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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic pancreatitis should be considered in all patients with unexplained abdominal pain. Management of abdominal pain in these patients continues to pose a formidable challenge. The importance of small duct disease without radiographic abnormalities is now a well-established concept. It is meaningful to determine whether patients with chronic pancreatitis have small duct or large duct disease because this distinction has therapeutic implications. Diagnostic evaluation should begin with simple noninvasive and inexpensive tests like serum trypsinogen and fecal elastase, to be followed where appropriate by more complicated measures such as the secretin hormone stimulation test, especially in patients with suspected small duct disease. No universal causal treatment is available. Non-enteric-coated enzyme preparations are useful for treatment of pain, whereas enteric-coated enzyme preparations are preferred for steatorrhea. Octreotide is used increasingly for abdominal pain that is unresponsive to pancreatic enzyme therapy. When medical therapy for chronic pancreatitis pain has failed, endoscopic therapy, endoscopic ultrasound-guided celiac plexus block, and thoracoscopic splanchnicectomy, performed by experts, may be considered for a highly selected patient population. Surgical ductal decompression is appropriate in patients with considerable pancreatic ductal dilation. The role and efficacy of cholecystokinin-receptor antagonists, antioxidants, and antidepressant drugs remain to be defined.
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PMID:Medical therapy for chronic pancreatitis pain. 1263 50

In the past year, numerous important papers were published on chronic pancreatitis, its causes, and its diagnosis; the cause of fibrosis; and pain in pancreatic cancer. More than 750 mutations have been described in the cystic fibrosis transmembrane regulator (CFTR) gene. Some mutations cause relatively mild reductions in CFTR function and may lead to disease in one organ without clinical involvement of other organs. Two groups of investigators recently reported that "idiopathic" chronic pancreatitis may be the sole manifestation of some CFTR mutations. Some recent reports may enhance our understanding of pancreatic fibrogenesis and may lead to therapies for painful chronic pancreatitis. Pancreatic stellate cells are vitamin A-containing cells that resemble hepatic stellate cells and were recently isolated from rat and human pancreas. They respond to inflammatory cytokines by producing collagen. Two studies show that endoscopic ultrasonography (EUS) correlates well with endoscopic retrograde cholangiopancreatography in moderate to severe chronic pancreatitis. However, in patients who have a few nondiagnostic abnormalities on EUS, these results have poor correlation with the results of endoscopic retrograde cholangiopancreatography and the secretin test. The clinical significance of these abnormalities is unclear, and the diagnosis of chronic pancreatitis should not be based on EUS findings alone. Painful chronic pancreatitis is a complex and difficult management problem. A recent study of alcoholic chronic pancreatitis suggests that the best predictors of pain relief are an intermittent pattern of pain and the presence of surgically correctable complications (eg, pseudocysts or biliary obstruction). An American Gastroenterological Association technical review of painful chronic pancreatitis emphasized the lack of controlled studies supporting any form of therapy. Further evidence that longstanding chronic pancreatitis is a premalignant condition has been provided by recent epidemiologic, pathologic, and molecular biology studies.
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PMID:Chronic pancreatitis. 1702 80

