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Bernadett Márkus Department of Family Medicine, Semmelweis University, Budapest, Hungary

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György Temesszentandrási Department of Internal Medicine and Hematology, Semmelweis University, Budapest, Hungary

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Krisztián Vörös Department of Family Medicine, Semmelweis University, Budapest, Hungary

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László Jakab Department of Internal Medicine and Hematology, Semmelweis University, Budapest, Hungary

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Béla Fekete Department of Internal Medicine and Hematology, Semmelweis University, Budapest, Hungary

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Henriette Farkas Department of Internal Medicine and Hematology, Semmelweis University, Budapest, Hungary
National Angioedema Center, Semmelweis University, Budapest, Hungary

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Zoltán Prohászka Department of Internal Medicine and Hematology, Semmelweis University, Budapest, Hungary
National Angioedema Center, Semmelweis University, Budapest, Hungary

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Tamás Masszi Department of Internal Medicine and Hematology, Semmelweis University, Budapest, Hungary

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László Kalabay Department of Family Medicine, Semmelweis University, Budapest, Hungary
Department of Internal Medicine and Hematology, Semmelweis University, Budapest, Hungary

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https://orcid.org/0000-0002-8329-3755
Open access

Abstract

Helicobacter pylori is a common pathogen causing gastric inflammation and malignancy. Fetuin-A is a multifunctional protein that is involved in the regulation of calcification, insulin resistance and inflammation. Reports on serum levels of fetuin-A in acute H. pylori infection are contradictory. We intended to see whether H. pylori post-infection status has a long-term effect on serum fetuin-A levels in a well-characterized series of systemic lupus erythematosus cases.

In this cross-sectional study 117 patients with systemic lupus erythematosus were enrolled. Helicobacter infection status and serum fetuin-A concentration were determined by ELISA and radial immunodiffusion, respectively. H. pylori positive patients had higher serum fetuin-A concentration than negative ones: 517 (456–603) vs. 476 (408–544) mg L−1, median (25–75% percentiles), P = 0.020. No other parameters differed between these groups. During univariate regression analysis fetuin-A levels were associated with Erythrocyte sedimentation rate (ESR), White blood cell count (WBC), C-reactive protein (CRP), serum total protein, albumin, and the SLEDAI index at the time of diagnosis but only serum albumin remained a significant determinant in multivariate regression study.

Abstract

Helicobacter pylori is a common pathogen causing gastric inflammation and malignancy. Fetuin-A is a multifunctional protein that is involved in the regulation of calcification, insulin resistance and inflammation. Reports on serum levels of fetuin-A in acute H. pylori infection are contradictory. We intended to see whether H. pylori post-infection status has a long-term effect on serum fetuin-A levels in a well-characterized series of systemic lupus erythematosus cases.

In this cross-sectional study 117 patients with systemic lupus erythematosus were enrolled. Helicobacter infection status and serum fetuin-A concentration were determined by ELISA and radial immunodiffusion, respectively. H. pylori positive patients had higher serum fetuin-A concentration than negative ones: 517 (456–603) vs. 476 (408–544) mg L−1, median (25–75% percentiles), P = 0.020. No other parameters differed between these groups. During univariate regression analysis fetuin-A levels were associated with Erythrocyte sedimentation rate (ESR), White blood cell count (WBC), C-reactive protein (CRP), serum total protein, albumin, and the SLEDAI index at the time of diagnosis but only serum albumin remained a significant determinant in multivariate regression study.

Introduction

Helicobacter pylori infection can lead to chronic gastritis, peptic ulcer and gastric cancer [1, 2]. In addition its association with obesity [3, 4], insulin resistance [5] and metabolic syndrome [6] is also known. There are studies suggesting that a H. pylori increases the risk of development of non-alcoholic fatty liver [7], whereas others debate it [8].

Human fetuin-A is a secretory multifunctional glycoprotein that is synthetized mainly in the liver in adulthood [9]. Fetuin-A inhibits ectopic calcification [10] and behaves as a negative acute phase reactant [11]. Low serum fetuin-A concentration is a good predictor of mortality in alcoholic liver cirrhosis [12] and end-stage renal disease [13]. Fetuin-A inhibits insulin receptor autophosphorylation and signaling, thereby increasing insulin resistance [14–17].

