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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Purtscher's syndrome (traumatic retinal angiopathy, posttraumatic retinopathy) belongs to rare posttraumatic retinopathies. The authors present a case of a bilateral occurrence of this syndrome after a head injury connected with pancreatitis. A 6-months long observation of the patient showed an improvement of the visual acuity from counting fingers to 0.1 and receding of the inflammatory-oedematous changes at the eye fundus; there remained a pallor of the temporal side of the optic discs.
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PMID:[Bilateral Purtscher's syndrome]. 130 Apr 4

Atherosclerotic vascular disease can give rise to provoked or spontaneous cholesterol crystal embolization to organ systems. Lodging in downstream arterioles, these crystals can produce granuloma formation, infarction, ulceration, and perforation. Histologic sections of the tissue concerned invariably show pathognomonic empty needle-shaped clefts left by the crystals after processing of the material. In the digestive system these events can cascade to many and often misleading presentations. They can be the cause of massive bleeding, acute acalculous cholecystitis, pancreatitis, or teleangiectasis with chronic intractable blood loss. Owing to the progressive nature of the disease the treatment options described in this paper can only give temporary, but nevertheless often worthwhile relief.
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PMID:Cholesterol crystal embolization and the digestive system. 177 43

A girl aged 1 year died of acute haemorrhagic pancreatitis while taking sodium valproate. Necropsy showed widespread vascular disease that may have contributed to the onset of pancreatitis. Previous reports of pancreatitis in children receiving valproic acid are reviewed and although the association is rare, a causal relation between pancreatitis and valproic acid seems to have been established.
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PMID:Pancreatitis during sodium valproate treatment. 640 11

The clinical and epidemiological literature is reviewed as to metabolic effects of oral contraceptives (OCs). Both the estrogens and the progestins in OCs cause biochemical alterations which have metabolic consequences. Changes in glucose, lipid, and protein metabolism suggest that the dosage of both estrogens and progestins should be minimized as much as possible. All studies with OCs show no changes in glucose tolerance, but all do consistently show elevated plasma insulin levels as a result of OC usage. This occurs because the pill causes a decrease in insulin sensitivity in healthy women. Increases in age and weight, regardless of OC usage, will also cause an increase in glucose tolerance. Oral glucose tolerance deteriorates in all OC user groups, the greatest deterioration being in the high-dose estrogen users. Women with a history of gestational diabetes or impaired glucose tolerance should be considered high-risk pill users. Lipid abnormalities as a result of pill usage are primarily due to estrogen content. Fasting triglyceride levels are increased in all estrogen users. High-risk factors to be considered in OC prescription are: moderate obesity; diabetes; history of gestational diabetes; hypertension; history of pancreatitis, gallbladder or liver disease; physical evidence of xanthomatosis; age over 30 and smoker; age over 35; family history of hyperlipidemia; and family history of early atherosclerotic vascular disease. Many of the pill-induced protein synthesis changes are similar to those which occur during pregnancy. These, too, are due to estrogen content.
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PMID:Metabolic effects of the birth control pill. 702 12

We retrospectively studied the clinical features of all 44 patients (35 men, 9 women, mean age 74.5 years) registered with a diagnosis of hepatic, biliary, and/or pancreatic cholesterol crystal embolization (CCE) in the Dutch National Pathology Information System (DNPIS) from 1973 through 1994. Liver CCE was found in 12 (11 autopsies and 1 biopsy), gallbladder CCE in 2 (resection specimens), pancreas CCE in 19 (18 autopsies and 1 biopsy), and both liver and pancreas CCE in 11 (all autopsies) patients. Five patients presented with focal liver cell necrosis, 1 with acalculous necrotizing cholecystitis, 1 with chronic cholecystitis, 10 with necrotizing pancreatitis, and 1 with chronic fibrosating pancreatitis. Four patients died of CCE-induced pancreatitis. Nineteen patients died as a consequence of other CCE sites. These were reported in 37 patients. All patients had a history of atherosclerotic vascular disease. In half the patients a possibly CCE provoking factor (vascular surgery and/or cannulation, anticoagulant treatment) was present. We conclude that liver cell necrosis, cholecystitis, and pancreatitis may be caused by CCE, particularly in elderly male patients with a history of atherosclerosis.
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PMID:Cholesterol crystal embolization to liver, gallbladder, and pancreas. 879 1