The pathogenesis of idiopathic chronic pancreatitis remains poorly understood despite the high expectations for ascribing the pancreatic damage in affected patients to genetic defects. Neither mutations in the cationic trypsinogen gene nor mutations of the cystic fibrosis conductance regulator gene account for the chronic pancreatitis noted in most patients with idiopathic chronic pancreatitis. Attempts to find an autoimmune basis for the pancreatitis in these patients have not been very successful. The diagnosis of small duct idiopathic chronic pancreatitis remains a great source of frustration for clinicians. Such patients with negative results of radiographic studies often cannot be diagnosed unless a hormone stimulation test such as a secretin test is performed. Although the porcine biologic form of secretin, which has been used to diagnose chronic pancreatitis, became unavailable because of widespread use in the treatment of children with autism, a synthetic form of porcine secretin has now been approved by the US Food and Drug Administration and is available. The true value of endoscopic ultrasonography in diagnosing small duct chronic pancreatitis remains to be fully defined. Endoscopic ultrasonography is becoming the test of choice in detecting radiographic abnormalities in both the parenchyma and ducts of the pancreas. Endoscopic ultrasonography-guided celiac plexus block can be performed relatively easily and very safely. It can provide excellent short-term pain relief in some patients, but reliable predictors of which patients will be successful with this therapy are not yet available. Because long-term follow-up data on the use of endoscopic ultrasonography in this respect are not available, and because the pain of chronic pancreatitis is, indeed, chronic, the role of endoscopic ultrasonography-guided celiac plexus block should be limited to treating those patients with chronic pancreatitis whose pain has not responded to other modalities.
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PMID:Chronic pancreatitis. 1703 33

Pancreas divisum (PD), the most common congenital variant of pancreatic duct anatomy, occurs when the ductal systems of the ventral and dorsal pancreatic ducts fail to fuse during the second month of gestation. With non-union of the ducts, the major portion of the pancreatic exocrine secretion enters the duodenum by way of the dorsal duct and minor papilla. It has been generally accepted that a relative obstruction to pancreatic exocrine secretory flow through the minor duct and minor papilla could result in pancreatitis in small numbers of patients with PD. The debate whether PD causes pancreatitis continues, although most authorities agree that PD is a definite cause in a subgroup of patients. Most patients with PD and well-documented acute recurrent pancreatitis have responded favorably to surgical sphincteroplasty of the minor papilla. Endoscopic retrograde cholangiopancreatography (ERCP) is the most common procedure for diagnosis PD in patients who have pancreatobiliary symptoms. MRCP is being increasingly used to establish the diagnosis and secretin stimulation can improve ductal images greatly. Endoscopic management of symptomatic patients with PD is evolving. Only a limited number of series are available, using endoscopic pancreatic stent placement, minor papilla endoscopic papillotomy, or both to decompress the dorsal duct in an effort to restore pancreatic exocrine secretory flow. Even with relatively small numbers of patients and a near absence of controlled, randomized trials, it appears that the patients most likely to benefit, as with surgery, are those with well-documented ARP rather than pain alone or chronic pancreatitis. Overall we recommend that pancreatic stenting and pancreatic sphincterotomy should be done only in large centers with experience in therapeutic ERCP. Further randomized trials would be of interest.
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PMID:[State-art: diagnosis and management in pancreas divisum]. 1746 16

Sphincter of Oddi dysfunction (SOD) is a poorly-understood disorder, typically presenting as postcholecystectomy, "biliary-type," right-sided abdominal and/or chest wall pain. Most patients referred to specialist clinics for work-up of presumed SOD do not, in fact, have anything wrong with their bile ducts or biliary sphincter mechanisms. A careful history and focused physical examination will often identify the true source of the pain syndrome, ranging from chest wall costochondritis and nerve injury at surgical trochar sites, to gastroparesis and visceral hypersensitivity ("irritable bowel"). The Rome III classification of functional gallbladder and biliary disorders defines SOD as episodic (not daily) pain lasting more than 30 min, which is disruptive of normal activities and not associated with bowel upset. It is not relieved by gastric acid suppression or antispasmodics. Other causes of abdominal pain must be excluded. Standard work-up includes endoscopic retrograde cholangiopancreatography (ERCP) with biliary manometry, which risks post-ERCP pancreatitis, especially in young women with normal bile ducts and liver serology. Noninvasive tests for SOD, such as timed ("gated") cholecystokinin (CCK)-stimulated hepatobiliary iminodiacetic acid (HIDA) scans and secretin-stimulated magnetic resonance cholangiopancreatography, are imperfect and still evolving. Although many doubt the very existence of SOD, a multidisciplinary approach to the management of pre- and postcholecystectomy abdominal pain syndromes is long overdue.
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PMID:Sphincter of Oddi dysfunction. 2042 85

