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)

Enteropeptidase (enterokinase) (EC 3.4.21.9), a highly specific processing protease, initiating a cascade of reactions activating the digestion enzymes. Catalyzing trypsinogen activation enteropeptidase exhibits unique properties for high efficiency hydrolysis of the polypeptide chain after lysine-15 residue in the -DDDDK15- sequence. In 1998 we found an unusual calcium-dependent autolysis of the enteropeptidase heavy chain leading to the drastic loss of its activity towards trypsinogen: after lysine-360 (-NNYEK360-INCN-), -), arginine-384 (-NEWER384-TQGS-), arginine-422 (-GRRER422-VGLL-) and lysine-465 (-QNMEK465-TIFQ-) residues. We used hepta-nona-peptides as the model substrates for autolysys: human angiotensin II--DRVYIHPF and cattle hemoglobin b-chain fragments: LTAEEKA and MLTAEEKAA. Kinetic parameters of enteropeptidase hydrolysis for these substrates were determined. Recent study demonstrates the ability of enteropeptidase to hydrolyze peptide bonds formed by carboxyl groups of Lys or Arg residues if less than four but at least one negative charged amino acid residue is in any of substrate P2-P5 positions. Ca(2+)-dependent autolysis of enteropeptidase heavy chain and of trypsin were compared; the second one serves as the natural defense mechanism against the undesirable premature proenzymes activation in pancreas leading to pancreatitis. The corresponding enteropeptidase inactivation in low Ca2+ environment ought to be the component of the same protective mechanism.
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PMID:[Hydrolysis by enteropeptidase of nonspecific (model) peptide sequences and possible physiological role of this phenomenon]. 1269 55

We report a case of blackwater fever with brown plasma due to the presence of methemalbumin. The discovery of plasma with this color is a rare event at the laboratory. This compound appears during intravascular hemolysis or hemorrhagic pancreatitis when the ability of haptoglobin and hemopexin to bind free hemoglobin has been exceeded. In these cases some of heme is oxidized to hematin and taken up by serum albumin to form an albumin-hematin complex called methemalbumin. The major clinical problem is to evoke the diagnosis of methemalbuminemia and not confuse with methemoglobinemia. In our case, methemalbumin was detected and quantified using a scanning spectrophotometer. Its diagnostic and clinicals consequences are discussed.
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PMID:[Methemalbuminnemia after massive hemolysis during blackwater fever]. 1280 12

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

Sixteen fatal dog envenomations by the snake Vipera palaestinae over a 14-y period are described. Most envenomations occurred during the late night hours in the warm months, and 8/16 dogs were bitten on the limbs. The most frequent clinical signs upon admission were soft tissue swelling and edema, local pain, depression, bleeding, lameness, dyspnea, and 6 dogs were in shock. Thrombocytopenia was present in 14/16 cases and increased hematocrit (13/16) and hemoglobin (9/16) concentration were the most common hematological abnormalities upon admission. Biochemical abnormalities included increased activities of muscle enzymes and alkaline phosphatase, hypocalcemia, and hypocholesterolemia. Creatine kinase activity was markedly increased in 2 dogs. During hospitalization serious complications in many dogs were disseminated intravascular coagulation, acute renal failure, seizures, cardiac arrhythmias, acute necrotizing pancreatitis and severe laryngeal edema; these required intensive and expensive therapies. Specific antivenin (10 ml) administered to 8/16 dogs did not prevent death. Glucocorticosteroids were given in 8 cases; however, their use was associated with complications. Four dogs suffered sudden death, 2 of which died 1-2 d after discharge. Necropsy performed on 3/16 dogs found soft tissue swelling and local bleeding at the envenomation sites as well as bleeding in several distal body organs and tissues.
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PMID:Fatal Vipera xanthina palestinae envenomation in 16 dogs. 1548 52

VitaResc (formerly Apex) is developing PHP-HT, pyridoxalated hemoglobin polyoxyethylene conjugate, for the potential treatment of nitric oxide-induced shock (characterized by hypotension), associated with various etiologies, initially in septic shock. A phase I safety study and an initial phase I/II patient trial for NO-induced shock have been completed, and VitaResc has enrolled patients in three of five planned cohorts in a continuation of these trials to include a protocol of continuous infusion and dose escalation [330680,349187,390918]. The results from the dose escalation trials are expected to provide the basis for a randomized, controlled phase II/III pivotal trial of PHP-HT [390918]. VitaResc has licensed PHP-HT exclusively from Ajinomoto for all indications, worldwide, except Japan [275263]. Ajinomoto originally developed the human derived and chemically modified hemoglobin preparation as a blood substitute, but no development has been reported by the company since 1997 [275277,303577]. The other potential indications of PHP-HT include shock associated with burns, pancreatitis, hemodialysis and cytokine therapies [275277]. VitaResc expects the annual market potential of PHP-HT to exceed 1 billion dollars [330680].
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PMID:PHP-HT (VitaResc Biotech). 1601 85

