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)

A 7-year experience with radiography-guided blockade of the celiac ganglia in patients suffering from pancreatic pain is described; 36 patients had carcinoma of the pancreas and nine had chronic pancreatitis. The importance of fluoroscopic guidance of deposition of the blocking agent is stressed. The success rate of this procedure is similar to operative intervention for interruption of the pathways of pain conduction. Radiography-guided celiac ganglion block along with enzymatic substitution for increasing pancreatic insufficiency are recommended for effective palliative treatment.
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PMID:Relief of pancreatic pain by radiography-guided block. 9 85

Cimetidine, a new histamine H2-receptor antagonist (H.H2.R.A.) is a potent inhibitor of basal and stimulated gastric acid secretion. Contrary to anticholinergics, it does not affect gastric emptying nor does it decrease lower oesophageal sphincter pressure; cimetidine may therefore be used as the treatment of reflux oesophagitis. After prolonged administration of currently used therapeutic doses, basal and post-prandial serum gastrin levels remain unchanged and the parietal cell mass is not increases. Cimetidine toxicity is very low. Cimetidine is effective in promoting healing and pain relief of gastric and duodenal ulcer. In the latter long-term treatment for prevention of relapse is efficient, but the appraisal of its safety remains debated. Efficiency of H.H2.R.A. in the prophylaxis of gastrointestinal haemorrhage in patients with fulminant hepatic failure has been proven. Furthermore, cimetidine has a dramatic ability to control haemorrhage from acute erosive lesions in any seriously-ill patient. It may also be of benefit in the treatment of bleeding from gastric or duodenal ulcer and, whatewer the lesion, in the prevention of bleeding recurrence. In the Zollinger-Ellison syndrome, good results have been obtained but cimetidine treatment must be decided and supervised only by well-informed specialists. Lastly, in patients with severe exocrine pancreatic insufficiency, cimetidine prevents gastric degradation of orally administered pancreatic extracts and decreases steatorrhea.
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PMID:[Cimetidine. Clinical pharmacology and toxicity (author's transl)]. 35 5

A retrospective study of 49 patients with chronic obstructive and chronic calcific pancreatitis is presented. All patients were operated upon and underwent either a partial pancreatectomy or internal drainage of the ductal system into a Roux-en-Y loop of jejunum. The criteria for selection of operation are discussed, and the follow-up of the two operative groups is given. In patients selected as described, internal drainage provided better relief of pain and was accomplished with a lower operative mortality and morbidity and with less postoperative pancreatic insufficiency.
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PMID:Surgery for chronic pancreatitis. Drainage versus resection. 44 18

After Whipple operations, follow-up examinations were conducted under hospital conditions in order to investigate the function of the remainder of the pancreas and the extent to which general health was adversely affected. General parameters such as vocational rehabilitation, history of pain, and weight were analyzed, as well as chemistry related to the severity of pancreatic malassimilation, e.g., stool weight, stool fat contents, fat utilization, chymotrypsin in stool, and PABA test. An exocrine pancreatic insufficiency was found in 80% of patients, but this was easily manageable using medications, sometimes in combination with a MCT fat diet. Subclinical diabetes mellitus was shown in 80% of patients using glucose tolerance tests. However, clinical manifestations of diabetes did not occur.
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PMID:[Function of the residual pancreas following partial duodeno-pancreatectomy]. 45 44

Information from 72 patients from 7 families in England and Wales confirms that hereditary pancreatitis is inherited as an autosomal dominant conditions with limited penetrance. The degree of penetrance is approximately 80%. These patients have had recurrent attacks of abdominal pain starting from childhood or young adult life. The mean age of onset in the 7 families studied was 13.6 years. There were two peaks, with maximum numbers at 5 years and 17 years. The second peak was thought to represent genetically susceptible individuals having pain brought on by alcohol rather than representing evidence of genetic heterogeneity. Five of the 7 families had members with both childhood and adult ages of onset. Only 4 patients out of 72 had life-threatening disease and in the majority of cases the attacks of pain were of nuisance value only. Hereditary pancreatitis was implicated in only 1 patient's death and this was not definite. Patients appear to get better after a period of symptoms usually as they approach middle age, or after a severe attack. In older patients alcohol, emotional upsets, and fatty food appear to precipitate attacks. Pancreatic insufficiency (5.5%), diabetes mellitus (12.5%), pseudocysts (5.5%), and haemorrhagic pleural effusion are uncommon complications. Portal vein thrombosis occurred definitely in 2 patients and was suspected in 3 others. Carcinoma of the pancreas was not found in any of 72 patients studied in detail; however, 2 members from a family not visited personally had chronic pancreatitis and malabsorption going on to carcinoma. They may have suffered from a different disease. Genetic linkage information was too slight for many definite conclusions. However, there was no suggestion of linkage with any of the markers tested.
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PMID:Hereditary pancreatitis in England and Wales. 67 83

