Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis has been suggested as a model for acute pancreatitis (AP), which allows evaluation of early alterations in the time course of the disease. The influence of the clinical course on procalcitonin (PCT), serum amyloid A (SAA), and several proinflammatory and inhibitory cytokines was evaluated in patients with AP following ERCP. Blood samples were prospectively collected from patients undergoing ERCP. The incidence of ERCP-induced pancreatic damage, defined as abdominal complaints, a threefold increase of serum lipase, and elevation of CRP from <10 to >20 mg/liter was 12.8% (12/94). Only mild clinical courses of acute pancreatitis were observed. PCT significantly increased in subjects with post-ERCP pancreatitis after 24 hr. However, PCT levels did not exceed 0.5 ng/ml in any patient. Interleukin-1 receptor antagonist (IL-1RA) began to differ from baseline 2 hr after ERCP, followed by interleukin-6 (IL-6, 6 hr), solubilized tumor necrosis factor-alpha receptor II (sTNF-alphaRII, 24 hr) and SAA (24 hr). Interleukin 10 (IL-10) showed marked interindividual variations with no obvious peak. Among all parameters evaluated, only peak values of IL-6 and IL-10 showed significant correlations with the reported pain score (r2 = 0.62/0.78), degree of ampullar irritation (r2 = NS/0.87), and the duration of ERCP (r2 = 0.58/0.76). No correlation was found with the volume of the injected contrast agent. We conclude that IL-10 and IL-6 appear to be useful to monitor patients after ERCP. The absence of any PCT elevation in the present study is in accordance with the clinical course of the patients who suffered from mild pancreatic damage without systemic or infectious complications.
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PMID:Diagnostic relevance of interleukin pattern, acute-phase proteins, and procalcitonin in early phase of post-ERCP pancreatitis. 972 66

A 33 years old woman presented with cramp-like abdominal pain. Ultrasound examination revealed multiple lesions in the liver of hyper- and hypoechoic echogenicity which in accordance to subsequently performed computed tomography and dynamic hepatobiliary scintigraphy were considered to be a focal nodular hyperplasia (FNH). A severe increase of the serum lipase concentration, suspected to be an acute pancreatitis, was treated conservatively and led to a short improvement of symptoms. Some months later, a severe progression of the pain symptoms occurred, along with a measurable expansion of the abdominal circumference and palpable tumors of the liver. The dynamic hepatobiliary imaging and the static liver scan showed a decreased perfusion and function of the nodes as well as a reduced RES activity, respectively. A subsequently performed Positron Emission Tomography (PET) with F-18-Fluorodeoxyglucose (FDG) showed a massively increased glucose metabolism of the liver tumors. The histologic result of several biopsies of the tumors revealed metastases of an acinus cell carcinoma of the pancreas. Under systemic and local chemotherapy, a temporary remission could be obtained that was clearly detectable in a second FDG-PET. Nevertheless, during the further course of the disease, a progression occurred being detectable in an additional control PET-study by an increase in tumor size as well as in tumor glucose metabolism. The patient died in liver coma 15 months after the histologic diagnosis was obtained.
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PMID:[Long-term follow-up and therapeutic control of a hepatic metastatic acinar cell carcinoma of the pancreas using FDG PET]. 972 47

Therapy of chronic pancreatitis rests on five arms: Avoidance of alcohol, treatment of pain, replacement therapy for exocrine and endocrine insufficiency and adequate nutrition. Alcohol withdrawal improves pain and the patient's compliance. It also seems to retard the chronic inflammatory process. Therapy of pain depends on the pathomechanism of pain. There is a lack of prospective, controlled studies comparing various treatment regimens. Thus, treatment options are partly dependent on the experience of the physician taking care of the patient and include i.e. for pseudocysts: surgical vs percutaneous or endoscopic drainage; for stenosis of the main pancreatic duct close to the papilla: surgical vs endoscopic drainage (stents); for distal bile duct stenosis: endoscopic stents vs biliodigestive anastomosis vs pancreatic head resection; for pancreatic stones: extracorporal shock wave lithotripsy followed by endoscopic stone extraction vs surgery (pancreaticojejunostomy), finally for inflammatory tumor of the pancreatic head combined with pain with or without compression of the distal bile duct or duodenum: duodenum-preserving pancreatic head resection vs Whipple resection. Patients with pain resistant to medical treatment may be candidates for a transcutaneous blockade of the plexus coeliacus or for epidural nerve blockade before one choses a surgical procedure. Application of pancreatic enzymes does not seem to have a major beneficial effect on pancreatic pain. Modification of nutrition has become less restrictive. Thanks to improved substitution with acid resistant porcine pancreatic extracts with high lipase activity, fat restriction is no longer of paramount importance. However, supply with sufficient calories is still difficult due to pain, inadequate compliance and hypermetabolism.
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PMID:[Chronic pancreatitis: nutrition and pain therapy]. 985 67

