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Effects Of Endogenous Alcohol On Liver Functions
Author: Aurelian Udristioiu
Publisher: Emergency County Hospital TARGU-JIU
13 pages
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In Western countries, up to 50% of cases of end-stage liver disease have the alcohol intake as a major etiologic factor. The mortality from alcoholic cirrhosis is higher than that of nonalcoholic cirrhosis, with a survival rate at 5 and 10 years of only 23% and 7%, respectively. Also, the liver disease was the 12-th leading cause of death in the United States, the annual deaths being reported 27.000 of cases in the statistic of the Centers for Disease Control and Prevention, (1).

In Portugal, were recently found that total costs of alcohol-related diseases was estimated to be €189.2 million, representing 0.13% of Gross Domestic Product and 1.25% of total national health expenditures, (2).

In Romania, the alcohol is the most common cause of chronic liver disease. Liver

diseases caused by alcohol abuse include fatty liver, hepatitis and cirrhosis. Cirrhosis,

which is an irreversible form of liver disease can occur in about 30% of excessive

drinkers. This form of cirrhosis is meted at men who consumed high amounts of alcohol

daily, time of 10-15 years and at women, in more less years.


of this work was to identify the patients admitted in hospital in 2012 year with the

diagnostic of alcoholic cirrhosis after an abuse alcohol consumption in last 10 years.


The retrospective study consisted of analysis in180 cases, adult men (mean age 55

years) and females (mean age 48 years), hospitalized and investigated for alcoholic liver

diseases, along years, in Emergency County Hospital Targu Jiu, region from south-east of


The diagnostics of admitted patients in internal medicine department has made initially on physical exam which emphasized portal hypertension, hepatomegaly, peripheral edema, spider angiomata, splenomegaly, jaundice and ascites. Melena, hematemesis, dyspnea on exertion and fatigue accompanied patients with gastrointestinal bleeding, increasing abdominal girth, shortness of air and peripheral edema (4). Patients with well-compensated cirrhosis exhibited only hepatomegaly and/or splenomegaly, although the liver was decreased in size as a fibrosis progresses. Confirmatory preclinical investigations were assessed on the hematological analyzer Coulter LH 750 with 26 parameters and on dry biochemistry analyzer Vitros 700.


The majority of patients with un-compensated liver cirrhosis (70%) have had elevation of AST, (379.9 U/L mean value,

SD =1.1)>ALT( 249.2 U/L, mean value, SD=

0.05),, in all cases, both below 400 U/L. Also, they have had an AST / ALT ratio > 1.52

(N = 1.33). The enzyme GGT levels (mean value, 123.8 U/L,

SD =1.33

), have proven to be more sensitive than ALT.

Elevation of total bilirubin (5.6 mg/d L, mean value,

SD =0.04

), prolongation of

prothrombin time (PT), [INR = 4.53 mean value,

SD =1.63] and hypoalbuminemia (1.2 mg d/ L, in mean value, SD =0.083

) were markers of severe alcoholic hepatitis and/or cirrhosis. However, specificity of these tests is very low and values are affected by multiple other factors including age, obesity and diabetes.

LDH-4 enzyme (mean value 500 U/L; SD =2.6), but especially LDH 5 (650 U/L mean value,

SD =1.6), were accelerated in chronic alcoholic hepatitis more that Alkaline Phosphatase (ALP mean value = 250 U/L, SD=2.4


Patients with alcoholic liver disease (ALD) have had leukocytosis cell, [(WBC) count in mean value of 13.9 x 10³μl,

SD = 2.66)] and thrombocytopenia (Platelets, X‾ = 133 x 10³μl, SD =1.91

), in 70% of cases.

Leukemoid reactions with leukocytes counts of > 60 x 10³ WBC/μl, in the absence of infection have been seen in patients with ALD (10%), while thrombocytopenia, that is secondary to heavy alcohol consumption, was persistently at patients with concomitant cirrhosis, < mean value of 70 x 10³μl. Results of liver enzymes and hematological parameters in our cohort study are encompassed in Table 1 and Table 2.