Reports on serum fetuin-A concentration in H. pylori infection are contradictory. Kebapcilar et al. observed decreased fetuin-A and elevated C-reactive protein (CRP) and macrophage migration inhibitory factor (MIF) levels in H. pylori infected patients with dyspepsia compared to healthy controls [18]. Concentrations of CRP and MIF decreased whereas those of fetuin-A increased following eradication [18]. In contrast with these observations Manolakis et al. found elevated serum fetuin-A concentrations in H. pylori positive patients [19]. The difference between H. pylori positive and negative patients remained following adjustment for age, gender, smoking habits, body mass index (BMI), blood lipids and CRP levels [19]. They described elevated serum insulin and HOMA-IR levels. Based on these findings and on the positive correlation between HOMA-IR and fetuin-A levels they suspected that fetuin-A could be responsible for the increased insulin resistance observed in H. pylori infection [19].

Based on these findings we found it interesting to see whether H. pylori postinfection status can affect fetuin-A levels in serum. We tested this hypothesis in a well-characterized cohort of patients with systemic lupus erythematosus.

Patients and methods

One-hundred and seventeen patients (14 men, 103 women, mean age: 43.6 years, median: 43 years, Q1–Q3: 31–55), who were treated at the Outpatient Service of Immunology, 3rd Department of Internal Medicine, Semmelweis University were included in the study. The study period was between 2000 and 2005. The diagnosis of SLE was established on international criteria [20]. None of the patients received eradication therapy in the past 6 months. Depending on their organ manifestations and severity of disease patients were on corticosteroid (oral prednisolone or methylprednisolone), azathioprine, chloroquine or cyclophosphamide treatment.

The study was approved by the Ethical Committee of the Hungarian Medical Research Council and all patients gave informed consent to participate in the study.

We determined serum fetuin-A concentration by radial immunodiffusion, as described earlier [21]. Anti-Helicobacter IgG was determined by ELISA using the NovaLisa kit (NovaTec, Dietzenbach, Germany). Values ≤1.0 were considered negative and >1.0 were positive.

Other laboratory examinations were determined by conventional methods.

Statistical analysis was performed with the IBM SPSS v23 statistical program (IBM-SPSS Inc., Armonk, NY, USA). We used non-parametric tests as not all parameters followed normal distribution.

Results

Comparison of Helicobacter pylori negative and positive patients with SLE

Comparison of H. pylori negative and positive patients is shown in Table 1. These two groups differed only in fetuin-A concentration.

Table 1.

Comparison of H. pylori negative and positive patients. Continuous variables are represented as median (Q1-Q3 values), categorical variables as frequency (percentage), respectively

Parameter H. pylori negative H. pylori positive P #
(n = 55) (n = 62)
Age, years 40 (31–49) 49 (31–58) 0.087
Gender (M/F) 9/46 5/57 0.167§
BMI, kg m−2 23 (22–26) 23 (20–27) 0.346
Fetuin-A, mg L −1 476 (408–544) 517 (456–603) 0.020
ESR, mm h−1 22 (14–40) 23 (10–38) 0.569
C3, g L−1 81 (47–113) 87 (65–125) 0.131
Anti-DNA, IU/mL 12 (5–42) 18 (5–48) 0.799
Anti-C1q, U/mL 18 (9–35) 17 (10–28) 0.792
CRP, mg L−1 3.98 (1.37–9.44) 3.45 (1.37–8.58) 0.669
Total protein, g L−1 73 (64–76) 72 (68–75) 0.439
Albumin, g L−1 42 (35–47) 43 (38–45) 0.661
IgG, g L−1 12.5 (10.0–15.3) 11.8 (10.3–13.3) 0.525
IgA, g L−1 2.44 (1.76–3.56) 2.26 (1.46–3.24) 0.303
IgM, g L−1 1.06 (0.71–1.71) 1.32 (0.76–1.77) 0.611
RBC, *106/µL 4.3 (4.0–4.7) 4.2 (4.0–4.4) 0.288
Hematocrit 0.38 (0.35–0.42) 0.37 (0.36–0.40) 0.304
Hemoglobin, g L−1 128 (115–141) 125 (115–134) 0.172
WBC,/µL 6,100 (5,100–8,570) 6,755 (5,075–9,273) 0.574
Glucose, mmol L−1 4.58 (4.15–5.02) 4.73 (4.31–5.47) 0.331
Creatinine, µmol L−1 70 (64–81) 68 (59–81) 0.535
Bilirubin, µmol L−1 8.9 (6.8–12.4) 7.6 (6.0–10.7) 0.110
ASAT, UL−1 23 (19–29) 18 (15–25) 0.055
ALAT, UL−1 19 (15–34) 17 (12–23) 0.081
Alkaline phosphatase, UL−1 91 (60–166) 70 (53–144) 0.242
INR 1.05 (0.94–1.10) 1.03 (0.94–1.10) 0.934
Cholesterol, mmol L−1 5.05 (4.13–5.61) 4.91 (4.02–5.61) 0.799
Triglyceride, mmol L−1 1.18 (0.93–1.71) 0.97 (0.70–1.65) 0.081
SLEDAI 6.0 (2–17) 4 (3–10) 0.245
Corticosteroid treatment, yes/no 34/21 39/23 0.904§

