Acta Medica Martiniana - Univerzita Komenského

ACTA 

MEDICA 

MARTINIANA 

JESSENII FACULTAS MEDICA MARTINENSIS 

Universitatis Comenianae 

ISSN 1335 - 8421 

Journal for Biomedical Sciences, 

Clinical Medicine and Nursing 

2011 

11/1 

ISSN 1339 - 4139 (online)

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Publishing of Acta Medica Martiniana 11/01 

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ISSN 1335-8421, ISSN 1338-4139 (online) Acta Med Mart 2011, 11(1) 

ACTA MEDICA 

MARTINIANA 

Journal for Biomedical Sciences, 

Clinical Medicine and Nursing 

Contents 

5 

Genetics of psoriasis – short resume 

Valentova V., Galajda P., Pec M., Mokan M., Pec J. 

14 

Activity of monoamine oxidases in rat female genital organs during 

preimplantation period of pregnancy 

Mihalik J., Kravcukova P., Hodorova I., Vecanova J., Rybarova S. 

21 

Renal ontogeny of P-glycoprotein/MDR1 in rat 

Hodorova I., Mihalik J., Vecanova J., Dankova M., Rybarova S. 

27 

Investigating dyspepsia in clinical practice – a trap for Giardia. 

Banovcin P. Jr., Demeter M., Bozikova J., Hyrdel R. 

35 

Point prevalence survey of nosocomial infections in University Hospital in Martin 

Zabkova E., Murajda L., Hudeckova H. 

Published by the Jessenius Faculty of Medicine in Martin, 

Comenius University in Bratislava, Slovakia

4 

A C T A M E D I C A M A R T I N I A N A 2 0 1 1 1 1 / 1 

Editor – in – Chief: 

Javorka Kamil, Martin, Slovakia 

International Editorial Board: 

Belej Kamil, Martin, Slovakia 

Belova Nina, Sofia, Bulgaria 

Bohlin Kajsa, Stockholm, Sweden 

Danko Jan, Martin, Slovakia 

Honzikova Natasa, Brno, Czech Republic 

Jakus Jan, Martin, Slovakia 

Javorka Kamil, Martin, Slovakia 

Kliment Jan, Martin, Slovakia 

Lehotsky Jan, Martin, Slovakia 

Mares Jan, Praha, Czech Republic 

Mechirova Eva, Kosice, Slovakia 

Mistuna Dusan, Martin, Slovakia 

Mokan Marian, Martin, Slovakia 

Mokry Juraj, Slovakia 

Musial Jacek, Krakow, Poland 

Plank Lukas, Martin, Slovakia 

Stasko Jan, Martin, Slovakia 

Stransky Albert, Martin, Slovakia 

Tatar Milos, Martin, Slovakia 

Zibolen Mirko, Martin, Slovakia 

Zubor Pavol, Martin, Slovakia 

Editorial Office: 

Acta Medica Martiniana 

Jessenius faculty of Medicine, Comenius University 

(Dept. of Physiology) 

Mala Hora 4 

036 01 Martin 

Slovakia 

Instructions for authors: http://www.jfmed.uniba.sk (Acta Medica Martiniana) 

© Jessenius Faculty of Medicine, Comenius University, Martin, Slovakia, 2011

ACTA MEDICA MARTINIANA 2011 11/1 

DOI: 10.2478/v10201-011-0001-0 

5 

GEnEtICS OF PSORIASIS – SHORt RESUME 

Valentova V. 1 , Galajda P. 2 , Pec M. 1 , Mokan M. 2 , Pec J. 3 

1 

Department of Medical Biology, Jessenius Faculty of Medicine, Comenius University, Martin, 2 Clinic 

of Internal Medicine I., Jessenius Faculty of Medicine, Comenius University, Martin, 3 Clinic of 

Dermatovenerology, Jessenius Faculty of Medicine, Comenius University, Martin, Slovak Republic 

ABStRACt 

Psoriasis is a disease with a genetic background (4). Several psoriasis susceptibility loci (PSORS) have been 

found on various chromosomes: PSORS1 on 6p21.3, PSORS2 on 17q, PSORS3 on 4q, PSORS4 on 1q21, 

PSORS5 on 3q21, PSORS6 on 19p, PSORS7 on 1p, PSORS8 on 16q, PSORS9 on 4q31, PSORS10 on 18p11, 

PSORS11 on 5q31-q33 and PSORS12 on 20q13. (27). However, the exact genes and their functions, or their 

respective malfunctions, in psoriasis and arthritis have not been unambiguously identified. Recently, it has 

been argued that PSORS1 may indeed be the HLA-Cw*06 allele encoding the HLA-Cw6 molecule (35). 

Psoriasis is a chronic inflammatory disease of skin that also often affects joints and nails. This disorder is 

characterized by hyperproliferation of keratinocytes, activation of angiogenesis, vasodilatation and mainly by 

lymphocyte infiltration of dermis and epidermis (45). The process of maturation of keratinocytes is accelerated 

and thus not quite terminated. Psoriatic lesion appears on skin. 

Skin manifestations are typically red bounded areas of different size and shape with characteristic silvery 

scales (9). Lesions appear mostly on the skin of elbows and knees, scalp including genitals. Individual 

manifestations differ in size and severity from localized lesions to whole body involvement. Very often psoriasis 

affects nails of hands and feet. It can also cause inflammatory changes on joints, named as psoriatic arthritis. 

Similarly to rheumatoid arthritis and sclerosis multiplex, psoriasis is classified as an immune mediated 

inflammatory disorder. Those disorders are characterized by chronic progression of an inflammatory process 

and important role of TNF alpha. Because of the role of TNF alpha in pathogenesis, we can use its inhibitors 

in therapy. It also affects progress of different comorbidities such as diabetes mellitus 2 and cardiovascular 

problems (21). Patients with psoriasis have often other risk factors for atherosclerosis such as lipid metabolism 

disorders and overweight (37). 

Key words: psoriasis, PSORS, HLA-Cw6 

IntRODUCtIOn 

Psoriasis is characterized by hyperproliferation and abnormal differentiation of epidermal 

keratinocytes, by lymphocytary infiltrate composed mainly of T-cells. Other features 

are change of endothelium, angiogenesis, dilatation and formation of high endothelial 

venules (HEV) (29). 

Exact pathogenesis of this disorder is unknown, but it is supposed that main role 

plays an immune system (42, 45). 

Theory that psoriasis is primarily keratinocyte proliferation disorder is based on abnormally 

fast mitotic activity of keratinocytes. T-cell hypothesis imply an abnormal activation 

of an acquired immunity. Knowing that TNF alpha therapies are very effective, 

suggests an important role of innate immunity in pathogenesis (5). 

Address for correspondence: 

Mgr. Vanda Valentova, Department of Medical Biology, Jessenius Faculty of Medicine, Comenius University 

Mala Hora Str. 4, 036 01 Martin, Slovak Republic, Phone: +4210434131425, E-mail: valentova@jfmed.uniba.sk

6 


SHORt REVIEw OF LOCI AnD CAnDIDAtE GEnES 

In the early 1970s psoriasis was placed into associations with the HLA complex on 

chromosome 6p. Russell et al. in 1972 first reported association with allele HLA-B13. 

After that, were identified strong associations with other two alleles, Cw6 and DR7 (22, 

49). These two alleles were estimated to be relative risk factors for the disease. 

There are two types of psoriasis (23): 

• a familial, early age of onset form (

A C T A M E D I C A M A R T I N I A N A 2 0 1 1 1 1 / 1 7 

It is possible that malfunction of CD4+CD25+ regulatory lymphocytes can be partially 

based on abnormal hematopoietic cells and with genetic background (55). 

table 1: PSORS loci (10) 

Locus name Chromosomal location Reference 

PSORS 1 6p21.3 Zhang et al., 2002 

PSORS 2 17q24-25 Samuelsson et al., 1999 

PSORS 3 4q34 Samuelsson et al., 1999 

PSORS 4 1q21 Capon et al., 1999 

PSORS 5 3q21 Enlund et al., 1999 

PSORS 6 19p13-q13 Lee et al., 2000 

PSORS 7 1p35-p34 Veal et al., 2001 

PSORS 8 16q Karason et al., 2003 

PSORS 9 4q31 Zhang et al., 2002 

PSORS 10 18p11.23 Asumalahlati et al., 2002 

PSORS 11 5q31-q33 www.ncbi.nlm.nih.gov/omim 

PSORS 12 20q13 www.ncbi.nlm.nih.gov/omim 

PSORS1 

The most studied locus is PSORS1 mapped to MHC complex on chromosome 6. This 

region contains genes coding proteins of immunological pathways and is strongly associated 

with genes of lymphocyte antigens also situated in this area (1, 11). Main marker 

of this area is HLA-Cw6 (48). This allele is most frequently mapped in population with 

early onset psoriasis (36). 

Human leukocyte antigen 

Psoriasis has signs of an autoimmune disease and there is no surprise that there was 

found association with certain HLA alleles. Also a role for CD8+ cells is favoured by the 

observed linkage of psoriasis to certain MHC I alleles, especially HLA Cw6 (20). 

Only about 10 % of HLA-Cw6-positive individuals develop psoriasis, suggesting a major 

role for additional genes and/or environmental triggers (30). 

The observation that a large, multiply affected family demonstrated linkage of psoriasis 

susceptibility to 17q25 (50) and not to HLA suggests that other genes can confer 

susceptibility. In a study of 23 multiply affected families was observed that 25 % are 

HLA-Cw6 positive. In one family, all three affected members are HLA-B27 (4, 33, 35). 

PSORS2 

Locus is situated near telomeres of chromosome 17q (50). Exact localization of risk allele 

is not known. In this area at least two candidate genes are expected, but last large 

study eliminated them both (47).

