Introduction

A thyroxine hormone shortage is the cause of the extremely common medical disease named hypothyroidism. The hormone thyroxine governs the body's metabolism, and an absence of it can lead to disorders with a number of organ systems. If left untreated, it could have an enormous adverse effect on the body's health and eventually result in death.¹ Thyroid diseases are most commonly caused by environmental iodine deficiency. The prevalence of primary hypothyroidism rises with age, peaking between the ages of 30 and 50. It affects women up to 8–9 times more frequently than it does men. Additionally, it seems that white people are more likely than black or Hispanic people to have hypothyroidism.²

Symptoms

Cognitive decline, cold intolerance, constipation, dry skin, edema, fatigue, infertility, lethargy, muscle cramps, voice changes, weakness and weight gain.³

Effects of hypothyroidism on different organ systems

Hypothyroidism affects almost all major organs; nevertheless, the cardiovascular system has received the most attention in study. Individuals showed symptoms such as decreased cardiac output, a decline in left ventricular function, and an increase in vascular resistance. In addition, people with hypothyroidism often exhibit metabolic syndrome symptoms, including elevated cholesterol (dyslipidemia), expanded waist circumference, and increased blood pressure (hypertension), as well as a higher prevalence of cardiovascular risk factors.¹

Types of hypothyroidism and their causes

There are generally 4 kinds of hypothyroidism: primary, secondary, tertiary, and peripheral. A T4 deficit causes primary hypothyroidism, a TSH inadequate induces secondary hypothyroidism, and a thyrotropin-releasing hormone deficiency creates peripheral hypothyroidism. Central hypothyroidism is the composite outcome of secondary and tertiary hypothyroidism. Just over one percent of individuals suffer from both central and peripheral hypothyroidism (extra thyroidal). Primary hypothyroidism is mainly caused by persistent autoimmune thyroiditis, also referred to as Hashimoto's thyroiditis, in areas that have suitable iodine levels. A large number of patients with Hashimoto's disease possess elevated levels of anti- thyroid antibodies, mainly thyroid peroxidase (TPO) antibodies, as well as anti- thyroglobulin antibodies. Nearly 12% of normal people have high thyroid peroxidase antibody counts. Thyroid peroxidase antibody levels among those with subclinical hypothyroidism are a useful marker of the disease's severity. Compared to non-smokers, smokers exhibit lower levels of thyroid peroxidase antibodies, and giving up smoking raises their risk to acquire autoimmune thyroiditis. Extra environmental factors that may lead to autoimmune thyroiditis involve a lack of vitamin D and selenium along with moderate alcohol intake. In both sexes, central hypothyroidism is equally common yet unusual. It generally includes both but is more commonly linked to pituitary and hypothalamic issues. Central hypothyroidism is marked as low levels of TSH and extremely low levels of free T4. at times there might be a modest rise in TSH, that is likely triggered by a decrease in bioactivity. More than half of cases of central hypothyroidism are triggered by pituitary adenomas. Other causes of central hypothyroidism involve radiation, brain trauma, Sheehan's syndrome, infiltrative illness, genetics, and impaired actions of the pituitary gland and hypothalamus brought on by pituitary apoplexy.¹

Congenital and acquired hypothyroidism

Hypothyroidism may appear later in life (acquired hypothyroidism) or be present from birth (congenital hypothyroidism). Around 85 percent and 15%, respectively, of persistent cases of congenital primary hypothyroidism are caused by thyroid dysgenesis and dyshormonogenesis. Few, if any, clinical symptoms of hypothyroidism show up in more than 95% of infants with congenital hypothyroidism. Programs for newborn screening make congenital hypothyroidism early detectable.⁴ One of the most common avoidable causes of intellectual disability in the world is congenital hypothyroidism (CH). Thyroid hormone (TH) levels are insufficient for the proper growth and activity of bodily tissues in people with CH, a genetic disorder. The majority of affected newborns have a permanent problem due to either an error in TH synthesis or unjust growth of the thyroid gland.⁵ In general, juvenile hypothyroidism is another term for acquired hypothyroidism. The root of hypothyroidism is inadequate thyroid hormone secretion, resulting in cellular metabolic and neurological issues. When thyrotropin (TSH) rises and thyroid hormone (T4 and T3) output falls, it can show up as overt hypothyroidism. Rarely is acquired hypothyroidism found before the age of 4 years old, usually manifesting between the ages of nine and eleven. At the time of diagnosis, nearly 80 percent of the children and adolescents display no symptoms.⁶

Diagnosis and treatment

There are many varied clinical signs and non-specific symptoms linked to hypothyroidism; no single symptom is able to identify if hypothyroidism is present. Moreover, symptoms usually manifest by the time circulating thyroxine levels fall, and sometimes even long after. In certain population groups, the use of symptoms to detect hypothyroidism is more successful than in others. So, the sole basis for the diagnosis of hypothyroidism is recurrent biochemical results.² The suggested course of action involves ingesting one levothyroxine pill on an empty stomach. The individual is then needed to fast for the following hour to prevent food from interfering with the absorption of the levothyroxine included in the tablet. Those having overt hypothyroidism ought to begin taking medicine daily at a dose of 1.5 to 1.8 mcg/kg. A full substitute doses of 2.0 to 2.4 mcg/kg of thyroxine is suitable for pregnant women to take. It is advised that people with coronary artery disease start consuming medicines at a dose of 12.5 to 25 mcg/day. The dosage needs to be adjusted according to with symptoms and blood levels of TSH. It is advised that elderly patients, specifically those who have multiple comorbidities, follow this treatment strategy. Young patients lacking comorbidities can frequently get on an adequate or complete dosage of the medicine right once, but they must be closely monitored to avoid over treating them; the levels of TSH are recorded.¹