The effect of severity of liver cirrhosis, an alcoholic and non-alcoholic genesis, on the results of serum lipids and lipoproteins was evaluated. Serum cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-Ch), and low-density lipoprotein cholesterol (LDL-Ch) were measured in the sera of 59 patients suffering from alcoholic cirrhosis and 34 patients with non-alcoholic cirrhosis. The level of serum triglycerides depends on the severity of liver damage in alcoholic liver cirrhosis, being the highest in Child-Pugh score B. The severity of liver damage significantly affects the HDL-Ch and LDL-Ch levels in cirrhosis of non-alcoholic origin, reaching the highest value for LDL-Ch and the lowest for HDL-Ch in score C. It should not be generalized that the levels of lipids and lipoproteins in liver cirrhosis progressively diminished with the deterioration of liver function. The serum HDL-Ch and LDL-Ch may be considered as markers of severity of liver damage in non-alcoholic cirrhosis, but the triglycerides only in disease of alcoholic origin.

Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), which are most abundant in the liver, are the main enzymes involved in ethanol metabolism in humans. Gender-related differences in total liver ADH and ALDH activity among different animal species have been observed in many studies. We measured total ADH and ALDH activity, and the activity of class I-IV ADH in the livers of male and female patients. Total ADH and class I and II ADH activities were significantly higher in males than in females (P=0.0052, P=0.0074, P=0.020, respectively). Class III and IV ADH and total ALDH activities were not significantly different between the genders (P=0.2917, P=0.0590, P=0.2940, respectively). The results of our study clearly show that there is a difference in enzymatic activity between male and female patients for those isoenzymes that actively participate in ethanol oxidation in the liver (class I and II ADH), although the main form of ADH in this organ is class III ADH.

The aim of this study was to evaluate the effect of liver diseases of different etiologies and clinical severity of liver cirrhosis on the serum level of hyaluronic acid. The results were compared with noninvasive markers of liver fibrosis: APRI, GAPRI, HAPRI, FIB-4 and Forn’s index. Serum samples were obtained from 20 healthy volunteers and patients suffering from alcoholic cirrhosis (AC)—57 patients, non-alcoholic cirrhosis (NAC)—30 and toxic hepatitis (HT)—22. Cirrhotic patients were classified according to Child–Pugh score. Hyaluronic acid concentration was measured by the immunochemical method. Non-patented indicators were calculated using special formulas. The mean serum hyaluronic acid concentration was significantly higher in AC, NAC and HT group in comparison with the control group. There were significant differences in the serum hyaluronic acid levels between liver diseases, and in AC they were significantly higher than those in NAC and HT group. The serum hyaluronic acid level differs significantly due to the severity of cirrhosis and was the highest in Child–Pugh class C. The sensitivity, specificity, accuracy, positive and negative predictive values and the area under the ROC curve for hyaluronic acid and all non-patented algorithms were high and similar to each other. We conclude that the concentration of hyaluronic acid changes in liver diseases and is affected by the severity of liver cirrhosis. Serum hyaluronic acid should be considered as a good marker for noninvasive diagnosis of liver damage, but the combination of markers is more useful.

Alcohol is one of the main factors of liver damage. The evaluation of the degree of liver fibrosis is of great value for therapeutic decision making in patients with alcoholic liver disease (ALD). Staging of liver fibrosis is essential to define prognosis and management of the disease. Liver biopsy is a gold standard as it has high sensitivity and specificity in fibrosis diagnostics. Taking into account the limitations of liver biopsy, there is an exigency to introduce non-invasive serum markers for fibrosis that would be able to replace liver biopsy. Ideal serum markers should be specific for the liver, easy to perform and independent to inflammation and fibrosis in other organs. Serum markers of hepatic fibrosis are divided into direct and indirect. Indirect markers reflect alterations in hepatic function, direct markers reflect extracellular matrix turnover. These markers should correlate with dynamic changes in fibrogenesis and fibrosis resolution. The assessment of the degree of liver fibrosis in alcoholic liver disease has diagnostic and prognostic implications, therefore noninvasive assessment of fibrosis remains important. There are only a few studies evaluating the diagnostic and prognostic values of noninvasive biomarkers of fibrosis in patients with ALD. Several noninvasive laboratory tests have been used to assess liver fibrosis in patients with alcoholic liver disease, including the hyaluronic acid, FibroTest, FibrometerA, Hepascore, Forns and APRI indexes, FIB4, an algorithm combining Prothrombin index (PI), α-2 macroglobulin and hyaluronic acid. Among these tests, Fibrotest, FibrometerA and Hepascore demonstrated excellent diagnostic accuracy in identifying advanced fibrosis and cirrhosis, and additionally, Fibrotest was independently associated with survival. Therefore, the use of biomarkers may reduce the need for liver biopsy and permit an earlier treatment of alcoholic patients.