Various hematological abnormalities including fall in serial values of hemoglobin or hematocrit, coagulation factor abnormalities, leukocytosis, acute hemolytic anemia, thrombocytopenia, and thrombotic thrombocytopenic purpura or hemolytic uremic syndrome have been reported in patients with acute pancreatitis. Similarly, abnormalities of blood coagulation factors consistent with disseminated intravascular coagulopathy (DIC) have also been noticed in patients with pancreatitis. We report a case of a 33-year-old female with acute pancreatitis who presented with one episode of epistaxis and abnormal prothrombin time and partial prothrombin time. Coagulation work-up revealed thrombin time 24.3 s fibrinogen 110 mg/dl, D-dimers >1 and < 2, and fibrin degradation products >22. Pancultures did not show any evidence of infection. The patient maintained a normal renal and mental status during her illness. Her D-dimers continued to decrease with resolution of acute pancreatitis as evidenced by decreased abdominal pain, relief of nausea, control of vomiting, and decrease in serum amylase and lipase levels. This case report suggests that coagulation abnormalities are encountered in patients with acute pancreatitis. It is hypothesized that such hemostatic abnormalities may be related to early intravascular consumption of coagulation factors secondary to circulating pancreatic enzymes, particularly trypsin, or secondary to vascular injury. Recognition of these hematological complications including DIC is paramount. Physicians caring for these patients should be aware of such a complication of acute pancreatitis.
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PMID:DIC secondary to acute pancreatitis. 1604 98

A patient with severe hypothermia presented with an initial rectal temperature of 28.3 degrees C coupled with a hemoglobin of 2.2 g x dL(-1) and acute pancreatitis. Although hypothermia decreases oxygen and substrate consumption by tissues and can be cerebro-protective, the ideal rewarming strategy is unclear when the oxygen-delivery system is profoundly deficient, as with severe anemia. In this patient, truncal active external rewarming with a forced-air system, heated inhalation, and slow warmed transfusion yielded a 1.5 degrees C x h(-1) rate of rewarming and a good outcome. We discuss the numerous protective and detrimental factors affecting oxygenation and ventilation during hypothermia coupled with profound anemia and the possible etiologic explanations for coexistent hypothermia and pancreatitis.
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PMID:Hypothermia with profound anemia and pancreatitis. 1653 43

We report a 54-year-old male patient with arteriovenous malformation located at the common bile duct and hereditary hemorrhagic telangiectasia. The patient was treated as gallstone pancreatitis at first. Three days after endoscopic nasobiliary drainage (ENBD) for biliary drainage to subside gallstone pancreatitis, hemobilia was drained from the ENBD tube and the serum hemoglobin level gradually decreased. Cholangioscopy and angiography revealed that hemobilia was due to a small arteriovenous malformation located at the common bile duct. Subsequently, the patient was successfully treated by endovascular intervention.
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PMID:Small arteriovenous malformation of the common bile duct causing hemobilia in a patient with hereditary hemorrhagic telangiectasia. 1802 22

A 7-year-old girl with severe hereditary pancreatitis underwent total pancreatectomy. A total of 160,000 islet equivalents (6400 islet/kg) were transplanted to the brachioradialis muscle of the right forearm. Her plasma C-peptide level was undetectable after pancreatectomy but increased to 1.37 ng/mL after 17 days; at this time point, her insulin requirement was 0.75 units of insulin/kg/day. At 5- and 27-months, her hemoglobin A1c (HbA1c) and insulin requirements were 4.5 and 5.3% and 0.3 and 0.18 units/kg/day, respectively. Basal and stimulated C-peptide levels were 0.67 +/- 0.07 and 3.36 +/- 1.37 ng/mL, respectively. Stimulated insulin levels were 30% higher in the islet-bearing arm compared to the contralateral arm after glucagon stimulation. After surgery and islet transplantation, the quality of life improved dramatically and she gained 8 kg of weight. In summary, a normal HbA1c, a low insulin requirement and the absence of recurrent hypoglycemia and the gradient of insulin between the arms indicate that the intramuscularly transplanted islets contribute to a long-term clinically significant metabolic control.
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PMID:Intramuscular autotransplantation of pancreatic islets in a 7-year-old child: a 2-year follow-up. 1809 67

During the last 100 years in medical literature, there are only 54 reports, including the report of Pasaoglu et al (World J Gastroenterol 2008; 14: 2915-2916), with clinical descriptions of agenesis of the dorsal pancreas in humans. Agenesis of the dorsal pancreas, a rare congenital pancreatic malformation, is associated with some other medical conditions such as hyperglycemia, abdominal pain, pancreatitis and a few other diseases. In approximately 50% of reported patients with this congenital malformation, hyperglycemia was demonstrated. Evaluation of hyperglycemia and diabetes mellitus in all patients with agenesis of the dorsal pancreas including description of fasting blood glucose, oral glucose tolerance test, glycated hemoglobin and medical treatment would be a future goal. Since autosomal dominant transmission has been suggested in single families, more family studies including imaging technologies with demonstration of the pancreatic duct system are needed for evaluation of this disease. With this letter to the editor, we aim to increase available information for the better understanding of this rare disease.
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PMID:Agenesis of the dorsal pancreas. 1847 21


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