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Best Practice & Research. Clinical... Jan 2020Graves' disease (GD) is characterized by thyrotoxicosis, caused by the presence of circulating thyroid stimulating antibodies (TSAb), that are determinant also in the... (Review)
Review
Graves' disease (GD) is characterized by thyrotoxicosis, caused by the presence of circulating thyroid stimulating antibodies (TSAb), that are determinant also in the pathogenesis of its extrathyroidal manifestations [Graves' ophthalmopathy (GO), pretibial myxedema]. T helper (Th)1 immune response prevails in the immune-pathogenesis of GD and GO, during the active phase, when Th1 chemokines, and their (C-X-C)R3 receptor, play a key role. In GD, the existing treatments are not ideal for hyperthyroidism (long-term remission with anti-thyroid-drugs only in 50% of patients; while radioiodine and surgery cause hypothyroidism). In GD, antigen-specific therapy has been recently published, with the induction of T cell tolerance via an immunization by TSH-R peptides. In GO, rituximab and drugs targeting cytokines have been evaluated. Furthermore, teprotumumab (a human monoclonal anti-IGF-1R blocking antibody) showed to be very effective in GO patients. Further researches are necessary to identify novel effective therapies targeting GD, or GO.
Topics: Autoimmunity; Chemokines; Cytokines; Diagnosis, Differential; Graves Disease; Graves Ophthalmopathy; Humans; Iodine Radioisotopes; Risk Factors
PubMed: 32059832
DOI: 10.1016/j.beem.2020.101388 -
Best Practice & Research. Clinical... Dec 2019The versatile clinical manifestations of the Hashimoto's chronic autoimmune thyroiditis often include psycho-neurological disorders. Although hypothyroidism disturbs... (Review)
Review
The versatile clinical manifestations of the Hashimoto's chronic autoimmune thyroiditis often include psycho-neurological disorders. Although hypothyroidism disturbs significantly the ontogenesis and functions of central nervous system, causing in severe cases of myxedema profound impairment of cognitive abilities and even psychosis, the behavioral, motor and other psychoneurological disorders accompany euthyroid and slightly hypothyroid cases and periods of Hashimoto's disease as well, thus constituting the picture of so called "Hashimoto's encephalopathy". The entity, although discussed and explored for more than 50 years since its initial descriptions, remains an enigma of thyroidology and psychiatry, because its etiology and pathogenesis are obscure. The paper describes the development of current views on the role of thyroid in ontogeny and functions of brain, as well as classical and newest ideas on the etiology and pathogenesis of Hashimot's encephalopathy. The synopsis of the world case reports and research literature on this disorder is added with authors' own results obtained by study of 17 cases of Hashimoto's thyroiditis with schizophrenia-like clinical manifestations. The relation of the disease to adjuvant-like etiological factors is discussed. Three major mechanistic concepts of Hashimoto's encephalopathy are detailed, namely cerebral vasculitis theory, hormone dysregulation theory and concept, explaining the disease via direct action of the autoantibodies against various thyroid (thyroperoxidase, thyroglobulin, and TSH-receptor) and several extrathyroid antigens (alpha-enolase and other enzymes, gangliosides and MOG-protein, onconeuronal antigens) - all of them expressed in the brain. The article demonstrates that all above mentioned concepts intermingle and prone to unification, suggesting the unified scheme of pathogenesis for the Hashimoto's encephalopathy. The clinical manifestations, criteria, forms, course, treatment and prognosis of Hashimoto's encephalopathy and its comorbidity to other diseases - are also discussed in brief. The relation between Hashimoto's encephalopathy and non-vasculitis autoimmune encephalomyelitides of paraneoplastic and non-paraneoplastic origin is emphasized [1 figure, bibliography - 200 references].
Topics: Brain; Brain Diseases; Encephalitis; Hashimoto Disease; Humans; Hypothyroidism; Thyroid Gland
PubMed: 31801687
DOI: 10.1016/j.beem.2019.101364 -
Der Internist Oct 2017Thyroid emergencies are rare life-threatening endocrine conditions resulting from either decompensated thyrotoxicosis (thyroid storm) or severe thyroid hormone... (Review)
Review
Thyroid emergencies are rare life-threatening endocrine conditions resulting from either decompensated thyrotoxicosis (thyroid storm) or severe thyroid hormone deficiency (myxedema coma). Both conditions develop out of a long-standing undiagnosed or untreated hyper- or hypothyroidism, respectively, precipitated by an acute stress-associated event, such as infection, trauma, or surgery. Cardinal features of thyroid storm are myasthenia, cardiovascular symptoms, in particular tachycardia, as well as hyperthermia and central nervous system dysfunction. The diagnosis is made based on clinical criteria only as thyroid hormone measurements do not differentiate between thyroid storm and uncomplicated hyperthyroidism. In addition to critical care measures therapy focusses on inhibition of thyroid hormone synthesis and secretion (antithyroid drugs, perchlorate, Lugol's solution, cholestyramine, thyroidectomy) as well as inhibition of thyroid hormone effects in the periphery (β-blocker, glucocorticoids).Cardinal symptoms of myxedema coma are hypothermia, decreased mental status, and hypoventilation with risk of pneumonia and hyponatremia. The diagnosis is also purely based on clinical criteria as measurements of thyroid hormone levels do not differ between uncomplicated severe hypothyroidism and myxedema coma. In addition to substitution of thyroid hormones and glucocorticoids, therapy focusses on critical care measures to treat hypoventilation and hypercapnia, correction of hyponatremia and hypothermia.Survival of both thyroid emergencies can only be optimized by early diagnosis based on clinical criteria and prompt initiation of multimodal therapy including supportive measures and treatment of the precipitating event.
