P.S.G.V.P. M’s College of Pharmacy, Shahada Dist. Nandurbar, 425409 (Ms), India.
*Corresponding Author E-mail: ppremsager124@gmail.com
ABSTRACT:
KEYWORDS: Gestational diabetes mellitus, Gestational hypertension, Gestational thyroid dysfunction, Maternal–fetal outcomes.
INTRODUCTION:
The period of time during which one or more babies develop inside a woman is called pregnancy, gravidity, or gestation. After the Last Menstrual Period (LMP), which the patient should be aware of, it typically lasts for about 40 weeks before ending with childbirth. Human gestation typically lasts 280 days, or 40 weeks. Human Chorionic Gonadotropin (hCG) is a hormone that is detected by both blood and urine test.1
There is a link between increased levels of estrogen and progesterone and vasodilation, and both increase significantly during pregnancy. Relaxin is a peptide hormone produced by the corpus luteum and circulated throughout pregnancy. It is detectable during the luteal stage of the ovulatory cycle. If conception occurs, serum concentrations peak at the end of the first trimester before falling to an intermediate level throughout the pregnancy. This hormone has been shown to have an endothelial- dependent vasodilatory role in pregnancy, affecting small arterial resistance vessels. In a Swedish observational study of pregnant women, the effects of serum progesterone, relaxin, and estradiol concentrations on arterial blood pressure were studied.2
· HIV (human immunodeficiency virus)
· Thyroid Disorders in Pregnancy
· Gestational Diabetes Mellitus
· Gestational Hypertension
The acronym HIV stands for Human Immunodeficiency Virus. The acronym AIDS stands for Acquired Immuno deficiency Syndrome. [3] In recent years, universal HIV prenatal testing, antiretroviral therapy (ART), scheduled cesarean delivery for HIV-positive women with elevated viral loads, appropriate ART for infants, and avoidance of breastfeeding have shown encouraging results. The Centers for Disease Control and Prevention now aims to eliminate HIV transmission from mother to child by reducing the incidence to <1 infection per 100,000 live births.4
HIV can be spread vertically through:
· In the amniotic fluid or across the placenta in utero.
· Direct contact with blood during the birth process, as well as infected maternal cervical and vaginal secretions.
· After birth through breast milk.5
HIV-positive pregnant women are at higher risk for bacterial pneumonia, UTIs, parasitic infestations, and other opportunistic infections. Tuberculosis is the most common in developing countries. Herpes zoster and, rarely, Kaposi's sarcoma can also occur in HIV-positive pregnant women.6
1) Postpartum Management:
All postpartum HIV-positive women should be screened for depression. Emphasize continued ART adherence, consider future pregnancies, contraceptive choice, and drug interactions when selecting postpartum ART. Inform patients about early ovulation without breastfeeding and advise on contraceptives and PrEP for partners in serodiscordant couples. All contraceptive methods are safe for HIV-positive women.