ALD is most often a clinical diagnosis, with a careful history being of vital importance. Physiological, the alcohol is readily absorbed from the gastrointestinal tract; however, alcohol cannot be stored and therefore, the body must oxidize it to get rid of it. Alcohol can only be oxidized in the liver, where enzymes are found to initiate the process. The enzyme alcohol dehydrogenases (ADH) comprise a group of several iso-enzymes that catalyse the oxidation of primary and secondary alcohols to aldehydes and ketones, respectively, and also can catalyse the reverse reaction.

ADH is an enzyme that makes it possible for humans to drink beer, wine, and other alcoholic beverages. However, its "real" function is thought to be the conversion of alcohol generated by bacteria in the intestine to other metabolic products. Individuals with some mutant forms of ADH may be especially sensitive to alcohol. The molecule is a dimer made either of two identical or two different chains, [Figure 1].

Alcohol dehydrogenase uses two molecular "tools" to perform its reaction on ethanol.

The first is a zinc atom, which is used to hold and position the alcoholic group of ethanol. The second is a large NAD cofactor (constructed using the vitamin niacin), which actually performs the reaction. A slightly-modified version of NAD was used in the structure analysis, so that the enzyme would not immediately attack the ethanol.

From biochemical view point, the first step in the metabolism of alcohol is the oxidation of ethanol to acetaldehyde catalyzed by alcohol/dehydrogenase containing the coenzyme NAD

+. The acetaldehyde is further oxidized to acetic acid and finally CO2 and water through the citric acid cycle. A number of metabolic effects from alcohol are directly linked to the production of an excess of both NADH and acetaldehyde: CH3CH2OH + NAD+ ---> CH3CH=O + NADH + H+

, [Figure 2].

Pyruvic Acid conversion to Lactic Acid:

The conversion of pyruvic acid to lactic acid requires NADH: Pyruvic Acid + NADH + H+ ---> Lactic Acid + NAD+. This pyruvic acid normally made by transamination of amino acids, is intended for conversion into glucose by gluconeogenesis. This pathway is inhibited by low concentrations of pyruvic acid, since it has been converted to lactic acid. The final result may be acidosis from lactic acid build-up and hypoglycemia from lack of glucose synthesis.2.

Synthesis of Lipids:

Excess NADH may be used as a reducing agent in two pathways--one to synthesize glycerol (from a glycolysis intermediate) and the other to synthesis fatty acids. As a result, heavy drinkers may initially be overweight.

3. Electron Transport Chain:

The NADH may be used directly in the electron transport chain to synthesize ATP as a source of energy. This reaction has the direct effect of inhibiting the normal oxidation of fats in the fatty acid spiral and citric acid cycle. Fats may accumulate or acetyl CoA may accumulate with the resulting production of ketone bodies. Accumulation of fat in the liver can be alleviated by secreting lipids into the blood stream. The higher lipid levels in the blood may be responsible for heart attacks.

Ethanol can also inhibit gene expression for inducible nitric oxide synthase, the enzyme responsible for generation of nitric oxide in alveolar macrophages and neutrophils in response to bacterial stimulation. Both acute and chronic alcohol treatment inhibited alveolar macrophage nitric oxide secretion in a recent study in rats, suggesting that decreased reactive oxygen radical generation by ethanol-exposed macrophages may contribute to the impaired antimicrobial defence after alcohol use (6).

Alcoholic liver disease (ALD) is associated with decreases in zinc (Zn). Zn supplementation attenuates ethanol-induced hepatic Zn depletion and suppresses ethanol-elevated cytochrome P450 2E1 (CYP2E1) activity. Zn also enhances glutathione-related antioxidant capacity in the liver. At the cellular level, Zn inhibits alcohol-induced hepatic apoptosis partially through suppression of the Fas/FasL-mediated pathway. Zn supplementation preserves intestinal integrity and prevents endotoxemia, leading to inhibition of endotoxin-induced tumor necrosis factor-alpha (TNF-alpha) production in the liver. Zn also directly inhibits the signaling pathway involved in endotoxin-induced TNF-alpha production, (7).