BMI: Body Mass Index; ESR: Erythrocyte Sedimentation Rate; C3: C3 complement component; CRP: C-reactive protein, RBC: Red blood cell count; WBC: White blood cell count; ASAT: Serum aspartate aminotransferase; ALAT, Serum alanine aminotransferase, INR: International Normalization Rate; SLEDAI: Systemic Lupus Erythematosus Disease Activity Index at the time of diagnosis. #: Mann-Whitney test; §: Chi2 test. Parameters typed in bold have statistically significant values (P < 0.05).

Correlation between serum fetuin-A levels and H. pylori status in patients with SLE

There was a weak but statistically significant correlation between H. pylori status and fetuin-A levels (r = 0.203, P = 0.028). Thus, compared to H. pylori negative patients a significantly higher portion of H. pylori positive patients was associated with higher fetuin-A concentration ranges (Table 2). Serum fetuin-A levels and H. pylori IgG levels, however, did not correlate significantly either in all (r = 0.141, P = 0.154, n = 117) or in H. pylori positive patients (r = 0.104, P = 0.448, n = 62).

Table 2.

The number of H. pylori positive and negative patients in serum fetuin-A level quartiles

Q1 Q2 Q3 Q4 Total
0–435 436–510 511–568 569-
H. pylori IgG negative 19 13 14 9 55
H. pylori IgG positive 10 19 13 20 62
Total 29 32 27 29 117
χ 2 = 7.736, P = 0.052; linear association coefficient = 4.867, ordinal by ordinal Spearman correlation: r = 0.205, P = 0.027

Q1–Q4: the four quartiles of a serum fetuin-A concentration (mg L−1).

The association between fetuin-A concentration and other parameters of patients

Univariate regression analysis between serum fetuin-A levels and the other parameters is shown in Table 3. We observed a significant association with Erythrocyte sedimentation rate (ESR), White blood cell (WBC) count, CRP, total protein and albumin levels, the SLEDAI index at the time of diagnosis but not with the other parameters listed in Table 1.

Table 3.

Univariate regression analysis between serum fetuin-A concentration and other laboratory parameters

Parameter Adjusted r 2 Standardized β P
Age −0.008 −0.026 0.780
BMI −0.005 0.085 0.440
ESR 0.123 −0.364 <0.001
WBC 0.111 −0.347 0.001
CRP 0.090 −0.300 0.002
Serum total protein 0.122 0.349 0.001
Serum albumin 0.168 0.409 <0.001
C3 0.024 0.181 0.051
Anti-DNA −0.002 0.086 0.369
Anti-C1q −0.009 0.001 0.997
H. pylori status (positive/negative) 0.049 0.239 0.010
SLEDAI 0.053 −0.278 0.010

BMI: Body mass index; ESR: Erythrocyte sedimentation rate; WBC: White blood cell count; CRP: C-reactive protein; C3: C3 complement component; SLEDAI: Systemic Lupus Erythematosus Disease Activity Index at the time of diagnosis. Parameters typed in bold have statistically significant values (P < 0.05).

Next, in a multiple regression model we analyzed the association of fetuin-A levels and the five parameters that were significant in the univariate regression analysis. We used serum albumin instead of total protein due to strong collinearity between these two parameters (r = 0.739, P = 4.55*10−16, Table 4). Only albumin (and marginally WBC) but not the H. pylori status or SLEDAI showed statistically significant association with fetuin-A.

Table 4.

Multiple regression analysis of fetuin-A levels and parameters positive during univariate variable analysis

Predictor Standardized β (95% C.I.) P
ESR −0.067 (−1.351–0.829) 0.634
WBC −0.215 (−0.011–0.000) 0.058
CRP −0.134 (−0.896–0.265) 0.281
Serum albumin 0.293 (0.421–7.526) 0.029
H. pylori status (positive/negative) 0.163 (−11.937–74.057) 0.154
SLEDAI 0.026 (−3.075–3.881) 0.818
Modell fit: r 2 = 0.275, adjusted r 2 = 0.207, P = 0.002

ESR: Erythrocyte sedimentation rate; WBC: White blood cell count; CRP: C-reactive protein; C3: C3 complement component; SLEDAI: Systemic Lupus Erythematosus Disease Activity Index at the time of diagnosis. Parameters typed in bold have statistically significant values (P < 0.05).