2) Newborn Management:
Infants of HIV-positive mothers should receive post-exposure ART within 6–12hours of birth. For mothers with viral suppression, give ZDV for 4 weeks unless there were genital ulcers, bleeding, or other STIs. Infants of mothers without viral suppression (HIV RNA >50) should get a 2- or 3-drug regimen for 6 weeks. If maternal HIV status is unknown, perform a rapid HIV test and give prophylaxis; stop if negative.7
Hyperthyrodism is the term used to describe elevated levels of thyroid hormone in the bloodstream, while hyperthyroidism is usually the disease process in which excessive TH is produced and eliminated. It can happen in up to 0.4% of pregnancies and about 1% of the population. The prevalence of thyroid dysfunction was 10.2%, while hyperthyroidism, hypothyroidism, and hypothyroxinemia were 1.8, 7.5, and 0.9%, respectively, according to a prior study by Wang et al.8
· TSH-induced hyperthyroidism:
· Pituitary resistance to thyroid hormone:
· Hyperthyroidism from thyroid stimulators other than TSH.8
Since tachycardia, sweating, dyspnea, and anxiety can all be signs of a healthy pregnancy, the clinical manifestation of hyperthyroidism may not be immediately apparent. Heart systolic flow murmurs can happen in both hyperthyroidism and a typical pregnancy. Routine measurements of circulating thyroid hormones and TSH using a sensitive assay are used to diagnose hyperthyroidism in pregnancy. Some people prefer free T4 and T3 assays over total T4 and T3 assays because the estrogen-stimulated rise in TBG concentrations does not interfere. According to recent national and international guidelines, labs should be encouraged to establish normal ranges for TSH, total T4 and T3 levels, but especially free T4 and T3 levels.9
Table No 2. Drugs used in hyperthyroidism10
|
Drug |
Mode of action |
Dose |
Adverse effect |
|
Propylthiouracil |
Inhibits thyroxine synthesis; inhibits peripheral conversion of thyroxine to triiodothyronine |
Starting: 300-450 mg/day; maintenance: 50-100 mg/day |
Rash, fever, agranulocytosis |
|
Carbimazole |
Inhibits thyroxine synthesis |
Starting: 15-40 mg/day; maintenance: 5-15 mg/day |
As above, plus aplasia cutis and methimazole embryopathy |
|
Propranolol |
Reduces adrenergic symptoms |
10-40 mg, 3-4 times/day (short term use only |
Bronchospasm, intrauterine growth restriction, neonatal hypoglycaemia |
One type of thyroid condition is hypothyroidism. Thyroid removal surgery, radiation therapy, and autoimmune diseases are common causes of hypothyroidism.11 Depending on the location of the functional defect we describe:
Primary disease = thyroid failure = low T3 and T4 production Secondary disease = pituitary failure = low TSH production Tertiary disease – hypothalamus failure = low TRH production.12
Few studies reported the frequency of long-term hypothyroidism when hypothyroidism was detected and treated during pregnancy.
According to the European Thyroid Association's 2014 recommendations, levothyroxine was administered to pregnant women between 2014 and 2020 if their TSH levels were greater than 2.5mU/L in the first trimester or greater than 3.0mU/L in the second. 36(34%) of 177 patients who were treated for hypothyroidism at the beginning of pregnancy and who were monitored for at least six months after giving birth showed signs of long-term hypothyroidism, especially when.
· levothyroxine was initiated early, at 11.7±4.7 versus 13.7±6.5 weeks of pregnancy (P = 0.77).
· TSH levels were higher: 4.1 versus 3.5mU/L (P = 0.005) at diagno-sis of thyroid insufficiency.
· a substantial dose of levothyroxine was required to restoreand maintain euthyroidism during pregnancy: 62.8±22.2 versus 50.7±13.9g/day (P = 0.005).13
The three main aims of therapy are:
i) To resolve symptoms, including physiological and biological indicators of hypothyroidism.
ii) To improve thyroid hormone concentrations while achieving normalization of serum TSH.
iii) To avoid iatrogenic thyrotoxicosis or overtreatment particularly in the elderly.14
Pregnancy-related hypothyroidism can be managed based on TSH levels. Usually, the amount of levothyroxine is increased by between 30% and 50% over the pre-pregnancy dosage. Every four to six weeks, thyroid function tests (TFTs) should be conducted to make sure that the dosage is appropriate for the TSH levels. It should be highlighted, nevertheless, that the "normal" TSH upper reference limit varies significantly among populations. During pregnancy, levothyroxine may normally need to be gradually increased every 4-6 weeks. To guarantee proper dosing in response to the TSH levels,15 taking one levothyroxine tablet on an empty stomach. Clinical symptoms and laboratory evidence of overt hypothyroidism are the first indicators of hypothyroidism. For stable people, switching brands of levothyroxine tablets is not recommended. Individuals with overt hypothyroidism must take medication every day, ideally at a dose of 1.5 to 1.8mcg/kg. A full replacement dosage of 2.0–2.4mcg/kg of thyroxine can be administered to pregnant women. It is recommended that patients with coronary artery disease begin taking the drugs at a dose of 12.5 to 25mcg per day; the dosage needs to be adjusted in accordance with symptoms and blood TSH levels.16
One type of hyperglycemia is GDM. Generally speaking, an insulin supply that is insufficient to satisfy tissue demands for appropriate blood glucose regulation leads to hyperglycemia. Research done in the latter stages of pregnancy, when insulin needs are high and only marginally different in normal and gestational diabetic women, consistently shows that women with GDM have lower insulin responses to nutrients. Research done either prior to or following pregnancy, when women with a history of GDM are typically more insulin resistant Compared to normal women (also covered below), they frequently exhibit insulin responses that are comparable between the two groups or only marginally lower in women who have previously had GDM.
