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 designed this study to define determinants of gastrointestinal complications after cardiac surgery. From January 1992 through December 2000, 11,058 patients underwent cardiac surgery on cardiopulmonary bypass at our institution. Data were prospectively collected and univariate and multivariate analyses conducted. A total of 147 gastrointestinal complications occurred in 129 patients (129/11,058; 1.2%) including gastroesophagitis (18, 12.2%), upper gastrointestinal hemorrhage (42, 28.6%), perforated peptic ulcer (7, 4.7%), cholecystitis (10, 6.8%), pancreatitis (13, 8.8%), intestinal ischemia (17, 11.5%), colitis (18, 12.2%), diverticulitis (5, 3.4%), intestinal occlusion (2, 1.1%), lower gastrointestinal hemorrhage (1, 0.7%), and mixed gastrointestinal complications (14, 9.5%). Patients with gastrointestinal complications were significantly older and had significantly higher comorbidity (unstable angina, chronic renal failure, and peripheral vascular disease), morbidity (prolonged mechanical ventilation, intraaortic balloon pumping, bleeding, acute renal failure, stroke, and infection), and mortality rates (22.5% vs 4%, P < 0.0001). They also had longer cardiopulmonary bypass times and higher valvular surgery rates. Multivariate analysis identified 6 independent predictors for gastrointestinal complications: prolonged mechanical ventilation (odds ratio [OR], 5.5), postoperative renal failure (OR, 4.2), sepsis (OR, 3.6), valve surgery (OR, 3.2), preoperative chronic renal failure (OR, 2.7), and sternal infection (OR, 2.4). Factors such as mechanical ventilation, renal failure, and sepsis are the stronger predictors for GI complications, causing splanchnic hypoperfusion, hypomotility, and hypoxia. Furthermore, excessive anticoagulation after valve replacement may lead to GI hemorrhage. Valve surgery, often requiring anticoagulation, increases bleeding. Monitoring mechanical ventilation and hemodynamic parameters, adopting early extubation and mobilization measures, preventing infections, and strictly monitoring renal function and anticoagulation may prevent catastrophic abdominal complications.
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PMID:Determinants of gastrointestinal complications in cardiac surgery. 1506 41

Mitochondriopathies (MCPs) are either due to sporadic or inherited mutations in nuclear or mitochondrial DNA located genes (primary MCPs), or due to exogenous factors (secondary MCPs). MCPs usually show a chronic, slowly progressive course and present with multiorgan involvement with varying onset between birth and late adulthood. Although several proteins with signalling, assembling, transport, enzymatic function can be impaired in MCP, most frequently the activity of the respiratory chain (RC) protein complexes is primarily or secondarily affected, leading to impaired oxygen utilization and reduced energy production. MCPs represent a diagnostic challenge because of their wide variation in presentation and course. Systems frequently affected in MCP are the peripheral nervous system (myopathy, polyneuropathy, lactacidosis), brain (leucencephalopathy, calcifications, stroke-like episodes, atrophy with dementia, epilepsy, upper motor neuron signs, ataxia, extrapyramidal manifestations, fatigue), endocrinium (short stature, hyperhidrosis, diabetes, hyperlipidaemia, hypogonadism, amenorrhoea, delayed puberty), heart (impulse generation or conduction defects, cardiomyopathy, left ventricular non-compaction heart failure), eyes (cataract, glaucoma, pigmentary retinopathy, optic atrophy), ears (deafness, tinnitus, peripheral vertigo), guts (dysphagia, vomiting, diarrhoea, hepatopathy, pseudo-obstruction, pancreatitis, pancreas insufficiency), kidney (renal failure, cysts) and bone marrow (sideroblastic anaemia). Apart from well-recognized syndromes, MCP should be considered in any patient with unexplained progressive multisystem disorder. Although there is actually no specific therapy and cure for MCP, many secondary problems require specific treatment. The rapidly increasing understanding of the pathophysiological background of MCPs may further facilitate the diagnostic approach and open perspectives to future, possibly causative therapies.
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PMID:Mitochondriopathies. 1500 63

The literature considers hyperthermic intraoperative intraperitoneal chemotherapy a safe and effective procedure for peritoneal carcinomatosis, but a technical improvement is necessary. Regional chemotherapy anticipates the "downfall" of tumoral cells in the peritoneum. The Authors considered 5 patients--female, age 27-45 years, ASA 2--operated of peritonectomy in ovaric neoplasia with peritoneal metastasis. The hyperthermic intraoperative intraperitoneal chemotherapy has been made at the end of the surgery with a hot solution (43 degrees C): 3000 ml of dextrose 1.5% with mytomicina C 25 mg e cysplatino 75 mg/m2. We considered variation of emodinamic parametres (blood pressure, central venous pressure, stroke volume, etc.) and biochemical parametres (Na, K, CI-, CO2, etc.). These parametres have been correlated with some complications: fistula, anastomotic leakage, pancreatitis and postoperative bleeding.
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PMID:[Anaesthesiologic problems about hyperthermic intraoperative intraperitoneal chemotherapy]. 1575 60