The metabolism of cancer is in many way different than in healthy cells. Increased metabolism of several carcinogenic substances may take place in cancer cells. The one of them was ethanol, that is oxidized by alcohol dehydrogenase (ADH) to high concentration of acetaldehyde, a toxic and carcinogenic compound. The enzyme responsible for oxidation of acetaldehyde is aldehyde dehydrogenase (ALDH). The aim of this study was to compare the capacity for ethanol metabolism measured by ADH isoenzymes and ALDH activity between gastric cancer and normal gastric mucosa. Total ADH activity was measured by photometric method with p-nitrosodimethylaniline (NDMA) as a substrate and ALDH activity by the fluorometric method with 6-methoxy-2-naphtaldehyde as a substrate. For the measurement of the activity of class I isoenzymes, we used fluorometric methods, with class-specific fluorogenic substrates. The activity of class III ADH was measured by the photometric method with n-octanol and class IV with m-nitrobenzaldehyde as a substrate. The samples were taken surgically during routine operations of gastric carcinomas from 55 patients. The activities of total ADH, and the most important in gastric mucosa, class IV ADH were significantly higher in cancer cells than in healthy tissues. The other tested classes of ADH and ALDH showed a tendency toward higher activity in cancer than in healthy mucosa. The activities of all tested enzymes and isoenzymes were not significantly higher in men than in women in wither gastric cancer tissues or normal mucosa. The increased ADH IV activity may be 1 of the factors intensifying carcinogenesis by the increased ability to acetaldehyde formation from ethanol.

Various isoenzymes of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) exist in human colorectal mucosa. In our last experiments we have shown that ADH and ALDH are present also in colorectal cancer cells. Moreover the activities of total ADH and class I isoenzymes were significantly higher in cancer tissue than healthy mucosa. This may suggest that these changes may be reflected by enzyme activity in the serum. Therefore, we have measured the activity of total ADH, and classes I-IV of this enzyme and ALDH in the sera of patients suffering from this cancer. Total ADH activity was measured by a photometric method with p-nitrosodimethylaniline (NDMA) as a substrate and ALDH activity by the fluorometric method with 6-methoxy-2-naphtaldehyde as a substrate. For the measurement of the activity of class I and II isoenzymes we employed fluorometric methods, with class-specific fluorogenic substrates. The activity of class III ADH was measured by the photometric method with formaldehyde and class IV with m-nitrobenzaldehyde as a substrate. Serum samples were taken for routine biochemical investigations from 52 patients with colorectal carcinoma before treatment. A statistically significant increase of class I ADH isoenzymes was found. Therefore the total ADH activity was also significantly increased. The total ALDH and the activity of other tested ADH isoenzymes were unchanged. We also observed the increasing tendency of ADH I activity in accordance with the advance of disease. The activity of class I ADH isoenzymes was elevated in the serum of patients with colorectal cancer. This activity was derived from colorectal cancer cells and probably from severely damaged liver by metastatic disease.

Glycosylation is the most common chemical process of protein modification and occurs in every living cell. Disturbances of this process may be either congenital or acquired. Congenital disorders of glycosylation (CDG) are a rapidly growing disease family, with about 50 disorders reported since its first clinical description in 1980. Most of the human diseases have been discovered recently. CDG result from defects in the synthesis of the N-and Oglycans moiety of glycoproteins, and in the attachment to the polypeptide chain of proteins. These defects have been found in the activation, presentation, and transport of sugar precursors, in the enzymes responsible for glycosylation, and in proteins that control the traffic of component. There are two main types of protein glycosylation: N-glycosylation and O-glycosylation. Most diseases are due to defects in the N-glycosylation pathway. For the sake of convenience, CDG were divided into 2 types, type I and II. CDG can affect nearly all organs and systems. The considerable variability of clinical features makes it difficult to recognize patients with CDG. Diagnosis can be made on the basis of abnormal glycosylation display. In this paper, an overview of CDG with a new nomenclature limited to the group of protein Nglycosylation disorders, clinical phenotype and diagnostic approach, have been presented. The location, reasons for defects, and the number of cases have been also described. This publication aims to draw attention to the possibility of occurrence of CDG in each multisystem disorder with an unknown origin.

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