8 


PSO0RS3 

Localized is on chromosome 4, in position 4q34. A relation with early onset psoriasis 

was found in this area (17). Responsible gene is mapped about 50kb from former marker 

of PSORS3 locus. The newest localization is for PSORS9 locus, mapped closer to centromere 

(4q31) in PSORS3 area (25, 56). In this region are situated different genes coding 

immunologically important proteins, including IL-15 gene (53). 

PSORS4 

Locus PSORS4 mapped to 1q21 of chromosome 4, in area of Epidermal differentiation 

complex. This region involves 13 genes coding S100 calcium binding proteins. Some of 

them, S100A7, S100A8 a S100A9 are known to be increased in keratinocytes of psoriatic 

patients (44). S100 proteins are responsible for chemotaxis of leukocytes. 

PSORS5 

Localized to 3q21 but his exact position is need to be confirmed by more studies (43). 

PSORS6 

Mapped to 19p13 and his position is also not exact. In this area is mapped also gene 

JUNB, which product is member of AP-1 family of transcriptional factors, that control 

differentiation of keratinocytes (54). 

PSORS7 

Locus is situated in position 1p. Veal et al. (52) referred to fact that gene EPS15 

coding intracellular substrate for EGF receptors, highly expressed in psoriatic skin, 

and is mapped to critical region in position of 1p. 

PSORS8 

This locus is mapped to 16q. Nair et al. (35) referred that PSORS8 area is overlapping 

with susceptibility locus for Crohn disease. They found that this locus contains NOD2/ 

CARD15 gene. They also found that psoriasis is more often in patients with Crohn disease, 

in comparison to control group. It shows a possibility that in this region is localized 

an immunomodulatory locus able to affect both diseases. 

PSORS9 

Locus is mapped to 4q position. 

IL-10 

IL-10 plays an important role in the pathophysiology of psoriasis. This disease is characterized 

by a relative IL-10 deficiency that can in part explain the predominance of a 

Th1 response. The IL-10 promoter region is very polymorphic and controls transcription 

of the IL-10 gene (3, 24). 

While the concept of an allele that makes an individual susceptible to a disease is easily 

understood, the concept of a protective allele of a predisposing gene is rather new in 

the genetics of psoriasis.


table 3: Frequencies and allele sizes of interleukin (IL)-10.G (a) - Allele nomenclature at the Genome Data 

Base (http://www.gdb.org) (24). 

Size (bp) Frequency GDB a 

132 0.022 Allele 12 

134 0.034 Allele 11 

136 0.399 Allele 10 

138 0.075 Allele 9 

140 0.079 Allele 8 

142 0.052 Allele 7 

144 0.240 Allele 6 

146 0.086 Allele 5 

148 0.011 Allele 4 

Other study analyzed the highly polymorphic IL10.G microsatellite to determine if IL- 

10 has a role in psoriasis susceptibility. Findings showed a possible role of IL-10 promoter 

polymorphism in disease susceptibility and the G13 allele at the IL10.G locus was 

found to be associated with psoriasis (3). 

Other allele, allele 3 (IL10.G9) apparently has a small protective effect and is the most 

frequent allele of this multiallelic polymorphism allele 3 (IL10.G9) was present in 80 % 

of the families (24). 

The effect of the IL10.G9 promoter polymorphism observed by Hensen et al. is small 

compared with the effect of the PSORS1 marker. They also observed a small effect for 

allele 8 (IL10.14). This allele was present in only 28 % of the families (24). 

SPP2 (Secreted phosphoprotein 2) 

Bandshift analysis showed that SPP2 is NF-κB dependent gene. High positive regulation 

of NF-κB dependent gene was detected in samples from affected skin of psoriatic 

patients (34). NF-κB induces expression of VCAM-1 trough homocysteine. Protein vCAM- 

1 enables adhesion of lymphocytes, monocytes, eosinophiles and basophiles to endothelium 

of blood vessels. It also has a function in signal transport between leukocytes and 

endothelial cell. 

VDR 

D vitamin receptor is one of the candidate genes in psoriasis. It has immunosuppressive 

effects and is involved in an antiproliferation and prodifferentiaton cascades in 

keratinocytes (18). Neutrophils are expressing VDR. Polymorphism in A allele, A-1012G, 

is linked to negative regulation of TH1 response trough Trans-acting T-cell-specific transcription 

factor GATA-3. Alleles F and T of Fok1 and Taq1 genes are involved in increased 

activity of VDR. A-1012G, Fok1 and Taq1 VDR gene polymorphism is linked to 

with answer to calcipotriol (synthetic vitamin D3). A-1012G and Fok1 have relationship 

with susceptibility to non-familial psoriasis (18).

10 


ADAM33 and other genes 

Polymorphism in locus ADAM33, first gene identified in asthma, is in these days given 

to relation with psoriasis (46). 

Li et al. have tested 15 SNPs form 7 expected psoriatic risk genes: rs597980 in allele 

ADAM33, rs6908425 in CDKAL1 and rs3789604 in PtPn22. Results have shown as 

significant for the same alleles as in previous studies. This data show, that ADAM33, 

CDKAL1, and PTPN22 are risk genes for psoriasis (32). 

Study of Oudota et al. in year 2009, confirmed linkage of other six candidate genes 

to susceptibility to psoriasis: SCL12A8, belongs to group of free transposing genes; 

FLG and tGM5, involved in epidermal differentiation; CARD15 and CYLD, that modulate 

transcriptional factor NF-κB and IL1Rn, coding antagonist receptor of IL-1. It was 

proved that an association exists between main risk allele HLA-Cw6 and CARD15, CYLD 

and TMG5 alleles. Together these results show that etiology of psoriasis and other disorders 

is cooperation of different genetic factors (40). 

One region is within the MHC complex on 6p21.3 (51) and includes the non-HLA gene– 

encoding corneodesmosin (CD) — a protein with homology to keratin-10 (2). The other 

region includes a cluster of genes on chromosome 1q21 (19, 38). Potential candidate 

genes encode markers of epidermal differentiation such as corneodesmosin, psoriasin, 

and CD1d, to name a few (19). 

IL-20R 

Complex of IL-20 receptor is composed from two chains IL20RA and IL20RB. Its ligands 

are three members from IL-19 subfamily, IL-19, IL-20 and IL-24. These cytokines 

are important for manifestation of psoriatic lesions and recently was described also a 

relation between IL20 gene polymorphism and psoriasis. In last studies the hypothesis 

is tested, that genetic variants of IL-20-RI influence susceptibility to psoriasis. To these 

days there isn’t proved relationship between SNP in that gene and psoriasis. SNPs in 

two risk haplotypes influence two transcriptional factors leading to differentiation of 

immune cells. Other studies are necessary to confirm genetic association of IL-20-RA 

haplotypes with psoriasis (27). 

Conclusion 

In the last few years, molecular genetics analyses have permitted novel insights into 

psoriasis, a disease characterized by uncontrolled proliferation of keratinocytes and 

recruitment of T cells into the skin. HLA studies revealed an association with certain 

alleles, notably HLA-Cw6. Despite this HLA component, psoriasis in some families is 

inherited as an autosomal dominant trait with high penetrance. 

Significant progress has been made in the understanding of the genetic, immune and 

pathogenetic aspects of psoriasis. 

Understanding the genetics of psoriasis, and why some people are affected and others 

are not could lead to more effective treatments. They could work blocking the action of 

concrete genes, changing their behaviour or by replacing mutated genes with healthy 

ones via gene therapy.


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51. Trembath RC, Lee Clough R, Rosbotham JL, Jones AB, Camp RDR, Frodsham A, Browne J, Barber R, 

Terwilliger J, Lathrop GM, Barker JNWN. Identification of a major susceptibility locus on chromosome 6p 

and evidence for further disease loci revealed by a two stage genome-wide search in psoriasis. Hum Mol 

Genet 1997; 6:813-820 

52. Veal CD, Clough RL, Barber RC, Mason S, Tillman D, Ferry B, Jones AB, Ameen M, Balendran N, Powis 

SH, Burden AD, Barker JNWN, Trembath RC. Identification of a novel psoriasis susceptibility locus at 1p 

and evidence of epistasis between PSORS1 and candidate loci. J Med Genet 2001; 38:7-13 

53. Villadsen LS, Schuurman J, Beurskens F, Dam TN, Dagnaes-Hansen F, Skov L, Rygaard J, Voorhorst- 

Ogink MM, Gerritsen AF, van Dijk MA, Parren PW, Baadsgaard O, van de Winkel JG. Resolution of psoriasis 

upon blockage of Il-15 biologic activity in a xenograft mouse model. J Clin Invest 2003; 112:1571-80 

54. Zenz R, Eferl R, Kenner L, Florin L, Hummerich L, Mehic D, Scheuch H, Angel P, Tschachler E, Wagner 

EF. Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins. Nat 

2005; 437:369-75 

55. Zhang K, Li X, Yin G, Liu Y, Niu X, Hou R. Functional characterization of CD4+CD25+ regulatory T cells 

differentiated in vitro from bone marrow-derived haematopoietic cells of psoriasis patients with a family 

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56. Zhang XJ, He PP, Wang ZX, Zhang J, Li YB, Wang HY, Wei SC, Chen SY, Xu SJ, Jin L, Yang S, Huang W. 

