Skip to main content
Download PDF

Determination of the relationships between hyperemesis gravidarum and systemic inflammation markers: a case‒control study

BMC Pregnancy and Childbirth volume 25, Article number: 331 (2025) Cite this article

Abstract

Background

We conducted our study to investigate the relationships between hyperemesis gravidarum (HEG) and inflammatory markers such as the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and monocyte-to-lymphocyte ratio (MLR).

Materials and methods

A total of 150 pregnant women diagnosed with HEG and 150 controls were included in our study. The data analysed included demographic variables, complete blood count results, and urinary ketonuria levels.

Results

We found that the NLR, PLR and MLR were significantly greater in HEG patients than in controls (p < 0.05), indicating a potential role of systemic inflammation in the pathophysiology of HEG. Receiver operating characteristic (ROC) analysis revealed that these markers had moderate discriminative power, suggesting their utility as adjunctive diagnostic tools in clinical settings. However, no correlation was found between inflammatory markers and the severity of ketonuria.

Conclusions

The NLR, PLR and MLR can be used as indicators of HEG as a result of the inflammatory process in pregnant women with HEG.

Peer Review reports

Introduction

Hyperemesis gravidarum (HEG) is a severe disease characterized by excessive nausea and vomiting during pregnancy, often leading to dehydration, weight loss, electrolyte imbalances, and even hospitalization. HEG occurs in approximately 0.3–3% of pregnancies and can significantly impact maternal health, potentially causing malnutrition and emotional distress throughout pregnancy [1]. The exact pathophysiology of HEG remains unclear; however, HEG is recognized as a multifactorial disorder involving hormonal changes, genetic predispositions, and possibly immunological responses [2, 3]. The importance of systemic inflammation in determining the aetiology of HEG has been shown in some studies [4, 5]. HEG patients have higher levels of haematologic inflammation indicators than healthy pregnant patients do. The monocyte-to-lymphocyte ratio (MLR), neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR) values were greater in the HEG group than in the control group [6]. The NLR and PLR values were also significantly greater in the HEG group [7]. In a recent study, the systemic immune inflammation (SII) index was greater in the severe HEG group than in the other groups [8].

The relationship between HEG and inflammation has been studied, and significant results have been reported in the literature. The existing information is inadequate to define the function of inflammation in the pathogenesis of HEG; however, it is likely that subclinical inflammation contributes to HEG development. HEG is considered a consequence of an overactive immune system, potentially linked to the production of pregnancy hormones [6].

Emerging research suggests that inflammatory responses may be central to the development and progression of HEG, as indicated by elevated levels of interleukin-6 (IL-6) and C-reactive protein (CRP) in affected patients [9, 10]. Additionally, systemic inflammatory markers, such as the NLR, PLR, and MLR, have been recognized as potential diagnostic and prognostic indicators for various inflammatory conditions and diseases [11, 12]. These markers, derived from haemograms, are convenient, cost-effective, and reliable measures of systemic inflammation, offering insights into a patient’s inflammatory status without the need for complex assays [13].

Given the ongoing interest in identifying reliable diagnostic markers for HEG, this study aimed to investigate the associations between HEG and inflammatory markers, specifically the NLR, PLR, and MLR. We hypothesize that these markers are elevated in pregnant women with HEG and that they may be correlated with the severity of the condition. Through retrospective analysis, we sought to determine the potential of the NLR, PLR, and MLR as adjunctive diagnostic tools in the clinical evaluation of HEG, contributing to a broader understanding of the inflammatory mechanisms underlying this challenging condition.

Materials and methods

This retrospective case‒control study was performed in the obstetrics and gynaecology department of a referral hospital from July 2019 to July 2023. In our study, 150 patients diagnosed with HEG and 150 patients not diagnosed with HEG were included in the control group. Patients who met the following criteria were included in the HEG group: nausea/vomiting, > 5% weight loss, positive ketonuria test results, and a singleton pregnancy at 11–13 weeks of gestation. The control group consisted of healthy women at similar gestational weeks who underwent routine outpatient clinic examinations. Patients who underwent ovulation induction, had eating problems for another reason, had multiple pregnancies, were smokers, had gastrointestinal system diseases, had thyroid diseases, had urinary tract infections or had any other infections were excluded.

