PMID:A case of acute pancreatitis presenting with electrocardiographic signs of acute myocardial infarction. 1473 Jan 76

The impact of alcohol intake on mortality from all causes has been described in a large number of prospective population studies from many countries. Most have shown a J-shaped relation between alcohol intake and subsequent mortality, indicating that there are both beneficial and harmful effects of ethanol on health. The risk of death from ischemic heart disease is seen to be significantly increased, and highest among abstainers, but not significantly increased among heavy drinkers. Some studies have found plausible mechanisms for the beneficial effect of light to moderate drinking. Subjects with a moderate alcohol intake have a higher level of high density lipoprotein than abstainers. Further, moderate drinkers are seen to have a lower low density lipoprotein. Also, alcohol has a beneficial effect on platelet aggregation, and thrombin level in blood is higher among drinkers than among non-drinkers. In the other end of the range of intake, the ascending leg of the U-shaped curve has been explained by the increased risk of cirrhosis, pancreatitis, and development oropharynx, oesophagus, and breast cancer. In exploring the French paradox, it has been suggested that wine may have beneficial effects additional to that of ethanol. Recently, several prospective population studies have supported this idea. It is, however, also likely that the apparent additional beneficial effect of wine on health in addition to the effect of ethanol itself is a consequence of confounding.
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PMID:Epidemiologic evidence for the cardioprotective effects associated with consumption of alcoholic beverages. 1500 14

Endothelin (ET) is among the strongest endogenous vasoconstrictors known and a potent mitogen. A rich body of experimental evidence suggests that ET contributes to vascular remodeling and end-organ damage in several cardiovascular conditions. Therefore, blockade of ET receptors has been suggested as an attractive target in a number of acute and chronic cardiovascular indications, including pulmonary arterial hypertension (PAH), systemic hypertension, and heart failure. To date, clinical studies have confirmed expectations in PAH and yielded promising initial results in systemic hypertension, which are currently awaiting confirmation in large-scale trials. In contrast, no added benefit could be demonstrated in large clinical trials on top of current standard treatment in both acute and chronic heart failure. Further clinical development in heart failure has therefore been suspended. Other indications that are currently being studied clinically or would possibly merit clinical trials include acute myocardial ischemia and reperfusion, cerebral vasospasm after intracranial bleeding, glaucoma, acute severe pancreatitis, systemic sclerosis, (diabetic) renal failure, restenosis after angioplasty/stent implantation, and late transplant rejection. This article critically reviews the available clinical data on ET receptor antagonism in cardiovascular indications against the background of the underlying preclinical research.
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PMID:Endothelin receptor antagonists: clinical realities and future directions. 1565 68

Diabetic ketoacidosis (DKA) is the most common hyperglycemic emergency in patients with diabetes mellitus. DKA most often occurs in patients with type 1 diabetes, but patients with type 2 diabetes are susceptible to DKA under stressful conditions, such as trauma, surgery, or infections. DKA is reported to be responsible for more than 100 000 hospital admissions per year in the US, and accounts for 4-9% of all hospital discharge summaries among patients with diabetes. Treatment of patients with DKA uses significant healthcare resources and accounts for 1 out of every 4 healthcare dollars spent on direct medical care for adult patients with type 1 diabetes in the US. Recent studies using standardized written guidelines for therapy have demonstrated a mortality rate of less than 5%, with higher mortality rates observed in elderly patients and those with concomitant life-threatening illnesses. Worldwide, infection is the most common precipitating cause for DKA, occurring in 30-50% of cases. Urinary tract infection and pneumonia account for the majority of infections. Other precipitating causes are intercurrent illnesses (i.e., surgery, trauma, myocardial ischemia, pancreatitis), psychological stress, and non-compliance with insulin therapy. The triad of uncontrolled hyperglycemia, metabolic acidosis and increased total body ketone concentration characterizes DKA. These metabolic derangements result from the combination of absolute or relative insulin deficiency and increased levels of counter-regulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). Successful treatment of DKA requires frequent monitoring of patients, correction of hypovolemia and hyperglycemia, replacement of electrolyte losses, and careful search for the precipitating cause. Since the majority of DKA cases occur in patients with a known history of diabetes, this acute metabolic complication should be largely preventable through early detection, and by the education of patients, healthcare professionals, and the general public. The frequency of hospitalizations for DKA has been reduced following diabetes education programs, improved follow-up care, and access to medical advice. Novel approaches to patient education incorporating a variety of healthcare beliefs and socioeconomic issues are critical to an effective prevention program.
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PMID:Diabetic ketoacidosis: risk factors and management strategies. 1587 46