Evidence for a major psoriasis susceptibility locus at 6p21 (PSORS1) and a novel candidate region at 4q31 

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Physiol Genomics 2003; 13:69-78 

Received: December,6,2010 

Accepted: January,7,2011

14 


DOI: 10.2478/v10201-011-0002-z 

ACtIVItY OF MOnOAMInE OxIDASES In RAt FEMALE GEnItAL 

ORGAnS DURInG PREIMPLAntAtIOn PERIOD OF PREGnAnCY 

Mihalik J. 1 , Kravcukova P. 2 , Hodorova I. 1 , Vecanova J. 1 , Rybarova S. 1 

1 

Department of Anatomy, P.J.Safarik University, Medical Faculty, Kosice, Slovak Republic 

2 

Neurobiological Institute, Slovak Academy of Sciences, Kosice, Slovak Republic 

ABStRACt 

Our objectives in the present study were to determine the activity of monoamine oxidases A and B (MAO AB) 

in rat ovary, oviduct and uterus during preimplantation period of pregnancy. It should help us to clarify and 

better understand possible involvement of both MAO enzymes in the reproductive process. Pregnant females 

were killed employing a lethal dose of thiopental on the first (D1), on the third (D3), and on the fifth (D5) 

days of pregnancy. Rats were perfused transcardially with the PBS to rinse out of the body as much blood as 

possible. Ovaries, oviducts and uteri were immediately removed and stored until the measurement was done. 

MAO activity was determined by fluorescent monoamine oxidase detection kit. In the ovaries we have found 

the highest MAO activity at D3, followed by D1, and the lowest levels were recorded at D5 of pregnancy. In 

the oviducts, the highest MAO activity was detected again at D3, followed by D5, and by D1 of pregnancy. But 

statistical analysis did not reveal any difference between individual days of pregnancy nor in the ovaries, neither 

in uterine tubes. Uteri were the only organs, in which statistically significant differences were detected (p


numerous, but information about the quantification of MAO in female gonads during 

pregnancy is limited. 

Recently we have observed an antagonistic effect of chronic treatment with deprenyl, 

a potent MAO-B inhibitor, at the dose 0.25 mg/kg on embryo development in rats. Significantly 

less degenerated embryos were isolated from experimental females, but on the 

other hand, a decreased mean cell number in blastocysts was recorded [5]. Our objectives 

in the present study were to determine the activity of MAO in rat ovary, oviduct and uterus 

during preimplantation period of pregnancy, which should help us to clarify and better 

understand possible involvement of both MAO enzymes in the reproductive process. 

MAtERIAL AnD MEtHODS 

Animals 

All procedures performed with animals adhered to the permission granted by the Committee 

for Ethical Control of Animal Experiments at Safárik University and the permission 

of the State Veterinary and Food Administration of the Slovak Republic (permission 

No. 715/08-221b). All efforts were made to minimize both the number of animals and 

their suffering. 

Experiments were carried out on 15 young, virgin female Wistar rats (200-240 g, 85-90 

days old) obtained from the animal facility of the University. The animals were given free 

access to standard diet and water and were maintained in a 12 h light/12 h dark cycle. Females 

were mated for two hours from 07:00-09:00 a.m. with males of the same strain. The 

first day on which a vaginal plug was present was designated as day 1 of pregnancy. Pregnant 

rats were killed by a lethal dose of thiopental (40 mg/kg; ICN Czech Pharma, Prague, 

Czech Republic) on the first (D1), on the third (D3), and on the fifth (D5) day of pregnancy. 

After a lethal injection of thiopental rats were perfused transcardially with 100 ml of 

room-temperature PBS (ph 7.4) to rinse out as much blood as possible. Ovaries, oviducts, 

and uteri were immediately removed and stored in Eppendorf tubes at -80 °C 

until the measurement was done. 

MAO AB activity 

Activity of MAO was measured by fluorescent monoamine oxidase detection kit (Bachem; 

Cat. No. S-90092) based on detection of H2O2 released from the conversion of a 

substrate to its aldehyde via both forms MAO A and MAO B. H2O2 oxidizes the detection 

reagent in a 1:1 stoichiometry to produce the fluorescent product. A standard curve was 

prepared from resorufin to determine moles of product produced. 

Briefly, organs were homogenized in five volumes (w/v) of the 25mmol/l TRIS-HCL (pH 

7.4) mixed with 1mmol/l EDTA and subsequently were centrifuged at 10,000xg for 15 

min at 4 °C. To a black 96 well plate 100 ml of samples and 100 ml of reaction cocktail 

were added into individual wells to incubate at room temperature for 30-60 minutes. 

Reaction cocktail was prepared obeying the manufacturer’s instructions and consisted 

of the detection reagent, horse radish peroxidase and dimethyl sulfoxide (DMSO). Samples 

were read using excitation at 570 nm and fluorescence was measured at 590-600 

nm employing the fluorescence plate reader. Activity of MAO expressed as the µmol/l 

resorufin was normalized on the basis of total protein content (µmol/l of resorufin/ 

mg of protein). Chemicals used for assessing of enzymes activity were purchased from 

Sigma-Aldrich (St. Louis, MO, USA). 

Statistical analysis 

Data are expressed as the mean ± SD. Differences in the MAO AB activity were analyzed by 

the Kruskal-Wallis test for multiple comparisons. P

16 


RESULtS 

Fig. 1 Activity of MAO in the rat ovary on the first (D1), third (D3), and on the fifth (D5) day of pregnancy. 

Results are depicted as a µmol/l of resorufin/mg of proteins ± S. D. (p>0.05) 

Concerning ovary (Fig. 1), we have found the highest MAO AB activity at D3 (72.44 ± 

22.66), followed by D1 (67.10 ± 32.12) and the lowest activity was recorded at D5 (57.90 

± 17.60) of pregnancy. Kruskal-Wallis test did not reveal any significant difference compared 

individual days of pregnancy (p>0.05). 

Fig. 2 Activity of MAO in the rat oviduct on the first (D1), third (D3), and on the fifth (D5) day of pregnancy. 

Results are depicted as the µmol/l of resorufin/mg of proteins ± S. D. (p>0.05) 

In regard to oviduct (Fig. 2), the highest MAO AB activity was detected at D3 (45.44 ± 12.97), 

followed by D5 (42.09 ± 27.40) and D1 (36.49 ± 16.91) of pregnancy. Statistical analysis did 

not confirm any significant difference between individual days of pregnancy (p>0.05).


Fig. 3 Activity of MAO in the rat uterus on the first (D1), third (D3), and on the fifth (D5) day of pregnancy. 

Results are depicted as the µmol/l of resorufin/mg of proteins ± S. D. (* it means p

18 


in the CL of rat ovary employing enzymatic histochemical method [17]. In our work we 

found the highest MAO activity on the D3 of pregnancy, when corpora lutea are already 

formed. Similar results were recorded in women employing monoclonal antibodies. MAO- 

A was intensely expressed in CL of pregnancy, especially in large luteal cells [18]. MAO 

enzymes were also detected in the intersticial gland cells and in the blood vessels of rat 

ovary [17]. It has been recorded [19], that MAO activities in the vessels of ovarian pedicle 

of pigs were the highest on the 13-14 day of the estrous cycle. Authors suggest that high 

MAO activity in the vessels may be a significant factor in the regulation of the ovarian 

vasotone and might be responsible for increasing in the ovarian blood flow during the 

luteal phase of ovarian cycle. Interstitial glands are situated near to the blood vessels in 

the ovarian stroma, and arise from the follicles, which undergo atrophic process. Probably 

this is the reason why the further catecholamine accumulation is not needed and 

these substances are rather metabolized through MAO enzymes. Taken together, results 

suggest that MAO activity in the ovary might be involved in follicular development and 

progesterone metabolism. 

High concentrations of NA have been detected in the human and cow oviductal compartments 

[20, 21]. The highest concentrations were found in the isthmus, where the 

adrenergic nerves are primarily related to smooth muscles [20]. Recently we have found 

that high doses of deprenyl (2.5 mg/kg), a potent MAO-B inhibitor, significantly slow 

down the movement of rat embryos through the female reproductive tract [22]. These 

findings need another investigation, because MAO-B and MAO-A are responsible for the 

DA degradation and DA was also detected in the human [20] and cow [21] oviduct compartments. 

Moreover, the addition of DA into the incubation bath significantly reduced 

the strength and frequency of spontaneous rhythmic contractions of the rat uterus [23]. 

NA was also identified in bovine oviductal fluid [24], and it could influence the oviduct 

epithelium via adrenergic receptors, which have been shown in the oviduct epithelian 

cells of several species [25, 26]. Recently, it was clearly demonstrated that mouse oocytes 

and embryos express α2C- and β2-adrenergic receptors, too [27]. As one could expect, 

MAO activity in the human oviduct has been detected on the same places, as their 

catecholamine substrates are located. It means in the epithelium and in the muscular 

layer [28]. Despite the fact that we have recorded the highest activity of monoamine oxidases 

on D3 and on D5, when embryo goes through the oviduct into the uterus, activity 

of MAO did not differ significantly compared the individual days of pregnancy. Probably, 

it could be the sign of similar metabolic MAO activity, as the oviduct almost permanently 

moves during the transport of spermatozoa in the time of fertilization and subsequently 

during the embryo passage down into the uterine cavity. Based on the works mentioned 

above, catecholamines play the pivotal role in this process. 

Uterus is the only one reproductive organ, in which significantly different MAO activity 

during preimplantation period of pregnancy was recorded. In the time, when the oocytes 

and subsequently embryos are located in the oviduct, extremely low MAO activity in rat 

uterus was detected. However, on the D5, when embryos are present in the uterine cavity 

and their implantation into the uterine wall occurs, MAO activity significantly increased 

several times. Successful implantation depends both on the quality of the embryo and on 

the endometrial receptivity. The later depends on the progesterone-induced changes in 

gene expression. One of the genes whose transcription appears to be enhanced during the 

receptive period is probably gene for MAO. Similar results were obtained in women [29]. 

MAO-A transcript levels increased in human uterus between the pre-receptive and receptive 

phase with a median increase of 25-fold. Conversely, prior failure of embryo implantation 

was associated with a 29-fold decrease in MAO-A mRNA levels and a substantial 

reduction in MAO-A protein immunofluorescent label score. These results show a strong 

association between endometrial receptivity and MAO-A expression in the endometrial 

epithelium, suggesting an important role for this enzyme in normal implantation.