Discussion

Although serum fetuin-A concentration significantly differed between patients with past H. pylori infection and without it further analysis indicated that this difference was not due to the H. pylori status.

In two cross-sectional studies both decreased [18] and increased [19] fetuin-A levels have been observed in active H. pylori infection. The decrease was attributed to the negative acute phase character of the protein. The elevation of fetuin-A was not explained by molecular mechanisms but was referred to the clinical observations on the metabolic effects of the molecule (increased insulin resistance and incidence of NAFLD) [5, 19, 22, 23]. In addition the acutely protective anti-inflammatory effect of fetuin-A has also been well known [24]. As compared by Polyzos et al. [7] these above-mentioned studies on the decrease [18] and elevation [19] of fetuin-A, however, markedly differed from each other in terms of patient recruitment (age, BMI) and the methods used to diagnose H. pylori infection [7]. Furthermore, fetuin-A levels differed from each other by four orders of magnitude in the two studies.

We did not intend to solve this issue but rather focused on the potential long-term effect on of H. pylori infection on fetuin-A levels. The diagnostic value of serological testing is to detect the postinfection status of the patient and is not suitable to detect active infection.

Although fetuin-A levels correlated with several parameters during univariate regression analysis only the association with albumin was found to be significant in the multivariate model, like in previous studies on alcoholic liver cirrhosis [12, 21]. Although – in contrast to alcoholic liver cirrhosis – none of our SLE patients had liver failure – we suppose that both parameters are indicators of the protein synthetizing capacity of the liver. The lack of significant regression with the positive acute phase protein CRP also supports this notion.

Parameters of SLE activity parameters did not seem to influence fetuin-A levels. We paid special attention to analyze the impact of SLE. Among SLE activity parameters only SLEDAI at the time of the diagnosis (but not anti-DNA, C3, anti-C1q) seemed to weakly predict fetuin-A levels on regression analysis, whereas SLEDAI did not differ between H. pylori positive and negative patients. Corticosteroid treatment had no effect on fetuin-A levels, either. This latter one was especially important since dexamethasone treatment has been shown to increase fetuin-A expression in rats [25].

In summary, in our cross-sectional study we could not confirm that H. pylori postinfection status by itself could determine serum fetuin-A concentration.

Acknowledgments

Authors thank Mrs. Nagyné V. M. for the skillful assistance to determine fetuin-A concentrations. This work was supported by Hungarian grant OTKA TO49266 (GF).

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  • 1.

    Kawaguchi H , Haruma K , Komoto K , Yoshihara M , Sumii K , Kajiyama G . Helicobacter pylori infection is the major risk factor for atrophic gastritis. Am J Gastroenterol 1996; 91(5): 95962.

    • Search Google Scholar
    • Export Citation
  • 2.

    Haruma K , Okamoto S , Sumii K , Yoshihara M , Tari A , Teshima H , et al. Helicobacter pylori infection and gastroduodenal disease: a comparison of endoscopic findings, histology, and urease test data. Hiroshima J Med Sci 1992; 41(3): 6570.

    • Search Google Scholar
    • Export Citation
  • 3.

    Azuma T , Suto H , Ito Y , Muramatsu A , Ohtani M , Dojo M , et al. Eradication of Helicobacter pylori infection induces an increase in body mass index. Aliment Pharmacol Ther 2002; 16 (Suppl. 2): 2404. https://onlinelibrary.wiley.com/doi/epdf/10.1046/j.1365-2036.16.s2.31.x.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 4.

    Fujiwara Y , Higuchi K , Arafa UA , Uchida T , Tominaga K , Watanabe T , et al. Long-term effect of Helicobacter pylori eradication on quality of life, body mass index, and newly developed diseases in Japanese patients with peptic ulcer disease. Hepatogastroenterology 2002; 49(47): 1298302.

    • Search Google Scholar
    • Export Citation
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    Eshraghian A , Hashemi SA , Hamidian Jahromi A , Eshraghian H , Masoompour SM , Davarpanah MA , et al. Helicobacter pylori infection as a risk factor for insulin resistance. Dig Dis Sci 2009; 54(9): 196670. https://link.springer.com/article/10.1007/s10620-008-0557-7.