Increased proinflammatory cytokines, particularly TNF alpha, play a central role in the pathogenesis of ALD. TNF alpha is tightly regulated at transcriptional and posttranscriptional levels. Recently, micro ARN miR-29a and miR-122a were reported to modulate intestinal membrane permeability. MiR-29a regulates intestinal membrane permeability in patients with irritable bowel syndrome (IBS). Increased expression of miR-29a was found in blood microvesicles, small bowel, and colon tissues of patients. MiR-29a targets the glutamine synthetase gene (GLUL), which in turn regulates intestinal membrane permeability (8, 9,).

The role of miRNAs in ALD is getting attention, and recent studies suggest that alcohol modulates miRNAs. Recently, we showed that alcohol induces miR-155 expression both in vitro (RAW 264.7 macrophage) and in vivo (Kupffer cells, KCs of alcohol-fed mice), (10). Induction of miR-155 contributed to increased TNF alpha production and to the sensitization of liver cells Kupffer (KCs) to produce more TNF alpha in response to LPS (11), [Figure 3].

Chronic alcohol abuse increases gut permeability resulting in high circulating endotoxin that reaches the liver via portal circulation. Endotoxin (lipopolysaccharide or LPS) is recognized by the Toll-like receptor (TLR-4 complex), on resident macrophages or Kupffer cells in the liver, leading to production of pro-inflammatory cytokines, TNF-α, and resulting in injury to liver cells (hepatocytes).

The typical inflammatory cytokines, such as TNF-α, IL-1, and IL-6, are primarily produced by inflammatory monocytes, macrophages, whereas other cell types including neutrophils, endothelial cells, lymphocytes, and activated tissue cells can also be a source during overwhelming inflammatory responses.(12).

One of the characteristics of the immune aberrations in chronic alcoholics is the elevated levels of serum antibodies (immunoglobulins), particularly those of IgG and IgA classes. Considering that immunoglobulins are produced by cells of B lymphocyte lineage, the elevated immunoglobulin levels in alcoholics indicate B cell dysfunctions. The recent studies imply that the decreased T cell proliferation after alcohol use might be due to impaired accessory cell/monocyte function. Additionally, the T cell proliferation inhibiting effects of ethanol-induced monocyte-derived cytokines (TGF-β, IL-10, PGE


) might be important (13).

Induction of inflammatory mediators and chemokines, particularly monocyte chemotactic protein-1(MCP-1), as a result of endothelial cell and monocyte activation, has been identified as a key element in initiation and progression of atherosclerotic plaque formation. Thus, decreased MCP-1 and inflammatory cytokine, IL-1 and TNF-α production seen after acute alcohol treatment of human monocytes and after binge drinking in mice has beneficial effects on the inflammatory component of atherosclerotic plaque formation (14).

The activity of NK cells can be suppressed by the presence of ethanol

in vitro; however, other studies reported no effect of ethanol treatment in vitro

on NK cell function (15). Lipopolysaccharide (LPS) is a major component of a Gram-negative bacterial cell wall, and it is detoxified in the liver via both parenchymal and non-parenchymal cells, It is believed that increased LPS in the circulation disrupts the liver homeostasis, resulting in Kupffer cell. Upon activation, KCs produce TNF alpha, which then induces the activation of other signaling cascades to amplify the inflammation, This suggests that alcohol-induced steatohepatitis is tightly associated with LPS-TLR4 signaling. Among bone morrow (BM), derived cells, Kupffer cells/macrophages highly express TLR-4 and produce inflammatory cytokines in response to LPS (16), [Figure 4].

Maddrey's Discriminant Function (MDF), which is calculated using the equation [4.6×(PT patient – PT control)+total bilirubin (mg/dl)], is the most commonly utilized tool for evaluating the severity of ASH. If this value exceeds 32, the mortality during the current hospitalization is in excess of 50%. In our cohort of study, MDR vas calculated in mean value of 20.19, [4.6 x (4.53- 1.2) + 5.6]. Other validated models for severity in ASH the Glasgow score, and others which can be recommended to become familiar with one [17].