In the present study, we determined activity of monoamine oxidases in rat ovary, 

oviduct and uterus on the first, on the third and on the fifth day of pregnancy. We can 

conclude that significant elevation of MAO activity was recorded in the rat uterus in the 

time of embryonic implantation. The data obtained extend our knowledge about MAO 

enzymes in rat reproductive organs during early period of embryo development. To our 

knowledge this is the first paper describing the MAO activity in female reproductive organs 

during the whole preimplanation period of pregnancy in mammals. 

Acknowledgement: This research work was supported by the VEGA Agency [grant 1/4227/07]. 

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DOI: 10.2478/v10201-011-0003-y 

21 

REnAL OntOGEnY OF P-GLYCOPROtEIn/MDR1 In RAt 

Hodorova I. 1 , Mihalik J. 1 , Vecanova J. 1 , Dankova M. 2 , Rybarova S. 1 

1 

Department of Anatomy, P. J. Safarik University, Faculty of Medicine, Kosice, Slovak Republic; 2 Department 

of Histology and Embryology, P. J. Safarik University, Faculty of Medicine, Kosice, Slovak Republic 

ABStRACt 

BACKGROUND: P-glycoprotein (Pgp/MDR1) is an ATP-dependent, integral plasma-membrane efflux pump 

that is constitutively expressed on adult apical brush-border epithelium of renal proximal tubules. This Pgp/ 

MDR1 tissue distribution and localization affects the absorption, distribution, metabolism, and excretion of 

Pgp/MDR1 substrates. The ontogeny of rat Pgp/MDR1 is still doubtful, and such knowledge may be helpful 

in understanding age-related pharmacokinetics. The purpose of this study was to determine, whether Pgp/ 

MDR1 expression is altered during development. 

METHODS: Postnatal expression of Pgp was determined using immunohistochemical method. Tissue from 

Wistar rat were isolated on the 1st day (D1), 7th day (D7), 14th day (D14), 21st day of life (D21) and from adult 

animals (60 days old; Ad). 

RESULTS: Our ontogeny study illustrated that expression of Pgp was relatively constant from birth to adulthood. 

CONCLUSIONS: Knowledge of the ontogeny of transport proteins involved in distribution and elimination of 

drugs is important for adequate interpretation of the results of toxicity studies in juvenile animals. 

Key words: Pgp/MDR1, rat, immunohistochemistry 

IntRODUCtIOn 

ATP-binding cassette (ABC) superfamily now includes about 300 proteins, among the 

transporters of quite different compounds (1,2,3). Proteins of this family are present in 

all living organisms. About fifty ABC proteins have been found in man and approximately 

the same number in mouse (4). Since a great number of ABC proteins were discovered 

only recently, many of them are still poorly studied. Studies of ABC proteins are important 

both for medicine and biology because they concern problems of protection of all 

living cells. Human proteins of the ABC family are divided to seven subfamilies (class A 

to G) (4,5). The affiliation of each protein to a subfamily is determined by its domain organization, 

namely by the number and combination of transmembrane domains (TMDs) 

and ATP-binding domains (NBDs, nucleotide-binding domains) (6). In total, there are 49 

protein members in this family, but only three are well known for their multidrug resistance 

(7). There are P-glycoprotein (Pgp/MDR1, ABCB1), MDR-associated protein (MRP1, 

ABCC1) and breast cancer resistance protein (BCRP, ABCG2). Pgp, paradigm ABC drug 

efflux transporter, is the first detected and to date the best characterized of the family of 

ABC drug efflux transporters. It gained worldwide attention about three decades ago for 

its role in the phenomenon of multidrug resistance in tumor cells (8,9). Subsequently, 

constitutive expression of Pgp/MDR1 has been described in a variety of other tissues including 

liver, intestine, kidney, pancreas, adrenal, capillary endothelium of blood-brain 

and blood-testis barrier, choroid plexus, placental trophoblast and others (10). The polarized, 

apical membrane localization of Pgp/MDR1 causes that its substrates are prefeerentially 

translocated from basolateral to the apical side of the epithelium. Thus, Pgp/ 

MDR1 limits the influx and facilitates the efflux of its substrates, eventually preventing 

their intracellular accumulation. Many in vitro and in vivo studies demonstrated high 


Hodorova Ingrid, MD, PhD, Department of Anatomy, P.J. Safarik University, Medical Faculty 

Srobarova Str. N. 2, 040 01 Kosice, Slovak Republic, Phone: ++ 421 055 6228866; e-mail: ingrid.hodorova@upjs.sk

22 


impact of Pgp/MDR1 on drug pharmacokinetics in these organs (10). It is likely that 

Pgp/MDR1 and other ABCs have evolved in these “normal” tissues to protect them from 

potentially damaging effect of toxic compounds. 

In the kidney, Pgp/MDR1 is expressed mainly at the apical (luminal) brush-border membrane 

of proximal tubular cells (11) and to lesser extent in the thick limb of Henle’s loop, 

collecting ducts, and glomerular mesangium. Many substances are actively transported by 

Pgp/MDR1, e.g. calcium channel blockers, immunosuppressants, cardioactive glycosides, 

antibiotics, antineoplastic and severel others peptides and steroids (12,13). Thus Pgp/MDR1 

functions as an efflux pump which represents a protective mechanism to exclude endogenous 

and exogenous toxins from normal cells and to ultimately excrete them into the bodily 

secretions. In humans, two genes (MDR1 and MDR2) encode this protein, whereas in rodents 

there are three homologs of this protein, mdr1 (mdr1b), mdr2, mdr3 (mdr1a) (14,15,16). 

The aim of the present study was to determine postnatal expression of Pgp/MDR1 in rat kidney 

by two widely used monoclonal antibodies for Pgp/MDR1: C219 and UIC2 .These antibodies 

are known to detect Pgp/MDR1 in paraffin-embedded histological tissue in many histopathological 

laboratories. The neonatal rat is a useful model for kidney developmental studies since 

rats are born with immature kidneys and there is considerable postnatal renal development. 


Animals 

All procedures performed with animals adhered to the permission of the Committee for 

Ethical Control of Animal Experiments at Safarik University and the permission of the 

State Veterinary and Food Administration of the Slovak Republic (permission No. 7881/04- 

220/3). All efforts were made to minimize both the number animals and their suffering. 

To acquire rat cubs, female Wistar rats were mated with males of the same strain overnight. 

Tissue from Wistar rat were isolated on the 1st day (D1), 7th day (D7), 14th day 

(D14), 21st day of life (D21) and from adult animals (60 days old; Ad) by ether anaesthesia. 

Three animals were killed on each day examined. The kidneys were obtained by medial 

laparotomy carried out in deeply anaesthetised animals. At the end of surgery rats were 

killed by overdose of ether. Rat kidneys were immersed in a neutral buffered formalin solution 

for 72 hours at room temperature. Tissue blocks were dehydrated in increasing alcohols 

and embedded in paraffin. Seven-micron-thick serial sections were cut and attached 

to the slide with alum gelatine. The slides were processed for immunohistochemistry. 

Antibodies: 

We have used the following primary monoclonal antibodies: mouse anti-MDR1, clone 

C219 (Signet Laboratories, Inc.) and mouse anti-MDR1, UIC2 – clone C494 (Santa Cruz 

Biotechnology, Inc.). 

Immunohistochemical detection of Pgp: 

For immunohistochemistry, paraffin embedded sections of the rat kidney were deparaffinized 

with xylene and rehydrated in decreasing ethanols to water. The slides were finally washed in 

phosphate-buffered saline containing 0.05 % Tween-20 (PBS-Tw), pH 7.6. Endogenous peroxidase 

activity was blocked by 0.3 % H202 in methanol for 30 minutes at room temperature. To 

re-establish an original conformation of epitopes modified after fixation, we performed antigen 

retrieval using a microwave (in sodium citrate solution for 2x5 minutes at 500 watts). Pgp/ 

MDR1 staining procedure continued by blocking nonspecific staining with milk buffer (5 % 

dry milk in TRIS buffer) for 30 minutes at room temperature. Primary antibodies were applied 

overnight in humidified chamber at 4˚C. After rinsing in PBS-Tw (3x5 minutes) the sections 

were subsequently incubated with the secondary antibody (30 minutes) and strepatavidin-


biotin (30 minutes) (Universal detection kit LSAB+KIT/HRP, Dako). Next, the sections were 

visualized with DAB (3.3’- diaminobenzidine tetrahydrochloride) at a concentration of 0.5 mg/ 

ml in Tris buffer, pH 7.6 and 0.015 % H2O2. Slides were stream-rinsed with tap water, counterstained 

with Mayer’s hematoxylin for 2 minutes, washed in tap water, dried, mounted and 

coverslipped. Sections processed with omission of primary antibody served as control. 

Semiquantitative evaluation 

Immunostaining was assessed by two independent observers blinded to animal 

characteristics. 

Expression of Pgp/MDR1 was evaluated separately using the following scale: 3+ = 

high level (91-100 % of positive cells), 2+ = medium level (11-90 % of positive cells), 1+ = 

low level (up to 10 % of positive cells), – = negative cells (0 % of positive cells). Samples 

with high [3+] and medium level [2+] of proteins expression were considered as positive. 

Samples scored as [1+] and [–] were considered as negative. 

RESULtS 

Kidney of rat cubs 

Using monoclonal antibody mouse anti-MDR1 clone C219 we have detected moderate 

immunopositivity for Pgp/MDR1 in all developmental stages (D1, D7, D14, D21). Employing 

semiquantitative evaluation of tissue samples we have found no differences in 

expression of Pgp/MDR1 in epithelial cells of proximal tubules. The remaining structures 

(epithelial cells of distal tubules, glomerulus and glomerular capsule) did not show any 

positivity for Pgp/MDR1. 

Using monoclonal antibody mouse anti-MDR1 UIC2 – clone C494 we have detected in all developmental 

stages the same spatial protein distribution but its signal was significantly weaker. 