Topics: Coma; Combined Modality Therapy; Critical Care; Diagnosis, Differential; Early Diagnosis; Emergencies; Humans; Myxedema; Prognosis; Risk Factors; Survival Analysis; Thyroid Crisis; Thyroid Function Tests
PubMed: 28939923
DOI: 10.1007/s00108-017-0306-0 -
The American Journal of Emergency... Jan 2021Decompensated hypothyroidism, formerly known as myxedema coma, is an endocrine emergency that commonly presents with altered mental status, as well as hypothermia and... (Review)
Review
BACKGROUND
Decompensated hypothyroidism, formerly known as myxedema coma, is an endocrine emergency that commonly presents with altered mental status, as well as hypothermia and depressed vital signs. The condition is often caused by an inciting event, which may lead to significant delays in the diagnosis and management of this disease. Although the incidence is low, this disease is associated with significant morbidity and mortality. Therefore, it is important for emergency clinicians to be aware of this condition.
OBJECTIVE
This narrative review evaluates the emergency medicine diagnosis and management of adult patients with decompensated hypothyroidism.
DISCUSSION
Decompensated hypothyroidism is a severe hypothyroid state associated with multiple organ failure. The diagnosis can be challenging due to similarities with more common diseases and lack of consideration of the diagnosis. Many patients may present with altered sensorium or depressed vital signs. Clinicians should obtain a thyroid stimulating hormone and free thyroxine level when considering the diagnosis. Management involves resuscitation, early steroid supplementation, thyroid hormone replacement, and treatment of the inciting event.
CONCLUSIONS
Decompensated hypothyroidism should be considered in the evaluation of patients with altered sensorium and depressed vital signs so as to not miss this critical diagnosis.
Topics: Coma; Combined Modality Therapy; Diagnosis, Differential; Emergencies; Emergency Medicine; Humans; Hypothyroidism; Multiple Organ Failure; Severity of Illness Index
PubMed: 33039222
DOI: 10.1016/j.ajem.2020.09.062 -
Travel Medicine and Infectious Disease 2022COVID-19 is a severe acute respiratory syndrome. Recent reports showed that autoimmune thyroiditis might occur following COVID-19 infection. We aimed to review the... (Review)
Review
COVID-19 is a severe acute respiratory syndrome. Recent reports showed that autoimmune thyroiditis might occur following COVID-19 infection. We aimed to review the literature to assess the prevalence, clinical features and outcome of autoimmune thyroid disorders triggered by COVID-19. We reviewed case reports, case series, and observational studies of autoimmune thyroiditis including Graves' disease, Hashimoto thyroiditis, and silent thyroiditis developed in COVID-19 patients by searching PubMed, SCOPUS and Web of Science and included in the systematic review. Our search yielded no prevalence study. We noted 20 reported cases: Fourteen cases of Graves' disease, 5 cases of hypothyroidism due to Hashimoto's thyroiditis and one case of postpartum thyroiditis. The majority (16/20, 80%) were middle-aged (mean age: 40 years) female patients. Autoimmune thyroiditis was diagnosed either concomitantly or 7-90 days after the COVID-19 infection. Eight out of 14 cases with Graves' disease had a known thyroid disorder and they were stable in remission. One out of 5 cases with Hashimoto's thyroiditis had known prior hypothyroidism. The majority of the patients achieved remission within 3 months. One patient with thyroid storm due to Graves' disease and one patient with myxedema coma have died. Current data suggest that COVID-19 may cause autoimmune thyroid disease or exacerbate the underlying thyroid disease in remission. It is reasonable to routinely assess the thyroid functions both in the acute phase and during the convalescence so as not to overlook a thyroid disorder and not to delay treatment especially in patients with preexisting autoimmune thyroid diseases.