The study from Fibromax tests can assess five biomarkers of fibrosis [FibroTest (FT)], steatosis [SteatoTest (ST)], necrosis, and inflammation, [alanine aminotransferase (ALT), ActiTest (AT), and NashTest (NT)]. FT, AT, and ST scores ranged from 0 to 1.00, with high score indicating greater probability of significant lesion. .Predetermined FT conversion for the METAVIR fibrosis stage scoring system was 0.00–0.27 for F0, greater than 0.27–0.48 for F1, greater than 0.48–0.58 for F2, greater than 0.58–0.74 for F3, greater than 0.74 for F4 [14]. Predetermined AT conversion for the METAVIR activity grade scoring system was 0.00–0.17 for A0, greater than0.17–0.52 for A1,

greater than 0.52–0.62 for A2, greater than 0.62 for A3 [21].Predetermined ST conversion for steatosis grade was0.00–0.57 for S0, greater than 0.57–0.69 for S1, and greater than 0.69–1.000 for S2–S3 [16].The NT is a 3-category score for predicting three NAS categories: 0.25 indicates ‘No-NASH’, 0.50 indicates possible NASH’, and 0.75 indicates ‘NASH’(22 ) .

Finally, an elevated creatinine can also be seen in patients with ALD and, in the setting of severe ASH without other causes of acute kidney injury, may indicate the ominous diagnosis of hepatorenal syndrome (18). Hypertriglyceridemia, hyperuremia, hypokalemia, hypomagnesemia, and an elevated MCV can also be seen with chronic alcohol consumption. Individuals with cirrhosis are also at increased risk of developing liver cancer (hepatocellular carcinoma).

In conjunction with the 2010 AASLD/ACG guidelines on the treatment of severe alcoholic hepatitis, pentoxifilin (PTX) should be considered an alternative to corticosteroids and appears to especially effective in ALD patients with renal dysfunction/hepato-kidney syndrome

The immediately studies confirmed that moderate wine consumption is associated with high plasma levels of omega-3 polyunsaturated fatty acids, reduction of blood viscosity, improved insulin sensitivity, lowering of platelets count and aggregation and, changes in coagulation protein plasma level, increasing HDL-Cholesterol about 50% of the cardio-protective effect., (19).

The concentration of ethanol in blood, breath or urine constitutes important evidence for prosecuting drunk drivers. For various reasons, the reliability of the results of forensic alcohol analysis are often challenged by the defence. One such argument for acquittal concerns the notion that alcohol could be produced naturally in the body, hence the term 'auto-brewery' syndrome.

Although yeasts such as Candida albicans readily produce ethanol in-vitro, whether this happens to any measurable extent in healthy ambulatory subjects is an open question. Over the years, many determinations of endogenous ethanol have been made, and in a few rare instances (Japanese subjects with very serious yeast infections) an abnormally high ethanol concentration (> 80 mg/dl) has been reported. In these atypical individuals, endogenous ethanol appeared to have been produced after they had eaten carbohydrate-rich foods. A particular genetic polymorphism resulting in reduced activity of enzymes involved in hepatic metabolism of ethanol and a negligible first-pass metabolism might explain ethnic differences in rates of endogenous ethanol production and clearance.

Other reports of finding abnormally high concentrations of ethanol in body fluids from ostensibly healthy subjects suffer from deficiencies in study design and lack suitable control experiments or used non-specific analytical methods.

The concentrations of endogenous ethanol in peripheral venous blood of healthy individuals, as well as those suffering from various metabolic disorders (diabetes, hepatitis, cirrhosis) ranged from 0-0.08 mg/dl. These concentrations are far too low to have any forensic or medical significance. The notion that a motorist's state of intoxication was caused by endogenously produced ethanol lacks merit, (20).

With respects to the types of alcoholic beverages, wine (ethanol with a variety of polyphenols including phenolic acids, tannins, resveratrol (a strong antioxidant) and flavonoids, it is seen to have the significantly higher antioxidant, anti-carcinogen and anti-inflammatory effects in contrast with gin (ethanol without polyphenols), or with abuse ethanol with carcinogenetic effect.(21). Finally, it is not important how much drink, but is very important what we daily drink.


Clinicians from all countries should be well versed on the diagnosis and treatment of

the wide spectrum of liver conditions associated with ethanol intake. In conjunction with the 2010 AASLD/ACG, we consider that have to a new guidelines on the treatment of severe alcoholic hepatitis will be necessary in all clinical centers of ALD treatment.


