Pancreatitis with

Chemiluminescence has been used to demonstrate increased free-radical activity after induction of caerulein pancreatitis, with levels peaking at about 20 min and decreasing rapidly to control values thereafter (Gough et al., 1990). Electron spin resonance has been used to demonstrate increased hydroxyl radical activity in choline-deficient diet pancreatitis in the mouse (Nonaka etal., 1989a). [Pg.152]

Only one study to date has been conducted on the treatment of acute pancreatitis with antioxidants. Clemens et al. (1991) were unable to show any difference in the incidence or severity of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis in a prospective, randomized, double-blind, placebo-controlled trial of allopurinol. However, Salim (1991) performed a similar trial of the effect of allopurinol and DMSO in patients with pain from recurrent pancreatitis, and found significant benefit. On the basis that depletion of antioxidants is important in the pathogenesis of chronic pancreatitis, the administration of a cocktail of antioxidants was assessed for its effect on pain in this disease. Treatment with a combination of organic selenium, d-carotene, vitamins C and E, and methionine was of benefit in the initial pilot study, and in a placebo-controlled trial (San-dilands etal., 1990 Uden et al., 1990). [Pg.153]

Studies of both acute and chronic pancreatitis in humans and in animals support the hypothesis that free radicals are involved in the pathogenesis of pancreatitis. There is some conflicting data from the animal work, which may in part be due to differences in the models used. It does also indicate that free radicals are not the only factors involved and su ests that activation of pancreatic enzymes are also imprortant, particularly in the development of haemorrhagic pancreatitis (Sanfey, 1991). The findings of decreased antioxidant defences and the success of treatment reported in chronic pancreatitis with a cocktail of antioxidants and with allopurinol surest further studies are required to establish the role of antioxidants in pancreatic disease and its prevention. [Pg.153]

The patient has been transferred from the CT scanner to the surgical intensive care unit for mechanical ventilation, blood pressure support, and surgical evaluation. A diagnosis of acute pancreatitis with pancreatic necrosis is made. [Pg.341]

Fig. 9. Effect of short-term rifaximin administration (400 mg t.i.d. for 7 days) on diarrhea (a) and fecal fat excretion (b) in patients with chronic pancreatitis with and without SIBO (from Trespi and Fer-rieri [201]).

Pancreatitis PN may be used in patients with severe pancreatitis with prolonged inadequate nutritional intake longer than 5-7 days who are not candidates for EN. PN should be used when EN exacerbates abdominal pain, ascites, or fistula output. [Pg.683]

Adverse effects include pancreatitis with symptoms of nausea, vomiting, severe abdominal or stomach pain and is more frequent in children. Paresthesia and peripheral neuropathy with tingling, burning, numbness or pain in the hands and feet are also more frequent in children. [Pg.340]

In addition, an open-label study was conducted examining the efficacy of valproate in ten adolescents with chronic temper outbursts and mood lability ( 193). The authors report that valproate was associated with improvement in all subjects, that discontinuation led to relapse, and that there was subsequent improvement on rechallenge in five of six subjects. Although encouraging, these data are modest in terms of both the numbers and design and must be balanced against the risk of toxicity (e.g., hepatic and pancreatic) with valproate in children. [Pg.284]

In a case-control study in 1.4 million people in Sweden, 462 who were hospitalized for pancreatitis without gallbladder disease were compared with 1781 randomly selected controls 6% of the cases and 3% of the controls had diabetes (118). Diet and insulin therapy were not associated with an increased risk, but the risk of pancreatitis with glibenclamide had a crude odds ratio of 3.2 and was higher in people aged over 70 years and in those taking beta-blockers. [Pg.447]

Due. Treatment of pain in chronic pancreatitis with pancreatic enzymes. Am-... [Pg.218]

Key findings that have been reported inclnde significant hypoxia, acidosis, and carbon dioxide retention (Sofer et al, 1989). Also hyperglycemia, hypokalemia, and lenkocytosis were observed in a case series of organophosphate exposures (Levy-Khademi et al, 2007). A prospective study done on 17 children with typical organophosphate or carbamate poisoning looked at laboratory abnormalities that are associated with acute pancreatitis. Five of the patients (30%) had laboratory values consistent with pancreatitis with elevated immunoreactive trypsin, amylase, and serum... [Pg.931]

Chronic pancreatitis with typical changes in ERCP is... [Pg.657]

Pancreatitis with other antiepileptic drugs is extremely rare. [Pg.282]

Two new cases of pancreatitis with captopril have been reported (12,13). It has been suggested that early detection of raised serum amylase and lipase activities can prevent the development of full-blown pancreatitis (13). [Pg.626]

Acute pancreatitis, with relapse on re-exposure, has been observed in a patient taking co-trimoxazole (114). [Pg.3514]

Inactivation or removal of plasma enzymes may be accomplished by several processes denaturation of the enzyme due to dilution in plasma or separation from its natural substrate or coenzyme presence of enzyme inhibitors (e.g., falsely decreased activity of amylase in acute pancreatitis with hyperlipemia) removal by the reticuloendothelial system digestion by circulating proteinases uptake by tissues and subsequent degradation by tissue proteinases and clearance by the kidneys of enzymes of low molecular mass (amylase and lysozyme). [Pg.124]

FIGURE 31-4. CT scan of the abdomen showing pancreatitis with calcification white arrow) and pancreatic pseudocyst black arrows). [Pg.609]

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