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)

In order to determine the composition of "normal" ascitic fluid, the results of analysis of the first paracentesis on 347 consecutive cirrhotic patients with ascites at the West Haven Veterans Administration Hospital between 1955 and 1976 were examined. The ascites was considered "normal" in 259 patients. Bacterial peritonitis was present in 51, malignant ascites in 18, pancreatitic ascites in 15, and ascites of other types in 4 patients. Normal ascites is sterile, usually clear, and contains 281 +/- 25 leukocytes/mm3 (mean +/- SEM), 27 +/- 2% of which are polymorphonuclear. In spontaneous bacterial peritonitis the fluid is usually cloudy, contains 6084 +/- 858 white blood cells/mm3, 77 +/- 4% of which were PMN and culture is positive for a single bacterial species, usually enteric in origin. Malignant and pancreatitis ascites are sterile, often cloudy, and contain an average of 696 +/- 273 and 1821 +/- 833 leukocytes/mm3, respectively, about half of which are polymorphonuclear. Amylase activity is increased in pancreatitic ascites, but not in other types of ascites. Stained smears of sediment for bacteria are often positive in bacterial peritonitis, but not in the other categories. Neither the specific gravity, protein concentration, nor glucose level is useful in the differential diagnosis of ascites. Based on the critical number of leukocytes alone, (500/mm3), one can accurately differentiate infected from uninfected fluid in over 90% of ascitic patients.
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PMID:Analysis of ascitic fluid in cirrhosis. 42 2

The first recognised outbreak of Marburg virus disease in Africa, and the first since the original epidemic in West Germany and Yugoslavia in 1967, occurred in South Africa in February 1975. The primary case was in a young Australian man , who was admitted to the Johannesburg Hospital after having toured Rhodesia. Two secondary cases occurred, one being in the first patient's travelling companion, and the other in a nurse. Features of the illness included high fever, myalgia, vomiting and diarrhoea, hepatitis, a characteristic maculopapular rash, leucopenia, thrombocytopenia, and a bleeding tendency. The first patient died on the seventh day from haemorrhage resulting from a combination of disseminated intravascular coagulation and hepatic failure. The other two patients were given vigorous supportive treatment and prophylactic heparin and recovered after an acute phase lasting about seven days. During this period on developed pancreatitis, the serum amylase remaining raised until the 32nd day after the onset of the illness. The other developed unilateral uveitis after having been asymptomatic for two months. This persisted for several weeks and Marburg virus was cultured from the anterior chamber of the eye.
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PMID:Outbreake of Marburg virus disease in Johannesburg. 81 15

The study was designed to determine the prevalence of alcoholism/problem drinking among emergency medical admissions. Of 203 emergency admissions to two medical wards, 18% were found to be problem drinkers, using the brief Michigan alcoholic screening test (MAST) questionnaire. Problem drinking was found in 31% of males and 5% of females. Most drinking was done with friends (77%) and at the "rum shop" (62%). Fifty-one per cent of problem drinkers started between the ages of sixteen and twenty years. Seventy per cent of all problem drinkers had a first degree family relative who drank compared to 28% of non-drinkers. A high prevalence of alcoholism (48%) was found among smokers. Housestaff detected just over half of male (56%) and female (60%) alcoholics who were MAST-positive. Medical diagnoses among MAST-positive patients were gastrointestinal (cirrhosis, pancreatitis and hepatitis) in 32%, neurological (delirium tremens, seizures and subdural hematoma) in 27% and cardiovascular (cardiomyopathy, heart failure and dysrhythmias) in 16%. The detected level of problem drinking is likely to cause significant morbidity, and allows an important opportunity for intervention. The use of questionnaire methods to screen for alcoholism needs further evaluation in the region.
West Indian Med J 1991 Jun
PMID:Questionnaire detection of problem drinkers among acute medical admissions. 189 23

