Effect of non-alcoholic compounds of alcoholic drinks on the pancreas.

Over the past 30 years the role of alcohol (ethanol) in the development of acute and chronic pancreatitis has been intensively investigated. However, ethanol is generally consumed in form of alcoholic beverages which contain numerous non-alcoholic compounds. At least on gastric acid secretion it has been convincingly demonstrated that alcohol and alcoholic beverages have markedly different effects. In the present article, we provide an overview about the effect of different non-alcoholic constituents of alcoholic beverages on the pancreas and their possible interaction with molecular mechanisms leading to 'alcoholic' pancreatitis. The present data indicate that pancreatic enzyme secretion in humans is stimulated by non-alcoholic constituents of beer which are generated by alcoholic fermentation of glucose. In addition, it has been shown that natural phenolic compounds (e.g. quercetin, resveratrol) of alcoholic beverages exert different effects on the pancreasin vitro, such as inhibition of pancreatic enzyme output, of pancreatic stellate cell activation and of pancreatic cancer growth as well as protective effects against oxidative stress and on experimental induced acute pancreatitis in rats. However, it should be pointed out that alcoholic beverages contain much more non-alcoholic ingredients. Since the effects of these are still unknown, caution is required in attempting to define alcoholic etiology of pancreatitis without considering the effect of non-alcoholic compounds of alcoholic beverages.

[Chronic pancreatitis: nutrition and pain therapy]. / Chronische Pankreatitis: Ernährung und Schmerztherapie.

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.

The impact of ethanol and Marinol/marijuana usage on HIV+/AIDS patients undergoing azidothymidine, azidothymidine/dideoxycytidine, or dideoxyinosine therapy.

Therapeutic observations suggest that azidothymidine (AZT)-resistant HIV+/AIDS patients are frequently offered AZT/dideoxycytidine (DDC) or dideoxyinosine (DDI) therapy. The latter therapies have been associated with the development of acute pancreatitis. During the initial portion of this study, when patients reported limiting ethanol consumption, an increase in CD4+, a decrease in amylase, and a decrease in lipase was observed in patients on DDI monotherapy. Marinol/marijuana usage was associated with depressed CD4+ counts and elevated amylase levels within the DDI subgroup. The purpose of this study was to follow these patients over 1 year and compare clinical indicators of pancreatitis and HIV progression. After 1 year, the remaining 56 patients were reexamined in the follow-up portion for clinical indicators of HIV disease progression and pancreatoxic/hepatotoxic effects. Those in the AZT group, who remained on this therapy throughout the year, had significantly increased amylase values from 55.3 to 69.3 IU/liter (p < 0.05). In the AZT/DDC group, those who remained on combination therapy throughout the year, 4 of the 5 clinical indicators of disease progression changed. Amylase, ALT, and AST all increased significantly from 55.2 to 77.8 IU/liter (p < 0.01), from 38.0 to 92.3 IU/liter (p < 0.05), and from 55.2 to 97.0 IU/liter (p < 0.05), respectively. Lipase levels decreased significantly (106.0 to 74.6 IU/liter, p < 0.05). The most remarkable changes occurred in the AZT/DDC group (who reduced ethanol consumption), wherein clinical indicators of pancreatitis and liver dysfunction declined, including amylase (65.0 to 20.0 IU/liter, p < 0.05), ALT (350.0 to 100.0 IU/liter, p < 0.01), and AST (240.0 to 95.0 IU/liter, p < 0.01). No significant changes were noted in the DDI or AZT groups. Marinol/marijuana use was associated with declining health status in both the AZT and AZT/DDC groups. In contrast, all clinical indicators of pancreatitis improved in the DDI patients who utilized Marinol/marijuana, including amylase (-34%), lipase (-30.8%), ALT (-21.4%), and AST (-20.1%). This paired follow-up study suggests that HIV+/AIDS patients on antiretroviral therapies should restrict their ethanol consumption. In HIV+/AIDS patients with the lowest CD4+ counts (those on DDI monotherapy), utilization of Marinol/marijuana does not seem to have a deleterious impact.