Data such as the white blood cell (WBC) count, neutrophil (NEU) count, lymphocyte (LYM) count, haemoglobin (Hb) level, monocyte (MON) count, platelet (PLT) count, mean platelet volume (MPV), urine density, urine pH and ketonuria test results were obtained retrospectively from hospital records. The timing of routine blood tests was recorded as the time when the patient initially presented to the gynaecology and obstetrics outpatient clinic or emergency room with complaints of HEG during the diagnostic phase prior to receiving therapies for HEG. The NLR, PLR and MNR were obtained as the ratios of absolute NEU, PLT and MON values to absolute LYM values, respectively. In the urine analysis, the ketonuria results were classified as + 1, +2, + 3 and + 4. Demographic data, maternal age, body mass index (BMI), gravidity, and parity were also recorded.

The study was approved by the Republic of Turkey Adana City Training and Research Hospital Scientific Research Ethics Committee Republic of Turkey (Date: 17.08.2023, Decision No: 2782).

Statistical analysis

We used the Shapiro‒Wilk test to determine whether continuous data were normally distributed. While the mean ± standard deviation was used for normally distributed continuous variables, the median [25-75%] was used for other variables. Categorical variables are presented as numbers and percentages. For the comparison of two independent groups, the Mann‒Whitney U test was used if the distribution was not normal, and the independent samples t test was used if the distribution was normal. The relationships between the degree of ketonuria and the NLR, PLR and MLR were investigated with the Kruskal‒Wallis test. The optimum cut-off values for the NLR, MNR and PLR to diagnose HEG with maximum sensitivity and specificity were determined by receiver operating characteristic (ROC) curve analysis. We considered p < 0.05 to indicate statistical significance. Multivariate analysis of variance (MANOVA) was used to provide a more comprehensive understanding of the underlying relationships between variables, which could reveal multivariate effects that the original two-independent sample t test missed. Logistic regression analysis was used to investigate the associations between HEG and clinical factors. The possible risk factors for HEG identified with univariate analysis (p < 0.10) were included in the multiple logistic regression analysis. Odds ratios (ORs) and their 95% confidence intervals were calculated.

Results

The study included 150 patients diagnosed with HEG and 150 controls. The patients’ serum inflammation markers, demographic characteristics and haematological values ​​ are shown in Table 1. In the statistical evaluation between the groups, no significant differences were detected in the WBC count, PLT count, NEU count, MON count or MPV. The median LYM counts of the HEG and control groups were 1.46 [0.04–2.99] and 1.85 [0.27–3.22], respectively. A statistically significant difference was found between the groups with respect to LYM counts. A significant difference was not detected between the groups with respect to demographic characteristics such as age, gravidity, parity and gestational week.

Table 1 Demographic and laboratory measurements of the study participants
Full size table

The median NLR of the HEG group was 4.37 [1.25–91.75], the median PLR was 177.37 [57.66–6750], and the median MLR was 0.34 [0.18–13.5]; for the control group, the values were 3.52 [0.93–27.41], 141.69 [59.63–875.6] and 0.32 [0.13–1.92], respectively. We found that the NLR, PLR and MLR values ​​were significantly greater in the HEG group (p < 0.05).

When the relationships among the NLR, PLR and MLR values ​​and the degree of ketonuria were compared, the p values ​​were 0.462, 0.574 and 0.631, respectively, and no statistically significant results were found (Table 2).

Table 2 Comparison of ketonuria and blood inflammation indicators
Full size table

ROC analysis was performed using the NLR, PLR and MLR to separate the HEG and control groups. The discriminatory power of the NLR, PLR and MLR between the HEG and control groups was intermediate and statistically significant. The AUC values ​​for the NLR, PLR and MLR were 0.648, 0.645 and 0.585, respectively (p < 0.001, p < 0.001 and p < 0.0093, respectively). The NLR, PLR and MLR cut-off values were as follows: 5.3179, with 43.3% sensitivity and 80% specificity; 137.4957, with 74.7% sensitivity and 49.3% specificity; and 0.4136, with 40% sensitivity and 74.7% specificity, respectively (Table 3) (Fig. 1).

