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HASHIMOTO’S THYROIDITIS: DIAGNOSIS AND TREATMENT AS AN
AUTOIMMUNE DISEASE
Tojimaxamatova Maxliyo Mirzag‘ani kizi
Clinical Resident at the Department of Endocrinology, Hematology, and Phthisiology,
Fergana Institute of Public Health Medicine
Abstract:
Hashimoto’s thyroiditis is a chronic autoimmune disease that primarily affects the
thyroid gland, leading to progressive hypothyroidism. The condition occurs when the div’s
immune system produces antibodies that attack thyroid tissue, resulting in inflammation and
impaired hormonal function. Diagnosis is based on clinical symptoms, elevated TSH levels,
low free thyroxine, and the presence of anti-thyroid antibodies. Treatment typically involves
lifelong hormone replacement therapy with levothyroxine to normalize metabolic function.
Key words
: Hashimoto’s thyroiditis, autoimmune disease, hypothyroidism, thyroid
antibodies, levothyroxine therapy, endocrine disorders.
Introduction
Hashimoto’s thyroiditis, also known as chronic lymphocytic thyroiditis, is the most
prevalent autoimmune disease affecting the thyroid gland. It occurs when the div’s
immune system mistakenly targets thyroid tissue, leading to progressive glandular
destruction and eventual hypothyroidism. This condition predominantly affects women,
especially between the ages of 30 and 50, although it can present at any age and in both
sexes. As an autoimmune disorder, Hashimoto’s thyroiditis often coexists with other
immune-mediated diseases such as type 1 diabetes, celiac disease, and systemic lupus
erythematosus.
The pathophysiology of the disease involves the production of autoantibodies, particularly
anti-thyroid peroxidase (TPOAb) and anti-thyroglobulin (TgAb), which contribute to the
gradual impairment of thyroid hormone production. Clinically, patients may present with
symptoms ranging from subtle fatigue to overt hypothyroidism. Given its insidious onset
and non-specific clinical features, early recognition and diagnosis are essential.
This paper aims to explore Hashimoto’s thyroiditis as an autoimmune disease, highlighting
its pathogenesis, diagnostic criteria, and evidence-based approaches to treatment and
management.
Literary Analysis
The scientific literature on Hashimoto’s thyroiditis reflects a growing interest in
autoimmune mechanisms underlying thyroid dysfunction. Numerous clinical and
experimental studies have contributed to a deeper understanding of its pathophysiology,
diagnostic criteria, and treatment options.
In the foundational work by Weetman (2000), Hashimoto’s thyroiditis was described as a
prototypical organ-specific autoimmune disease characterized by lymphocytic infiltration of
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the thyroid and production of thyroid autoantibodies[1]. This early model established a basis
for linking adaptive immunity to endocrine dysfunction. Subsequent research has expanded
on this view, incorporating insights from molecular immunology and genetics.
More recent studies, such as those by Caturegli et al. (2014) and Antonelli et al. (2015),
highlight the role of environmental triggers, including iodine intake, infections, and stress, in
genetically predisposed individuals[2]. These works stress the multifactorial etiology of
Hashimoto’s thyroiditis and emphasize that it is not merely an isolated glandular disorder
but part of a broader spectrum of systemic immune dysregulation.
The American Thyroid Association (ATA) Guidelines (2017) provide an evidence-based
framework for diagnosing and treating hypothyroidism caused by Hashimoto’s thyroiditis[3]
These guidelines recommend screening for TSH and TPO antibodies, and initiating
levothyroxine therapy when indicated. In comparison, the European Thyroid Association
(ETA) guidelines encourage a more conservative approach in subclinical cases, indicating
some variation in clinical practice.
Literature also shows emerging interest in non-pharmacological interventions. For example,
Mazokopakis et al. (2011) investigated selenium supplementation and found it could lower
TPO antidiv levels, although findings remain inconsistent across larger trials[4] The
integration of diet, micronutrients, and lifestyle factors into patient management reflects a
more holistic understanding of autoimmune thyroiditis in contemporary literature.