Kidney of rat adults 

Using both monoclonal antibodies (mouse anti-MDR1:clone C219 and mouse anti- 

MDR1:UIC2 – clone C494) we have observed expression of Pgp/MDR1 in epithelial cells of 

proximal tubules in adult kidney, too. Employing semiquantitative evaluation we have found 

no differences in expression of Pgp/MDR1 in all tissue samples. The immunoreactivity for 

this protein was strongly restricted to the apical membrane and weakly to the cytoplasm of 

proximal tubular cells. No signal for this protein in the other cells of rat kidney was found. 

A 

B 

Fig. 1. 1-day old rat kidney – D1. Immunohistochemical detection of Pgp/MDR1 by monoclonal antibody: 

mouse anti-MDR1 - clone C219 (A), UIC2 – clone C494 (B). Positive expression of Pgp/MDR1 in proximal 

tubular epithelial cells of rat kidney – cytoplasmic staining (A, B).

24 


A 

B 

Fig. 2. Pgp/MDR1 was expressed in epithelial cells of proximal tubules in 7-day old rat kidney - D7 (A) and adult 

kidney (B) by mononoclonal antibody: mouse anti-MDR1 – clone C219. The remaining structures (epithelial cells 

of distal tubules, glomerulus and glomerular capsule) did not show any positivity for Pgp/MDR1. 

DISCUSSIOn 

Knowledge of the ontogeny about transport proteins involved in distribution and elimination 

of drugs is important for adequate interpretation of the results of safety studies 

in juvenile animals. Since rat is one of the most frequently species used in non-clinical 

testing we used this species in our study on the age-dependent changes in Pgp/MDR1 

expression. We focused on the age shortly after birth until early adulthood of the animals 

(D1, D7, D14, D21, Ad). The transport proteins in the kidney are involved in the passage of 

compound through the tubular epithelial cells, prior to urinary excretion. Urinary excretion 

of drugs is a complex interplay of three mechanisms: glomerular filtration, tubular 

secretion, and tubular reabsorption. The basic prerequisite for excretion into urine is water 

solubility of drug and/or its metabolites as no transporting carrier is available in this body 

fluid. Accordingly, the primary mechanism for drug excretion is glomerular filtration, a 

passive process influenced by molecule size, concentration of unbound fraction of drug in 

plasma and renal blood perfusion. Tubular secretion and partly also reabsorption are active 

mechanisms requiring transporters. The function of renal proximal tubular epithelial 

cells is the most significant factor for active drug renal excretion (17). 

The large differences in ontogeny of the individual transport proteins were observed, 

with some transporters having the highest expression at birth (MRP1 and MRP3), and 

other having a more or less constant expression during development (MRP2 and BCRP) 

(18). It was reported that Pgp/MDR expression increased up to Day 26, with a subsequent 

decrease to adult levels at Day 42 (18). On the other hand, other authors found 

continuously increasing level of Pgp/MDR1 up to Day 60 (19). In our study we have 

found relatively constant levels of Pgp/MDR1 protein from the birth to the adulthood. 

It should be noted that all our data on transport protein is limited to actual functionality 

of Pgp/MDR1. The mRNA expression of this transporter was not studied such 

as in previous mentioned publications. The reason for the differences between the data 

obtained in our study and those already published, as well as the differences between 

individual publications, are most likely related to differences in methodology (sample 

preparation, differences in diet, etc.). 

Despite these differences, the results indicate that expression of majority of the transport 

proteins studied vary during development. Cellular and tissue distribution as well 

as elimination of transported substrates will therefore also change during development. 

Knowledge of these ontogenic differences in absorption, distribution, metabolism and 

excretion (ADME) processes of test compound in development may help to interpret differences 

in toxicity observed between adult, neonate and young animals.


REFEREnCES 

1. Ambudkar SV, Dey S, Hrycyna CA, Ramachandra M, Pastan I, Gottesman MM. Biochemical, cellular, and 

pharmacological aspects of the multidrug transporter. Annu Rev Pharmacol Toxicol. 1999; 39:361-98. 

Review. 

2. Stavrovskaya AA. Cellular mechanisms of multidrug resistance of tumor cells. Biochemistry (Mosc). 

2000; 65(1):95-106. Review. 

3. Higgins C. F. Multiple molecular mechanisms for multidrug resistance transporters. 

4. Nature 2007; 446, 749-757. 

5. Dean M, Rzhetsky A, Allikmets R. The human ATP-binding cassette (ABC) transporter superfamily. 

Genome Res. 2001; 11(7):1156-66. Review. 

6. Neyfakh AA. Mystery of multidrug transporters: the answer can be simple. Mol Microbiol. 2002; 

44(5):1123-30. Review. 

7. Sarkadi B, Homolya L, Szakács G, Váradi A. Human multidrug resistance ABCB and ABCG transporters: 

participation in a chemoimmunity defense system. Physiol Rev. 2006; 86(4):1179-236. Review. 

8. Stavrovskaya AA, Stromskaya TP. Transport proteins of the ABC family and multidrug resistance of 

tumor cells. Biochemistry (Mosc). 2008; 73(5):592-604. Review. 

9. Bosch I, Croop J. P-glycoprotein multidrug resistance and cancer. Biochim Biophys Acta. 1996; 

1288(2):F37-54. Review. 

10. Goldstein LJ, Gottesman MM, Pastan I. Expression of the MDR1 gene in human cancers. Cancer Treat 

Res. 1991; 57:101-119. Review. 

11. Schinkel AH, Jonker JW. Mammalian drug efflux transporters of the ATP binding cassette (ABC) family: 

an overview. Adv Drug Deliv Rev. 2003; 55(1):3-29. Review. 

12. Thiebaut F, Tsuruo T, Hamada H, Gottesman MM, Pastan I, Willingham MC. Cellular localization of the 

multidrug-resistance gene product P-glycoprotein in normal human tissues. Proc Natl Acad Sci U S A. 

1987; 84(21):7735-7738. 

13. Ernest S, Bello-reuss E. P-glycoprotein functions and substrates: possible roles of MDR1 gene in the 

kidney. Kidney Int 1998; 65: S11-S17. 

14. Shinkel AH. The physiological function of drug-transporting P-glycoproteins. Semin Cancer Biol 1997; 

8:161-170. 

15. Eraly SA, Blantz RC, Bhatnagar V, Nigam SK. Novel SK. Novel aspects of renal organic anion and cation 

transporters. Curr Opin Nephrol Hypertens 2003; 12: 551-558. 

16. Gottesman MM and Pastan I. Biochemistry of multidrug resistance mediated by multidrug transporter. 

Annu Rev Biochem 1993; 62: 385-427. 

17. Inui KI, Masuda S, Saito H. Cellular and molecular aspects of drug transport in the kidney. Kidney Int 

2000; 58: 944-958. 

18. Lash LH, Putt DA, Cai H. Drug metabolism enzyme expression and activity in primary cultures of human 

proximal tubular cells. Toxicology 2008, 244:56-65. 

19. de Zwart L, Scholten M, Monbaliu JG, Annaert PP, Van Houdt JM, Van den Wyngaert I, De Schaepdrijver 

LM, Bailey GP, Coogan TP, Coussement WC, Mannens GS. .The ontogeny of drug metabolizing enzymes 

and transporters in the rat. Reprod Toxicol. 2008, 26(3-4):220-230. 

20. Rosati A, Maniori S, Decorti G, Candussio L, Giraldi T, Bartoli F. Physiological regulation of P-glycoprotein, 

MRP1, MRP2 and cytochrome P450 3A2 during rat ontogeny. Dev Growth Differ. 2003 Aug;45(4):377-387. 

Acknowledgement: This work was supported partly by grant VEGA 1/0388/08 and partly by grant VVGS 

25/10-11. 

Received: November,12,2010 

Accepted: December,16,2010

26 


DOI: 10.2478/v10201-011-0004-x 

InVEStIGAtInG DYSPEPSIA In CLInICAL PRACtICE – A tRAP 

FOR GIARDIA 

Banovcin P. Jr., Demeter M., Bozikova J., Hyrdel R. 

Department of Internal Medicine - Gastroenterology, Jessenius Faculty of Medicine, Commenius University 

and University Hospital Martin, Slovak Republic 

ABStRACt 

Introduction: Dyspepsia is a very common condition with significant morbidity and economic implications. 

Dyspeptic symptoms have heterogeneous pathogenic mechanisms, including several organic, systemic or 

extragastrointestinal causes, however, origin of the most cases of dyspepsia remains unclear. This study aimed 

to focus on potential causes in patients with nonspecific dyspeptic symptoms in absence of organic, systemic 

or biochemical and hematological findings that readily explain their symptoms. 

Methods: We studied presence of persistent abdominal symptoms (heartburn, dull epigastric pain, epigastric 

cramps, epigastric fullness, flatulence, diarrhoea), weight loss. All patients (116 patients, 29 males/87 females) 

had normal laboratory tests, negative abdominal ultrasound evaluation and upper endoscopy findings. 

Presence of Giardia intestinalis (GI), Helicobacter pylori (HP) infection and coeliac disease (CD) was evaluated 

by obtaining biopsy samples and duodenal fluid aspiration during upper endoscopy. We determined the effect 

of eradication treatment on dyspepsia symptoms 2 months after therapy. 

Results: HP infection was present in 28 %, coeliac disease in 6 %, GI infection was diagnosed in 27 % patients 

GI and HP in 12 %, CD and HP in 1 %, GI and CD in 2 %. None of these causes were presented in 39 %. Most 

frequent symptoms were epigastric fullness (69 %), dull epigastric pain (38 %), heartburn (35 %), flatulence 

(34 %), abdominal cramps (31 %) and diarrhoea (16 %). We documented the remission of symptoms in 79 % 

examined patients 2 month after eradication therapy. 