Table 3 Analysis of cut-off points of the NLR, PLR and MLR values to diagnose HEG
Full size table
Fig. 1
figure 1

ROC curves for the NLR, PLR and MLR

Full size image

MANOVA was used to determine how the HEG and control groups differed in terms of the NLR, MLR and PLR. The NLR, MLR and PLR were used as the three dependent variables, and the group was used as the independent variable. Since the homogeneity of variance‒covariance matrices, which is among the assumptions required to conduct this test, was not provided, Pillai’s trace test was used. As a result of the analysis, it was determined that the groups had significant differences in the combined dependent variables (F = 4.938, p = 0.002, Pillai’s trace = 0.048). When the dependent variables were examined separately, statistically significant results were found for all the dependent variables depending on the group variable (p < 0.001 for the NLR, p = 0.016 for the MLR and p = 0.007 for the PLR).

In this analysis, logistic regression revealed significantly greater NLRs (OR 1.144, 95% CI: 1.072–1.221; p < 0.001), Hb levels (OR 1.478, 95% CI: 1.200–1.821; p < 0.001), urine pH levels (OR 0.540, 95% CI: 0.363–0.802; p = 0.002) and urine density levels (OR 1.064, 95% CI: 1.025–1.104; p = 0.001) in the HEG patients than in healthy controls (Table 4).

Table 4 Multiple logistic regression analysis of factors related to HEG
Full size table

Discussion

HEG is characterized by a complex pathophysiological mechanism in which inflammation is thought to be an important contributor [6]. Although many factors have been found to be involved in the aetiology of HEG, the effect of inflammation on the development of HEG has only begun to be accepted in recent years. Interest in the use of inflammatory indicators as diagnostic tools is increasing, although it remains limited. This study contributes to the literature by exploring the connection between HEG and inflammatory markers, with the hypothesis that patients with HEG present elevated values of these markers. The findings revealed that pregnant individuals with HEG presented elevated NLRs, PLRs, and MLRs compared with those with low-risk pregnancies. These results suggest that inflammation is part of the pathogenesis of HEG and that these indicators may be valuable in determining the severity of disease.

While HEG is diagnosed in patients with severe nausea and vomiting during pregnancy, it may lead to malnutrition and electrolyte imbalances and may be an indication for hospitalization [14]. Although the exact aetiology of HEG is not clearly known, it is suggested that HEG may occur due to various factors. These include psychological factors, hormonal changes, and abnormal gastrointestinal motility [15]. However, the overall influence of these factors has yet to be clearly defined. Furthermore, inflammation-related markers such as CRP and IL-6 levels are elevated in HEG patients, indicating that inflammation may be a part of the pathogenesis of the disease [16, 17].

Recent research has shown that systemic inflammatory markers such as the MPV, NLR, and PLR determined from complete blood counts have significant predictive and prognostic value in various conditions, including inflammatory and autoimmune disorders; gynaecological and gastrointestinal cancers; and preeclampsia and visual problems [11, 12, 18]. One study reported that both the NLR and the PLR were significantly greater in patients with HEG [7, 19, 20]. We found that the NLR, PLR and MLR values ​​were significantly greater in the HEG group and were related to the severity of HEG. Our ROC curve revealed that the NLR, PLR, and MLR have moderate discriminative power in differentiating HEG patients from healthy pregnant women. While the sensitivity and specificity values for these markers are not high enough to serve as definitive diagnostic tools, they provide valuable insights into the inflammatory status of patients and may serve as adjunctive markers in the clinical evaluation of HEG.

Although patients with HEG should have haemoconcentration due to vomiting and dehydration, studies have shown that the Hb levels and WBC counts in HEG patients are not significantly different from those in control individuals [21, 22]. In our study, no significant difference was found in the WBC count and PLT levels between the HEG and control groups; however, a significant difference was detected in terms of the Hb level. Although LYM counts are typically thought to be greater in women with HEG [23], the literature presents conflicting findings. Some studies have shown that there is no change in LYM counts [21, 24], whereas others have shown lower counts in the HEG group [7]. In our study, we did not observe any significant difference in LYM counts between the HEG group and the control group. The MPV is an indicator of PLT activation and indicates changes in PLT size. This parameter can be easily assessed using a complete blood count device. Markers indicating PLT activation have been utilized in the diagnosis of various inflammatory diseases [25]. However, no statistically significant difference was reported in the literature when the MPV was investigated in patients diagnosed with HEG [7, 20], whereas a significant difference was found in one study [26].

