Discussion

Hypothyroidism is a chronic condition linked with deficiency in the thyroid hormones

triiodothyronine (T3) and thyroxine (T4). If left untreated hypothyroidism could lead to

cardiovascular disease, infertility, and neurological symptoms. Generally, the lack of

sufficient amounts of readily available iodine in the environment is the usual cause of thyroid

disorders like hypothyroidism. The disease affects about 5 % of the population, while it is

also estimated that 5 % of the total population may have undetected thyroid malfunction

(Chiovato et al., 2019). The effect of undetected or inadequately treated hypothyroidism is

therefore noteworthy, particularly with respect to expenses that come with maternal

hypothyroidism, or some patients having co-morbidities like diabetes mellitus.

Hypothyroidism has a variable medical presentation and non-specific indicators such

as fatigue, weight gain, depression, inferior concentration, muscle pain, constipation, and

menstrual abnormalities, with no individual symptom tentatively predicting hypothyroidism.

Moreover, T4 deficiency makes the symptoms more visible even long after the decrease in

T4 levels (Chiovato et al., 2019). Consequently, patients with chronic hypothyroidism display

more symptoms but only a number of them like dry skin, constipation, hair loss, and fatigue

are more consistent with thyroid malfunction. While not very conclusive, use of symptoms to

detect hypothyroidism works better in certain populations compared to others. Symptoms

correctly indicate overt hypothyroidism in males than in females, and in youthful populations,

especially in younger men than in older women. For this reason, the analysis of

hypothyroidism is fully derived from replicated biochemical outcomes

Research studies conducted on patients reveal a disparity between ROS and the anti-

oxidant protection system. The imbalance leads to a raised oxidative pressure, which is

evident in patients and animal models of hypothyroidism. The toxic pro-oxidant surrounding
created by hypothyroidism could facilitate the atherosclerotic processes usually consistent

with this condition. In a scientific hypothyroidism model, the overall nitric oxide synthase

(NOS) action improved (Chiovato et al., 2019). However, serum analysis of anti-oxidant and

pro-oxidant species is at present excluded from the diagnostic developments of patients with

hypothyroidism.

Chiovato et al. (2019) affirm that the use of the thyroid hormone to cure

hypothyroidism was first recorded in the late 1800s when medical experts grafted an ovine

thyroid gland into a patient with chronic hypothyroidism (myxoedema). Later, thyroid extract

from sheep was administered to patients with chronic hypothyroidism and their condition

improved. Further advancements in medical research led to the availability of synthetic

thyroxine formulations that have been utilized since the 1950s. Levothyroxine was presented

in 1962 and is currently one of the most prescribed medications for hypothyroidism globally.

World Health Organization recognizes levothyroxine as a crucial medicine for fundamental

health care.

Levothyroxine is categorized as a narrow therapeutic index drug, signifying that strict

dose prescription must be ensured to promote therapeutic success and avoid detrimental drug

reactions resulting from differences in blood concentration. The main objective of

levothyroxine medication is to reduce symptoms and avoid long-term damage. Normally,

management of the condition is easily attained, with complete recovery after replacement of

thyroid hormones (Chiovato et al., 2019). Eventually, the dose of levothyroxine may need to

be adjusted based on advancement of the condition or if the patient’s thyroid hormone

metabolism is affected. Other reasons for levothyroxine dose adjustment include dietary

habits, changes in body mass, use of concomitant medications and noncompliance to

prescription.
 A major unresolved concern regarding hypothyroidism is the treatment of subclinical

hypothyroidism using levothyroxine. Interestingly, there is accordance in regards to the use

of levothyroxine to cure subclinical hypothyroidism in expectant women and women

considering pregnancy (Biondi et al., 2019). However, to reduce the risk of complications

and negative impacts on infant cognitive growth, treatment of patients who are not pregnant

stays controversial. Subclinical hypothyroidism is reflected upon as an indicator of early

thyroid malfunction (Chiovato et al., 2019). As a result, treatment using levothyroxine may

inhibit development of subclinical hypothyroidism to overt hypothyroidism.