Topics: Adult; COVID-19; Female; Graves Disease; Hashimoto Disease; Humans; Hypothyroidism; Middle Aged; Thyroiditis; Thyroiditis, Autoimmune
PubMed: 35307540
DOI: 10.1016/j.tmaid.2022.102314 -
Endocrine Practice : Official Journal... Aug 2014To develop diagnostic criteria for myxedema coma (MC), a decompensated state of extreme hypothyroidism with a high mortality rate if untreated, in order to facilitate...
OBJECTIVE
To develop diagnostic criteria for myxedema coma (MC), a decompensated state of extreme hypothyroidism with a high mortality rate if untreated, in order to facilitate its early recognition and treatment.
METHODS
The frequencies of characteristics associated with MC were assessed retrospectively in patients from our institutions in order to derive a semiquantitative diagnostic point scale that was further applied on selected patients whose data were retrieved from the literature. Logistic regression analysis was used to test the predictive power of the score. Receiver operating characteristic (ROC) curve analysis was performed to test the discriminative power of the score.
RESULTS
Of the 21 patients examined, 7 were reclassified as not having MC (non-MC), and they were used as controls. The scoring system included a composite of alterations of thermoregulatory, central nervous, cardiovascular, gastrointestinal, and metabolic systems, and presence or absence of a precipitating event. All 14 of our MC patients had a score of ≥60, whereas 6 of 7 non-MC patients had scores of 25 to 50. A total of 16 of 22 MC patients whose data were retrieved from the literature had a score ≥60, and 6 of 22 of these patients scored between 45 and 55. The odds ratio per each score unit increase as a continuum was 1.09 (95% confidence interval [CI], 1.01 to 1.16; P = .019); a score of 60 identified coma, with an odds ratio of 1.22. The area under the ROC curve was 0.88 (95% CI, 0.65 to 1.00), and the score of 60 had 100% sensitivity and 85.71% specificity.
CONCLUSION
A score ≥60 in the proposed scoring system is potentially diagnostic for MC, whereas scores between 45 and 59 could classify patients at risk for MC.
Topics: Adult; Aged; Aged, 80 and over; Coma; Female; Humans; Logistic Models; Male; Middle Aged; Myxedema
PubMed: 24518183
DOI: 10.4158/EP13460.OR -
Frontiers in Cellular and Infection... 2021Graves' disease (GD) is a clinical syndrome with an enlarged and overactive thyroid gland, an accelerated heart rate, Graves' orbitopathy (GO), and pretibial myxedema... (Review)
Review
Graves' disease (GD) is a clinical syndrome with an enlarged and overactive thyroid gland, an accelerated heart rate, Graves' orbitopathy (GO), and pretibial myxedema (PTM). GO is the most common extrathyroidal complication of GD. GD/GO has a significant negative impact on the quality of life. GD is the most common systemic autoimmune disorder, mediated by autoantibodies to the thyroid-stimulating hormone receptor (TSHR). It is generally accepted that GD/GO results from complex interactions between genetic and environmental factors that lead to the loss of immune tolerance to thyroid antigens. However, the exact mechanism is still elusive. Systematic investigations into GD/GO animal models and clinical patients have provided important new insight into these disorders during the past 4 years. These studies suggested that gut microbiota may play an essential role in the pathogenesis of GD/GO. Antibiotic vancomycin can reduce disease severity, but fecal material transfer (FMT) from GD/GO patients exaggerates the disease in GD/GO mouse models. There are significant differences in microbiota composition between GD/GO patients and healthy controls. , , and often increase in GD patients. The commonly used therapeutic agents for GD/GO can also affect the gut microbiota. Antigenic mimicry and the imbalance of T helper 17 cells (Th17)/regulatory T cells (Tregs) are the primary mechanisms proposed for dysbiosis in GD/GO. Interventions including antibiotics, probiotics, and diet modification that modulate the gut microbiota have been actively investigated in preclinical models and, to some extent, in clinical settings, such as probiotics () and selenium supplements. Future studies will reveal molecular pathways linking gut and thyroid functions and how they impact orbital autoimmunity. Microbiota-targeting therapeutics will likely be an essential strategy in managing GD/GO in the coming years.
Topics: Animals; Gastrointestinal Microbiome; Graves Disease; Graves Ophthalmopathy; Humans; Mice; Quality of Life; Receptors, Thyrotropin
PubMed: 35004341
DOI: 10.3389/fcimb.2021.739707 -
European Journal of Endocrinology Jan 2017Patients with moderate to severe hypothyroidism and mainly patients with myxedema may exhibit reduced sodium levels (<135 mmol/L). (Review)
Review
BACKGROUND
Patients with moderate to severe hypothyroidism and mainly patients with myxedema may exhibit reduced sodium levels (<135 mmol/L).
