Metabolic comorbidity of endometritis after caesarean section

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Abstract

Background. The present study is aimed at evaluation of the occurrence of postpartum (postoperative) infection by analyzing the information content of its predictors in patients with a somatic burden for the subsequent development of recommendations for treatment and prevention.

Objective. Assessment of the prevalence and structure of metabolic and endocrine diseases in puerperas with endometritis after caesarean section to determine their prognostic value as an independent predictor of the development of postoperative infectious and inflammatory complications.

Methods. A retrospective study of case histories and data from primary medical documentation of 406 puerperas with endometritis after caesarean section was carried out.

Results. The prevalence of pregravid obesity in puerperas with endometritis was 21.4% (every fifth patient with a BMI ≥30.00 kg/m2). Approximately with the same frequency (20.4%), various disorders of carbohydrate metabolism were diagnosed, gestational diabetes mellitus prevailed in their structure (78.3%). Obesity complicated the course of pregnancy 1.7 times more often in puerperas with endometritis compared with puerperas with an uncomplicated postoperative course (21.4 vs. 12.4%; χ2=8.36; P=0.004), and carbohydrate metabolism disorders – by 2.2 times (20.4 vs. 9.1%; χ2=14.391; P<0.001).

Conclusion. Concomitant metabolic diseases are significant predictors of the development of postoperative infectious and inflammatory complications in obstetrics.

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About the authors

Nikolay A. Korobkov

North-Western State Medical University n.a. I.I. Mechnikov; Sestroretskaya Multidisciplinary Clinic

Author for correspondence.
Email: nikolai_korobkov@mail.ru
ORCID iD: 0000-0001-7279-2535
SPIN-code: 4191-3581

Cand. Sci. (Med.), Associate Professor at the Department of Obstetrics and Gynecology n.a. S.N. Davydov, North-Western State Medical University n.a. I.I. Mechnikov, St. Petersburg, Russia

Russian Federation, St. Petersburg; St. Petersburg

N. V. Bakulina

North-Western State Medical University n.a. I.I. Mechnikov

Email: nikolai_korobkov@mail.ru
ORCID iD: 0000-0003-4075-4096
Russian Federation, St. Petersburg

N. V. Borovik

Sestroretskaya Multidisciplinary Clinic

Email: nikolai_korobkov@mail.ru
ORCID iD: 0000-0003-0835-6741
Russian Federation, St. Petersburg