Ketonuria is commonly used in the diagnosis of HEG [27]. Ketonuria serves as a parameter to assess the metabolic consequences and clinical outlook of patients with HEG; however, its relationship with the severity of HEG remains unclear. Various studies have explored this connection. One study reported that ketone levels in HEG patients were associated with longer hospital stays [28]. In contrast, some studies have shown that ketone levels have no direct relationship with the clinical severity of HEG [29, 30]. One study reported a positive correlation between the level of ketones in urine and the NLR and PLR [31]. We evaluated the same relationship in HEG patients. However, we did not find any significant relationships between ketonuria and inflammatory markers such as the NLR, PLR and MLR.

Our study has several limitations. First, our study had a retrospective design. Dehydration and malnutrition may increase the systemic inflammatory response. This point should be considered. Owing to the retrospective nature of the study, this question could not be answered according to the study results. Second, we did not use a scoring system that would allow more specific assessment of HEG. Third, we could not include the CRP level, sedimentation rate, or IL-6 level in our study because these parameters were not measured via routine screening in all patients.

In conclusion, our study demonstrated that the NLR, PLR, and MLR are elevated in pregnant women with HEG, supporting the hypothesis that inflammation is a part of the pathophysiology of this condition. However, the lack of correlation between these markers and the severity of ketonuria suggests that the relationship between inflammation and HEG is complex and multifaceted. New studies should be conducted to elucidate the mechanisms of HEG development and to investigate the advantages of the use of these markers in its management.

Data availability

The datasets used and analysed during the current study are available from the corresponding author on reasonable request.

References

  1. Fiaschi L, Nelson-Piercy C, Tata LJ. Hospital admission for hyperemesis Gravidarum: a nationwide study of occurrence, reoccurrence and risk factors among 8.2 million pregnancies. Hum Reprod. 2016;31(8):1675–84.

    CAS  PubMed  Google Scholar 

  2. Verberg MF, Gillott DJ, Al-Fardan N, Grudzinskas JG. Hyperemesis gravidarum, a literature review. Hum Reprod Update. 2005;11(5):527–39.

    CAS  PubMed  Google Scholar 

  3. Ismail SK, Kenny L. Review on hyperemesis gravidarum. Best Pract Res Clin Gastroenterol. 2007;21(5):755–69.

    PubMed  Google Scholar 

  4. Zahorec R. Neutrophil-to-lymphocyte ratio, past, present and future perspectives. Bratisl Lek Listy. 2021;122(7):474–88.

    CAS  PubMed  Google Scholar 

  5. Jiang S, He F, Gao R, Chen C, Zhong X, Li X, et al. Neutrophil and Neutrophil-to-Lymphocyte ratio as clinically predictive risk markers for recurrent pregnancy loss. Reprod Sci. 2021;28(4):1101–11.

    CAS  PubMed  Google Scholar 

  6. Soysal C, Isikalan MM, Biyik I, Erten O, Ince O. The relationship between inflammation markers and ketonuria in hyperemesis gravidarum. J Obstet Gynaecol Res. 2021;47(9):3078–83.

    CAS  PubMed  Google Scholar 

  7. Cintesun E, Akar S, Gul A, Cintesun FNI, Sahin G, Ezveci H, et al. Subclinical inflammation markers in hyperemesis gravidarum and ketonuria: A case-control study. J Lab Physicians. 2019;11(2):149–53.

    CAS  PubMed  PubMed Central  Google Scholar 

  8. Bayram F, Ozgen G, Karasin SS, Ozgen L. The predictive value of HALP score and systemic immune inflammation (SII) index in hyperemesis gravidarum. J Obstet Gynaecol Res. 2023;49(7):1729–35.

    CAS  PubMed  Google Scholar 

  9. Kurt RK, Guler A, Silfeler DB, Ozcil MD, Karateke A, Hakverdi AU. Relation of inflammatory markers with both presence and severity of hyperemesis gravidarum. Ginekol Pol. 2014;85(8):589–93.

    PubMed  Google Scholar 

  10. Kaplan PB, Gucer F, Sayin NC, Yuksel M, Yuce MA, Yardim T. Maternal serum cytokine levels in women with hyperemesis gravidarum in the first trimester of pregnancy. Fertil Steril. 2003;79(3):498–502.

    PubMed  Google Scholar 

  11. Bhat T, Teli S, Rijal J, Bhat H, Raza M, Khoueiry G, et al. Neutrophil to lymphocyte ratio and cardiovascular diseases: a review. Expert Rev Cardiovasc Ther. 2013;11(1):55–9.