Conclusion: The most common cause of dyspepsia was Helicobacter pylori infection and chronic giardiasis. 

Although H. pylori and coeliac disease are widely well known, we pointed out Giardia intestinalis as another 

possible cause of dyspepsia. Chronic giardiasis leads in selected individuals to dyspeptic symptomatology that 

mimics functional dyspepsia and irritable bowel syndrome. We recommend test for G. intestinalis infection in 

all patients with chronic dyspeptic complaints of unknown origin. 

Key words: Dyspepsia, functional dyspepsia, Giardia intestinalis, Helicobacter pylori, coeliac disease 

IntRODUCtIOn 

Dyspepsia is a very common condition with significant morbidity and economic implications. 

Around 25-40 % of adults in the general population have dyspepsia, but the prevalence 

and incidence depend on population study design, observation period, and definition 

of dyspepsia, itself (1,2). According to the Czech study, the prevalence of long-lasting 

dyspeptic symptoms in uninvestigated dyspepsia was 17 % (3). Dyspepsia accounts for 

2-5 % of primary care consultations, but patients that are most affected often do not seek 

medical care (4). A large number of patients in clinical practice present symptoms such 

as epigastric pain, abdominal cramps, excessive belching, early satiation, postprandial 

fullness or nausea. The dyspeptic symptoms can have several organic, systemic or extragastrointestinal 

causes. However, the origin of most of the cases of dyspepsia remains 

unclear. When these symptoms are chronic and occur in the absence of organic disease 

that readily explains them, patients are considered to have a functional gastroduodenal 

disorder (5). Functional dyspepsia remains a diagnosis of exclusion. The therapeutical 


Banovcin P.Jr. MD, Clinic of Internal Medicine, Gastroenterology Dept., Jessenius Faculty of Medicine 

CU and University Hospital in Martin, Kollarova Str. N. 2, 03601 Martin, Slovak Republic 

email: pbanovcin@gmail.com


and diagnostical processes are often not optimal and still controversial. Due to these 

facts we focused on potential causes of non-specific dyspeptic symptomatology. 

Giardia intestinalis (also known as Giardia lamblia and Giardia duodenalis) is an 

enteric protozoan pathogen found in a variety of mammalian hosts, including humans, 

and causes one of the most common parasitic infections worldwide. It contributes to 

estimate of 280 million symptomatic human infections per year (6). One of the major 

sources of infection in humans is contaminated water; however, there is evidence that 

the parasite is transmitted by human-to-human contact or by the contact with the 

domestic or wild animals (7). The symptoms of human giardiasis are highly variable. 

They vary from asymptomatic to severe form with diarrhoea, fever, weight loss and malabsorbtion. 

Most prominent clinical symptoms are abdominal pain, vague abdominal 

discomfort, bloating, flatulence and diarrhoea. Various extra-intestinal manifestations 

have been reported such as maculopapular rush, pulmonary infiltrates, polyarthritis 

and urticaria (8, 9). Chronic courses are common, but are mostly asymptomatic or presented 

by non-specific mild symptoms that may result in a low clinical index of suspicion 

for the diagnosis. Chronic infection may be linked to the phenomenon of antigenic 

variation and individual response of the host. Recent data show that Giardia intestinalis 

infection has been found to trigger abdominal symptoms of functional gastrointestinal 

disorder such as irritable bowel syndrome or functional dyspepsia. (10,11,12) 


We enrolled to our study 116 patients (29 males/87 females) aged 18 years and over attending 

Gastroenterology Outpatient Unit due to chronic dyspeptic symptoms. Patients 

with persistent abdominal dyspeptic symptoms in duration at least 3 months were considered 

for the study. Patient with the alarm features (such as dysphagia, odynophagia, 

vomiting, bleeding or rapid weight loss) as well pregnant women and patients familiarly 

for malignant disease were excluded. All patients underwent complex physical examination, 

routine biochemical and hematological blood laboratory tests. 

Furthermore, ultrasound evaluation including hepatobiliary tract, pancreas, kidneys and 

upper endoscopy were performed. All examination had not produced relevant explanation 

for dyspepsia. Upper gastrointestinal endoscopy was accompanied by obtaining of 

multiplied biopsy samples from gastric antrum to investigate presence of Helicobacter 

pylori (H. pylori) infection. Duodenal biopsy samples (D2-D3) and serum anti-gliadin, 

anti-endomysial and anti-transglutaminase antibodies estimation was used to evaluate 

coeliac disease. Presence of Giardia intestinalis infection was performed by direct 

examination of duodenal juice aspirate. Aspiration of duodenal fluid was performed on 

the fasting patient, during the endoscopy so the position of the aspiration tube was correctly 

placed in the distal duodenum or proximal jejunum. Aspirates were immediately 

transported in sterile containers in a tempered medium to microbiology laboratory. The 

samples were processed within 2 hours for microscopic examination. 

We studied presence of H. pylori infection, G. intestinalis and coeliac disease and its 

relative contribution to overall dyspeptic symptoms (heartburn, dull epigastric pain, epigastric 

cramps, epigastric fullness, flatulence, diarrhoea). After identification of possible 

cause, appropriate treatment was initiated (eradication of H. pylori, gluten-free diet in coeliac 

disease and therapy with metronidazole 250 mg tid. In the case of giadriasis, we determined 

the effect of eradication treatment on functional dyspepsia symptoms 2 months 

after therapy. Statistical analysis was performed using the program PAST version 1.80.

28 


RESULtS 

One hundred and sixteen patients (87F, 29M) fulfilled the inclusion criteria. The mean 

age of patients was 37.3 (18-67years). Giardia intestinalis infection was diagnosed in 27 

% of the patients. H. pylori infection was found in 28 %, coeliac disease in 6 %. Both 

G. intestinalis and H. pylori were present in 12 %, coeliac disease and H. pylori in 1 %, 

giardiasis and coeliac disease in 2 %. There were 39 % of the patients that did not exemplify 

any of the causes mentioned. Figure1. Most frequent symptoms were epigastric fullness 

(69 %), dull epigastric pain (38 %), heartburn (35 %), flatulence (34 %), abdominal 

cramps (31 %), and diarrhoea (16 %) Figure 2. Comparing frequency of symptoms, we 

didn’t confirmed statistically significant differences among investigated groups. Average 

lenght of dyspeptic syndrome history was 18.5 months and average weight loss was 2 kg. 

45% 

40% 

39% 

35% 

30% 

25% 

27% 

28% 

20% 

15% 

12% 

10% 

5% 

0% 

6% 

2% 

1% 

GI -total HP - total CD - total HP + GI HP + CD GI + CD Unkonwn 

Fig. 1. Summary of potential dyspepsia causes in study patients (totally). Giardia intestinalis (GI), Helicobacter 

pylori (HP) and coeliac disease (CD). 

80% 

70% 

60% 

50% 

40% 

30% 

Total=116 

Females n=87 

Males n=29 

20% 

10% 

0% 

Dull pain Cramps Heartburn Epigastric 

fullness 

Flatulence 

Diarrhoea 

Fig. 2. Prevalence of selected dyspepsia symptoms in study patients (totally)


In the Giardia positive group was the most frequent symptom was epigastric fullness 

(86 %), dull epigastric pain (50 %). Frequencies of other symptoms are shown in Figure 

3. Average length of dyspeptic syndrome was 23.3 months in total G. intestinalis 

infection (32 months in isolated infection) with weight loss of 2.8kg (3.5 giardia isolated). 

Fourteen patients with giardiasis (43 %) had simultaneous H. pylori infection. We 

documented the remission or significant improvement of symptoms in 79 % of Giardia 

positive patients 2 month after therapy (treatment with metronidazole). Approx. 7 % of 

patients did not response to therapy, and 14 % of the patients cancelled their follow up, 

thus we do not have any response for that group. Figure 4. 

100% 

90% 

80% 

70% 

60% 

50% 

40% 

30% 

20% 

10% 

0% 

38% 

50% 

Dull 

epigastric 

pain 

22% 

29% 

Abdominal 

cramps 

35% 

43% 

Heartburn 

80% 

86% 

Epigastric 

fullness 

35% 

36% 

Flatulence 

19% 

29% 

Diarrhoea 

GI total /n=31/ 

GI isolated /n=14/ 

Fig. 3. Prevalence of symptoms in Giardia intestinalis positive patients. 

Fig. 4 Effect of 14 days metronidasole 250mg tid. treatment on dyspepsia symptoms. Evaluated 2 months 

after treatment. 

Persistence of symptoms after therapy in patienst with GI 

7% 

14% 

remission 

persist 

not known 

79%

30 


DISCUSSIOn 

Dyspepsia is common and global problem with board differential. This study aimed 

to focus on patients with nonspecific dyspeptic symptoms in absence of organic, systemic 

or biochemical and hematological findings that explain their symptoms. In order 

to prevent serious illness, patient complaining of alarm symptoms were excluded. The 

negative aspect of this study was our failure to fulfill the diagnosis of functional gastrointestinal 

disorders according to ROME III criteria. However, the aim of the study was 

to identify other possible agents that may contribute to development of gastrointestinal 

symptoms. The role of H. pylori in functional disease has been controversial. Recent 

meta-analyses suggest some benefit from H. pylori eradication (13). In our findings was 

the H. pylori infection most common agent. After eradication therapy, 72 % of patients 

reported benefits from this therapy. 

Coeliac disease was diagnosed in 6 %. As expected, flatulence fullness and diarrhoea 

were the dominant symptoms, but not significantly different from other groups. On the 

other hand, in our study were not sufficiently many patients with coeliac disease to 

conclude any decision. 

Incidence of giardiasis varies from 20 % to 60 % in endemic areas and 2-7 % in industrialized 

countries depending on region and age (6). We found out that 27 % of studied 

patients had giardia infection. The rate is higher compared to general population in 

western countries mostly due to selection of symptomatic patients. 

