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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Embolization of cholesterol crystals from ulcerated atheromatous lesions can produce distinct syndromes that mimic more common disease processes. Cholesterol emboli can present as renal failure, hypertension, spells of numbness, abdominal pain, and myocardial infarction, or as a multisystem disease that closely approximates the presentation, clinical course, and even biopsy picture of polymyositis or periarteritis nodosa. A review of this problem with particular attention to the clinical presentations should help in the early diagnosis and treatment of cholesterol emboli and avoid unnecessary and inappropriate therapies.
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PMID:Cholesterol embolism: the great masquerader. 37 Oct 3

Screening for dyslipoproteinemias should be undertaken in all individuals older than 20 years of age at least once every 5 years. The initial screening, as recommended by the Adult Treatment Guidelines Panel of the National Cholesterol Education Program, is to determine the concentration of total blood cholesterol. This initial determination can be made on blood obtained in the nonfasting state. Further evaluation of the patient's lipoprotein concentrations is dependent upon the presence of other cardiovascular risk factors. in the absence of definite coronary heart disease, hypertension, diabetes mellitus, a family history of coronary artery disease, cigarette smoking, or severe obesity, the patient with a total blood cholesterol concentration less than 200 mg/dL requires no specific instruction and should have a repeated screening performed within 5 years. Patients with blood cholesterol concentrations greater than 200 mg/dL should have their lipoprotein profiles determined if they have atherosclerotic cardiovascular disease or two other cardiovascular disease risk factors. The lipoprotein profile includes the determination of fasting cholesterol and triglyceride and HDL cholesterol concentrations. From these values, the LDL cholesterol concentration can be calculated. This LDL cholesterol concentration is central in selecting the appropriate therapy. HDL cholesterol concentrations may be useful in evaluating patients with ischemic heart disease. Concentrations of HDL cholesterol less than 35 mg/dL are associated with increased risk for coronary artery disease. Although there is currently no convincing evidence that support the specific treatment of depressed HDL cholesterol concentrations, therapy directed to modulating lipoprotein metabolism in patients with heart disease and low HDL concentrations may be of benefit. Patients with recurrent abdominal pain, pancreatitis, and eruptive xanthomatosis frequently have fasting hypertriglyceridemia concentrations exceeding 1000 mg/dL. These patients should be identified in order to effectively reduce their triglyceride concentrations, which can prevent these complications.
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PMID:Detection and evaluation of dyslipoproteinemia. 219 76

Xanthogranulomatous cholecystitis often presents as a severe chronic cholecystitis associated with abdominal pain, fever, and leukocytosis. Gallstones are present in most cases. At operation, there are adhesions to surrounding tissues, and sometimes a mass is found, mimicking tumor of the gallbladder. The gross and microscopic appearances are characteristic with multiple intramural nodules composed of foamy histiocytes and inflammatory cells. Cholesterol contents of these nodules are high. Involvement of the Rokitansky-Aschoff sinuses with liberation of bile lipids into the adjacent tissue is implicated in the pathogenesis of this lesion.
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PMID:Xanthogranulomatous cholecystitis. A clinical and pathologic study of twelve cases. 291 7

Seventy-five patients affected by chronic constipation were treated for 4 weeks with an Ispaghula Husk preparation (Fibrolax), a bulk-forming laxative. Frequency, stool consistency, abdominal pain and signs of venous stasis improved after treatment. No important side-effect was recorded. Cholesterol, HDL-cholesterol and triglycerides did not show significant changes.
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PMID:Treatment of chronic constipation by a bulk-forming laxative (Fibrolax). 685 60

A 47-year-old woman with stones in the gall-bladder suddenly developed severe upper abdominal pain. Cholesterol concentration was elevated, as were amylase (555 U/l) and lipase (408 U/l) concentrations, suggesting biliary pancreatitis. Endoscopic retrograde cholangiography demonstrated a cyst, about 10 cm in diameter, in the left lobe of the liver, connected to the biliary tract system. Ultrasonography and computed tomography additionally showed a smaller cyst in the right lobe. Infection with Echinococcus granulosus was proven microbiologically on bile (demonstration of hooklets and protoscolices) as well as serologically. Transpapillary cholangioscopy demonstrated daughter cysts within the echinococcal cyst. The main cyst was rinsed with 20% NaCl for 10 days via a nasocystic catheter. In addition, mebendazole (three times daily 1000 mg) was administered for 13 months. The signs if inflammation receded and the cyst shrank to a small residual volume. Surgical intervention became unnecessary.
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PMID:[Acute pancreatitis due to the rupture of an echinococcal cyst into the bile duct system]. 751 77

