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Oral corticosteroid (OCS) use during pregnancy was not linked to gestational diabetes, although there was a small risk increase during early pregnancy, according to a nationwide cohort study of more than a million women. When adjusted for covariates, a pooled estimate for crude risk ratio of oral corticosteroid exposure in weeks 1 through 27 of pregnancy showed a slight increase in gestational diabetes risk, but it was attenuated to null.

However, they reported in JAMA Internal Medicine that oral corticosteroid exposure between 4 and 6 weeks of gestation was associated with a slight increase in the risk of gestational diabetes (weighted RR 1.10, 95 percent CI 1.03-1.17). However, the authors found no correlations in subgroup analyses of maternal age, indication, duration of action, dosage, timing, or duration of exposure.

Clinicians treating autoimmune or chronic inflammatory conditions during pregnancy, where corticosteroid therapy may be crucial for the health of both the mother and the fetus, will find these findings comforting. Oral corticosteroids are increasingly being used in pregnancy to manage chronic conditions, autoimmune diseases, and disease flares.

The authors pointed out that despite their widespread use, OCSs are known to impair glucose metabolism by increasing peripheral insulin resistance, encouraging hepatic gluconeogenesis, and possibly reducing pancreatic β-cell function, all mechanisms that may contribute to hyperglycemia and the development of gestational diabetes. They added that much of the previous research on this relationship had small sample sizes or insufficient adjustment for confounders.

The National Health Information Database of South Korea, which gathers claims information from the public health insurance system, was utilized in the population-based cohort study. Researchers examined pregnancies resulting in live births from January 1, 2010, to December. 31, 2021. Approximately 1.3 million of the roughly 3.8 million pregnancies that resulted in live births during the study period qualified for analysis; 6% of these pregnancies were exposed to oral contraceptives between 1 and 27 weeks of gestation.

Gestational diabetes occurred in 9.5 percent of pregnancies exposed to oral corticosteroids and 7.36 percent of unexposed pregnancies. Women with gestational diabetes, preexisting diabetes, no history of health screening before pregnancy, and exposure to oral corticosteroids starting 30 days before pregnancy without a prescription during the first 27 weeks of pregnancy were all excluded.

Pregnancy was divided into three weeks, from 1 week to 27 weeks’ gestation, as gestational diabetes is not typically tested after 28 weeks. Women who had not started oral corticosteroids or had been diagnosed with gestational diabetes before or during that period were included in each interval.

Women in the exposed group had more comorbidities than those in the unexposed group, including migraine (8.1 percent vs. 5.4 percent), asthma (7.2 percent vs. 2.2 percent), and immune-mediated inflammatory disease (2.5 percent vs. 0.4 percent). The majority of baseline characteristics were similar. Most patients in the full study population had a mean age of 30-34 and a BMI of 18.5-22.9. Additionally, the authors performed four sensitivity analyses, limiting the cohort to those with a known family history of diabetes, nulliparous pregnancies, singleton pregnancies, and one using women who had previously taken oral corticosteroids but not during pregnancy as the reference group. The results of these analyses were consistent with the main findings.

Shin and co-authors noted that “early pregnancy represents a critical developmental window when the endocrine pancreas anticipates increased insulin demands through adaptive-cell priming, occurring before the physiologic insulin resistance typically develops around 24 weeks’ gestation, indicating the limited risk at 4-6 weeks’ gestation. During this vulnerable period, corticosteroid exposure may disrupt foundational pancreatic-cell adaptation mechanisms, prematurely induce insulin resistance, and create a cumulative metabolic burden through prolonged exposure duration that overwhelms maternal compensatory capacity before the substantial insulin secretion increases required in later pregnancy.

Study limitations included the fact that prescription of oral corticosteroids may not guarantee actual medication intake, and the definition of gestational diabetes relied on diagnostic codes. Also, there was the overall potential for residual confounding. The study was restricted to live births, thereby introducing potential selection bias. Lastly, the authors noted that the findings might not apply to other populations with different baseline characteristics.

They concluded that “clinical decision-making regarding corticosteroid use should continue to prioritize maternal disease control while maintaining vigilance in monitoring glucose metabolism, particularly in women with preexisting risk factors” and that these results “suggest that appropriate corticosteroid therapy during pregnancy is metabolically safe with respect to gestational diabetes risk.

Reference:
https://pmc.ncbi.nlm.nih.gov/articles/PMC5604866/
https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2842158#:~:text=Conclusions%20and%20Relevance%20In%20this,of%20OCSs%20when%20clinically%20indicated.
https://www.medpagetoday.com/obgyn/pregnancy/118780

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