Elevated plasma viscosity is a predictor of atherosclerotic vascular disease and is a potential mechanism by which hypertriglyceridemia increases cardiovascular risk. Previous studies of plasma viscosity reduction in hypertriglyceridemic patients used medications that lowered both triglyceride and fibrinogen levels. Because fibrinogen is a major determinant of viscosity, it is unclear whether triglyceride reduction alone is sufficient to reduce plasma viscosity. The purpose of this study was to determine whether triglyceride-lowering therapy reduces plasma viscosity. This was a prospective study of 24 adult patients with severe hypertriglyceridemia (> or = 5.67 mmol/l). Fasting lipid, total serum protein, fibrinogen, plasma viscosity and serum viscosity levels were measured before and after therapy with 1200 mg/d of gemfibrozil. Triglyceride levels decreased by 70% (P < 0.001). Mean plasma and serum viscosity levels decreased by 0.082 mPa/s (P = 0.003) and 0.086 mPa/s (P = 0.013), respectively. Fibrinogen levels did not change significantly. Triglyceride-lowering therapy reduced plasma and serum viscosity without changes in fibrinogen levels. Since serum samples are deplete of fibrinogen, the serum viscosity reduction observed is corroborative evidence for an independent effect of triglyceride-lowering therapy on plasma viscosity. This observation provides a physiological rationale for triglyceride-lowering therapy in patients at risk for atherosclerotic vascular disease, the chylomicronemia syndrome and pancreatitis.
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PMID:Treatment of severe hypertriglyceridemia lowers plasma viscosity. 962 83

We reviewed the clinical and pathologic finding of 22 resected allografts from 19 of the 83 children who underwent a variety of small intestinal transplant procedures in the years 1990-2000 at the Children's Hospital of Pittsburgh. Resections were compared with prior mucosal biopsies because resections allow for evaluation of the entire bowel thickness, including the feeding vessels, and obviate the problems of limited sampling. Partial resections that were done soon after the transplant, or soon after additional surgery, were for surgical problems such as leaks, adhesions, and volvulus. None had biopsy features suggestive of rejection or infection. Partial resections done late (6 months or more) after transplantation were more likely to be related to allograft immune biology; two had a sclerosing peritonitis that was confined to the allograft, and one had an obstructing carcinoma arising in the allograft mucosa. One patient had a localized stricture, demonstrated to be due to graft vascular disease at partial resection, and this patient went on to have the allograft removed a year later for chronic rejection. Early complete allograft enterectomies were for refractory acute cellular rejection, 1-2 months following transplant. One was removed for pancreatitis and liver failure from operative complications. Late allograft enterectomies were generally for chronic rejection, some with residual acute rejection, but there were also a number of patients who had multiple superimposed conditions such as cytomegalovirus, Epstein-Barr virus, and post-transplant lymphoproliferative disorder in various combinations. One had idiopathic scarring and developed an adynamic bowel that remains unexplained. Examination of the resected specimens allows for dissection of the multiple contributions to graft failure, especially the vascular disease that can rarely be seen on mucosal biopsy. An unexpected finding was the impressive hypertrophy of neural elements, nerves, and ganglion cells in many of the patients, the significance of which requires further investigation.
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PMID:Pediatric intestinal transplantation: the resected allograft. 1181 64

Splenic artery aneurysms are an uncommon form of vascular disease that have a significant potential for rupture, resulting in life-threatening intraperitoneal hemorrhage. We describe the case of a 33-year-old man who died suddenly and unexpectedly due to the rupture of a splenic artery aneurysm. At medicolegal autopsy, 3000 mL of fluid blood were recovered from the peritoneal cavity. The source of bleeding was a sack-like aneurysm of the splenic artery, measuring 2 cm in diameter. Histologic examination of the splenic artery aneurysm revealed fibromuscular dysplasia. No atherosclerotic lesions or any inflammatory changes were apparent within the wall of the splenic artery. Portal hypertension and pancreatitis, previously described as important factors promoting splenic artery aneurysm formation, were excluded by autopsy and histology. From the forensic pathologist's viewpoint, this rare case underlines the importance of splenic artery aneurysm rupture as a relevant differential diagnosis of intraperitoneal hemorrhage and sudden death, respectively, since such cases may be misinterpreted as a result of blunt-force trauma.
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PMID:Sudden, unexpected death due to splenic artery aneurysm rupture. 1572 82

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 role of homocysteine role in inflammation and malignancy has been studied experimentally. Some researchers suggest that a relationship exists between pancreatitis and homocystinuria, possibly being secondary to occlusive vascular disease of the pancreas. To date, plasma homocysteine levels in pancreatic disease have not been studied. We aimed to analyze the homocysteine status in patients with acute pancreatitis, and the changes of the plasma homocysteine level at the acute phase of the disease and six months after hospital discharge. Fourteen acute pancreatitis patients and 14 healthy subjects were studied. Plasma homocysteine, vitamin B12, folate, amylase, lipase, C-reactive protein, total, HDL and LDL cholesterol, triglycerides, blood urea nitrogen, white blood cells, and creatinine were measured in the two groups of subjects. Plasma levels of homocysteine were significantly higher in patients with acute pancreatitis as were serum creatinine, blood urea nitrogen, WBC counts, amylase, lipase, and C-reactive protein. An impaired creatinine clearance was also found in these patients but this did not reach statistical significance. Serum total, HDL, and LDL cholesterol concentrations were not significantly different between the two groups of subjects. Our data suggest that homocysteine may play a role in inflammatory diseases of the pancreas. Increased plasma homocysteine levels in acute pancreatitis may be a reason, or a marker, for the diagnosis of acute pancreatitis. In conclusion, this is the first report showing that patients with acute pancreatitis have higher plasma homocysteine levels than healthy subjects.
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PMID:Changes in plasma levels of homocysteine in patients with acute pancreatitis. 1846 55


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