SUMMARY
The aim of this short review is the presentation of the mechanisms of hyponatremia and of the available data regarding its implications and treatment in patients with hypothyroidism. Hypothyroidism is one of the causes of hyponatremia, thus thyroid-stimulating hormone determination is mandatory during the evaluation of patients with reduced serum sodium levels. The main mechanism for the development of hyponatremia in patients with chronic hypothyroidism is the decreased capacity of free water excretion due to elevated antidiuretic hormone levels, which are mainly attributed to the hypothyroidism-induced decrease in cardiac output. However, recent data suggest that the hypothyroidism-induced hyponatremia is rather rare and probably occurs only in severe hypothyroidism and myxedema. Other possible causes and superimposed factors of hyponatremia (e.g. drugs, infections, adrenal insufficiency) should be considered in patients with mild/moderate hypothyroidism. Treatment of hypothyroidism and fluid restriction are usually adequate for the management of mild hyponatremia in patients with hypothyroidism. Patients with possible hyponatremic encephalopathy should be urgently treated according to current guidelines.
CONCLUSIONS
Severe hypothyroidism may be the cause of hyponatremia. All hypothyroid patients with low serum sodium levels should be evaluated for other causes and superimposed factors of hyponatremia and treated accordingly.
Topics: Disease Management; Endocrine System Diseases; Humans; Hyponatremia; Hypothyroidism; Sodium
PubMed: 27484454
DOI: 10.1530/EJE-16-0493 -
Cureus Sep 2023Hypothyroidism means an underactive thyroid gland. This leads to a decrease in the functioning of the thyroid gland. It is a very common endocrine disorder that causes... (Review)
Review
Hypothyroidism means an underactive thyroid gland. This leads to a decrease in the functioning of the thyroid gland. It is a very common endocrine disorder that causes under-secretion of thyroid hormones, mainly thyroxine (T4) and triiodothyronine (T3). It affects people of every age group but is more commonly found in women and older people. The symptoms of hypothyroidism can go unnoticed, may not be specific, and may overlap with other conditions, which makes it harder to diagnose it in some cases. Common symptoms include fatigue, weight gain, increased sensitivity to cold (cold intolerance), irregular bowel movements (constipation), and dry skin (xeroderma). These conditions are mostly the result of a low metabolic rate in the body. Weight gain occurs due to a decrease in fat-burning rate and cold intolerance due to a decrease in heat production by the body. This condition can be caused by a variety of factors, including autoimmune diseases, radiation therapy, thyroid gland removal surgeries, and certain medications. The diagnosis of hypothyroidism is based on laboratory tests that measure the levels of thyroid hormones (T3 and T4) in the blood. Treatment typically involves lifelong hormone replacement therapy with synthetic thyroid hormone replacement medication, such as levothyroxine, to help regulate hormone levels in the body. People with hypothyroidism may need to have their medication dosage adjusted over time. If hypothyroidism is left untreated, it can lead to severe complications like mental retardation, delayed milestones, etc., in infants and heart failure, infertility, myxedema coma, etc., in adults. With appropriate treatment, the symptoms of hypothyroidism can be effectively managed, and most people with the condition can lead normal, healthy lives. Lifestyle modifications like eating healthy food and exercising regularly can help manage the symptoms and improve the quality of life.
PubMed: 37908940
DOI: 10.7759/cureus.46241 -
Trends in Cardiovascular Medicine Jul 2019Although amiodarone is considered the most effective antiarrhythmic agent, its use is limited by a wide variety of potential toxicities. The purpose of this review is to...
Although amiodarone is considered the most effective antiarrhythmic agent, its use is limited by a wide variety of potential toxicities. The purpose of this review is to provide a comprehensive "bench to bedside" overview of the ways amiodarone influences thyroid function. We performed a systematic search of MEDLINE to identify peer-reviewed clinical trials, randomized controlled trials, meta-analyses, and other clinically relevant studies. The search was limited to English-language reports published between 1950 and 2017. Amiodarone was searched using the terms adverse effects, hypothyroidism, myxedema, hyperthyroidism, thyroid storm, atrial fibrillation, ventricular arrhythmia, and electrical storm. Google and Google scholar as well as bibliographies of identified articles were reviewed for additional references. We included 163 germane references in this review. Because amiodarone is one of the most frequently prescribed antiarrhythmic drugs in the United States, the mechanistic, diagnostic and therapeutic information provided is relevant for practicing clinicians in a wide range of medical specialties.
Topics: Amiodarone; Animals; Anti-Arrhythmia Agents; Humans; Predictive Value of Tests; Prognosis; Risk Assessment; Thyroid Diseases; Thyroid Function Tests; Thyroid Gland
PubMed: 30309693
DOI: 10.1016/j.tcm.2018.09.005