Traditional diagnosis of giardiasis is set by the direct detection of trophozoites or cysts 

in a stool sample; however, repeated stool examinations are needed to avoid false-negative 

results, because cyst excretion may be intermittent. This may be difficult sometime 

in outpatient units because of patient compliance. The data show that histological examination 

of duodenal biopsies is unsuitable (15,16,17). In recent years, rapid diagnostic 

tests that use antigen detection methods or PCR have been employed. These tests are 

both highly specific and sensitive, but still expensive (14). The specificity and sensitivity 

is also questionable in case of chronic giardiasis. Diagnosis of Giardia intestinalis in our 

study was performed by microscopic evaluation of duodenal juice aspirate. There are 

studies that show yields of microscopic examination of duodenal aspirate that vary from 

0.7 % to 47.6 % (15,16). There is disadvantage to duodenal fluid aspiration in that it is 

performed during endoscopy therefore it is not suitable for routine screening. Another 

disadvantage of this evaluation is that aspirate should be preceded within 2 hours of 

aspiration and transported in temperate medium. 

Giardia intestinalis infection in humans has a wide spectrum of clinical manifestation 

ranging from asymptomatic to serious diarrhoea. In our study the most frequent symptom 

was abdominal fullness and diarrhoea followed by heartburn, dull epigastric pain 

abdominal cramps, and flatulency. There were no symptoms or symptom-complex that 

reliably allowed the recognition of giardiasis. Again our results were similar to previously 

published studies. (17,18) 

The pathophysiology of these symptoms in giardia infection has not been well understood. 

The possible mechanisms include direct damage to the intestinal brush and 

mucosa resulting in secondary lactose intolerance, reduced intestinal absorption and 

deconjugation of bile salts. Recent hypothesis also suggests induction of apoptosis in 

intestinal epithelial cells and disruption of tight junctional zona-occludens followed by 

increased epithelial permeability across epithelial monolayers. (19,20, 23) Compared to 

other studies, diarrhoea was not so common feature in our study. as reported from in 

endemic areas. This difference might be caused by low initial dose of giardia cysts, in 

non-endemic area therefore the host is able to maintain parasite count at very low level, 

or it may be due to the distribution of different pathogenic strains. But this assumption 

is highly speculative. The association with clinical manifestation and parasite genotype 

is not definitive to date (18,21,22).


In our study, the mean age of patients with giardiasis was slightly lower (not significantly) 

compared to patients with H. pylori infection and in the group without any findings. 

It is well know, that giardiasis is more common in children and adolescents (28). 

From this point of view, age may have some attribution in diagnostic process in uninvestigated 

dyspepsia and related symptoms. 

Duration of symptoms was longest in patients with giardiasis. Possible reason of delayed 

diagnosis is that the G.intestinalis is generally considered to be on low degree of 

suspicion in non-endemic countries in comparison with the well-known H. pylori. 

Importantly, we documented total remission of symptoms in 79 % examined patients 

with G. intestinalis infection after 14-days course treatment with metronidazole at 

250mg tid. There were no statistically significant differences in symptoms distribution 

or metronidazole therapy effect on them in all G. intestinalis positive patients. 

Another finding was that giardiasis was associated with H. pylori infection. H. pylori 

was found in 14 patients of the 31 patients with giardiasis. This possibly reflects the 

fact that both G. intestinalis and H. pylori share similar risk factors (24). There is existing 

literature and data supporting possible synergy effect of infections, however, in our 

study were no significant differences between the giardia groups in symptoms presentation 

or distribution. Some authors suggest possible synergistic participation leading to 

metronidasole resistance and gastrointestinal neoplasia (24,25,26,27). 

Causal treatment of dyspesia led to resolution of dyspeptic symptoms; however in 

almost 39 % patients we did not find the cause of dyspepsia. Such patients are hypothesized 

to have functional gastrointestinal disorder. Given that functional gastrointestinal 

disorders are the diagnosis per exlusionem, further examinations are needed to proof 

the diagnosis according to ROME III criteria. 

COnCLUSIOn 

Chronic dyspeptic syndrome is a frequent problem of patients visiting gastroenterology 

outpatient unit. In our study most common cause of dyspepsia were Helicobacter 

pylori infection, chronic giardiasis and coeliac disease. Although H. pylori and coeliac 

disease are widely well known, we pointed out another possible cause of dyspepsia. According 

to our data, we are suggesting that chronic Giardia intestinalis infection leads 

to nonspecific dyspeptic symptomatology in selected individuals that mimics functional 

dyspepsia and irritable bowel syndrome. We recommend test GI infection in all patients 

with chronic dyspeptic complaints of unknown origin, 

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5. Tack J, Talley NJ, Camilleri M et al. Functional gastroduodenal disorders. Gastroenterology 2006;130:1466– 

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Water, 2nd edition. Addendum; 2002. 

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32 


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10. Hanevik K, Dizdar V, Langeland N, Hausken T. Development of functional gastrointestinal disorders after 

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DOI: 10.2478/v10201-011-0005-9 

33 

POInt PREVALEnCE SURVEY OF nOSOCOMIAL InFECtIOnS In 

UnIVERSItY HOSPItAL In MARtIn 

Zabkova E., Murajda L., Hudeckova H. 

Department of Public Health, Jessenius Faculty of Medicine, Comenius University, Slovak Republic 

Abstract 

Nosocomial infections (NI) are a serious problem not only in Slovakia but in all countries. The European 

Commission decided on their standardized surveillance in the whole European Union. According methodology 

elaborated by experts from the European Centre for Disease Control and Prevention (ECDC) in Stockholm we 

performed a point prevalence survey in the University Hospital Martin (UHM). In this article we present the 

results which show that the prevalence of NI in UHM (5.5 %) is comparable with the average in other European 

hospitals. In comparison with occurrence of NI (0.64 %) reported through the Epidemiological Information 

System of the Slovak Republic, our results are 8.5-times higher. The highest point prevalence of NI was found 

at the Clinic of Hematology and Transfusiology – 7 patients (out of 15 hospitalized) which is 46.7 %. The most 

common type of NI was sepsis (25.9 %) and urological infection (22.2 %). Based on the results obtained we 

recommend to continue in international projects of NI surveillance, so that it would be possible to acquire 

more accurate data on NI prevalence in UHM and do the benchmarking among hospitals in countries of the 

European Union. 

Key words: nosocomial infection, prevalence, University Hospital Martin 

IntRODUCtIOn 

A nosocomial infection (NI) is defined in Slovak legislation as an infection of internal 

or external origin, which occurred in direct relation with hospital stay or healthcare 

performance in a healthcare facility or social care facility (1). 

Centers for Disease Control and Prevention (CDC) in USA defines nosocomial infections 

as infections which occurred in a healthcare facility, were not present at admission 

and the patient was not in incubation period of the relevant infection at admission. If 

incubation period is unknown, an infection is considered nosocomial when occurred 

later than 48-72 hours after admission to hospital. Infection present at admission can 

be considered as nosocomial only if it is epidemiologically related to a precedent hospitalization. 

All other infections are considered as community acquired. The CDC has also 

specific diagnostic criteria for the infection types. Using these criteria and same methods 

of surveillance enables mutual comparability of the acquired data (2). 

The NI occurrence is watched in Slovakia through an obligatory reporting. Regulation 

of the Ministry of Health of Slovak Republic No. 553/2007 on requirements for healthcare 

facilities about health protection, sets for providers of healthcare and for healthcare 

workers a duty to avoid NI and to register NI in patient records and in a diary of NI, to 

perform an analysis of NI occurrence and of the reasons of their occurrence and to apply 

measures to decrease the occurrence, stop spread of NI and prevent them. 

The chief doctor of a ward has to inform the Regional Public Health Authority in 48 

hours by a written form. If there is an outbreak or clinically serious NI, death or suspicion 

of death for NI, reporting is performed immediately – personally, by telephone, fax 

or email. NI outbreak is an incidence of at least three cases of the same NI, which are in 

epidemiological relationship (3). 


Eva Zabková, Department of Public Health JFM CU 

Sklabinská Str. N. 26, 036 01 Martin, Slovak Republic, e-mail: evka.zabkova@gmail.com.

34 


Analysis of occurrence of NI is annually published in the Annual report on activities 

of public health authorities in the Slovak Republic, published by the Public Health Authority 

of the Slovak Republic. Through the Regional Public Health Authority in Banská 

Bystrica the information on NI has been published since 2006 on web pages of the Epidemiological 

Information System (EPIS), too. 

MEtHODS 

We used a point prevalence survey to estimate prevalence of nosocomial infections in 

University Hospital Martin. 

The survey was realized from June 22nd till July 8th, 2010. Performing of the study 

was approved by the Ethical Committee of the Regional Public Health Authority in Martin. 

Collection of data at each ward had to be finished during the same day it started. The 

maximum lenght of survey for the whole hospital was set to three weeks. For privacy 

protection, every patient in the survey was given a code and his/her data were registered 

in database only under this code. 

We used the definitions of different types of NI from the Codebook by ECDC (4). 

There were two criteria for the study group. First, regarding the wards – only the acute 

care wards were included and the long-term care wards were excluded. The second was 

about patients – all patients admitted to the ward before 8.00 am and not discharged 

from the ward at the time of the survey were included. 

Our team consisted from researchers from the Department of Public Health of the Jessenius 

Faculty of Medicine, Comenius University, Regional Public Health Authority in Martin 

and the University Hospital Martin. These visited in three weeks according a set schedule all 

acute care wards of the hospital and in collaboration with appointed doctors at the wards 

they assessed data from patient records and registered active nosocomial infections according 

the definitions used in the survey. We processed and analyzed the results in Microsoft Excel. 

