Regardless of notable progress in science, doctors keep treating patients with adverse pregnancy outcomes (APO) such as gestational diabetes mellitus (GDM), antenatal hypertension, pre-eclampsia & perinatal development malformations. GDM is the most alarming of these, while it has an effect on 7–25% of pregnancies which are clinically confirmed globally. GDM is defined by the American Diabetes Association as any level of glucose intolerance experienced during pregnancy in a pregnant women who have never been diagnosed as type 1 or type 2 diabetics before. In accord with latest study, few of the features which give to the beginning of GDM comprise being overweight, consuming poorly, malnutrition, advanced maternal age, and a family record of either diabetes or resistance to insulin. Resistance to Insulin resistance and decreased insulin production are considered to have a major role in GDM pathophysiology, although the basic reasons of the condition are obscure.

As of right now, there is no widely accepted method for preventing or treating GDM. The only treatments available are insulin therapy and lifestyle modifications, both of which have limited effectiveness because insulin resistance is a prevalent manifestation in GDM patients. Regularly consumed medications, like metformin and glyburide, have revealed agreeable results, there have been concerns about the long-established influence of these drugs on pregnant women and their children. An untimely recognition of GDM is mandatory to keep down unfavourable after-effect for mother-newborn duo.
UA is the end-product of purine metabolism, which decreases by 25–35% in the early stages of pregnancy before increasing towards normal values near term in a healthy pregnancy. Multiple studies have demonstrated that high amounts of uric acid are harmful to metabolic health because they impede insulin signalling, which leads to insulin resistance. In light of this, hyperuricemia has been suggested as a part of the metabolic syndrome linked to insulin resistance.

Moreover, there may be a link between UA levels and resistance to insulin in expectant women with prenatal hypertension. Compared to women without the illness, women with gestational diabetes have greater amounts of uric acid throughout the early phases of pregnancy. Despite a great deal of study being done in this area, the occurrence of GDM hasn’t been invariably linked to UA levels throughout pregnancy. The possible impact of elevated UA levels on the potential of GDM is a topic of debate. Thus, so as to successfully handle this medical condition among this high-risk population, an in-depth knowledge of this problem is required. To verify whether elevated levels of UA throughout pregnancy can raise the chance of subsequently developing GDM, independent of already recognised risk factors, authors Jankar et al set out to conduct a systematic review.
The articles have been chosen from the databases PubMed, Embase and Scopus. They discussed all applicable publications that explored the interrelation between serum UA and GDM, accompanying the formerly recorded articles. Other articles independent of this field are refrained from. This systematic review exhibited a bond between GDM and serum UA levels.
120 articles were chosen using the structured literature search. 30 duplicate papers were removed, while 38 articles were left out due to titles and abstracts, 9 studies were found using pertinent references, 24 articles were eliminated on the grounds of inclusion criteria, and nineteen articles that satisfied both exclusion and inclusion criteria were chosen. 9 observational studies, 8 cohort studies, 1 descriptive case series study, and 1 case-control study were incorporated in the literature review.
A major factor in GDM is insulin resistance. Numerous investigations have revealed that the ingenious molecule uric acid plays a role in insulin resistance. In addition to interfering with insulin function; uric acid also has a propensity to cause inflammation and oxidative stress. The delicate equilibrium in the body can be severely disrupted by these two troublemakers, which can result in the development of gestational diabetes. Uric acid also has an impact on those priceless pancreatic beta cells that make insulin. These cells may be harmed by uric acid, which could reduce their ability to produce enough insulin to regulate blood sugar levels.
Increased renal excretion and the uricosuric impact of elevated oestrogen levels during pregnancy lead to decreased serum UA levels. Pregnancy causes a 25% drop in blood concentration from 6 to 12 mL/min to 12 to 20 mL/min due to the faster clearance of UA. The changes in renal processing have been associated with variations in blood uric acid levels during pregnancy. Raised serum UA levels are linked with a number of unfavourable pregnancy outcomes. It may result in cardiovascular illness, renal dysfunction, and oxidative stress—conditions that are frequently seen in severe preeclampsia. A number of theories have been put forth to explain how hyperuricemia affects the course of pregnancy.
The results of this study demonstrated that perinatal discomfort is more common in children born to mothers who have hyperuricemia. If neglected, glucose intolerance which is initially identified during pregnancy, can have negative effects on both the mother and the foetus. GDM usually appears in the latter half of the second or third trimester of pregnancy and lastsIt is already known that hyperuricemia independently predisposes people to diabetes mellitus, cardiovascular morbidityand metabolic syndrome. Non-pregnant females experiencing hyperuricemia without symptoms experience increased insulin resistance due to release of inflammatory cytokines and oxidative stress, this eventually causes blood glucose levels to rise. Similarly, it raises the incidence of GDM and is a major risk factor for insulin resistance during pregnancy. Elevated UA is linked to pregnancy related insulin resistance. Therefore, the main emphasis of this review was on the role that hyperuricemia plays in pregnant women’s development of GDM until delivery.
The development and mechanism of insulin resistance resulting from hyperuricemia are identical in non-pregnant and pregnant females. An increased incidence of insulin resistance and GDM is associated with hyperuricemia. This is typically caused by the activation of oxidative changes in adipose tissues through the production of UA by adipocytes, the suppression of nitric oxide release by endothelial cells, and the facilitating involvement of inflammatory cytokines. Additional research is required to firmly demonstrate a link between hyperuricemia and GDM. In addition, we must determine the pathophysiologic mechanisms that underlie this connection and the part that various predisposing variables play in the progression to GDM when conjunction with increased UA levels. It may be possible to expedite early diagnosis and screening with more research. By treating gestational diabetes early on, both the mother and the foetus can be spared the possibility of adverse effects.
Source: Jankar et al. / Indian Journal of Obstetrics and Gynecology Research 2024;11(3):315–324; https://doi.org/10.18231/j.ijogr.2024.061