However, a significant impairment in pancreatic β ce l function is a consistent finding in women with a history of GDM when insulin levels and responses are expressed in relation to each person's level of insulin resistance. There are many unidentified potential causes of insufficient β ce l function. There are three general settings outside of pregnancy.17
1. Type 1 diabetes (T1D)
2. Type 2 Diabetes (T2D)
3. Gestational Diabetes Mellitus (GDM).18
The pancreas secretes the hormone insulin, which enables the body to use glucose effectively. However, the pancreas produces insufficient insulin in diabetics, which raises blood sugar levels. A condition known as β-cell hyperplasia occurs when the pancreas produces excessive amounts of insulin at postprandial during a natural pregnancy. (FIG NO.3) Insulin resistance rises as placental hormone release increases, especia ly in the third trimester. Therefore, when β ce l activity fails to overcome insulin resistance, GDM develops. Insulin resistance is thus brought on by pregnancy. Increased maternal obesity and placental products with insulin-dependent effects can both contribute to pregnancy-related insulin resistance. such as prolactin, estrogen, and placental human lactogen.19
an abnormal oral glucose tolerance test (GTT) serves as the basis for the diagnosis. Women undergoing a GTT must fast overnight before going to the hospital the next day. Two blood samples are typically obtained. The woman is given a sugary drink with 75 g of glucose (100 g is more frequently used in the US) after the first is taken upon arrival. Two hours later, a second blood sample is collected. It is challenging to define gestational diabetes precisely due to the controversy surrounding the GTT's exact diagnostic values.20
Table No.3 Diagnosis of Gestational Diabetes (WHO)21
|
Diagnosis of Gestational Diabetes (WHO) |
|
Blood glucose level is 10-15 percent ≤ plasma, but recent blood glucose monitors measure plasma glucose, so there is no confusion.
A fasting patient is given a one-step 75 gm glucose load, with the following parameters: |
|
1. Fasting ≥92 mg% is threshold for GDM. 2. One-hour ≥180 mg% is threshold for GDM 3. Two hours ≥153 mg% is threshold for GDM. |
|
In the 1st trimester, a fasting level 292 mg%, or in 2nd or 3rd trimester 1 hour ≥180 mg% or 2 hours ≥ 153 mg% with 75g m OGTT. |
Following diagnosis, weight management, exercise, and medical nutrition therapy are the first lines of treatment, contingent on pregestational weight.22
Most women with a history of GDM lead sedentary lives, eat few fruits and vegetables, and are overweight or obese. 99 On the other hand, it is advised to consume five or more servings of fruits and vegetables each day, engage in physical activity of $2.5hours per week of moderate aerobic activity or 75minutes per week of vigorous-intensity aerobic activity, or an equivalent of $100, and aim for weight targets of 25kg/m2.23
Pharmacotherapy:
1. Insulin and insulin analogs
2. Metformin
3. Glyburide
4. Acarbose
5. Supplementation and traditional treatment options
Any numerical definition or classification of hypertension is somewhat arbitrary due to the ongoing relationship between blood pressure and cardiovascular risk. Consequently, the level of arterial blood pressure linked to a doubling of long-term cardiovascular risk is typically considered to be the definition of hypertension.
