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)

Proteases have a wide range of functions: digestion (pancreatic proteases), protein catabolism (lysosomal proteases), blood coagulation, immune defences (complement), cellular division and proliferation, generation of biologically active oligopeptides (kinins, hormones) from inactive polypeptide precursors, inactivation of these oligopeptides, etc. The body protects itself against its own proteases, either by confining them to a given compartment (lysosome), by synthesising them in the form of inactive precursors (trypsinogen, prothrombin, etc.), or by synthesising proteins with an antiprotease activity. Any disturbance in one of the elements of this protective system may lead to severe pathological consequences: acute hemorrhagic pancreatitis with shock, coagulation disturbances (deficient hepatic synthesis of coagulation factors, congenital antithrombin III deficiency), angioneurotic oedema (congenital deficiency of C'l esterase inhibitor) pulmonary emphysema (local secretion of leukocyte elastase, congenital deficiency of alpha a-antitrypsin).
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PMID:[Problems in intensive care posed by imbalance in the protease--protease inhibitor system]. 611 Dec 72

Although the association between acute pancreatitis and pleuropulmonary damage is well documented, so far no information on lung function in patients with chronic pancreatitis is available. In this study functional, radiological, and clinical investigations have been carried out in 42 patients affected by chronic calcific pancreatitis (CCP) and in 50 controls in a case-control study. An impairment of pulmonary diffusing capacity has been detected in CCP patients, while all the parameters of ventilatory function were not different from controls. This finding suggests the presence of early lung parenchymal damage in chronic pancreatitis secondary to either emphysema or pulmonary fibrosis.
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PMID:Pulmonary involvement in chronic pancreatitis. 647 80

The surgery of the gall bladder by gallstones, bile duct and alterations of the duodenal papilla are conducted with an increase of lethality. This increased lethality is caused by accompanying ill effects, especially chronical pancreatitis, cholangitis, disturbances of the liver. The indications to operate old patients are occlusions of duodenal papilla relapsing colics with or less occlusing icterus, emphysema of gall bladder or perforation. A careful narcosis is necessary by disease of circulation, diabetes, bronchitis and emphysema of the lung. Simple cholestectomies in old patients have a mortality of 0-1%. Interventions on bile ducts, transduodenal papillotomia, choledochoduodenotomy have an mortality of 4-8%. The intraoperative cholangiography is always necessary. Operations on bile duct are finished by inserting a T-drain. The distal portion of the T-drain are not emissed through the duodenal papilla, because a pancreatitis can be released. The principal postoperative complication is the pancreatitis, consumption coagulopathy, bronchopneumonia, cholangitis with intermitting fever and injuries of the liver parenchym. The persisting pancreatitis can be treated with infusions.
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PMID:[Surgical interventions on the gallbladder and the biliary tract in the aged]. 712 73

A retrospective analysis was done of 88 cases of laparoscopic cholecystectomy performed by the first author from November 1990 to March 1992 at the Toa Payoh Hospital. There were 61 female and 27 male patients; the average age was 47.1 years. The most common presenting symptom was biliary colic (85.3%), followed by acute cholecystitis (10.2%) and gallstone pancreatitis (4.5%). In the vast majority of patients, the diagnosis was established by ultrasound (96.6%) while the remainder was diagnosed by oral cholecystography (3.4%). The operation was performed using the usual 4 puncture approach with the single-handed technique of dissection. Antibiotic prophylaxis with a broad-spectrum agent was used in all patients and there was no incidence of wound infection. A low complication rate of 4.5% was experienced--consisting of 1 case each of subcutaneous emphysema, abdominal colic, fever and bile duct injury. There was no mortality in our series. The conversion rate was 9.1% and this was due to our policy of performing laparotomy whenever the safety of laparoscopic surgery was in doubt. The mean duration of postoperative hospitalisation was 3 days and 7 days after laparoscopic and converted cholecystectomies respectively. The majority of patients (61.4%) returned to work after 2 weeks.
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PMID:Experience with laparoscopic cholecystectomy at the Toa Payoh Hospital. 826 71

The clinical pattern and the pathophysiological mechanism of the hereditary disorder alpha 1-antitrypsin deficiency are outlined. It appeared that the patient described suffered not only from emphysema, cirrhosis of the liver and hepatocellular carcinoma, but also from acute haemorrhagic pancreatitis. The combination of acute pancreatitis and alpha 1-antitrypsin deficiency has not been described before. Screening of relatives is important because of possible treatment.
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PMID:[Acute pancreatitis in a patient with alpha 1-antitrypsin deficiency. Is there a causal relationship?]. 841 21

Acute biliary pancreatitis (ABP) still retains high morbidity (15-50%) and mortality (20-35%). Therefore it appears to be crucial clearly assessing the aetiological factors (50% of idiopathic are in fact biliary pancreatitis) and establishing the severity in order to plan the appropriate treatment. Forty-nine ABP patients were diagnosed by ultrasound (75.5%) or by laboratory findings (22.5%). Following Ranson and APACHE II scoring, 15 cases (30.6%) were classified as severe, 34 (69.3%) as mild. All patients with severe ABP had emergency ERCP + ES (within 24-48 hours) followed by LC (< or = 10 days). Patients with mild ABP had LC within 10 days; in these cases IOC was always done. In severe cases operative endoscopy cured pancreatic inflammation in 11 cases. Subsequent LC never showed serious morbidity, but subcutaneous emphysema in one case. In 4 cases laparotomy was required since pancreatic necrosis was present, with 75% mortality. In patients with mild pancreatitis LC was successfully performed in all cases, with 8.8% morbidity. IOC showed choledochal stones in 32.5% of cases, while in severe cases stones in the biliary tree were showed in 80% of cases. In conclusion ABP treatment is always surgical, and almost always with minimally-invasive procedures in severe cases (ERCP + ES with LC < or = 10 days) if surgery is performed within 24-48 hours as well as in mild cases (LC + IOC) when surgery is done within 10 days.
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PMID:[Acute biliary pancreatitis: mini-invasive treatment]. 952 95