Intercurrent illness and episodes of hospitalization and surgery are common in an aging population, who, at the same time, are experiencing age-related bone loss. The objective was to test the hypotheses (1) that intercurrent illness severe enough to require hospitalization produces clinically important bone loss, and (2) that antiresorptive therapy will reduce that loss. The study was a retrospective analysis of bone mineral density (BMD) change at hip and spine in subjects of the risedronate postmenopausal osteoporosis phase III trials experiencing serious adverse events (SAEs). Subjects were 243 hospitalized for non-skin cancers, pneumonia, myocardial infarction, cerebrovascular accident, gallbladder disease, and pancreatitis, on whom BMD data were available both before and after the SAE; and 286 non-hospitalized control subjects matched to those with SAEs by age, height, weight, prevalent fracture, and visit interval. In hospitalized, placebo-treated participants, the annualized percent change in BMD (mean+/-SEM) across the period of hospitalization was -0.65+/-0.39 at lumbar spine, -1.13+/-0.55 at femoral neck, and -2.66+/-0.58 at femoral trochanter; the corresponding values for the non-hospitalized, placebo controls were +0.46+/-0.28, -0.77+/-0.34, and -0.67+/-0.34. These values were more negative at all three sites for the hospitalized subjects, and significantly so at lumbar spine and femoral trochanter (P=0.019 and 0.002, respectively). By contrast, in the risedronate-treated participants, all sites exhibited bone gain and there was no significant difference between hospitalized and non-hospitalized participants. Intercurrent illness resulting in hospitalization produced a rapid bone loss across the period of illness comparable in magnitude to documented age-related loss. Risedronate in a dose of 5 mg/day effectively abolished this loss.
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PMID:Hospitalization-related bone loss and the protective effect of risedronate. 1613 44

(1) For patients aged over 60 years who have essential thrombocythaemia, and are considered to be at increased risk of thromboembolism, the standard cytotoxic agent is hydroxycarbamide (hydroxyurea), which reduces the risk of thrombocytosis but adversely affects other blood cell lines. It may also increase the risk of progression to cancer. (2) Anagrelide, initially studied as an antiplatelet drug, was approved in Europe for the treatment of essential thrombocythaemia in high-risk patients when other treatments fail or are poorly tolerated. (3) Evaluation data includes a trial versus hydroxycarbamide that was prematurely halted because of an excess of cardiovascular events among patients on anagrelide. Among 809 patients who were also receiving aspirin as an antithrombotic (and who may not have met strict criteria for essential thrombocythaemia), arterial or venous thrombosis and haemorrhage were significantly more frequent with anagrelide, during a median follow-up of 39 months (55 versus 36 patients). (4) According to the results of 3 non comparative trials involving about 500 patients, and the European Medicines Agency report analysing these and other study populations, anagrelide reduces the platelet count to below 600 times 10 to the 9th power/litre in two-thirds of patients. No data are available on the clinical implications of this reduction in platelets. (5) Between 10% and 20% of patients treated with anagrelide experience cardiovascular adverse effects (palpitations, myocardial infarction, heart failure) or neurological adverse effects (headache, stroke, transient ischaemic attack). Gastrointestinal disturbances are also frequent (diarrhoea, nausea, abdominal pain, pancreatitis). Some of these adverse effects can be fatal. (6) Follow-up is too short to show whether anagrelide affects the risk of progression to cancer. (7) In practice, anagrelide has a less favourable risk-benefit balance than hydroxycarbamide, which remains the first-line cytotoxic agent in this setting. Anagrelide therapy can be considered if hydroxycarbamide fails or is poorly tolerated, provided patients are included in a long-term clinical trial.
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PMID:Anagrelide: new drug. Essential thrombocythaemia: further evaluation needed for this last-resort treatment. 1676 90

Activated protein C (APC), a plasma serine protease, is best known for its ability to inhibit blood clot formation. APC acts as an anticoagulant by degrading coagulation cofactors Va and VIIIa, thereby attenuating the coagulation cascade. Over the past 15 years, impressive research advances have provided novel insights into the diverse biological activities of this molecule. APC is now viewed not only as an anticoagulant but also as a signaling molecule that provides a pivotal link between the pathways of coagulation, inflammation, apoptosis, and vascular permeability. The protective effect of APC supplementation in patients with severe sepsis likely reflects the ability of APC to modulate multiple pathways implicated in sepsis pathophysiology. This review attempts to summarize key studies that support the therapeutic potential of APC in conditions beyond sepsis such as stroke, ischemia-reperfusion injury, lung injury, asthma, pancreatitis, wound healing, and angiogenesis. A comprehensive PUBMED literature review up to May 2006 was conducted.
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PMID:Activated protein C in sepsis and beyond: update 2006. 1712 35