Gastrointestinal bleeding and increased intestinal permeability have been observed in marathon runners. We sought to determine if L-arginine would be useful for prevention of these complications. Twenty-three runners were randomized to receive L-arginine (A) or glycine (placebo) (G), 10 grams 3 times daily for 14 days prior to the 1997 Houston-Methodist Marathon. Serum, stool hemoccults and lactulose:mannitol permeabilities were obtained at baseline, immediately after completion of the marathon and approximately 48 hours later. Runners rated their symptoms of nausea and vomiting, belching and indigestion, abdominal pain and bloating, diarrhea, and extremity pain on a 1-5 scale of increasing severity. The L:M was unchanged in either group during the three collections. Occult bleeding occurred in 8%/20% in A and G groups, respectively, p = NS) immediately post-marathon. No runners had occult bleeding 48 hours post-race. Gastrointestinal symptom scores were minimal to nonexistent. Extremity pain scores were similar for groups A and G (2.1+/-1.4 and 2.8+/-1.6, respectively, (p = NS). Fluid intake was similar between both groups (1875+/-1547 vs. 1506+/-970 ml, p = NS). Serum amylase was normal at baseline and remained virtually unchanged. Serum lipase was normal at baseline and immediately post-race in both groups, but increased at 48 hours post-race (82.2+/-34.3 to 121.5+/-53.3 mg/dl [A], p = 0.02 and 114.3+/-55.7 to 181.9+/-162.2 mg/dl [G], p = 0.09). CPK increased significantly and similarly in both groups immediately post-race, and even more dramatically 48 hours post-race (130.3+/-130.8 to 738.8+/-902.9, p = 0.007 to 1966.5+/-3.166.0 mg/dl [A] and 140.9+/-77.9 to 863.0+/-772.3, p = 0.003 to 5619+/-10636.8mg/dl [G]). Modest post-race decreases were seen in most serum amino acids in both groups. Finish times were longer than predicted (23+/-21 and 9+/-7 min for A and G groups, respectively, p = 0.049). Our study failed to show a clear benefit of arginine supplementation for the prevention of intestinal ischemia/reperfusion injury associated with endurance running, but either a detrimental affect on performance with arginine, or enhanced performance with glycine. Skeletal muscle injury was unaffected by arginine or glycine supplementation. The delayed increase in serum lipase suggests mild pancreatic injury, affected by either arginine or glycine supplementation.
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PMID:The effect of arginine or glycine supplementation on gastrointestinal function, muscle injury, serum amino acid concentrations and performance during a marathon run. 1045 29

Recently an ELISA using specific antibodies to detect elastase-1 in serum has become available. Earlier studies using a radioimmunoassay reported a prolonged elevation of serum elastase as compared to other pancreatic enzymes in acute pancreatitis. The aim of the present study was to compare the changes of serum levels of ELISA-elastase-1, lipase and amylase in acute pancreatic damage following ERCP. Blood samples were prospectively collected at five time points before and after the endoscopic procedures in 212 patients. Samples were analyzed for pancreatic serum enzymes, acute phase proteins and routine parameters. A pain score was used for clinical evaluation. Relevant post ERCP pancreatic damage was defined as CRP elevation from < 10 mg/l to > 10 mg/l in the presence of persistent abdominal pain without laboratory evidence of cholangitis and without clinical or laboratory signs of pancreatitis before the endoscopic procedures. Elastase-1 time course paralleled the courses of lipase and amylase peeking at six hrs. There was no prolonged elevation of elastase-1. Ten out of 204 patients (4.9%) were found to have relevant pancreatic damage. Depending on the cut off point used, sensitivity/specificity were as follows: lipase 80-100%/30.9-71.6%; amylase 70-90%/44.3-88.7%; elastase-1 60-90%/64.9-81.4%. In conclusion ELISA-elastase-1 is a marker of acute pancreatic damage similar to lipase and amylase. Although elastase-1 may show a better specificity than the other enzymes, this seems to be a matter of definition of the normal range. The determination of serum ELISA-elastase-1 does not provide additional information in acute pancreatic damage as compared to a combination of lipase and amylase.
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PMID:Determination of elastase-1 serum levels in post ERCP/EST pancreatic damage. 1049 4

