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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with recurrent acute pancreatitis should be treated with the same supportive and symptom-oriented measures as those with acute pancreatitis. The need for specific treatment depends on the cause of the pancreatitis. Patients should discontinue alcohol use, putative causative medications, and exposure to toxins or helminths in endemic areas. Metabolic abnormalities need to be corrected, and appropriate treatment should be initiated for associated infections, autoimmune diseases, vasculitis, and hypercoagulable states. For patients with gallstone pancreatitis, endoscopic retrograde cholangiopancreatography is indicated if biliary obstruction persists or if cholangitis is present. Elective cholecystectomy may be performed in appropriate patients; otherwise, consider biliary sphincterotomy and ursodeoxycholic acid for prevention of recurrent attacks. Transpapillary stenting or sphincterotomy of the minor papilla benefits some patients with pancreas divisum and no other explanation for recurrent pancreatitis. Surgical sphincteroplasty is reserved for those failing endoscopic treatment. Biliary sphincterotomy benefits more than 50% of patients with sphincter of Oddi dysfunction and recurrent acute pancreatitis. Some authors advocate pancreatic sphincter manometry and sphincterotomy for persistent pancreatic segment hypertension in patients who have recurrent pancreatitis after biliary sphincterotomy. In patients with pancreatic duct strictures, transpapillary stent placement serves as a short-term measure; most patients ultimately require surgery.
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PMID:Recurrent Acute Pancreatitis. 1156 Jul 83

Some clinical cases published in literature show that angiotensin-converting enzyme (ACE)-inhibitor administration may cause acute pancreatitis. In this work, the authors report a case of a patient affected by hypertension. Upon admission, the authors started antihypertensive therapy using captopril, which caused an important amylase and lipase rise within 13 days. When the ACE-inhibitor therapy was stopped, a rapid decrease of the serum enzyme was observed within 3 days. The high levels of serum amylase and lipase were linked to neutrophilia but were not associated with relevant symptomatic findings or features of pancreatopathy. The absence of the usual conditions that may cause pancreatitis, such as biliary stasis, hypercalcemia, or alcohol abuse, and the rapid decrease of serum enzyme levels after drug suspension suggested an ACE-inhibitor-induced pancreatitis. This is the first clinical report of an ACE-inhibitor-induced pancreatitis in which captopril administration was found after hospitalization. The drug suspension probably prevented other complications. This case report suggests that, when ACE-inhibitor administration is started, serum amylase and lipase should be monitored in order to prevent acute pancreatitis without waiting for clinical evidence of a pancreatopathy.
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PMID:Angiotensin-converting-enzyme inhibitor administration must be monitored for serum amylase and lipase in order to prevent an acute pancreatitis: a case report. 1157 Jun 65

Gallstone pancreatitis was first recognized as an entity by Opie in 1901 (1), and since then has generated volumes of literature which have attempted to explain its pathophysiology. Multiple animal experiments and human clinical studies in the past thirty years have led to a better understanding of both macro- and microscopic events which lead to pancreatic inflammation in the setting of a passing or impacted gallstone. Evidence suggests that pancreatic duct outflow obstruction is the initial event. Several possible sequelae of duct obstruction, including refluxed biliary-pancreatic secretions, pancreatic duct hypertension, and/or aberrant acinar cell secretion may result in pancreatic duct injury and release of pancreatic enzymes into the glandular interstitium, thus triggering a bout of acute pancreatitis. The details of many events related to gallstone pancreatitis remain unclear; this chapter attempts to present the pathophysiology of this disease as it is known today. Additionally, clinical presentation and treatment of gallstone pancreatitis will be reviewed briefly.
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PMID:Pathophysiology of gallstone pancreatitis. 1157 66