105 patients with intractable pain due to chronic pancreatitis were selected for treatment by lateral pancreatico-jejunostomy (according to the procedure of Partington Rochelle) after pre operative endoscopy had revealed a dilatation of the main pancreatic duct (mean : 6 mm). Pancreatico-jejunostomy was the unique procedure in 59 patients; it was associated with a biliary or duodenal diversion in 46 others patients. 2 patients died post-operatively and 12 required a second operation some years subsequent to the pancreatic drainage, for biliary stenosis due to the progress of the sclerosis. 8 of the 22 late death were in direct relation with the persistence of alcohol intake and 4 others died from an extra pancreatic cancer. Peptic ulcer complicating pancreatico-jejunostomy appeared in three patients and two of them died from hemorrhage. Mean observation time was 65 years. Long term results were excellent or improved in 93.4% what pain relief concern, but the progression of exocrine or endocrine pancreatic insufficiency indicates that decompression of the dilated pancreatic duct does not prevent continuing destruction of pancreatic glandular tissue. In spite of these good results, the rational for duct drainage as a mean to decrease the intraductal pressure secondary to stricture is unclear. Neither the patency of the anastomosis, nor the presence or not of pancreatic lithiasis or the size of the dilated pancreatic duct seem to be crucial for pain relief after pancreatico-jejunostomy. Notwithstanding of the dubiousness of the mechanism of action of the drainage procedure, pancreato-jejunostomy remains the most effective procedure for relief of pain in chronic pancreatitis with dilated duct.
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PMID:[Role of pancreaticojejunostomy in the treatment of chronic pancreatitis. A study of 105 operated patients]. 181 18

Potentialities of current chemotherapy of chronic pancreatitis are delineated. An individual approach is advocated for patients with the primary and secondary disease varying in etiology, for those with and without external and internal pancreatic insufficiency. Indications are validated for application of drugs distinct from each other by mechanism of action and intended for pain relief, of kallikrein-protease and other trypsin inhibitors, replacement polyenzymatic therapy, stimulators of pancreatic exocrine secretion, antihistamine drugs, parenteral feeding, vitamins, detoxicating, immunomodulating and psychopharmacological agents. Approaches to management of chronic pancreatitis and its complications as well as associated diseases are detailed. Chronic pancreatitis sufferers must be followed up and undergo prophylactic treatment.
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PMID:[Drug therapy of chronic pancreatitis]. 187 77

The goals of treatment with pancreatic extracts in patients with chronic relapsing pancreatitis are twofold: pain relief and control of maldigestion caused by exocrine pancreatic insufficiency. Experience with the use of pancreatic enzymes for analgesic purposes suggests that the less severe the pain, the greater the analgesic effect of these enzymes. However, the number of trials, as well as the number of patients treated, is fairly small and more studies in larger patient populations are needed. The use of pancreatic enzymes for maldigestion owing to exocrine pancreatic insufficiency which is secondary to chronic pancreatitis, pancreatectomy, cystic fibrosis, or GI bypass surgery incurs several problems. These problems are primarily caused by gastric inactivation of the enzymes, low enzyme activity of many commercial preparations and/or poor patient compliance. Treatment with conventional enzyme products (powdered extracts, enteric-coated tablets or capsules) has been disappointing. At best, results were inconsistent, showing a high degree of individual variation. The introduction of enzyme preparations in the form of pH-sensitive enteric-coated microspheres in hard gelatin capsules represents a significant advance. These microspheres are superior to conventional enzyme preparations in improving the symptoms of pancreatic insufficiency, particularly steatorrhea, where low doses of microspheres are as effective as large doses of conventional enzyme preparations. Steatorrhea, however, is rarely completely resolved. In cases refractory to therapy, treatment with the combination of pH-sensitive enteric-coated microspheres and H2-antagonists or prostaglandins has met with some success.
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PMID:Management of chronic pancreatitis. Focus on enzyme replacement therapy. 270 47

Pancreatic enzyme therapy may be beneficial to all patients with chronic pancreatitis, even those in whom the condition is very mild. The goal of enzyme therapy should be to restore normal gastrointestinal physiology as completely as possible. Monitoring of body weight is recommended as the main measure of treatment efficacy. Most pancreatic enzyme preparations presently employed are porcine in origin and must meet certain standards of quality for human consumption. The amount of active lipase in the duodenum determines the quantity of enzymes to be given. An appropriate diet is also important for relieving symptoms of pancreatic insufficiency and improving nutritional status. Although administration of large amounts of proteases has provided pain relief in some patients, the rationale for using enzymes to relieve pain in chronic pancreatitis has not been generally accepted. Gastric acid plays a role in malabsorption, since administered enzymes may be destroyed by gastric acid. Also, acidic conditions in the duodenum decrease the efficacy of pancreatic enzymes administered with meals. Histamine-H2-receptor antagonists may decrease gastric acidity but there are certain drawbacks to long-term use of these agents. The use of enteric-coated microspheres overcomes many of the problems associated with enzyme destruction. Patients with chronic pancreatitis display considerable individual variation in their treatment requirements. Therapy must be tailored to meet the need for adequate disease control as well as for social and emotional acceptability by the patient. The attending physician and the patient share the responsibility for maintaining appropriate therapy.
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PMID:Theory and practice in the individualization of oral pancreatic enzyme administration for chronic pancreatitis. 270 51

A 43-year-old man presented with loose stools, abdominal pain and a weight loss of 15 kg. Investigations revealed a pancreatic insufficiency and an enteropathy with villous atrophy. Coeliaki was suspected. In spite of treatment with a gluten-free diet in hospital the patient did not improve and the villous atrophy remained unchanged. Other causes than coeliaki to villous atrophy were ruled out. The patient had a heavy consumption of alcohol and after prolonged abstinence the patient gained weight, the pain disappeared and the stools were normalized. The jejunal biopsy was now normal. This case report raises the possibility that enteropathy and villous atrophy may be causally related to alcohol overconsumption.
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PMID:Can villous atrophy be induced by chronic alcohol consumption? 226 54


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