RESULtS 

There were 495 patients included in the survey, 268 men (54.1 %) and 227 women 

(45.9 %), with average age 51.5 years (min. 0, max. 89 years).Out of all patients included 

in the survey, there were 5.5 % patients found with an active NI. The average age of patients 

with NI was 50 years (min.0, max.85 years). We found NI in 44.4 % of women (12 

NI) and in 55.6 % of men (15 NI). 

22.2% 

18.6% 

11.1% 

22.2% 

PN 

UTI 

BSI 

EENT 

OTH 

25.9% 

Fig. 1. Prevalence of nosocomial infections at University Hospital Martin Legends for Fig.1 and Fig.5: 

PN – Pneumonia; UTI – Urinary tract infection; BSI – Bloodstream infection; EENT – Eye, Ear, Nose or Mouth 

infection; OTH – other; (according CDC definitions).


The NI prevalence according age groups is on Figure 2. 

HI (abs.) 

7 

6 

5 

4 

3 

2 

1 

0 

0-4 5-9 10-14 15-19 20-24 25-34 35-44 45-54 55-64 65-74 75-84 85- 

age groups 

Fig. 2. Prevalence of nosocomial infections according age groups 

We present character distribution of NI found at the clinics visited on the following 

picture. 

PED 

25,93% 

14,81% 

14,81% 

11,11% 11,11% 

11,11% 

11,11% 

OR THO 

I.INT 

II. INT 

NE ON 

HAE M 

OTH 

Fig. 3. Proportion of nosocomial infections at clinics of University Hospital Martin 

Legends for Fig. 3, Fig. 4 and Fig. 5: PED – Paediatrics; ORTHO – Orthopaedics and 

Traumatology; I. INT – General Medicine; II. INT – Gastroenterology; NEON – Neonatology; 

HAEM – Haematology; NEUROL – Neurology; I.SUR - General Surgery; II.SUR – 

Transplant and Vascular Surgery; OTH – Other. 

On Figure 4 there is prevalence of NI at the clinics of UHM. At nine clinics the prevalence 

of NI was from 2.8 % to 46.7 %. At other clinics there was not found any NI during 

the survey.

36 


HI% 

50 

46,7 

45 

40 

35 

30 

25 

20 

15 11,8 

10 10,3 

8,1 

8 

10 

5,9 

6 

5 

2,8 

0 

PED 

OR THO 

NE UR OL 

I. S UR 

II. SUR 

I.INT 

II. IN T 

NE ON 

Fig. 4. Prevalence of nosocomial infections at clinics of University Hospital Martin. 

HAE M 

On Figure 5 we present character of found NI according clinics of the hospital. 

100% 

90% 

80% 

70% 

60% 

50% 

40% 

30% 

20% 

10% 

0% 

PE D 

OTR HO 

I.INT 

II.INT 

NEON 

HAE M 

I. S UR 

II. S UR 

NEUROL 

PN 

UTI 

BSI 

EENT 

OTH 

Fig. 5. Character of nosocomial infections at clinics of University Hospital Martin. 

DISCUSSIOn 

The European Union put an effort on harmonisation of policies of surveillance of communicable 

diseases including nosocomial infections. In this context, the EU-funded 

HELICS project in 1993-2004 undertook a systematic overview of the national surveillance 

policies and organisation to identify similarities and discrepancies and to plan 

further progress to be made. Totally, around 2000 European hospitals participate in 

a surveillance network. The participation is voluntary and the estimated coverage is 

quite high: around 30 % (5). 

Based on the IPSE project (Improving Patient Safety in Europe) in hospitals in the 

European Union a need was defined for a surveillance of nosocomial infections on European 

level to estimate and watch the burden of nosocomial infections. 

Because a general continuous incidence surveillance is very expensive, the prevalence 

hospital surveys are considered efficient.


In 2009 the experts from European Centre for Disease Control and Prevention (ECDC) 

and experts from member states of the European Union elaborated a protocol of the 

European point prevalence survey (6). 

Prevalence here means the number of all cases – new and also old but still present in population. 

Because this number is counted for a specific date, it is a point prevalence study (7). 

Currently, the average NI incidence among hospitalized patients in hospitals in developed 

countries is about 6-8 %. In less developed countries it is even more than 25 %. 

Infections, deaths and economic costs related to acquiring NI have been growing mainly 

in past thirty years. Although estimations of proportion of preventable NI differ, there is 

a general consent that it could be more than 20 % in developed countries and even more 

than 40 % from all NI in less developed countries (8). 

The biggest proportion of NI was the sepsis (25.9 %). In men it was 33.0 % from all 

found NI, in women 16.0 %. Then there were urological infections, which occurred in 

22.2 %. In men in 20.0 % and in women 25.0 % of all NI. Other infections were found in 

22.2 % of all NI. To this group we put the infections of gastrointestinal system, central 

nervous system, surgical site infections (SSI) and bone and joint infections. 

It results from the data from EPIS that in 2009 the most common reported NI were the 

SSI (22.96 %) and urological infections (20.41 %). 

We found most of the NI in the age group of 65-84 years, 12 cases (22.2 %). High number 

of NI occurred also in children under one year of age – 4 cases (14.8 %). In both these groups 

there was the highest number of hospitalized patients, too. We think that one of the most 

important causes underlying the high prevalence in these is the weak immune system. 

The highest proportion of NI found at the University Hospital Martin (UHM) was from 

the Clinic of Hematology and Transfusiology (25.9 %). There occurred all types of serious 

NI. This was probably due to characteristic weak immune system of the patients 

hospitalized at the clinic and to an aggressive chemotherapy. 

At the Clinic of Children and Adolescents there were 14.8 % of all NI in the hospital 

and equally 11.1 % at the Clinic of Orthopedics and Traumatology, Clinic of Internal 

Medicine I, Clinic of Internal Medicine-Gastroenterology and Clinic of Neonatology. 

Some clinics with lower NI prevalence (Clinic of Neurology, Clinic of Surgery, Clinic of 

Transplant and Vascular Surgery) represent 14.8 % from total number of found NI. 

There were no found NI at other clinics. When looking at data from EPIS, the highest 

number of NI in 2009 was reported from the Clinic of Surgery (25.51 %). 

The highest point prevalence - the proportion of NI from the total number of hospitalized 

patients at a clinic – was at the Clinic of Hematology and Transfusiology: 7 patients 

(46.7 %). In 2009 there was no NI reported to EPIS from this clinic. We assume that it was 

due to insufficient reporting. Similarly, in the Annual report on activities of public health 

authorities in the Slovak Republic in 2009 we may read that the low number of reported 

NI from all healthcare facilities in Slovakia is probably due to insufficient reporting, too. 

At the Clinic of Children and Adolescents we found 4 cases of NI (11.8 %), at Clinic of 

Neonatology we found 3 NI cases (10.3 %) and at Clinic of Internal Medicine-Gastroenterology 

3 NI cases (10.0 %). We found less than 10 % of NI cases among the patients 

at the Clinic of Orthopedics and Traumatology, Clinic of Neurology, Clinic of Surgery, 

Clinic of Transplant and Vascular Surgery and Clinic of Internal Medicine I. 

Summarizing, the prevalence of NI found in patients at the University Hospital Martin 

was higher (5.5 %) in comparison with the reported occurrence in the Epidemiological 

information system where NI represent 0.64 % (9). We are convinced that this is due to 

insufficient reporting of NI. There could be more reasons for that. Our main assumption 

is that there is a belief that a higher number of reported NI could lead to a negative assessment 

of quality of healthcare of the hospital. 

However, our results are in accord with data on reported NI in developed countries. Marcel 

et al. (10) state that the prevalence of NI in European hospitals is about 6-12 % (10).

38 


We suggest that the reporting of NI would be improved at the University Hospital 

Martin and that there would continue the participation in international projects of surveillance 

of NI and the infection control, so that it would enable benchmarking and 

consecutive improvement. 

REFEREnCES 

1. Act of the Parliament of the Slovak Republic No. 355/2007 on protection, promotion and development of 

public health. Code of laws, 2007 (154): 2402-75. 

2. Centers for Disease Control and Prevention: Definitions of Nosocomial Infections. [online ] [cit. 2009-03- 

10] Available on Internet: http://www.health2k.state.nv.us/sentinel/Forms/ UpdatedForms105/CDC_ 

Defs_Nosocomial.pdf 

3. Regulation of Ministry of Health of the Slovak Republic No. 553/2007 on requirements for health 

protection in healthcare facilities. 

4. Point Prevalence Survey of Healthcare-Associated Infections and Antimicrobial Use in European Acute 

Care Hospitals, Pilot Protocol 3.3 - Codebook, ECDC, June 2010. 

5. IPSE, Improving Patient Safety in Europe, IPSE Annual Report 2005. Available on Internet: http://helics. 

univ-lyon1.fr/deliverables/IPSE_Annual_Report_2005_25oct06.pdf 

6. Point Prevalence Survey of Healthcare-Associated Infections and Antimicrobial Use in European Acute 

Care Hospitals, Pilot Protocol (final), Version 3.3, ECDC, June 2010. 

7. Bakoss, P. et al.: Epidemiológia. Bratislava, Univerzita Komenského, 2005. 488 p. 

8. Stefkovicova, M.: Prevencia nozokomiálnych nákaz je ako beh na dlhé trate. In: Nozokomiálne nákazy, 

2003 (2): 1-2. 

9. Annual Report on Activities of Regional Public Health Authorities in the Slovak Republic in 2009. 

Bratislava, Public Health Authority of the Slovak Republic, 2009. 776 p. Available on Internet: http:// 

www.slovanet.sk/uvzsr/docs/vs/vyrocna_sprava_SR_09.pdf 

10. Marcel, J.P. et al.: Healthcare-associated infections: think globally, act locally. Clin Microbiol Infect. 

October 2008;14(10):895-907. 

Received: November,30,2010 

Accepted: February,14,2011

Acta Medica Martiniana - Univerzita Komenského

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