Despite the etiology of endometriosis still being unknown, many articles highlight the

relationship between thyroid dysfunction and endometriosis (Peyneau et al., 2019). AITD has

long been associated with endometriosis-linked infertility, but the systematic explanation for

the part thyroid dysfunction plays on endometriosis evolution has not been clarified (Wu et

al., 2019). This review shows no considerable increase in thyroid disease in female patients

with endometriosis. Based on findings from the study, the population of women battling with

endometriosis is at a low risk of getting thyroid disease (Shafrir et al., 2018). Thus, it is not

necessary to screen these women for endometriosis.

Interestingly, the prevalence of AITD in the control group was higher than in female

patients with endometriosis. These instances of thyroid dysfunction in the control subjects

were linked with the presence of antithyroid antibodies, while in the patients with

endometriosis, instances of thyroid dysfunction certainly involved antithyroid antibodies

(Peyneau et al., 2019).

Drawing from the ex vivo analysis on thyroid transcripts in endometriosis patients,

raised levels of TSH (hypothyroidism) or T4 hormone (hyperthyroidism) could be proposed

as a contributing aspect of endometriosis evolution. In vitro analyses were done to investigate

the action of TSH, T3, and T4 on endometriotic and endometrial cells from patients and

control subjects (Symons et al., 2018). From the study, it was deduced that T3 only affects

epithelial cells while TSH has a proliferative effect on all control and endometriotic cells

whereas T4 specifically acted on stromal and epithelial ectopic endometrial cells (Peyneay et

al., 2019). Moreover, thyroid hormones enhance ROS production in ectopic endometrial

cells.

Falcone & Flyckt (2018) reported that endometriosis is an inflammatory disorder

distinguished by a critical leukocytic penetration in the ectopic endometrium. High amounts

of thyroid antigens such as thyroid hormones, thyroglobulin, or TSHR in endometriotic cells

may enhance their contact with the immune system in an immunostimulant surrounding that

could activate the break of tolerance and the autoimmune response toward the thyroid

antigens (Peyneau et al., 2019). The impact of thyroid function on the evolution of

endometriosis was examined in vivo using three mouse replicas. These models enabled the

evaluation of the influence of hypothyroidism, hyperthyroidism, euthyroidism, and thyroid

autoimmunity on endometriosis progression.

The local production of thyroid hormones can trigger macrophages and neutrophils to

facilitate a nearby proinflammatory surrounding and ROS creation that may promote

endometriotic cell proliferation. As such, the endometriosis model that the researchers used

was an autologous graft replica of the uterine horn, which ensured the mice maintained a

normal immune response (Peyneau et al., 2019). The endometriosis model was also

combined with a hypothyroid model, an autoimmune thyroid state with euthyroidism, and an

autoimmune thyroiditis with hyperthyroidism. To determine whether the findings could be

interpreted to humans, the researchers conducted a backward analysis on endometriosis

patients whose clinical details were present. They deduced that patients with thyroid
disorders and endometriosis experienced more severe pelvic pain, and had a more critical

clinical score compared to endometriosis patients without thyroid dysfunction (Peyneau et al.,

2019).

Statistically, complaints of symptoms related with hypothyroidism were more

frequent among endometriosis patients and were not actually linked to thyroid dysfunction.

Nonetheless, the presence of endometriosis was not ascertained using laboratory tests; hence

the indicators of thyroid dysfunction were not prognostic of the disease. Ek et al. (2019) also

elucidate that endometriosis patients exhibited degraded quality of life, including symptoms

like fatigue, reduced body mass, and a higher incidence of depression compared to women

without the disorder. Medical experts and the patients acknowledge emotional susceptibility

and fatigue as being predominantly significant to the impact of hypothyroidism.