It was indicated that injuries of liver, pancreas, salivary glands, and muscle occurred in asymptomatic or oligosymptomatic chronic alcoholics. SUMMARY: Biochemical and hematimetric indicators of inflammation and cell damage were correlated with bilirubin and hepatic and pancreatic enzymes in 30 chronic male alcoholics admitted into psychiatric hospital for detoxification and treatment of alcoholism. Abusive chronic alcohol intake causes degenerative, inflammatory, and necrotic damage in various tissues, frequently leading to development of hepatic, pancreatic, muscular, and neural diseases.
Alterations of enzymes and other substances that occur in degenerative, inflammatory, and necrotic processes may reflect damage in more than one organ since they are rarely tissue-specific Furthermore, the types of laboratory tests and their success in identifying physiopathologic response to high alcohol intake vary widely.
The majority of studies evaluating the behavior of biochemical indicators of inflammation and cell necrosis relate to patients with exuberant clinical symptoms. Observations are scarce at stages where clinical manifestations are not evident or are very mild. Structural and functional alterations of these patients have been found most frequently in the liver, which occupies a key position in alcohol metabolism and is the most commonly damaged organ, isolated or in association with others, in alcoholics.
Serum alterations of liver enzymes may indicate different processes. Alteration of aspartate aminotransferase may indicate microsomal induction or liver cell damage while that of alanine aminotransferase occurs in liver or muscle cell injury. Alteration of alkaline phosphatase may reflect, at least partially, failure in bile excretion through damage of bile channels or cholestasis secondary to pancreatopathy.
This study evaluates the relationship of levels of plasma components employed to identify occurrence of inflammation and necrosis with those of liver and pancreatic enzymes in asymptomatic and oligosymptomatic alcoholics. Thirty male chronic alcoholics admitted into the psychiatric hospital for detoxification were considered asymptomatic or oligosymptomatic at the admittance physical exam and clinical anamnestic-structured interview 3.
The majority belonged to the low and average subgroups of the middle class, as judged from mean income. None of them had used illicit drugs or any medicine in the 30 days before admission. After being carefully informed, they consented to undergo, in the first 24 hours, laboratory exams: hematimetric analyses and biochemical plasma determinations of bilirubins total, TB, and fractions , aminotransferases AT; aspartate aminotransferase, AST, and alanine aminotransferase, ALT , alkaline phosphatase AP , gamma-glutamyltransferase GGT , albumin and globulins, fibrinogen, prothrombin activity and time, lactic dehydrogenase LDH , creatine phosphokinase CPK , amylase, iron, total capacity of iron binding TCIB , and transferrin saturation index TSI.
No tests were done for viral antigens, and parasitologic exams were negative for Schistosoma mansoni eggs. Comparisons were made by chi-squared or Fisher's one-tailed tests when occurrences were less than 5, and by Student's t-test for quantitative variables Variables were correlated using linear regression, correlation coefficient, and Pearson's significance test Demographic characteristics and pattern of alcoholism of the sample are presented in table 1.
Average plasma TB was significantly higher in individuals with elevated AT. Prevalence of alteration of alpha-1 globulin was not correlated to those of hepatic enzymes or TB. There were no significant differences between prevalence of leucocytosis and alterations of bilirubin, liver enzymes, or amylase. Prevalence of hyperamylasemia among cases with elevated AST was 1 : 4. Prevalence of alterations and plasma levels of liver enzymes and amylase were not related to time and daily intake of alcohol.
Except for the better socioeconomic conditions and lower age of patients in this study, the pattern of alcoholism and general clinical conditions did not differ significantly from those observed in our previous study of patients with the same symptomatic profile and in the same hospital 4.