To further elucidate the incidence and potential mechanism of asparaginase-associated lipid abnormalities in children with acute lymphoblastic leukemia (ALL), we serially obtained fasting lipid and lipoprotein studies on 38 of the 43 consecutively diagnosed children with ALL before, during, and after asparaginase therapy. We also evaluated a second population of 30 long-term survivors of childhood ALL; a fasting lipid and lipoprotein profile was obtained once at study entry. The mean peak triglyceride level during asparaginase of 465 mg/dL (standard deviation [SD] 492) was significantly higher (P = .003) than the level of 108 mg/dL (SD 46) before the initiation of asparaginase therapy. Sixty-seven percent of the newly diagnosed patients had fasting triglyceride levels greater than 200 mg/dL during asparaginase therapy; 15 patients (42%) had levels greater than 400 mg/ dL, 7 with levels greater than 1,000 mg/dL. The incidence of hypertriglyceridemia did not vary by type of asparaginase or risk status of ALL (defined by white blood cell count and age). None of the 7 patients with triglyceride levels greater than 1,000 mg/dL developed pancreatitis. In contrast, 4 of the 13 patients without triglyceride elevation developed pancreatitis; 3 of the 4 patients had fasting studies at the height of their abdominal pain. Nuclear magnetic resonance analysis of lipid subclasses showed a significant increase in the smaller, denser forms of very low density lipoprotein (VLDL) and negligible chylomicron fraction in a subset of patients with marked triglyceride elevation. Lipoprotein lipase activity was consistently above normative values for all levels of triglyceride and could not be explained by obesity or hyperglycemia. Apolipoprotein B(100) levels increased during asparaginase therapy, although the mechanism of this remains unclear. LDL reciprocally decreased with increased VLDL during asparaginase therapy. After asparaginase therapy, triglyceride levels (mean, 73 mg/dL [SD 33]) were significantly lower than levels obtained during asparaginase therapy. Triglyceride levels for survivors did not differ from the normal range or postasparaginase levels in the newly diagnosed patients. These data show a striking temporal association between asparaginase therapy and hypertriglyceridemia. Changes in cholesterol, in contrast, were not temporally related to asparaginase treatment. Cholesterol levels were elevated (>200 mg/dL) in 20% of the patients after asparaginase, which may be due to continued treatment with corticosteroids. The mean cholesterol level of long-term survivors of 177 mg/dL was significantly higher than the norm (P = .045). High-density lipoprotein (HDL) levels were significantly lower than normal at all time periods and for both populations; 25% of survivors had HDL levels less than 35 mg/dL. We conclude that modifications in asparaginase therapy are not necessary. In cases of triglyceride elevation greater than 2,000 mg/dL when the risk of pancreatitis is increased, close clinical monitoring is imperative. Larger studies are needed to determine the incidence of dyslipidemia in long-term survivors of ALL as well as the relationship between lipid abnormalities and other late effects of treatment, notably obesity and cardiomyopathies.
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PMID:Asparaginase-associated lipid abnormalities in children with acute lymphoblastic leukemia. 905 8

Rosuvastatin (Crestor), an HMG-CoA reductase inhibitor (statin), has a favorable pharmacologic profile, including its selective uptake by hepatic cells, hydrophilic nature, and lack of metabolism by cytochrome p450 (CYP) 3A4 isoenzyme. This last property means that the potential for CYP3A4-mediated drug interactions and, as a consequence, adverse events is low in those requiring concomitant therapy with a statin and agents metabolized by CYP3A4. In a broad spectrum of adult patients with dyslipidemias, oral rosuvastatin 5-40 mg once daily effectively and rapidly improved lipid profiles in several large, randomized, mainly double-blind, multicenter trials of up to 52 weeks' duration. After 12 weeks' treatment, rosuvastatin was significantly (all p < 0.05) more effective at milligram equivalent dosages than atorvastatin, pravastatin, and simvastatin in improving the overall lipid profiles of patients with hypercholesterolemia (intent-to-treat analyses). Moreover, overall a significantly (all p < 0.001) higher proportion of patients achieved National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III low-density lipoprotein-cholesterol (LDL-C) goals with rosuvastatin 10 mg/day than with therapeutic starting dosages of these other statins after 12 weeks' treatment in pooled analyses. Rosuvastatin treatment for up to 52 weeks was generally well tolerated in patients with dyslipidemias in clinical trials. The most commonly reported treatment-related adverse events were myalgia, constipation, asthenia, abdominal pain, and nausea; these were mostly transient and mild. The incidence of proteinuria or microscopic hematuria with rosuvastatin 10 or 20 mg/day was <1% versus <1.5% with rosuvastatin 40 mg/day; these events were mostly transient and not associated with acute or progressive deterioration in renal function at recommended dosages. Importantly, very few patients experienced elevations in serum creatine phosphokinase (CPK) levels of over [corrected] 10-fold the upper limit of normal (0.2-0.4% of patients) or treatment-related myopathy (<or=0.1%) [i.e. muscle aches or weakness plus the same elevated serum CPK levels] at dosages of 5-40 mg/day. In conclusion, rosuvastatin treatment effectively and rapidly improves the lipid profile in patients with a broad spectrum of dyslipidemias. In those with hypercholesterolemia (including high-risk patients), rosuvastatin was more efficacious than and generally as well tolerated as atorvastatin, simvastatin, and pravastatin, with significantly more rosuvastatin recipients achieving their NCEP ATP III target LDL-C levels. Thus, rosuvastatin has emerged as a valuable choice for first-line treatment in the management of low- to high-risk patients requiring lipid-lowering drug therapy.
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PMID:Rosuvastatin: a review of its use in the management of dyslipidemia. 1504 23