Author Contributions:

Effects of endogenous alcohol on liver functions

Undersigned, Aurelian Udristioiu, as corresponding author


I confirm that I have contributed together with the co-author Manole Cojocaru, to the intellectual content of this paper and we have met the following 3 requirements: (a) significant contributions to the conception and design, acquisition of data, or analysis and interpretation of data; (b) drafting or revising the article for intellectual content; and (c) final approval of the published article.

Authors’ Disclosures of Potential Conflicts of Interest:

No authors declared any potential conflicts of interest. All authors have read the journal's policy on conflicts of interest and have none to declare.

Role of Sponsor:

The funding organizations played no role in the design of study, choice of enrolled patients, review and interpretation of data, or preparation or approval of manuscript.

Aurelian Udristioiu,

Clinical Laboratory, Department of Hematology, Emergency County Hospital Targu Jiu & UCB University, Romania, E-mail:


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4. Szabo G, Mandrekar P. Focus On: Alcohol and the Liver. Alcohol and Health 2010; 33(1/2): 25-33.

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6. Oekonomaki E, Notas G. Mouzas AI, Binge V. Drinking and Nitric Oxide Metabolites in Chronic Liver Disease


Alcohol and Alcoholism 2004; 39 (2): 106-109.

7. Kang YJ, Zhou, Z. Zinc prevention and treatment of alcoholic liver disease. Mol Aspects Med 2005; 26(4-5):391-404.

8. Bala S, Marcos M, Szabo G. Emerging role of microRNAs in liver diseases. World Journal of Gastroenterology 2009; 15 (45): 5633–5640.

9. Bartel P.D. Micro RNAs: Target Recognition and Regulatory Functions. Cell 2009; 136(2): 215–233.

10. Sato F, Tsuchiya S, Meltzer, JS Shimizu K. MicroRNAs and epigenetics. FEBS J, 2011; 278(10):1598-609.

11. Bala S, Szabo G. MicroRNA Signature in Alcoholic Liver Disease. International Journal of Hepatology 2012; (10): 1155-1161.

12. Hong FK, Tian WH, Jaruga BZ et al. Elevated interleukin-6 during ethanol consumption acts as a potential endogenous protective cytokine against ethanol-induced apoptosis in the liver: involvement of induction of Bcl-2 and Bcl-x(L) proteins. Oncogene 2002; 21(1):32-43.

13. Szabo G. Consequences of alcohol consumption on host defence. Alcohol and Alcoholism 1999; 34(6): 830-841.

14. Weihua Ni, Egashira K. Kitamoto S, Kataoka C

. New Anti–Monocyte Chemoattractant Protein-1 Gene Therapy Attenuates Atherosclerosis in Apolipoprotein E–Knockout Mice. Circulation 2004

(103): 2096-2101

15. Zhou J, Meadows GG. Alcohol Consumption Decreases IL-2–Induced NF-_B Activity in Enriched NK Cells from C57BL/6 Mice. Toxicological Scientes 2003; 73: 72–79.

16. Nicholas J, Kelly BL. Suppression of LPS-induced inflammatory responses in macrophages infected with Leishmania. Journal of Inflammation 2010; 7:8.

17. Ali S, Hussain SH, Shas, AA. Comparison of Maddrey Discriminant Function, Child-Pugh Score and Glasgow Alcoholic Hepatitis Score in predicting 28-day mortality on admission in patients with acute hepatitis. Ir J Med Sci 2012; 138(6):831-836.

18. Frazier HT, Stocker MA, Kershner AN, Marsano LS. Treatment of alcoholic liver disease. Therap Adv Gastroenterol 2011; 4(1): 63–81.

19. Di Castelnuovo A. Costanzo S, Donati BM, Iacoviello L et al. Prevention of cardiovascular risk by moderate alcohol consumption: epidemiologic evidence and plausible mechanisms. Internal and Emergency Medicine 2010; 5(4): 291-297.

20. Logan BK, Jones AW. Endogenous ethanol 'auto-brewery syndrome' as a drunk-driving defence challenge. Med Sci Law. 2000; 40(3): 206-15

21. Rehm J


The Risks Associated With Alcohol Use and Alcoholism. Alcohol Research & Health 2007; 34(2): 4-8.