    CAS  PubMed  Google Scholar 

  12. Templeton AJ, McNamara MG, Seruga B, Vera-Badillo FE, Aneja P, Ocana A, et al. Prognostic role of neutrophil-to-lymphocyte ratio in solid tumors: a systematic review and meta-analysis. J Natl Cancer Inst. 2014;106(6):dju124.

    PubMed  Google Scholar 

  13. Zhang X, Wei R, Wang X, Zhang W, Li M, Ni T, et al. The neutrophil-to-lymphocyte ratio is associated with all-cause and cardiovascular mortality among individuals with hypertension. Cardiovasc Diabetol. 2024;23(1):117.

    CAS  PubMed  PubMed Central  Google Scholar 

  14. Boelig RC, Barton SJ, Saccone G, Kelly AJ, Edwards SJ, Berghella V. Interventions for treating hyperemesis Gravidarum: a Cochrane systematic review and meta-analysis. J Matern Fetal Neonatal Med. 2018;31(18):2492–505.

    PubMed  Google Scholar 

  15. London V, Grube S, Sherer DM, Abulafia O. Hyperemesis Gravidarum: A review of recent literature. Pharmacology. 2017;100(3–4):161–71.

    CAS  PubMed  Google Scholar 

  16. Kuscu NK, Yildirim Y, Koyuncu F, Var A, Uyanik BS. Interleukin-6 levels in hyperemesis gravidarum. Arch Gynecol Obstet. 2003;269(1):13–5.

    CAS  PubMed  Google Scholar 

  17. Desdicioglu R, Yildirim M, Kocaoglu G, Demir Cendek B, Avcioglu G, Tas EE, et al. Soluble urokinase-type plasminogen activator receptor (suPAR) and interleukin-6 levels in hyperemesis gravidarum. J Chin Med Assoc. 2018;81(9):825–9.

    PubMed  Google Scholar 

  18. Yildirim M, Turkyilmaz E, Avsar AF. Preoperative Neutrophil-to-Lymphocyte ratio has a better predictive capacity in diagnosing Tubo-Ovarian abscess. Gynecol Obstet Invest. 2015;80(4):234–9.

    PubMed  Google Scholar 

  19. Yildirim SB, Ayaydin Yilmaz KI, Altuntas NB, Tekin YB. Relationship between combined systemic inflammatory indices with presence and severity of hyperemesis gravidarum. Eur Rev Med Pharmacol Sci. 2023;27(18):8868–76.

    CAS  PubMed  Google Scholar 

  20. Beyazit F, Ozturk FH, Pek E, Unsal MA. Evaluation of the hematologic system as a marker of subclinical inflammation in hyperemesis Gravidarum: a case control study. Ginekol Pol. 2017;88(6):315–9.

    PubMed  Google Scholar 

  21. Sari N, Ede H, Engin-Ustun Y, Gocmen AY, Caglayan EK. Hyperemesis gravidarum is associated with increased maternal serum ischemia-modified albumin. J Perinat Med. 2017;45(4):421–5.

    CAS  PubMed  Google Scholar 

  22. Bulanik M, Sagsoz N, Sayan CD, Yeral MI, Kisa U. Comparison of serum Ykl-40 and ischemia modified Albulmin levels between pregnant women with hyperemesis gravidarum and normal pregnant women. Med Arch. 2019;73(2):97–100.

    PubMed  PubMed Central  Google Scholar 

  23. Niemeijer MN, Grooten IJ, Vos N, Bais JM, van der Post JA, Mol BW, et al. Diagnostic markers for hyperemesis Gravidarum: a systematic review and metaanalysis. Am J Obstet Gynecol. 2014;211(2):e1501–15.

    Google Scholar 

  24. Tayfur C, Burcu DC, Gulten O, Betul D, Tugberk G, Onur O, et al. Association between platelet to lymphocyte ratio, plateletcrit and the presence and severity of hyperemesis gravidarum. J Obstet Gynaecol Res. 2017;43(3):498–504.

    PubMed  Google Scholar 

  25. Korniluk A, Koper-Lenkiewicz OM, Kaminska J, Kemona H, Dymicka-Piekarska V. Mean platelet volume (MPV): new perspectives for an old marker in the course and prognosis of inflammatory conditions. Mediators Inflamm. 2019;2019:9213074.

    PubMed  PubMed Central  Google Scholar 

  26. Timur B, Guney G. The role of serum ADAMTS-1 levels in hyperemesis gravidarum. BMC Pregnancy Childbirth. 2022;22(1):499.