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The author instruction is available in PDF.
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Senior editors

Editor-in-Chief: Prof. Dóra Szabó (Institute of Medical Microbiology, Semmelweis University, Budapest, Hungary)

Managing Editor: Dr. Béla Kocsis (Institute of Medical Microbiology, Semmelweis University, Budapest, Hungary)

Co-editor: Dr. Andrea Horváth (Institute of Medical Microbiology, Semmelweis University, Budapest, Hungary)

Editorial Board

  • Prof. Éva ÁDÁM (Institute of Medical Microbiology, Semmelweis University, Budapest, Hungary)
  • Prof. Sebastian AMYES (Department of Medical Microbiology, University of Edinburgh, Edinburgh, UK.)
  • Dr. Katalin BURIÁN (Institute of Clinical Microbiology University of Szeged, Szeged, Hungary; Department of Medical Microbiology and Immunobiology, University of Szeged, Szeged, Hungary.)
  • Dr. Orsolya DOBAY (Institute of Medical Microbiology, Semmelweis University, Budapest, Hungary)
  • Prof. Ildikó Rita DUNAY (Institute of Inflammation and Neurodegeneration, Medical Faculty, Otto-von-Guericke University, Magdeburg, Germany; Center for Behavioral Brain Sciences (CBBS), Magdeburg, Germany)
  • Prof. Levente EMŐDY(Department of Medical Microbiology and Immunology, University of Pécs, Pécs, Hungary.)
  • Prof. Anna ERDEI (Department of Immunology, Eötvös Loránd University, Budapest, Hungary, MTA-ELTE Immunology Research Group, Eötvös Loránd University, Budapest, Hungary.)
  • Prof. Éva Mária FENYŐ (Division of Medical Microbiology, University of Lund, Lund, Sweden)
  • Prof. László FODOR (Department of Microbiology and Infectious Diseases, University of Veterinary Medicine, Budapest, Hungary)
  • Prof. József KÓNYA (Department of Medical Microbiology, University of Debrecen, Debrecen, Hungary)
  • Prof. Yvette MÁNDI (Department of Medical Microbiology and Immunobiology, University of Szeged, Szeged, Hungary)
  • Prof. Károly MÁRIALIGETI (Department of Microbiology, Eötvös Loránd University, Budapest, Hungary)
  • Prof. János MINÁROVITS (Department of Oral Biology and Experimental Dental Research, University of Szeged, Szeged, Hungary)
  • Prof. Béla NAGY (Centre for Agricultural Research, Institute for Veterinary Medical Research, Budapest, Hungary.)
  • Prof. István NÁSZ (Institute of Medical Microbiology, Semmelweis University, Budapest, Hungary)
  • Prof. Kristóf NÉKÁM (Hospital of the Hospitaller Brothers in Buda, Budapest, Hungary.)
  • Dr. Eszter OSTORHÁZI (Institute of Medical Microbiology, Semmelweis University, Budapest, Hungary)
  • Prof. Rozália PUSZTAI (Department of Medical Microbiology and Immunobiology, University of Szeged, Szeged, Hungary)
  • Prof. Peter L. RÁDY (Department of Dermatology, University of Texas, Houston, Texas, USA)
  • Prof. Éva RAJNAVÖLGYI (Department of Immunology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary)
  • Prof. Ferenc ROZGONYI (Institute of Laboratory Medicine, Semmelweis University, Budapest, Hungary)
  • Prof. Joseph G. SINKOVICS (The Cancer Institute, St. Joseph’s Hospital, Tampa, Florida, USA)
  • Prof. Júlia SZEKERES (Department of Medical Biology, University of Pécs, Pécs, Hungary.)
  • Prof. Mária TAKÁCS (National Reference Laboratory for Viral Zoonoses, National Public Health Center, Budapest, Hungary.)
  • Prof. Edit URBÁN (Department of Medical Microbiology and Immunology University of Pécs, Pécs, Hungary; Institute of Translational Medicine, University of Pécs, Pécs, Hungary.)