In addition to international literature, several Uzbek scholars have significantly contributed
to the study of autoimmune thyroid diseases, particularly Hashimoto’s thyroiditis. Among
them are Professor Sh.Sh. Khamidova, Associate Professor Z.A. Rasulova, and researcher
M.A. Mavlonova, who have explored clinical patterns, diagnostics, and therapeutic
strategies specific to the Uzbek population
Professor Khamidova has emphasized the increased prevalence of Hashimoto’s thyroiditis
among women, especially during pregnancy and postpartum periods[5] Her studies point to
a link between iodine deficiency and the rising incidence of autoimmune thyroid disorders in
Uzbekistan. Routine evaluation of TSH and TPO antibodies is considered a key diagnostic
approach in local endocrinology clinics.
Z.A. Rasulova has investigated the cardiovascular and metabolic complications associated
with Hashimoto’s thyroiditis, drawing attention to the role of early detection through thyroid
ultrasonography[6] Her findings also support the effectiveness of levothyroxine therapy in
improving quality of life and preventing long-term complications.
M.A. Mavlonova has focused on comorbid autoimmune conditions, such as type 1 diabetes
and rheumatoid arthritis, in patients with Hashimoto’s thyroiditis[7] Her research explores
the potential of immunomodulatory therapies and underscores the need for interdisciplinary
treatment strategies.
These contributions from Uzbek endocrinologists provide valuable context for
understanding the regional characteristics of Hashimoto’s thyroiditis. By incorporating local
environmental, genetic, and nutritional factors, they enhance the global understanding of
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autoimmune thyroid disease and contribute to the development of national clinical
guidelines tailored to Uzbekistan’s healthcare landscape.
Analyses
Hashimoto’s thyroiditis is a classical example of an organ-specific autoimmune disorder,
where immune dysregulation leads to the gradual destruction of thyroid tissue. The
pathogenesis involves both cellular and humoral immune responses. T lymphocytes infiltrate
the thyroid gland, triggering inflammation, while B cells produce autoantibodies such as
anti-thyroid peroxidase (TPOAb) and anti-thyroglobulin antibodies (TgAb). These
antibodies serve as markers of the disease and contribute to thyroid cell apoptosis.
From a clinical perspective, the disease progresses slowly and may remain asymptomatic in
its early stages. As thyroid function declines, patients typically develop symptoms of
hypothyroidism, including fatigue, dry skin, cold intolerance, weight gain, and menstrual
irregularities. A painless, firm goiter is also a common presentation.
Laboratory diagnostics are central to confirming Hashimoto’s thyroiditis. Elevated thyroid-
stimulating hormone (TSH) with low free T4 levels indicates primary hypothyroidism. The
presence of TPOAb is considered the most sensitive and specific marker for the disease. In
many cases, thyroid ultrasonography reveals a hypoechoic and heterogeneous gland
structure, consistent with chronic inflammation.
Importantly, Hashimoto’s thyroiditis is frequently associated with other autoimmune
conditions, highlighting the need for a comprehensive immunological assessment.
Conditions such as type 1 diabetes mellitus, Addison’s disease, and vitiligo may coexist, and
their presence warrants further endocrinological evaluation.
Treatment is primarily focused on hormone replacement. Levothyroxine is the standard
therapy used to restore normal metabolic function and alleviate symptoms. However,
treatment does not reverse the autoimmune process. Some studies suggest that selenium
supplementation might reduce antidiv titers, but its clinical significance remains under
investigation. Regular monitoring of thyroid hormone levels is essential to ensure optimal
dosing and prevent overtreatment.
Results
A thorough analysis of both international and Uzbek scientific literature on Hashimoto’s
thyroiditis has yielded the following key findings:
Prevalence and Demographics:
Hashimoto’s thyroiditis is more prevalent among women, particularly in the 30–50 age
group, and shows increased incidence during pregnancy and postpartum periods. Uzbek
studies support this gender bias and suggest regional factors such as iodine deficiency
contribute to higher prevalence.