A hiccup is involuntary, paroxysmal inspiratory movements of the chest wall associated with diaphragm and accessory respiratory muscle contractions, with the synchronized closure of glottis. The mechanism underlying this common primitive reflex plays an important role in protecting airways against esophageal aspiration. The hiccup reflex mechanism is based on the afferent pathway (vagus and phrenic nerve and sympathetic fibers innervating chest organs, the abdomen, the ear, the nose and the throat stimulation, and the stimulation of hiccup center in the central nervous system, mainly reflecting psychogenic or metabolic disorders) and the efferent pathway (phrenic nerves). An incidental hiccup is a common problem, usually resolves spontaneously and does not present a clinical issue. The clinical issue arises in the case of pathologic persistent hiccups or symptomatic secondary hiccups which may lead to significant fatigue, insomnia or depression. Generally, pathologic hiccups are associated with considerable discomfort concerning both the "stigmatized" person and his or her personal surroundings in which it evokes different emotions, from amusement through impatience to uneasiness and the suggestion of a medical visit as an expression of concern for a given person. The most common causes of pathologic symptomatic hiccups are nervous system diseases, either the central nervous system (proliferative, angiogenic, inflammatory disorders), or the peripheral nervous system: the irritation of the phrenic nerve (proliferative disorders, goitre) and the vagus nerve (otolaryngologic diseases, meningitis, esophageal, stomach and duodenal diseases, hepatitis, pancreatitis, enteritis). The vagus nerve irritation with subsequent hiccups may be caused by chest disorders (injury, surgery) and heart diseases (myocardial infarction). In the present paper we describe the case of a 62-year-old male with recurrent hiccups associated with exertion as a secondary symptom of myocardial ischemia.
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PMID:Hiccups as a myocardial ischemia symptom. 1847 62

No previous reports are available about the potential dramatic effects resulting from the combination of acquired long QT interval not associated to bradycardia and myocardial ischemia. We report the case of a man that during acute necrotic pancreatitis presented QT interval prolongation without bradycardia, TdP, and two episodes of cardiac arrest. A coronary angiogram revealed a subocclusive stenosis of left anterior descending coronary artery, treated with a percutaneous coronary intervention. After myocardial revascularization, even in presence of long QT interval, no arrhythmic events occurred suggesting the key role of myocardial ischemia in triggering TdP in acquired long QT even without bradycardia. ECG performed six months later, after complete recovery from pancreatitis, showed a normal QT interval.
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PMID:Partners in crime in the setting of recurring cardiac arrest. 2140 70

Endoscopic necrosectomy (EN) for walled-off pancreatic necrosis (WOPN) is less invasive than surgical treatment and has become the first choice for pancreatic abscess. EN is usually carried out with several devices including snares, baskets, and grasping forceps. Occasionally, we have encountered cases in which EN has not been satisfactorily carried out, and there is pressure for further innovation in EN. Here, we describe a case of a large area of WOPN that was successfully treated by EN with endoscopic submucosal dissection and associated techniques, which facilitated removal of necrotic tissues. A 60-year-old man was referred to our hospital for WOPN as a complication of necrotizing pancreatitis. As a result of his complicating conditions including ischemic heart disease, uncontrollable arrhythmia, chronic renal failure, and persistent pleural effusion, he was deemed a poor surgical candidate. Although EN with conventional devices was carried out for five sessions, we could not remove the dense and massive necrotic tissues. At the sixth EN session, the Clutch Cutter device (Fujifilm, Tokyo, Japan) was used to remove the necrotic tissues, without major complications. This is believed to be the first report of EN using the Clutch Cutter for successful treatment of WOPN.
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PMID:Large area of walled-off pancreatic necrosis successfully treated by endoscopic necrosectomy using a grasping-type scissors forceps. 2374 85

Atherosclerosis is strongly associated with dyslipoproteinaemia, and especially with increasing concentrations of low-density lipoprotein and decreasing concentrations of high-density lipoproteins. Its association with increasing concentrations of plasma triglyceride is less clear but, within the mixed hyperlipidaemias, dysbetalipoproteinaemia (Fredrickson type III hyperlipidaemia) has been identified as a very atherogenic entity associated with both premature ischaemic heart disease and peripheral arterial disease. Dysbetalipoproteinaemia is characterized by the accumulation of remnants of chylomicrons and of very low-density lipoproteins. The onset occurs after childhood and usually requires an additional metabolic stressor. In women, onset is typically delayed until menopause. Clinical manifestations may vary from no physical signs to severe cutaneous and tendinous xanthomata, atherosclerosis of coronary and peripheral arteries, and pancreatitis when severe hypertriglyceridaemia is present. Rarely, mutations in apolipoprotein E are associated with lipoprotein glomerulopathy, a condition characterized by progressive proteinuria and renal failure with varying degrees of plasma remnant accumulation. Interestingly, predisposing genetic causes paradoxically result in lower than average cholesterol concentration for most affected persons, but severe dyslipidaemia develops in a minority of patients. The disorder stems from dysfunctional apolipoprotein E in which mutations result in impaired binding to low-density lipoprotein (LDL) receptors and/or heparin sulphate proteoglycans. Apolipoprotein E deficiency may cause a similar phenotype. Making a diagnosis of dysbetalipoproteinaemia aids in assessing cardiovascular risk correctly and allows for genetic counseling. However, the diagnostic work-up may present some challenges. Diagnosis of dysbetalipoproteinaemia should be considered in mixed hyperlipidaemias for which the apolipoprotein B concentration is relatively low in relation to the total cholesterol concentration or when there is significant disparity between the calculated LDL and directly measured LDL cholesterol concentrations. Genetic tests are informative in predicting the risk of developing the disease phenotype and are diagnostic only in the context of hyperlipidaemia. Specialised lipoprotein studies in reference laboratory centres can also assist in diagnosis. Fibrates and statins, or even combination treatment, may be required to control the dyslipidaemia.
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PMID:Dysbetalipoproteinaemia: a mixed hyperlipidaemia of remnant lipoproteins due to mutations in apolipoprotein E. 2440 72


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