The peroxisome proliferator-activated receptor (PPAR) family of genes plays a major role in metabolic regulation. Unfortunately, the results of two recent, large event trials of PPAR agonists have been mixed. High rates of crossover to statin use confound the interpretation of the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial, which found a less than expected reduction in coronary and stroke events with fenofibrate. Of concern, nonsignificant increases in coronary and sudden deaths, thrombotic events, and pancreatitis occurred in the fenofibrate group. The PROspective pioglitAzone Clinical Trial In macroVascular Events (PROACTIVE) also found a reduction in coronary and stroke events with pioglitazone compared with placebo in a population with diabetes and cardiovascular disease, but this benefit was counterbalanced by an increase in congestive heart failure as well as symptomatic edema. Further research is needed to determine the role of PPAR agonists in the prevention of cardiovascular disease.
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PMID:Update on PPAR agonists: the clinical significance of FIELD and PROACTIVE. 1716 49

HIV protease inhibitors are an integral part of effective anti-HIV therapy. The drugs block HIV protease, prevent proper packaging of HIV virions, and decrease the HIV viral burden in the peripheral blood of infected individuals. In addition to direct anti-viral effects, the HIV protease inhibitors also modulate apoptosis. A growing body of work demonstrates the anti-apoptotic effects of HIV protease inhibitors on CD4+ and CD8+ T cells during HIV infection. The mechanism of this apoptosis inhibition is supported by several proposed hypotheses for how they alter the fate of the cell, including preventing adenine nucleotide translocator pore function, which consequently prevents loss of mitochondrial transmembrane potential. More recently, the anti-apoptotic effects of the HIV protease inhibitors have been tested in non-HIV, non-immune cell, whereby protease inhibitors prevent apoptosis, and disease in animal models of sepsis, hepatitis, pancreatitis and stroke. Interestingly, when HIV protease inhibitors are used at supra-therapeutic concentrations, they exert pro-apoptotic effects. This has been demonstrated in a number of tumor models. Although it is unclear how HIV protease inhibitors can induce apoptosis at increased concentrations, future research will define the targets of the immunomodulation and reveal the full clinical potential of this intriguing class of drugs.
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PMID:HIV protease inhibitors modulate apoptosis signaling in vitro and in vivo. 1745 62

Abdominal apoplexy is an uncommon disorder typically due to atheromatous vascular disease, inflammatory processes such as pancreatitis eroding into large blood vessels or vasculitis. We describe an unusual case due to unrecognised syphilis masquerading as pancreatitis.
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PMID:An unusual case of intra-abdominal apoplexy. 1836 Oct 21

The hyperosmolar hyperglycemic nonketotic state (HHNS) is an acute metabolic complication occurring characteristically in elderly type-2 diabetic patients. It may account for 10 up to 47% of cases of severe hyperglycemia with or without ketoacidosis. Many factors associated with advanced age may explain the predilection of both elderly subjects in general and older diabetics in particular to develop hyperosmolar coma, including reduced glomerular filtration rate and elevated renal threshold for glucose (which fail to correct hyperglycemia by osmotic diuresis), lack of thirst appropriate to the state of hydratation and some iatrogenic factors. In HHNS the age of the patients is the best known prognostic indicator. The increased mortality rate in the elderly diabetics depends on the severity of precipitating acute diseases (gastrointestinal hemorrhage, cardiovascular accident, pneumonia, pancreatitis, etc.), but the frequent compromises of the hemodynamic state and renal function of aged subjects substantially contributes. However, the role of erroneous management is not negligible and difficulties may be encountered in conciliating correction of metabolic disorder with treatment of precipitating illness. Insulin, water and electrolytes are the most important therapeutical tools for the treatment of hyperglycemic emergencies. In HHNS, the aggressive fluid replacement with isotonic or hypotonic NaCl solutions have first priority. Such a type of strategy is difficult to perform in patients suffering from cerebral stroke (which needs of anti-edema therapy) or congestive heart failure (necessitating to avoid fluid excess). According to the literary data, in our experience these two precipitating factors are frequent causes of death. We outline the validity of prefixed protocols of management; on the other hand, we think that the pathophysiological understanding of HHNS in the single patient is essential to decide the proper corrections and to permit a successful outcome. The primary way aiming at diminishing mortality by HHNS is its prevention; it is fundamental to warrant an appropriate fluid intake and to utilize with caution some drugs (thiazides, steroids, phenytoin, etc.) in aged diabetics, especially when nephropathic or unable, or living in nursing homes.
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PMID:Diabetic non ketotic hyperosmolar state: a special care in aged patients. 1865 40


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