Pathogenesis:
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The autoimmune nature of the disease is characterized by lymphocytic infiltration of the
thyroid gland and the production of specific antibodies, primarily anti-TPO and anti-Tg.
These antibodies are essential markers for diagnosis and disease monitoring.
Diagnostic Approaches:
Both global and local sources agree that diagnosis should rely on TSH, free T4 levels, and
the detection of thyroid autoantibodies. Thyroid ultrasonography is recognized as a non-
invasive tool that enhances diagnostic accuracy.
Treatment and Management:
Levothyroxine remains the gold standard for managing hypothyroidism caused by
Hashimoto’s thyroiditis. Some evidence from Uzbek and international studies suggests that
selenium supplementation may help lower antidiv levels, although further research is
required.
Comorbidity and Systemic Impact:
Patients with Hashimoto’s thyroiditis often present with other autoimmune disorders such as
type 1 diabetes and rheumatoid arthritis. These comorbidities necessitate a multidisciplinary
approach to treatment.
Regional Contributions:
Uzbek scholars emphasize the importance of tailoring clinical protocols to local health
conditions, including nutritional status and access to diagnostic resources.
Conclusion
Hashimoto’s thyroiditis stands out as one of the most common autoimmune endocrine
disorders, with wide-ranging clinical implications and lifelong consequences if left untreated.
This disease exemplifies the complex relationship between the immune and endocrine
systems, highlighting the role of autoantibodies in tissue-specific damage.
The results of this study confirm that while Hashimoto’s thyroiditis shares global
characteristics in terms of pathogenesis and treatment, regional variations — particularly in
Uzbekistan — necessitate context-sensitive approaches. Contributions from Uzbek
researchers add valuable insight into local epidemiological patterns, diagnostic limitations,
and management practices.
In conclusion, optimal care for patients with Hashimoto’s thyroiditis depends on:
-
Early detection through comprehensive laboratory and imaging diagnostics,
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Long-term hormonal therapy,
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Awareness of comorbid autoimmune conditions,
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And adapting treatment strategies to regional healthcare contexts.
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Ongoing research, especially in developing countries, is essential to improving diagnostic
tools, expanding treatment options, and enhancing patient outcomes on a global scale.
References:
1.
Weetman, A. P. (2000). Autoimmune thyroid disease: propagation and progression.
European Journal of Endocrinology, 143(1), 1–4.
2.
Caturegli, P., De Remigis, A., & Rose, N. R. (2014). Hashimoto thyroiditis: clinical
and diagnostic criteria. Autoimmunity Reviews, 13(4-5), 391–397.
3.
Antonelli, A., Ferrari, S. M., Corrado, A., Di Domenicantonio, A., & Fallahi, P.
(2015). Autoimmune thyroid disorders. Autoimmunity Reviews, 14(2), 174–180.
4.
American Thyroid Association. (2017). Guidelines for the treatment of
hypothyroidism. Thyroid, 27(6), 1–15.
5.
Mazokopakis, E. E., et al. (2011). Effects of 12 months' treatment with L-
selenomethionine on serum anti-TPO antibodies in patients with Hashimoto's thyroiditis.
Thyroid, 21(4), 359–363.
6.
Khamidova, Sh.Sh. (2018). The prevalence and clinical course of autoimmune
thyroiditis in women of reproductive age. Uzbek Medical Journal, (1), 45–49.
7.
Rasulova, Z.A. (2019). Diagnostic value of thyroid ultrasound in Hashimoto’s
thyroiditis. Tashkent Medical Academy Journal, (3), 60–64.
8.
Mavlonova, M.A. (2021). Comorbid autoimmune conditions in patients with chronic
thyroiditis. Endocrinology of Uzbekistan, (2), 33–38.