    CAS  PubMed  PubMed Central  Google Scholar 

  27. Koot MH, Boelig RC, Van’t Hooft J, Limpens J, Roseboom TJ, Painter RC, et al. Variation in hyperemesis gravidarum definition and outcome reporting in randomised clinical trials: a systematic review. BJOG. 2018;125(12):1514–21.

    CAS  PubMed  Google Scholar 

  28. Derbent AU, Yanik FF, Simavli S, Atasoy L, Urun E, Kuscu UE, et al. First trimester maternal serum PAPP-A and free beta-HCG levels in hyperemesis gravidarum. Prenat Diagn. 2011;31(5):450–3.

    CAS  PubMed  Google Scholar 

  29. Koot MH, Grooten IJ, Post J, Bais JMJ, Ris-Stalpers C, Naaktgeboren CA, et al. Ketonuria is not associated with hyperemesis gravidarum disease severity. Eur J Obstet Gynecol Reprod Biol. 2020;254:315–20.

    CAS  PubMed  Google Scholar 

  30. Morris ZH, Azab AN, Harlev S, Plakht Y. Developing and validating a prognostic index predicting re-hospitalization of patients with hyperemesis gravidarum. Eur J Obstet Gynecol Reprod Biol. 2018;225:113–7.

    PubMed  Google Scholar 

  31. Aslan MM, Yeler MT, Biyik I, Yuvaci HU, Cevrioglu AS, Ozden S. Hematological parameters to predict the severity of hyperemesis gravidarum and ketonuria. Rev Bras Ginecol Obstet. 2022;44(5):458–66.

    PubMed  PubMed Central  Google Scholar 

Download references

Acknowledgements

Not applicable.

Funding

No funding was received for this study.

Author information

Authors and Affiliations

  1. Department of Obstetrics and Gynecology, Adana City Training and Research Hospital, Adana, Turkey

    Fikriye Işıl Adıgüzel, Sadık Kükrer, Gülsüm Uysal & Cevdet Adıgüzel

  2. Department of Obstetrics and Gynecology, Antalya City Hospital, Antalya, Turkey

    Serhat Altınkaya

  3. Department of Perinatology, Mersin University, Mersin, Turkey

    Ahmet Zeki Nessar

Authors
  1. Fikriye Işıl Adıgüzel
    View author publications

    You can also search for this author inPubMed Google Scholar

  2. Serhat Altınkaya
    View author publications

    You can also search for this author inPubMed Google Scholar

  3. Sadık Kükrer
    View author publications

    You can also search for this author inPubMed Google Scholar

  4. Ahmet Zeki Nessar
    View author publications

    You can also search for this author inPubMed Google Scholar

  5. Gülsüm Uysal
    View author publications

    You can also search for this author inPubMed Google Scholar

  6. Cevdet Adıgüzel
    View author publications

    You can also search for this author inPubMed Google Scholar

Contributions

All authors listed have made a substantial, direct, and intellectual contribution to the work as follow: Conceptualization, C.A. and G.U.; methodology, A.Z.N., S.A., and G.U.; software, F.I.A.; formal analysis, F.I.A. and S.K.; investigation, S.K. and C.A.; resources, G.U.; responsible for data collection, S.A.; data curation, S.A.; writing-original draft preparation, S.K., F.I.A.; writing-review and editing, A.Z.N., F.I.A.; visualization, A.Z.N.; supervision, C.A.; All authors have read and agreed to the published version of the manuscript.

Corresponding author

Correspondence to Fikriye Işıl Adıgüzel.

Ethics declarations

Ethics approval and consent to participate

The study was conducted in accordance with the guidelines of the Helsinki Declaration. Written informed consent was obtained from all participants. The study was approved by the ethics committee of the University of Health Science Adana City Training and Research Hospital (Date: 17.08.2023, Decision No: 2782).

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.

Consort statement

Our study adheres to the Consort guidelines.

Additional information

Publisher’s note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Adıgüzel, F.I., Altınkaya, S., Kükrer, S. et al. Determination of the relationships between hyperemesis gravidarum and systemic inflammation markers: a case‒control study. BMC Pregnancy Childbirth 25, 331 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12884-025-07399-1

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12884-025-07399-1

Keywords

BMC Pregnancy and Childbirth

ISSN: 1471-2393

Contact us