 

Editorial Office:
Akadémiai Kiadó Zrt.
Budafoki út 187-187, A/3, H-1117 Budapest, Hungary

Editorial Correspondence:
Acta Microbiologica et Immunologica Hungarica
Institute of Medical Microbiology
Semmelweis University
P.O. Box 370
H-1445 Budapest, Hungary
Phone: + 36 1 459 1500 ext. 56101
Fax: (36 1) 210 2959
E-mail: amih@med.semmelweis-univ.hu

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  • Science Citation Index Expanded

2022  
Web of Science  
Total Cites
WoS
689
Journal Impact Factor 1.5
Rank by Impact Factor

Immunology (Q4)
Microbiology (Q4)

Impact Factor
without
Journal Self Cites
1.3
5 Year
Impact Factor
1.7
Journal Citation Indicator 0.34
Rank by Journal Citation Indicator

Immunology (Q4)
Microbiology (Q4)

Scimago  
Scimago
H-index
31
Scimago
Journal Rank
0.333
Scimago Quartile Score

Immunology and Microbiology (miscellaneous) (Q3)
Infectious Diseases (Q3)
Medicine (miscellaneous) (Q3)
Microbiology (medical) (Q3)

Scopus  
Scopus
Cite Score
2.8
Scopus
CIte Score Rank
General Immunology and Microbiology 29/53 (46th PCTL)
Infectious Diseases 186/304 (38th PCTL)
Microbiology 85/124 (31st PCTL)
Scopus
SNIP
0.484

2021  
Web of Science  
Total Cites
WoS
696
Journal Impact Factor 2,298
Rank by Impact Factor Immunology 141/161
Microbiology 118/136
Impact Factor
without
Journal Self Cites
2,143
5 Year
Impact Factor
1,925
Journal Citation Indicator 0,39
Rank by Journal Citation Indicator Immunology 146/177
Microbiology 129/157
Scimago  
Scimago
H-index
29
Scimago
Journal Rank
0,362
Scimago Quartile Score Immunology and Microbiology (miscellaneous) (Q3)
Medicine (miscellaneous) (Q3)
Scopus  
Scopus
Cite Score
3,6
Scopus
CIte Score Rank
General Immunology and Microbiology 26/56 (Q2)
Infectious Diseases 149/295 (Q3)
Microbiology (medical) 66/118 (Q3)
Scopus
SNIP
0,598

2020  
Total Cites 662
WoS
Journal
Impact Factor
2,048
Rank by Immunology 145/162(Q4)
Impact Factor Microbiology 118/137 (Q4)
Impact Factor 1,904
without
Journal Self Cites
5 Year 0,671
Impact Factor
Journal  0,38
Citation Indicator  
Rank by Journal  Immunology 146/174 (Q4)
Citation Indicator  Microbiology 120/142 (Q4)
Citable 42
Items
Total 40
Articles
Total 2
Reviews
Scimago 28
H-index
Scimago 0,439
Journal Rank
Scimago Immunology and Microbiology (miscellaneous) Q4
Quartile Score Medicine (miscellaneous) Q3
Scopus 438/167=2,6
Scite Score  
Scopus General Immunology and Microbiology 31/45 (Q3)
Scite Score Rank  
Scopus 0,760
SNIP
Days from  225
submission
to acceptance
Days from  118
acceptance
to publication
Acceptance 19%
Rate

2019  
Total Cites
WoS
485
Impact Factor 1,086
Impact Factor
without
Journal Self Cites
0,864
5 Year
Impact Factor
1,233
Immediacy
Index
0,286
Citable
Items
42
Total
Articles
40
Total
Reviews
2
Cited
Half-Life
5,8
Citing
Half-Life
7,7
Eigenfactor
Score
0,00059
Article Influence
Score
0,246
% Articles
in
Citable Items
95,24
Normalized
Eigenfactor
0,07317
Average
IF
Percentile
7,690
Scimago
H-index
27
Scimago
Journal Rank
0,352
Scopus
Scite Score
320/161=2
Scopus
Scite Score Rank
General Immunology and Microbiology 35/45 (Q4)
Scopus
SNIP
0,492
Acceptance
Rate
16%

 

Acta Microbiologica et Immunologica Hungarica
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Acta Microbiologica et Immunologica Hungarica
Language English
Size A4
Year of
Foundation
1954
Volumes
per Year
1
Issues
per Year
4
Founder Magyar Tudományos Akadémia
Founder's
Address
H-1051 Budapest, Hungary, Széchenyi István tér 9.
Publisher Akadémiai Kiadó
Publisher's
Address
H-1117 Budapest, Hungary 1516 Budapest, PO Box 245.
Responsible
Publisher
Chief Executive Officer, Akadémiai Kiadó
ISSN 1217-8950 (Print)
ISSN 1588-2640 (Online)

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