Pancreatic sphincter hypertension (PSH) is one of the causes of recurrent pancreatitis. The diagnosis can be established by direct measurement of pancreatic sphincter pressures at pancreatic sphincter manometry. This procedure is not without risks, and in cases with PSH, it certainly carries a higher risk of post procedure pancreatitis. The treatment of this disorder is pancreatic sphincterotomy, which on its own carries risk of acute pancreatitis. Therefore it is important to establish the diagnosis reliably before undertaking this procedure. In order to overcome the false positive readings that are possible in sphincter manometry, we proposed to use secretin stimulated endoscopic ultrasound (SSEUS) to measure pancreatic ductal response as an adjunctive method to aid and supplement the diagnosis. Here we describe 3 cases in which this was carried out to optimal effect.
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PMID:The use of endoscopic ultrasound and intravenous secretin as an investigative tool to aid diagnosis in pancreatic sphincter hypertension. 1173 88

A cystic fibrosis (CF) heterozygote incidence higher than in the general population has been repeatedly reported in conditions which include clinical features found in CF, like pancreatitis, disseminated bronchiectasis, and allergic bronchopulmonary aspergillosis. Some cases may be explained by an unidentified compound heterozygosity; others could be manifesting heterozygotes. This study was aimed at detecting the incidence of CF-related clinical features in a population of carriers. A group of 261 obligate heterozygotes (mean age, 44 years) and a control group, composed of 201 individuals negative for a standard mutation panel (mean age, 36 years), were surveyed for possibly CF-related conditions (asthma, bronchiectasis, pneumothorax, allergic bronchopulmonary aspergillosis, sinusitis, nasal polyps, gallstones, liver cirrhosis, diabetes, pancreatitis, bone fractures, plus hypertension). A questionnaire was administered, and the accuracy of the statements was evaluated by phone interviews. There was no difference between heterozygotes and controls, with the exception of hypertension (carriers 28/261, controls 7/201, p = 0.004), and, in males, nasal polyps (carriers 7/126, controls 0/102, p value = 0.0178), and, again, hypertension (carriers 17/126, controls 5/102, p value = 0.0407). To avoid age bias, 126 heterozygotes matched to controls of the same gender and age were separately processed: these two groups showed no significant differences. CF-related clinical manifestations in obligate CFTR mutation heterozygotes are not more represented than in individuals with a low risk of being carriers.
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PMID:A pilot survey of cystic fibrosis clinical manifestations in CFTR mutation heterozygotes. 1178 92

The discovery of the kinin system is not recent, but its study in clinical field has been done only in the last years. This system is composed by substrates (kininogens) and plasma and tissue kallikreins are the specific activators of these substrates producing two vasoactive peptides called bradykinin and kallidin. The biologic effects of kinins are mediated by specific receptors called B1 and B2. The activation of this system is particularly important in blood pressure regulation and in inflammatory reactions. The kinin system is involved in many clinical situations including respiratory allergic reactions, septic shock, hypertension and its treatment, hypotensive transfusion reactions, heart diseases, pancreatitis, hereditary and acquired angioedema, Alzheimer's disease and liver cirrhosis with ascites. The study of the kinin system in clinical field, which had been limited by methodological difficulties, has now received an important stimulus by the recent availability of specific and sensitive methods of dosage.
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PMID:[The kinin system: biological mechanisms and clinical implications]. 1182 1

Not only is the renin angiotensin system or its components found morphologically in many organs, it also exerts many different regulatory functions such as contributing to systemic homeostasis as well as to organ-specific regulation. The presence of the components of the renin angiotensin system in the pancreas was discovered only a few years ago. Physiological and pathophysiological stimuli were able to modify, in part, the gene expression and the occurrence of some of these components. Because of the important clinical significance of pancreatic diseases such as pancreatitis, research should follow every traces of the renin angiotensin system in the pancreas: impairment of microcirculation via hypoxia mediated up-regulation with the subsequent further deterioration of the oxygen supply seems to be the most obvious mechanism. There are many possible approaches to a better understanding of problems that are associated with diseases such as different kinds of pancreatitis; basic studies in animal models are oriented toward microcirculation, cellular function and the time course of modified gene expression after stimuli such as hypoxia; a clinical approach must reevaluate different correlations between clinical parameters of hypertension and those of pancreatic diseases.
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PMID:The renin-angiotensin system: from the renal basis to an organ-specific subsystem in the pancreas. 1186 16