Background A 53-year-old man with a history of hypertension and gout was referred to our clinic for severe hypertriglyceridemia, diagnosed 3 years previously. He was asymptomatic and had no history of abdominal pain, pancreatitis or diabetes, but consumed six cans of beer per night. Over the previous 2 years, he had been treated unsuccessfully with multiple medications; during this period his fasting triglycerides ranged from 5.41 mM to 55.04 mM (479 to 4,871 mg/dl). Investigations Physical examination including fundoscopy, medication review, and laboratory tests.Diagnosis Severe hypertriglyceridemia due to a genetic combined hyperlipidemia, exacerbated by persistent excessive alcohol intake and metabolic syndrome. Management Cessation of alcohol intake, initiation of a fat-restricted diet, and fibrate therapy, with close follow-up. Once serum triglycerides were controlled, attention was turned to lowering LDL-cholesterol concentration according to The National Cholesterol Education Program, Adult Treatment Panel III guidelines.
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PMID:Severe hypertriglyceridemia with a history of treatment failure. 1692 66

Formation of an abdominal chylous cyst is a rare event, predominantly occurring after spinal, vascular or urologic retroperitoneal surgery. As far as we know, the presented case is the first report in the literature of chylous cyst formation after laparoscopic fundoplication. A 57-year-old man with a history of a conservatively treated spinal compression fracture (T11/12) underwent laparoscopic fundoplication in 1996 for recurrent heartburn with insufficient response to treatment with PPI. His reflux symptoms disappeared but over the following years he developed intermittent abdominal pain in the right upper quadrant. Gastroscopy in 2002 revealed a slight compression of the distal esophagus. CT scan revealed a cystic formation next to the distal esophagus which was initially interpreted to be part of the fundoplicate itself. Aggravation of symptoms and weight loss was noted in 2006. A further CT scan revealed a 7 cm cyst along the fundoplicate and the lesser curvature of the stomach. The cyst was subsequently drained laparoscopically. Cholesterol (351 mg/d), LDL-cholesterol (263 mg/dl), triglycerides (334 mg/dl) and chylomicrons led to the diagnosis chylous cyst and the patient was put on a medium-chain triglyceride diet. After 12 weeks the discharge stopped and the drain was removed. The patient remained symptom-free for seven months but then presented again with the same complaints. This time an even larger cyst was diagnosed, extending from the lesser curvature of the stomach through the esophageal hiatus up to the right atrium. A Roux-en-Y chylous cystojejunostomy was then performed and has solved the problem up to the present. A chylous cyst may develop after laparoscopic fundoplication. If simple drainage fails, a cystojejunostomy can solve this problem.
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PMID:Chylous cyst formation following laparoscopic fundoplication. 1815 7

This study reports the clinical, clinicopathological and ultrasonographic findings from dogs with chronic pancreatitis (CP). Fourteen dogs with clinical signs consistent with CP and histological confirmation of the disease were evaluated. Abdominal ultrasound and clinical pathology results were recorded. Sensitivities of pancreatic enzymes for diagnosis of CP were calculated with two different cut-off values. The mean age of affected dogs was 9.1 years. Spaniels were the most common breed with CP, representing seven of the 14 dogs in this study. CP was histologically severe in nine cases. Most dogs showed chronic low-grade gastrointestinal signs and abdominal pain. Five dogs had exocrine pancreatic insufficiency and five dogs had diabetes mellitus. The sensitivity of elevated trypsin-like immunoreactivity for CP was 17 per cent. The sensitivities of canine pancreatic lipase immunoreactivity, lipase and amylase for CP were 44 to 67 per cent or 14 to 28 per cent depending on the cut-off value used. Cholesterol was elevated in 58 per cent of samples. Liver enzymes were often elevated. The pancreas appeared abnormal on 56 per cent of ultrasound examinations. Ten dogs had died by the end of the study period; only one case was due to CP.
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PMID:Observational study of 14 cases of chronic pancreatitis in dogs. 2126 13


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