In this study, higher prevalence of AT, especially AST, alteration was observed, relative to other studies of asymptomatic or oligosymptomatic alcoholics 5,15,16, In chronic alcoholics, ALT alteration is a better indicator of liver damage than AST since expression of ALT is restricted to the liver 38 , while AST may be altered through induction in the liver or after extra-hepatic complications myopathy, pancreatopathy, hemolysis due to alcoholism AP was lightly altered in only one-fourth of the cases and, while the average level of the enzyme remained normal, that of GGT was about 4-fold the normal value.
The divergent behavior of GGT and AP, also reported by others 36,43 , could result from both GGT induction 20,35 and from specific actions at the different sites of production of the enzymes GGT may be altered in pancreatitis 0. In alcoholic hepatitis, especially in intense acute forms, increased synthesis and elevation of alpha-globulins has been reported Otherwise, they were reduced in chronic inflammation with mesenchymal reaction, in parallel with albumin levels In the present study, prevalence and degrees of alteration were different for their fractions, low for alpha-1 and high for alpha-2 globulin.
The differences could be related to biologic and physico-chemical characteristics of their constituent glycoproteins and lipoproteins as well as to concomitant alterations of other substances. Previous observations 38 were consistent with our findings of correlation between alpha-1 globulin and albumin, where low alpha-1 globulin occurred in cases with hypoalbuminemia.
The possibility of relating the significant increase of alpha-2 globulin with that of the GGT glycoprotein is not supported by our finding of lack of correlation between them. This may contribute to that acute biliary pancreatitis may result in more increase in pancreatic enzyme secretion or passage of these enzymes into the circulation when compared to nonbiliary pancreatitis.
In practical purposes, when these five markers were elevated during admission to the hospital, the biliary evaluation should have priority not to delay in treatment. CRP and leukocyte number did not differ between biliary and nonbiliary pancreatitis. They both are predictive in detecting the severity of pancreatitis rather than etiology.
This shows the less sensitivity of these individual parameters in our patients in distinguishing etiology. Clinical and radiological evaluation should complete the biochemical markers to find the exact cause of acute pancreatitis. MRCP is a noninvasive procedure which could be the first diagnostic method when the suspicion of biliary pancreatitis occurred.
Endoscopic ultrasonography would be useful in these patients in aspect of rapid diagnosis; furthermore, therapeutic intervention by ERCP could be applied on the same session if required [ 12 , 18 ]. As a conclusion, because of these high rates of negative MRCP and ERCP, biochemical parameters gain an important role in the selection of initial biliary evaluation for acute pancreatitis.
This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Article of the Year Award: Outstanding research contributions of , as selected by our Chief Editors. Read the winning articles. Academic Editor: J. Received 26 Oct Accepted 24 Nov Published 14 Dec Abstract Background and Aim. Introduction Acute pancreatitis is a disease that could result in systemic inflammatory response, sepsis, multiorgan failure, and death. Results The analysis demonstrated that PPV: positive predictive value. NPV: negative predictive value.
Table 1. The biochemical markers whose values were significantly different between biliary and nonbiliary pancreatitis. Figure 1. The ROC curve of all of the measured serum biochemical markers. Diagonal segments are produced by ties. Figure 2. The ROC curve of the significantly increased biochemical markers in biliary pancreatitis.
References G. Wang, C. Gao, D. Wei, C. Wang, and S. View at: Google Scholar C. Johnson and P. Frossard, M. Steer, and C. Chang, S. Lo, B. Stabile, R. Lewis, and C. Cohen, L. Slezak, C. Wells, D. Andersen, and M. Roston and I. View at: Google Scholar J.
Smotkin and S. Chan, A. Yaghoubian, D. Rosing et al. Moon, Y. Cho, S. Cha et al. Matull, S. Pereira, and J. Liu, S.
Fan, C. Lo et al. Choi, N. Kang, and S. Davidson, J. The case presented here exemplifies the predictive use of aminotransferase liver enzymes in patients with biliary cholecystectomy but abdominal ultrasound that is negative for cholelithiasis and choledocholithiasis. The case is a 55 year old patient whose clinical picture was consistent with acute biliary pancreatitis.