Major papilla pancreatic sphincter dysfunction, a variant of sphincter of Oddi dysfunction, causes pancreatitis and pancreatic-type pain. The gold standard for diagnosis is sphincter of Oddi manometry, most commonly performed at endoscopic retrograde cholangiopancreatography (ERCP). Noninvasive testing, such as secretin-stimulated transabdominal or endoscopic ultrasound assessment of pancreatic duct diameter, is less reliable and has relatively low sensitivity. Two thirds of patients with biliary sphincter of Oddi dysfunction have elevated pancreatic basal sphincter pressure. To maximize the diagnostic yield of sphincter of Oddi dysfunction, both the biliary and pancreatic sphincter pressures should be measured. Patients with sphincter of Oddi dysfunction may respond to biliary sphincterotomy alone, but evaluation of their pancreatic sphincter is warranted if symptoms persist after biliary therapy alone. Whether both biliary and pancreatic sphincters should be treated at the first ERCP session is controversial. Biliary and pancreatic endoscopic sphincterotomies are associated with two- to fourfold increased incidence of pancreatitis following the procedure in patients with pancreatic sphincter hypertension. Prophylactic pancreatic duct stenting reduces the frequency and severity of complications by greater than 50%.
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PMID:Sphincter of Oddi (pancreatic) hypertension and recurrent pancreatitis. 1190 Jun 81

Endoscopic retrograde cholangiopancreatography (ERCP) plays a pivotal role in the management of patients with acute and chronic pancreatitis. Whereas endoscopic observation during ERCP permits recognition of abnormalities involving the major and minor duodenal papillae such as papillary tumors or choledochocele, radiographic evaluation enables the detection of structural abnormalities of pancreaticobiliary ducts like strictures or calculi. Sphincter of Oddi manometry, a technical advance of ERCP, is essential for the diagnosis of sphincter of Oddi dysfunction, which may present clinically as recurrent pancreatitis. Because structural alterations of the pancreatic duct forms the hallmark of chronic pancreatitis, ERCP is highly sensitive and specific in diagnosing chronic pancreatitis. Apart from its diagnostic role, ERCP offers a variety of possibilities for therapeutic interventions in selected problems associated with pancreatitis. Endoscopic papillectomy and mucosal resection for tumors of the papilla, unroofing of a choledochocele, and sphincterotomy for sphincter ablation in sphincter of Oddi dysfunction are some of the therapeutic interventions possible during ERCP. Pancreatic ductal hypertension, which is considered to be the major pathophysiologic mechanism for disabling abdominal pain in chronic pancreatitis, also can be managed by ERCP-directed treatments. Pancreatic sphincterotomy, dilation of strictures, lithotripsy, extraction of calculi, and deployment of endoprosthesis constitute the commonly used therapeutic techniques in this situation. Besides offering a noninvasive alternative, these treatments are associated with a favorable clinical outcome comparable with that of operative treatments. Nevertheless, complications such as acute pancreatitis, bleeding, perforation, or sepsis may occur in 5% to 10% of patients undergoing these procedures. Therefore, careful selection of patients, appropriate preoperative care, and a team approach, including surgeon, interventional radiologist, and endoscopist, are important.
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PMID:The role of endoscopic retrograde cholangiopancreatography in acute and chronic pancreatitis. 1196 71

Reported causes of pancreatitis in pregnancy include: gallstone disease, hyperlipidemia, alcohol ingestion, viral, and idiopathic. Few reports associate pancreatitis with pregnancy-induced hypertension. A 35-year-old women with pregnancy-induced hypertension and spontaneous rupture of membranes was admitted for induction of labor. Her postpartum course was complicated by acute renal failure that responded well to treatment with Lasix and Albumin. Subsequently, the patient developed acute pancreatitis and recovered following conservative treatment. It is possible that the pancreatic ischemia due to generalized vasoconstriction of preeclampsia and loop diuretics in the setting of oliguria with renal failure, had a synergistic effect on the pancreas. Therefore, we suggest that in postpartum women with pregnancy-induced hypertension and acute renal failure, diuretics should be cautiously used because they may increase the risk of pancreatitis.
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PMID:Pregnancy-induced hypertension complicated by postpartum renal failure and pancreatitis: a case report. 1201 78


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