References

  1. Hauguel-de Mouzon S., Guerre-Millo M. The placenta cytokine network and inflammatory signals. Placenta. 2006;27(8):794–98. doi: 10.1016/j.placenta.2005.08.009.
  2. Mor G., Cardenas I., Abrahams V., et al. Inflammation and pregnancy: the role of the immune system at the implantation site. Ann Ny Acad. Sci. 2011;1221:80–7. doi: 10.1111/j.1749-6632.2010.05938.x.
  3. Rowlands I., Graves N., de Jersey S., et al. Obesity in pregnancy: Outcomes and economics. Semin Fetal Neonatal Med. 2010;15(2):94–9. doi: 10.1016/j.siny.2009.09.003.
  4. Gregor M.F., Hotamisligil G.S. Inflammatory mechanisms in obesity. Ann Rev Immunol. 2011;29:415–45. doi: 10.1146/annurev-immunol-031210-101322.
  5. Retnakaran R., Hanley A., Raif N., et al. C-reactive protein and gestational diabetes: the central role of maternal obesity. J Clin Endocrinol Metab. 2003;88(8):3507–12. doi: 10.1210/jc.2003-030186.
  6. Pantham P., Aye, I., Powell T. Inflammation in maternal obesity and gestational diabetes mellitus. Placenta. 2015;36(7):709–15. doi: 10.1016/j.placenta.2015.04.006.
  7. Jung E., Romero R., Yeo L., et al. The fetal inflammatory response syndrome: the origins of a concept, pathophysiology, diagnosis, and obstetrical implications. Semin Fetal Neonatal Med. 2020;25(4):101146. doi: 10.1016/j.siny.2020.101146.
  8. Petrakis D., Margina D., Tsarouhas K., et al. Obesity a risk factor for increased COVID 19 prevalence, severity and lethality. Mol Med Rep. 2020;22(1):9–19. doi: 10.3892/mmr.2020.11127.
  9. St-Germain L., Castellana B., Baltayeva J., et al. Maternal obesity and the uterine immune cell landscape: the shaping role of inflammation. Int J Mol Sci. 2020;27;21(11):3776. doi: 10.3390/ijms21113776.
  10. Hotamisligil G.S. Inflammation and metabolic disorders. Nature. 2006;444(7121):860–67. doi: 10.1038/nature05485.
  11. Rudnicka E., Suchta K., Grymowicz M., et al. Chronic low grade inflammation in pathogenesis of PCOS. Int J Mol Sci. 2021;22(7):3789. doi: 10.3390/ijms22073789.
  12. Адамян Л.В., Артымук Н.В., Белокриницкая Т.Е. Септические осложнения в акушерстве: клин. рекомендации (протокол лечения): (утверждено Обществом акушерских анестезиологов-реаниматологов и Рос. обществом акушеров-гинекологов). Минзрав РФ. М., 2017. 63 с. [Adamyan L.V., Artymuk N.V., Belokrinitskaya T.E. Septic complications in obstetrics: clinical guidelines (treatment protocol). Ministry of Health of the Russian Federation. M., 2017. 63 p. (In Russ.)]. doi: 10.1111/j.1471-0528.2012.03452.x.
  13. Wloch C., Wilson J., Lamagni T., et al. Risk factors for surgical site infection following caesarean section in England: results from a multicentre cohort study. BJOG. 2012;356:1324–33.
  14. Nagendra L., Boro H., Mannar V. Bacterial Infections in Diabetes. 2022 Apr 5. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000.
  15. World Health Organization. Obesity: preventing and managing the global epidemic. 1997, Geneva: WHO.
  16. Scheithauer T., Rampanelli E., Nieuwdorp M., et al. Gut Microbiota as a Trigger for Metabolic Inflammation in Obesity and Type 2 Diabetes. Front Immunol. 2020;16(11):571731. doi: 10.3389/fimmu.2020.571731.
  17. McElwain C., McCarthy F., McCarthy C. Gestational Diabetes Mellitus and Maternal Immune Dysregulation: What We Know So Far. Int J Mol Sci. 2021;20;22(8):4261. doi: 10.3390/ijms22084261.
  18. Zhou W., Sailani M., Contrepois K., et al. Longitudinal multi-omics of host–microbe dynamics in prediabetes. Nature. 2019;569:663–71. doi: 10.1038/s41586-019-1236-x.
  19. Nemeth E., Valore E.V., Territo M., et al. Hepcidin, a putative mediator of anemia of inflammation, is a type II acute-phase protein. Blood J Am Soc Hematol. 2003;101(7):2461–63. doi: 10.1182/blood-2002-10-3235.
  20. Tussing-Humphreys L., Pustacioglu C., Nemeth E., et al. Rethinking iron regulation and assessment in iron deficiency, anemia of chronic disease, and obesity: introducing hepcidin. Journal of the Academy of Nutrition and Dietetics. 2012;112(3):391–400. doi: 10.1016/j.jada.2011.08.038.
  21. Fisher A.L., Nemeth E. Iron homeostasis during pregnancy. Am J Clin Nutrit. 2017;106(6):1567–74. doi: 10.3945/ajcn.117.155812.

Supplementary files

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2. Fig. 1. Structure and frequency of involved body systems in puerperas with endometritis after CS (n=648)

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3. Fig. 2. Structure and frequency of pregravid obesity in the examined patients (%)

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4. Fig. 3. Structure and frequency of detected disorders of carbohydrate metabolism in the examined patients (%)

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