Blood pressure readings below 120/80mmHg are considered normal. Prehypertension is defined as a systolic blood pressure of 120–139mmHg or a diastolic blood pressure of 80–89mmHg. These patients are more likely to develop hypertension in the future. Systolic blood pressure of 140mmHg or diastolic blood pressure of 90 mmHg are considered hypertensive. (Table No. 4)
There are two Phases to Hypertension:
· Stage 1 includes patients with systolic blood pressure 140–159mmHg or diastolic blood pressure 90–99 mmHg.
· Stage 2 includes patients with systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥100 mmHg.
Table No 4. Classification of Blood Pressure for Adult Aged ≥ 18 years24
|
BP Classification |
Systolic (mmHg) |
Diastolic BP |
|
Normal |
<120 |
<80 |
|
Prehypertension Stage 1 |
120-139 |
80-89 |
|
Hypertension State 2 |
140-159 |
90-99 |
|
Hypertension |
≥160 |
≥100 |
The following are among the differential diagnoses for pregnancy-related hypertension:
· Antiphospholipid syndrome
· Aortic coarctation
· Cushing syndrome
· Eclampsia
· Glomerulonephritis25
Classification of Hypertension:
There are four categories of HTNP
1. Chronic (pre-existing) hypertension (>140/90) that either predates pregnancy or develops before 20 weeks of gestation.
2. Gestational hypertension (without proteinuria).
3. Pre-existing hypertension plus superimposed gestational hypertension with proteinuria.
4. Antenatally unclassified hypertension.26
1) α-adrenergic agonists:
Methyldopa is among the drugs with the longest history of use during pregnancy. Methyldopa can cause a number of adverse effects, such as sedation and irregular sleep patterns, because it works centrally by lowering sympathetic tone.
2) Beta-blockers:
In general, beta-blockers are safe and well-tolerated during pregnancy. One of the most popular treatments for pregnancy-related hypertension is labetalol.
3) Calcium channel blockers:
Calcium channel blockers can influence the course of labor and are also strong tocolytics. The concurrent use of magnesium sulfate for seizure prevention while taking calcium channel blockers during pregnancy raises serious concerns because it has been shown to result in circulatory collapse and neuromuscular blockade.
4) Diuretics:
The most often prescribed drug for women with chronic hypertension who are of childbearing age is a diuretic. Vascular volume contraction is a potential side effect of all diuretics that, ironically, may lead to further blood pressure increases in preeclamptic women. Compared to women with normal pregnancies, preeclamptic women have lower plasma volumes. Volume contraction may activate the renin-angiotensin-dosterone axis, leading to additional increases in peripheral vascular resistance and exacerbation of hypertension. With the exception of spironolactone, which may have anti-androgen effects on the fetus, a woman who takes a diuretic before becoming pregnant can continue taking it during her pregnancy.
5) Renin-Angiotensin-Aldosterone System Blockade:
Blockers of the renin-angiotensin-aldosterone system (RAAS), such as ACE inhibitors and ARBs, are very good at lowering blood pressure and are very helpful in proteinuric disorders. At first, these drugs were thought to be reasonably safe in the first trimester and only linked to problems in the second, when they could cause oligohydramnios, anuria, and fetal renal failure. [27]
CONCLUSION:
The present study highlights the significant burden of Pregnancy Induced Hypertension, Gestational Diabetes Mellitus, thyroid dysfunction, and HIV among pregnant women, underscoring their importance as major public health concerns in antenatal care. These conditions were found to contribute substantially to maternal and fetal morbidity when not identified and managed in a timely manner. The findings emphasize the need for routine screening, early diagnosis, and integrated management of these disorders during pregnancy. Strengthening antenatal surveillance, improving awareness among pregnant women, and ensuring access to appropriate treatment can significantly reduce adverse pregnancy outcomes. Overall, a comprehensive and multidisciplinary approach to maternal healthcare is essential to improve both maternal and neonatal health outcomes.
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Received on 05.02.2026 Revised on 07.03.2026 Accepted on 01.04.2026 Published on 05.05.2026 Available online from May 09, 2026 A and V Pub J. of Nursing and Medical Res. 2026;5(2):87-92. DOI: 10.52711/jnmr.2026.18 ©A and V Publications All right reserved
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