Pituitary adenylate cyclase-activating peptide-38 (PACAP38) and vasoactive intestinal peptide (VIP) belong to the same secretin-glucagon superfamily and are present in nerve fibers in dura and skin. Using a model of acute cutaneous pain we explored differences in pain perception and vasomotor responses between PACAP38 and VIP in 16 healthy volunteers in a double-blind, placebo-controlled, crossover study. All participants received intradermal injections of 200 pmol PACAP38, 200 pmol VIP and placebo into the volar forearm. Measurements included pain intensity on a visual analog scale (VAS), blood flow by laser Doppler flowmetry, visual flare and wheal. Pain intensities after PACAP38 and VIP were mild and limited to a short time of about 100 s after injection. The area under the VAS-time curve was larger following PACAP38 (P = 0.004) and VIP (P = 0.01) compared to placebo. We found no statistical difference in pain perception between PACAP38 and VIP. Skin blood flow increase, flare and wheal were larger after both PACAP38 (P = 0.011) and VIP (P = 0.001) compared to placebo. VIP induced a considerably larger increase in skin blood flow, flare and wheal than PACAP38 (P = 0.002). In conclusion, we found that peripheral nociceptive cutaneous responses elicited by PACAP38 and VIP are similar in healthy volunteers. This suggests that acute pain and vasomotor responses following intradermal injections of PACAP38 and VIP are primarily mediated by VPAC receptors.
J Headache Pain 2010 Aug
PMID:Cutaneous nociception and neurogenic inflammation evoked by PACAP38 and VIP. 2045 93

The most important advances in chronic pancreatitis concern its etiopathogenesis, nutritional aspects, and improvements in diagnostic techniques and some treatment options. In the etiopathogenesis of this disease, the importance of smoking and its association with alcohol have been confirmed. Exocrine pancreatic insufficiency (EPI) secondary to chronic pancreatitis is associated with bone metabolism alterations (osteopenia and osteoporosis), a reduction in liposoluble vitamins and alterations in essential amino acid levels. Endoscopic ultrasound has been confirmed as the most highly developed technique for the diagnosis of chronic pancreatitis, especially due to new image optimization technologies. Breath tests for the diagnosis of EPI continue to be developed (optimization of the C-13 mixed triglyceride test and the development of a new test based on C-13-labelled bicarbonate determination). Modest results in pain treatment have been achieved with the use of antioxidants, pancreatic enzymes and/or intravenous secretin. The association of chronic pancreatitis with pancreatic cancer requires strict follow-up, especially in patients with inflammatory masses in the context of chronic pancreatitis.
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PMID:[Latest advances in chronic pancreatitis]. 2301 13

This review describes the history of secretin discovery, identification, purification, and structural determination; cloning of secretin and its receptor; synthetic secretin; and highly specific and sensitive radioimmunoassay to define the characteristic physiological role on postprandial pancreatic fluid and bicarbonate secretion, which requires robust potentiation by cholecystokinin. Secretin plays a key role in the negative and positive regulatory mechanisms of exocrine pancreatic secretion. Secretin-releasing peptides were discovered in duodenal acid perfusates of both rat and dog and in canine pancreatic juice. The release and action of secretin and secretin-releasing peptides are in part mediated via vagovagal reflex mechanism involving afferent sensory neurons in proximal intestine and efferent cholinergic neurons in the pancreas. Besides acetylcholine, many neurotransmitters or neuromodulators influence release and action of secretin. The action of secretin in the pancreas depends on insulin, which also suppresses local release of somatostatin and pancreatic polypeptide. Thus, release and action of secretin are mediated via neurohormonal interaction. Clinical conditions with hypersecretinemia and hyposecretinemia are discussed. Synthetic human secretin is used for studies of exocrine pancreatic secretion, secretin-enhanced magnetic resonance cholangiopancreatography combined with exocrine pancreatic function test and diagnosis of gastrinoma syndrome. Therapeutic use of secretin is considered for the relief of severe pain in chronic pancreatitis.
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PMID:Secretin: historical perspective and current status. 2451 94