To determine the role of magnesium deficiency in the pathogenesis of hypocalcemia in acute pancreatitis, we measured magnesium levels in serum and in peripheral blood mononuclear cells in 29 patients with acute pancreatitis, 14 of whom had hypocalcemia and 15 of whom had normal calcium levels. Only six patients had overt hypomagnesemia (serum magnesium less than 0.70 mmol per liter [1.7 mg per dl]). The mean serum magnesium concentration in hypocalcemic patients was not significantly lower than in normocalcemic patients, but the mononuclear cell magnesium content in hypocalcemic patients with pancreatitis was significantly lower than in normocalcemic patients with pancreatitis (P less than .01). The serum magnesium level did not correlate with that of serum calcium or the mononuclear cell magnesium content, but the latter did significantly correlate with the serum calcium concentration (r = .81, P less than .001). Most patients with hypocalcemia had a low intracellular magnesium content. Three normomagnesemic, hypocalcemic patients with alcoholic pancreatitis also underwent low-dose parenteral magnesium tolerance testing and showed increased retention of the magnesium load. We conclude that patients with acute pancreatitis and hypocalcemia commonly have magnesium deficiency despite normal serum magnesium concentrations. Magnesium deficiency may play a significant role in the pathogenesis of hypocalcemia in patients with acute pancreatitis.
West J Med 1990 Feb
PMID:Low intracellular magnesium in patients with acute pancreatitis and hypocalcemia. 240 29

This article describes the surgery of tropical pancreatitis as practiced in a region of high incidence, based on the experience at 2 centers: the Department of Surgical Gastroenterology and Proctology, Government General Hospital, Madras, Tamilnadu (a tertiary-care referral unit) where 52 patients were diagnosed and 40 were operated on between 1982 and 1987; and the Department of Gastroenterology, Deva Matha Hospital, Koothattukulam (a specialized center located in the main endemic area of Kerala), where 116 patients were diagnosed and 33 operated on between 1983 and 1988. The latter series is described in detail with emphasis on the preoperative imaging, operative findings, surgical procedures, complications, and results of surgery. The experience of other centers in southern India is summarized and discussed. The disease is obviously different from chronic pancreatitis in the West. Special problems of tropical pancreatitis, particularly the management of diabetes and the association of pancreatic carcinoma at a young age, are discussed.
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PMID:Observations and surgical management of tropical pancreatitis in Kerala and southern India. 240 37

Colonic complications are rare in acute pancreatitis. Over the last 9 years at St. Mary's Hospital, London, UK, we have managed severe acute pancreatitis by intensive supportive therapy followed by sub-total pancreatic resection and/or debridement in those who fail to improve. Of the 22 patients who have undergone this form of surgery, nine were found to have colonic involvement in the form of either necrosis or perforation. In addition, one patient presenting at West Middlesex University Hospital, Isleworth, UK, had severe acute pancreatitis and almost total colonic necrosis as an unexpected finding at emergency laparotomy. These ten patients comprised seven men and three women of median age 59 years and with a median of four Ranson criteria. In seven patients, colonic involvement was discovered at the time of pancreatic surgery or laparotomy for pancreatitis and in the remainder it presented between 1 and 3 weeks later as either a faecal fistula (n = 2) or persistent abdominal sepsis (n = 1). The ascending colon was involved in one patient, the splenic flexure and descending colon in one, the transverse colon in three, the splenic flexure alone in four, and one patient had almost total colonic involvement. All patients underwent resection of the involved colon and exteriorization with either a proximal colostomy (n = 7) or ileostomy (n = 3) and a distal mucous fistula. Pathological examination of the resected colons revealed a spectrum of changes from pericolitis through to ischaemic necrosis suggesting at least two possible mechanisms. Six patients died from overwhelming sepsis between 1 day and 4 weeks (median 11 days) after colonic resection. Severe acute pancreatitis must be recognized as a cause of colonic ischaemia and necrosis; this complication is associated with a very poor prognosis despite surgical intervention.
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PMID:Colonic complications of severe acute pancreatitis. 265 21