22.Lassaillyb G, Caiazzoc R, Hollebecquea A, Buob Det al. European Journal of Gastroenterology & Hepatology 2011; 23(6): 409-505.

Results of cases

Mean Value

( Σ X¯/n)

Reference Intervals

Adult Females

Reference Intervals

Adult males

White blood cell (WBC) count = 13.9 x 10³μl


4.4 - 11.3 x 109/L


4.8 - 10 x 109/L


Red blood cell (RBC) count = 3.8 x 10³μl


4.1 - 5.1 x 1012/L


4.2 - 5.50 x 1012/L


Hemoglobin (HGB)= 9.5 g/dL


12.3 - 15.3 g/dL


13 - 17 g/dL


Hematocrit (HCT) = 36.5%


35.9 - 44.6%


42 - 52%


MCV = 65.9 fL


81 - 99 pg


80 - 94 pg

About the publisher:

- My Book written in Clinical Laboratory Medicine, “ Hematological and Metabolical Aspects from Laboratory Medicine” , confirm the aria of my interest in discovery of carcinogenesis mechanisms, especially in onco-haematology field, Leukemia.


Also, my new e-Book: e-BOOK: Hematological and Metabolical Aspects of Laboratory Medicine (Hematological and Metabolical Aspects from Laboratory Medicine) ( Second Edition ) [Large Print] [Paperback].

Publisher: Aurelian Udristioiu, 2 edition (September 9, 2013) Full Color on White paper, 122 pages. ISBN-13: 978-1492186816 (CreateSpace-Assigned) ISBN-10: 1492186813, BISAC: Medical / Laboratory Medicine, USA. Sold by   

Please, see the Blog of my Medical Book :   




1. Udristioiu A. The Assessment of Uncertainty in Measurement of Cholesterol; A Model of Calculation. Biophysical Journal; Volume 96, Issue 3, Supplement 1, February 2009; Page 504a.

2. Udristioiu A, Florescu Cristina, Popescu Manuela Andrei. “High Concentration of anaerobic ATP implicated in aborted apoptosis from CLL”. LabMedicine, American Journal of Clinical Pathology-ASCP, Manuscript 09-08-LM-S-SCI-0122R1, Published in 04-05/2010.

3. Aurelian Udristioiu. First Hematological Signal of Latent Anemia to Aging Population. Nature Publishing Group. Advance Search 0.1038 npre 2009.3285.1. Creative Common Attribution 3.0 License, accepted for the work online posted.

4. Udristioiu A, Cojocaru M, Florescu C. Screening Tests for Latent Anemia in Hospitalized Adults Over 65.   LabMedicine, American Journal of Clinical Pathology-ASCP, Manuscript  09-11-LM-S-SCI-0156.R1,  Published  in 07-05/2010.USA American Journal of Clinical Pathology p-ISSN: 0002-9173 ICV 38.53 LabMedicine ; Ascp Press) , Impact Factor ISI, IF = 2.853 , 18 Index Copernicus Journals Master List 2006.


1 University of Medicine and Pharmacy “Carol Davila, Faculty of Pharmacy, Department of Microbiology, Traian Vuia 6, Sect. 2, 020956,Bucharest, Romania. 6“Stefan S. Nicolau” Virology Institute, Bucharest, Romania. FARMACIA 2010; (57); 3: 420-427 IMPACT FACTOR ISI THOMSON 0.144 .

6. Moleular Biological  Tchiniques  user for identification  of Candida SPP. MANUELA-ANDA RADU-POPESCU1*, SILVIA DUMITRIU2, SIMONA ENACHE-SOARE3,  AURELIAN UDRISTOIU4. 1 University of Medicine and Pharmacy “Carol Davila, Faculty of Pharmacy. FARMACIA 2010; (58); 4: 422-429

7. Udristioiu A. Role of Mg2+ ion as cofactor ATP in assurance of energetic environment cells( Abstract). Magnesium Research 2011; 24 (1): 22-6.