Chronic pancreatitis (CP) is an inflammatory disorder characterized by inflammation and fibrosis, resulting in a progressive and irreversible destruction of exocrine and endocrine pancreatic tissue. Clinicians should attempt to classify patients into one of the six etiologic groups according to the TIGARO classification system. MRI/MRCP, if possible with secretin enhancement, is considered the imaging modality of choice for the diagnosis of early-stage disease.In CP, pain is the most disabling symptom, with a significant impact on quality of life. Pain should be assessed using the Izbicki score and preferably treated using the "pain ladder" approach. In painful CP, endoscopic therapy (ET) can be considered as early as possible. This procedure can be combined with extracorporeal shock-wave lithotripsy (ESWL) in the presence of large (> 4 mm), obstructive stone(s) in the pancreatic head, and with ductal stenting in the presence of a single main pancreatic duct (MPD) stricture in the pancreatic head with a markedly dilated MPD. Pancreatic stenting should be pursued for at least 12 months in patients with persistent pain relief. On-demand stent exchange should be the preferred strategy. The simultaneous placement of multiple, side-by-side, pancreatic stents can be recommended in patients with MPD strictures persisting after 12 months of single plastic stenting. We recommend surgery in the following cases: a) technical failure of ET ; b) early (6 to 8 weeks) clinical failure ; c) definitive biliary drainage at a later time point; d) pancreatic ductal drainage when repetitive ET is considered unsuitable for young patients; e) resection of an inflammatory pancreatic head when pancreatic cancer cannot be ruled out; f) duodenal obstruction. Duodenopancreatectomy or oncological distal pancreatectomy should be considered for patients with suspected malignancy. Pediatricians should be aware of and systematically search for CP in the differential diagnosis of chronic abdominal pain. As malnutrition is highly prevalent in CP patients, patients at nutritional risk should be identified in order to allow for dietary counseling and nutritional intervention using oral supplements. Patients should follow a healthy balanced diet taken in small meals and snacks, with normal fat content. Enzyme replacement therapy is beneficial to symptomatic patients, but also in cases of subclinical insufficiency. Regular follow-up should be considered in CP patients, primarily to detect subclinical maldigestion and the development of pancreatogenic diabetes. Screening for pancreatic cancer is not recommended in CP patients, except in those with the hereditary form.
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PMID:Belgian consensus on chronic pancreatitis in adults and children: statements on diagnosis and nutritional, medical, and surgical treatment. 2476 91

This article summarizes some of the recent and clinically relevant advances in chronic pancreatitis. These advances mainly concern the early diagnosis of the disease, the treatment of symptoms and complications, mainly pain and pancreatic exocrine insufficiency, and the diagnosis and therapy of autoimmune pancreatitis. The multimodal dynamic endoscopic ultrasound-guided secretin-stimulated evaluation of the pancreas provides relevant morphological and functional information for the diagnosis of chronic pancreatitis at early stages. Extracorporeal shock wave lithotripsy in patients with calcifying pancreatitis and endoscopic pancreatic stent placement are effective alternatives for pain therapy in patients with chronic pancreatitis. Presence of pancreatic exocrine insufficiency in patients with chronic pancreatitis is associated with a significantly increase of mortality rate. Despite that, pancreatic enzyme replacement therapy is not prescribed in the majority of patients with pancreatic exocrine insufficiency, or it is prescribed at a low dose. The newly developed and commercialized needles for endoscopic ultrasound-guided pancreatic biopsy are effective in retrieving appropriate tissue samples for the histological diagnosis of autoimmune pancreatitis. Maintenance therapy with azathioprine is effective and safe to prevent relapses in patients with autoimmune pancreatitis.
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PMID:[Latest advances in chronic pancreatitis]. 2652 Feb 1


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