The role of alcohol metabolism enzymes in chronic alcoholic pancreatitis (review)

Author(s):  
Г.Р. Алиева

Алкогольный метаболизм является решающим биологическим фактором, значительно влияющим на злоупотребление алкоголем, развитие алкоголизма и алкогольное повреждение органов. Основной путь метаболизма этанола - это алкогольдегидрогеназный путь превращения в ацетальдегид, который переходит в митохондрии и окисляется до уксусной кислоты. Через этот путь проходит 80-90% всего этанола. За окисление 10-20% этанола отвечает алкогольоксидаза (цитохром P450), также называемая «микросомальная этанолокисляющая система» (MEOS/CYP2E1). Основные ферменты метаболизма алкоголя проявляют генетический полиморфизм и этническую изменчивость. В данном обзоре представлены достижения последних десятилетий в понимании функциональных полиморфных локусов генов ADH и ALDH и их метаболических, физиологических и клинических корреляций. Alcohol metabolism is a decisive biological factor that significantly affects alcohol abuse, the development of alcoholism and alcohol damage to organs. The main pathway of ethanol metabolism is the alcohol dehydrogenase pathway to acetaldehyde, which passes into the mitochondria and is oxidized to acetic acid. 80-90% of all ethanol passes through this path. Alcohol oxidase (cytochrome P450), also called microsomal ethanol oxidation system (MEOS/CYP2E1), is responsible for the oxidation of 10-20% of ethanol. The main alcohol metabolizing enzymes exhibit genetic polymorphism and ethnic variation. This review presents recent advances in understanding the functional polymorphisms of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) and their metabolic, physiological, and clinical correlations.

2020 ◽  
Vol 2020 (12) ◽  
Author(s):  
Jonathon N Holt ◽  
Heinrich E Schwalb

Abstract Splenic artery pseudoaneurysm is a rare phenomenon most associated with chronic pancreatitis or previous trauma. Complications can include erosion and rupture into local structures, a situation that carries a reported mortality of 10–40%. A 58-year-old male with chronic alcoholic pancreatitis and a known splenic artery pseudoaneurysm presented to the emergency department of a regional hospital with rectal bleeding and sepsis. Computed tomography revealed a peri-splenic mass communicating with the splenic flexure. The patient was taken for an emergency splenectomy and left hemicolectomy and was confirmed to have rupture of the splenic artery aneurysm into the large bowel. This case presented with comparable features reported in the literature and demonstrates that access to emergency specialist surgical services in a regional setting offers the capability to manage rare, life threatening surgical emergencies.


1998 ◽  
Vol 114 ◽  
pp. A503
Author(s):  
T. Tanaka ◽  
T. Fujii ◽  
Y. Matsugu ◽  
Y. Kodoh ◽  
K. Koide ◽  
...  

2011 ◽  
Vol 48 (2) ◽  
pp. 112-118 ◽  
Author(s):  
Maria Beatriz Sobral-Oliveira ◽  
Joel Faintuch ◽  
Dulce Reis Guarita ◽  
Claudia P. Oliveira ◽  
Flair J. Carrilho

CONTEXT: Alcoholism may interfere with nutritional status, but reports are often troubled by uncertainties about ingested diet and organ function, as well as by ongoing abuse and associated conditions. OBJECTIVE: To identify nutritional and body compartment changes in stable alcoholics without confounding clinical and dietetic variables, a prospective observational pilot study was designed. Three well-matched populations were considered: subjects with chronic alcoholic pancreatitis, alcoholics without visceral disease, and healthy never-drinking adults (controls). METHODS: Subjects (n = 60) were asymptomatic males with adequate diet, no superimposed disease or complication, and alcohol-free for at least 6 months. After exclusions, 48 patients were compared. Variables encompassed dietary recall, bioimpedance analysis, biochemical profile and inflammatory markers. Main outcome measures were body fat, lean body mass, serum lipids, C-reactive protein, and selected minerals and vitamins. RESULTS: Both alcoholic populations suffered from reduced lean body mass (P = 0.001), with well-maintained body fat.Magnesium was depleted, and values of vitamin D and B12 correlated with alcohol abuse. LDL and total cholesterol was increased in alcoholics without pancreatitis (P = 0.04), but not in those with visceral damage. C-reactive protein and serum amyloid A correlated with duration of excessive drinking (P = 0.01). CONCLUSIONS: Undernutrition (diminished lean body mass, risk of magnesium and vitamin deficiencies) contrasted with dyslipidemia and increased cardiovascular risk. This second danger was masked during chronic pancreatitis but not in alcoholics without visceral disease. Further studies should focus special requirements of this population.


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