This study is a retrospective analysis of clinical parameters and pulmonary function in seven male patients receiving lung transplantation between June 1993 and February 1996 as a treatment for pulmonary emphysema. The patients were suffering severe airway obstruction, functional class III-IV, and were dependent on home therapy with oxygen. Their mean age was 54.9 years (+/- 5.4 years) and their mean waiting list time was 266 +/- 158 days. Transplantation was sequential bilateral (TPb) in one case and unilateral (Tpu) in the remaining 6. A triple inmunosuppresant protocol was employed (Cyclosporina A--Azathioprin-Prednisone) and bronchoscopy was performed on a regular basis and on evidence of infection or rejection. The patient who received the bilateral transplant died 76 days later due to necrohemorrhagic pancreatitis. The 6 unilateral transplant patients were discharged in good condition 31.3 +/- 9.0 days after transplant. One patient died 69 days after transplantation due to hypertensive pneu-mothorax of the native lung. All patients presented acute rejection between 10 and 86 days after transplantation, responding well to treatment with Methylprednisone or increased immunosuppression. All patients receiving unilateral transplantation showed marked improvement in functional class, gas exchange, and pulmonary function.
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PMID:[Lung transplantation in emphysema]. 967 19

The less frequent complications of colonoscopy include pneumothorax, pneumoperitoneum, emphysema of the retroperitoneum or of the subcutis, septicemia and injuries of visceral organs (mainly the spleen). Since the mid 1970 s more than 30 splenic injuries during colonoscopy have been described. Any cause of increased splenocolic adhesions (inflammatory bowel disease, pancreatitis or prior abdominal surgery) might be a predisposing factor for splenic injury during colonoscopy. Other contributing factors are techniques that result in a strong torsion of the spleno-colic ligament. Patients with left shoulder and abdominal pain, hypotension, and a drop in hemoglobin without rectal bleeding after colonoscopy should be suspected to have splenic injury. Many physicians are not aware of splenic injuries as a potential complication of colonoscopy. Therefore the diagnosis of splenic injury during colonoscopy is often described in the literature as delayed (hours until 10 days). Since a colonoscopic splenic injury can be fatal, this exceedindly rare event must be considered when a patient shows the above-mentioned symptoms and no signs of colon perforation.
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PMID:[Splenic trauma--a rare complication during colonoscopy]. 1519 Apr 46

Serine proteases are attractive targets for the design of enzyme inhibitors since they are involved in the etiology of several diseases. Within the class of serine proteases, HLE is one of the most destructive enzymes in the body. It is implicated in the promotion or exacerbation of a number of diseases including pancreatitis, acute respiratory syndrome, rheumatoid arthritis, atherosclerosis, pulmonary emphysema, and cystic fibrosis. Thrombin, a trypsin-like serine protease, plays a dual role in thrombogenesis, including fibrin formation and platelet activation. As a result, thrombin constitutes one of the most widely studied targets for antithrombotic strategy. Numerous inhibitors of serine proteases have been reported during the past three decades. Among them, coumarin-type molecules displayed a high inhibitory potency towards various serine proteases. At that time, halomethyl dihydrocoumarins have been shown to behave as the first general suicide inhibitors of serine protease. These molecules inhibit several proteases such as human leucocyte elastase, porcine pancreatic elastase, thrombin, urokinase and human plasmin. Isocoumarins are very effective as mechanism-based inhibitors of serine proteases. Pharmacomodulation on the 3-alkoxy-4-chloroisocoumarins and the 3-alkoxy-7-amino-4-chloroisocoumarins led to strong inhibitors of numerous serine proteases such as HLE, human factor XIa and XIIa, thrombin, urokinase and kallikrein. Recently, a series of coumarins characterised by an alkyl, aryl ester, amide, thioester or ketone in the position 3 and an electrophilic chloromethyl moiety in the position 6 have been developed. These compounds were found to be high inhibitors of alpha-chymotrypin, HLE and human thrombin.
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PMID:Coumarin and isocoumarin as serine protease inhibitors. 1557 71

The identification of a Btk mutation in a male patient with <2% CD19(+) B cells warrants making the diagnosis of X-linked Agammaglobulinemia (XLA). Herein we report the case of a 31 year-old male with a gradual decline of peripheral B lymphocytes and low IgA and IgM but normal IgG levels. His clinical history revealed recurrent respiratory and skin infections, sclerosing cholangitis and chronic obstructive pancreatitis. Molecular studies revealed a novel aminoacidic substitution in Btk protein (T316A). His mother, maternal aunts and a maternal female cousin were heterozygotes for the same Btk mutation and were variably affected with pulmonary emphysema. This is a puzzling case where the patient's clinical history and laboratory findings divorce molecular genetics. Either this case confirms the variable expressivity of XLA disease or the T316A change in Btk SH2 domain is a novel non-pathogenic mutation and another unknown gene alteration is responsible for the disease.
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PMID:Identification of a Btk mutation in a dysgammaglobulinemic patient with reduced B cells: XLA diagnosis or not? 1861 43


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