The diagnosis was made and endoscopic treatment was recommended. Acute pancreatitis AP is one of the disorders that is seen most frequently in hospital gastroenterology services 1. It is the result of inflammation and necrosis of the pancreatic tissue which generate a generalized inflammatory response that can lead to systemic involvement with multi-organ dysfunction.
The identification of biliary AP is very important for the possibility of endoscopic treatment to control the condition and to reduce the risk of recurrence 5. Unfortunately during the initial phase of AP, the initial diagnostic imaging methods used to identify lithiasis in the bile ducts have little sensitivity and often report false negative results. This makes diagnosing biliary AP a real challenge 3, 5 , but there are easily measurable biochemical alterations that predict biliary AP 1, 3, 6, 8, 9.
The patient was a 55 year old man who was admitted to the emergency room with abdominal pain that had suddenly developed three hours earlier. The pain was intense but did not radiate. It was accompanied by occasional vomiting. The patient had had a cholecystectomy.
He did not use drugs or have any other relevant medical history. A physical examination upon admittance showed normal vital signs, tenderness in the epigastric area but no signs of peritoneal irritation. Sodium, potassium, chloride and creatinine were all within normal limits. Measures of arterial blood gases showed PaO2 Hepatobiliary ultrasound indicated fatty liver disease, showed a previous cholecystectomy, and indicated normal caliber intrahepatic and extrahepatic bile ducts.
A diagnosis of mild acute pancreatitis without systemic complications was made. Supportive of treatment intravenous fluids, intravenous meperidine for pain control and a liquid diet was begun.
Because of the indications of altered liver function, lithiasis and biliary AP were suspected. Magnetic resonance cholangiopancreatography MRCP was ordered to evaluate the bile ducts. Liver profiles at 48 and 72 hours after admission showed marked reduction in aminotransferase levels and bilirubin Table 1.
The MRCP showed an 11 mm bile duct with 5 mm stones at its distal end. The patient-s pancreas was normal Figure 1. Endoscopic retrograde cholangiopancreatography ERCP with sphincterotomy was requested. After the procedure there was significant improvement of the abdominal pain. AP is the most common acute pancreatic disease 1. In the USA, the incidence is 13 to 45 cases per , people 1. The ratio between biliary origins and alcoholic origins may vary in different geographical areas.
The prevalence of PD in the population is 7. Although the hypothesis that it can cause AP is still controversial, it is currently believed that AP can develop when a patient with PD also has associated genetic mutations such as the gene for cystic fibrosis CFTR gene and the serine protease inhibitor Kazal-type 1 SPINK1 gene Figure 2 1, 5, 9, While the pathophysiological mechanisms of AP have not yet been fully elucidated, it is now considered that many of the etiological factors can cause obstruction at the ampulla of Vater.
This increases pressure in pancreatic and biliary ducts resulting in retrograde flow of pancreatic and biliary secretions producing trypsin activation and self-digestion of the pancreatic parenchyma In the initial pathophysiological phases, zymogen granules within acinar cells are not exported and join the rich lysosomes in cathepsin B which converts trypsinogen to trypsin 1, This mechanism is considered to be the "classical trypsin theory". Recently it has become controversial because many cases have demonstrated that this series of events does not always occur but rather nuclear factor kappa B NF-kB is activated within acinar cells independently of the presence of trypsin 1, Therefore, at present it is considered that both mechanisms are active causes of AP.
The activation of NF-kB, involved in both the initial outbreak of the disease and its perpetuation by inducing the production of pro-inflammatory substances In cases of cholelithiasis, there are several risk factors for biliary obstruction including the presence of 20 or more small stones of less than 5 mm each, cystic ducts with diameters greater than 5 mm, and anatomical variations of the pancreaticobiliary ducts.
These can include longer than usual common bile ducts, increased angles of convergence between the biliary and pancreatic ducts, and papillary diverticula 5.
0コメント