Spontaneous massive gastrointestinal hemorrhage occurring in patients with pancreatitis is an uncommon and difficult clinical problem, especially in a tropical third world country where the underlying causes of pancreatitis and facilities for its diagnosis and management are different from those in the developed West. Of 7 such cases seen by us in 3 years, 2 were due to hemosuccus pancreaticus, 2 were due to gastric variceal hemorrhage consequent to splenic vein obstruction, and one each due to contiguous pancreatic inflammation involving the duodenum, an aneurysmal bleed from the left gastric artery and a pseudocyst rupturing into the transverse colon. A fiberoptic endoscopic examination was helpful in all the 7 cases and delineated the cause of bleeding, whereas angiography, performed in 4 patients contributed little to management. The mortality rate was 14%. It is suggested that a timely endoscopic examination during active bleeding, which may be repeated if necessary, is extremely rewarding in the diagnosis and management of such patients and often obviates the necessity of angiography which is a time-consuming and cumbersome investigation in a critically ill patient and facilities for which are usually not available in most third world country hospitals.
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PMID:Spontaneous massive gastrointestinal hemorrhage in patients with pancreatitis. 326 Dec 69

Spontaneous bacterial peritonitis (SBP), a fascinating disease that had been reported perhaps 50 times in varying guises over the preceding century, suddenly burst forth in the 1960s and was recognized in clusters of cases almost simultaneously in Paris, London, and West Haven, Connecticut. The spectrum of the disease has broadened. Initially, it was associated almost exclusively with alcoholic cirrhosis, but it has now been found in association with posthepatitic cirrhosis, cryptogenic cirrhosis, chronic active liver disease, and, occasionally, in biliary cirrhosis and cardiac cirrhosis. Recently, it has been reported in alcoholic hepatitis and acute viral hepatitis. It occurs occasionally in malignant ascites and in pancreatitis in the absence of cirrhosis. It is surprisingly common in disseminated lupus, in which it occurs relatively more commonly than in alcoholic cirrhosis. A similar syndrome, primary peritonitis, occurs frequently in children with nephrotic ascites. The clinical pattern of SBP has broadened. Initially it consisted of abdominal pain, fever, rebound tenderness, hypoactive bowel sounds, hypotension, encephalopathy, and cloudy ascites with large numbers of polymorphonuclear leukocytes in ascitic fluid. Each and every symptom, sign, and laboratory abnormality may be absent; indeed, the syndrome can be completely silent. Initially, the causative bacteria appeared to be almost exclusively enteric, but now the list of bacteria isolated in cases of SBP looks like a bacteriology textbook. Anaerobes are rare. Multiple organisms usually suggest nonspontaneous origin such as perforation or vasopressin induction. The differentiation between spontaneous and nonspontaneous bacterial peritonitis is crucial in the differential diagnosis. The great majority of cases of SBP develop in the hospital, 80% more than one week after admission. It is therefore a nosocomial disease that may be precipitated by procedure-induced bacteremia, gastrointestinal bleeding, or diarrhea, and it tends to occur in patients with low ascitic fluid protein (complement) concentrations and severe portal-systemic shunting.
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PMID:Spontaneous bacterial peritonitis: variant syndromes. 368 33

A West German family with hereditary pancreatitis is described. Four members are definitely known to have had pancreatitis, while three additional members are suspected of having the disease. The mean age of onset of symptoms was 14 years. Known causes of secondary pancreatitis and amino aciduria were ruled out in each case. HLA-segregation was analysed on the A, B, C, and DR loci in all members of the family, but no coupling between distribution of HLA haplotypes and incidence of pancreatitis was detected.
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PMID:Hereditary pancreatitis. Presentation of an additional family. 398 24

Macroamylase is a circulating complex of immunoglobulin linked to normal amylase in most cases. Its physical properties are heterogeneous, but its large size impairs renal filtration. Macroamylasemia usually causes hyperamylasemia and an amylase clearance:creatinine clearance (C(AM):C(CR)) ratio of less than 1 percent. Macroamylasemia occurs in 2.5 percent of hyperamylasemic patients, and 1 percent of apparently healthy subjects with normal amylase levels. It often accompanies diseases of aberrant immunity or conditions in which pancreatitis must be ruled out. This disorder should be considered in a patient with asymptomatic hyperamylasemia because its detection can obviate a prolonged diagnostic workup. The condition requires no treatment and may be transient. Macroamylasemia is one of several immunoglobulin-complexed enzyme (ICE) disorders. MacroLDemia, an ICE disorder of lactate dehydrogenase (LD), shares features with macroamylasemia. These and other ICE disorders appear to represent nonspecific dysproteinemic responses to disease.
West J Med 1980 Nov
PMID:Macroamylasemia and other immunoglobulin-complexed enzyme disorders. 616 78


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