8. -Aurelian Udristioiu, Radu G. Iliescu, Cristina Popescu. Variability of bilirubin values in serum samples with high triglycerides; interference or congenital liver syndromes. J Biosci Tech Volume 2, Issue 4 (JULY 2011).

9. Aurelian Udristioiu¹*,Radu G. Iliescu², Lucian Udristioiu¹ and Manole Cojocaru. A new approach of abnormal apoptosis as a cause of autoimmunity and malignancy. Biotechnology and Molecular Biology Review Vol. 6(8), pp. 166-171, November 2011 . Available online at <>

10. Aurelian Udristioiu, Cristina Popescu, Manole Cojocaru, Sorina Comisel, Valentina Uscatescu. Relation between LDH and Mg as Factors of Interest in the Monitoring and Prognoses of Cancer. Journal of Bioanalysis & Biomedicine. Ref.:  Ms. No. JBABM-11-48R1 accepted on Jan 27, 2012

11. UDRISTIOIU A. Florescu C, Popescu C, Cojocaru M "Significance of Neutrophil Alkaline Phosphatase versus Isoenzymes ALP in Acute or Chronic Diseases,"accepted for publication in LabMedicine, LabMedicine Manuscript 11-03-LM-U-MR-0052.R2/11/12/2011.

12. Aurelian Udristioiu¹, Radu Iliescu ², Manole Cojocaru³. Errors in Counting Platelets in Hemodialysis Patients by Use of Optical Microscopy. Review of Applied Physics (RAP) Volume 2 Issue 1, March 2013; p: 17-22

13. Aurelian Udristioiu¹, Radu Iliescu ², Manole Cojocaru³. Energetic Levels of Metabolic Pathways in Malignant B and T Cells Mini-Review. Advances in Chemical Science Volume 2 Issue 4, December 2013; 2; 90-95

14. Aurelian Udristioiu¹, Manole Cojocaru² Hemolytic Anemia Drugs Induced by Antihypertensive Agents: A case of Laboratory. 13 Scholars Journal of Medical Case Reports ISSN 2347- 6559. Sch J Med Case Rep 2013; 1(1):8-11

15. Aurelian Udristioiu1*, Radu G. Iliescu2, Manole Cojoraru Molecular mechanisms of bone reconstruction in new dental implant technology. Integrated Journal of British. Volume 1 2014 Issue 1(5-6), pg: 1-7; IJBRITISH.


1.Aurelian Udristioiu. Cicloergometrul si Sanatatea. Ed. Medicala 1990, Bucuresti. ISBN: 973-39-01105-9; Formatul 16/10 x 100; Nr pagini: 78.

2.Aurelian Udristioiu. “Bioenergetica Celulara si Maligna” Ed. Academica Brancusi 2002, Targu Jiu, Bun de tipar, Bucuresti, Tipografia Everest 2001; ISBN 973 85342-6-7; Formatul 16/14 x 100; Nr. Pagini: 307.

3. Aurelian Udristioiu, Manole Cojocaru, Radu Iliescu., Hematological and Metabolic Aspects from Laboratory Medicine" (ISBN 978-3-8473-0775-4). LAP LAMBERT Academic Publishing GmbH & Co. KG Heinrich-Böcking-Str. 6-8 , 66121, Saarbrücken, Germany, 2012.

4. Book title: Renal Diseases / Book 2 (ISBN 979-953-307-704-7). Chapter title: Variability of Biological Parameters in Blood Samples between Two Consecutive Schedules of Hemodyalsis

Authors: Aurelian Udristioiu, Manole Cojocaru, Victor Dumitrascu, Daliborca Cristina Vlad, Alexandra Dana Maria Panait and Radu Iliescu, Publishing Group 2011., Volume 2, Issue 4 (JULY 2011)

5. e-BOOK: Hematological and Metabolical Aspects of Laboratory Medicine (Hematological and Metabolical Aspects from Laboratory Medicine) ( Second Edition ) [Large Print] [Paperback].


Publisher: Aurelian Udristioiu, 2 edition (September 9, 2013) Full Color on White paper, 122 pages. ISBN-13: 978-1492186816 (CreateSpace-Assigned) ISBN-10: 1492186813, BISAC: Medical / Laboratory Medicine, USA. Sold by  

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