Pancreatic enzyme replacement therapy has proved useful in the treatment of malabsorption and persistent pain in patients with chronic pancreatitis. The formulation of pancreatic enzyme preparation varies considerably. Treatment of chronic pain is facilitated by the use of a high-protease enzyme preparation, preferably non-microsphere encoated. Treatment of steatorrhea is optimized by use of high-lipase-containing preparations.
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PMID:Enzymatic therapy in patients with chronic pancreatitis. 1050 44

Chronic pancreatitis is characterized by progressive and irreversible loss of pancreatic exocrine and endocrine function. In the majority of cases, particularly in Western populations, the disease is associated with alcohol abuse. The major complications of chronic pancreatitis include abdominal pain, malabsorption, and diabetes. Of these, pain is the most difficult to treat and is therefore the most frustrating symptom for both the patient and the physician. While analgesics form the cornerstone of pain therapy, a number of other treatment modalities (inhibition of pancreatic secretion, antioxidants, and surgery) have also been described. Unfortunately, the efficacy of these modalities is difficult to assess, principally because of the lack of properly controlled clinical trials. Replacement of pancreatic enzymes (particularly lipase) in the gut is the mainstay of treatment for malabsorption; the recent discovery of a bacterial lipase (with high lipolytic activity and resistance to degradation in gastric and duodenal juice) represents an important advance that may significantly increase the efficacy of enzyme replacement therapy by replacing the easily degradable porcine lipase found in existing enzyme preparations. Diabetes secondary to chronic pancreatitis is difficult to control and its course is often complicated by hypoglycaemic attacks. Therefore, it is essential that caution is exercised when treating this condition with insulin. This paper reviews recent research and prevailing concepts regarding the three major complications of chronic pancreatitis noted above. A comprehensive discussion of current opinion on clinical issues relating to the other known complications of chronic pancreatitis such as pseudocysts, venous thromboses, biliary and duodenal obstruction, biliary cirrhosis, and pancreatic cancer is also presented.
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PMID:Chronic pancreatitis: complications and management. 1050 49

A 51 year old man presents with a short history of acute onset severe upper abdominal pain. It is predominantly epigastric, radiating to the back. The pain is exacerbated by lying flat, improves on sitting upright, and is associated with nausea and vomiting. Both serum amylase and serum lipase levels are elevated. A CT scan of the abdomen was performed (Figures 1, 2).
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PMID:Imaging of pancreatitis. 1056 97

The medical treatment has an important role in patients with chronic pancreatitis. Pain is the most frequent symptom, at least in the initial phases of the disease. In about 60% of patients it can be successfully treated by medical therapy; in the remaining 40% it requires surgery. Malabsorption of fat and protein and diabetes usually appear in the advanced stages of the disease. The treatment of these complications is based on the administration of pancreatic extracts and insulin. There are several types of pancreatic extracts; the most useful are those with high lipase content and high lipase-protease ratio. Moreover, they should be protected against gastric acid and should have a gastric emptying simultaneously with chyme, with a rapid liberation of enzymes into the duodenum. The treatment of diabetes usually requires low-moderate doses of insulin. Diabetic ketoacidosis is rare, while microvascular changes have the same frequency as in type 1 diabetes.
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PMID:Medical treatment of chronic pancreatitis. 1082 21

Severe acute necrotizing pancreatitis is a disease that is caused by premature activation of pancreatic enzymes. Cytokine release contributes to systemic manifestations such as systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome (MODS), adult respiratory distress syndrome (ARDS), and sepsis. Diagnosis is based on a history of abdominal pain, laboratory values such as serum amylase and lipase levels, and CT scan. Medical management focuses on fluid and electrolyte balance, antibiotic therapy, pain control, and decreasing systemic complications. Surgery is indicated when infectious pancreatic necrosis has been identified. This article addresses incidence and etiology; pathophysiology; clinical manifestations; diagnostics; and medical and surgical patient care management.
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PMID:Necrotizing pancreatitis: pathophysiology, diagnosis, and acute care management. 1086 31


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