What are the potential complications of untreated Hashimoto’s disease. How does Hashimoto’s affect life expectancy. What are the most effective treatments for Hashimoto’s disease. Can Hashimoto’s lead to other health problems if left unchecked.

Understanding Hashimoto’s Disease: An Autoimmune Thyroid Condition

Hashimoto’s disease, also known as chronic lymphocytic thyroiditis, is an autoimmune condition that primarily affects the thyroid gland. In this disorder, the immune system mistakenly attacks the thyroid, leading to inflammation and impaired function. While Hashimoto’s disease itself is not typically life-threatening, it can lead to serious complications if left untreated.

The thyroid gland plays a crucial role in regulating metabolism, heart rate, body temperature, and various other bodily functions. When Hashimoto’s disease compromises thyroid function, it often results in hypothyroidism – a condition where the thyroid doesn’t produce enough hormones to meet the body’s needs.

Key Facts About Hashimoto’s Disease

• It is the most common cause of hypothyroidism in the United States
• Affects approximately 5 in 100 Americans
• 4 to 10 times more prevalent in women than men
• Can occur at any age but becomes more common as people get older
• Has a genetic component, increasing risk for those with family history

Recognizing the Symptoms of Hashimoto’s Disease

Hashimoto’s disease often progresses slowly, and symptoms may not be noticeable in the early stages. As thyroid function declines, various signs and symptoms can emerge. It’s important to note that these symptoms can mimic other conditions, making proper diagnosis essential.

Common Symptoms of Hashimoto’s Disease

• Fatigue and weakness
• Weight gain
• Increased sensitivity to cold
• Dry, thinning hair
• Constipation
• Depression
• Joint or muscle pain
• Irregular or heavy menstrual periods
• Slowed heart rate
• Goiter (enlarged thyroid gland)

What is the first noticeable sign of Hashimoto’s disease? Often, the development of a goiter – an enlarged thyroid gland – is the initial visible symptom. This swelling in the front of the neck can sometimes make swallowing difficult.

Diagnosis and Treatment Options for Hashimoto’s Disease

Proper diagnosis of Hashimoto’s disease typically involves a combination of physical examination, medical history review, and blood tests. Healthcare providers use these methods to assess thyroid function and detect the presence of antibodies associated with the condition.

Diagnostic Procedures for Hashimoto’s Disease

1. Physical examination: The doctor checks for signs of thyroid enlargement and other physical symptoms.
2. Blood tests: These measure levels of thyroid hormones (T3 and T4), thyroid-stimulating hormone (TSH), and thyroid antibodies.
3. Thyroid ultrasound: In some cases, imaging may be used to examine the structure of the thyroid gland.

What is the primary treatment for Hashimoto’s disease? The mainstay of treatment is thyroid hormone replacement therapy, typically with levothyroxine (synthetic T4). This medication helps restore normal thyroid hormone levels and alleviate symptoms of hypothyroidism.

Potential Complications of Untreated Hashimoto’s Disease

While Hashimoto’s disease itself is not usually life-threatening, leaving it untreated can lead to serious health complications. The long-term effects of untreated hypothyroidism can impact various body systems and overall quality of life.

Possible Complications of Untreated Hashimoto’s Disease

• Heart problems: Increased risk of heart disease, enlarged heart, and heart failure
• Mental health issues: Depression, cognitive decline, and in severe cases, myxedema coma
• Fertility problems: Difficulty conceiving and increased risk of miscarriage
• Birth defects: Untreated hypothyroidism during pregnancy can lead to developmental issues in the baby
• Myxedema: A rare, life-threatening condition characterized by intense cold intolerance and drowsiness

Can Hashimoto’s disease be fatal if left untreated? While death directly from Hashimoto’s disease is rare, severe untreated hypothyroidism can lead to myxedema coma, a life-threatening condition that requires immediate medical intervention.

Managing Hashimoto’s Disease: Lifestyle and Dietary Considerations

In addition to medical treatment, certain lifestyle changes and dietary modifications can help manage Hashimoto’s disease and improve overall well-being. While these strategies don’t replace medical treatment, they can complement it effectively.

Lifestyle Recommendations for Hashimoto’s Disease

• Stress management: Practice relaxation techniques like meditation or yoga
• Regular exercise: Engage in moderate physical activity to boost metabolism and mood
• Adequate sleep: Aim for 7-9 hours of quality sleep per night
• Avoid environmental toxins: Minimize exposure to endocrine disruptors

Dietary Considerations for Hashimoto’s Disease

• Iodine balance: Avoid excessive iodine intake, which can worsen thyroid function
• Gluten-free diet: Some individuals with Hashimoto’s may benefit from eliminating gluten
• Nutrient-rich foods: Focus on foods high in selenium, zinc, and omega-3 fatty acids
• Avoid goitrogenic foods in excess: Limit raw cruciferous vegetables if they seem to affect thyroid function

How can diet impact Hashimoto’s disease management? While no specific diet has been proven to treat Hashimoto’s, some dietary changes may help reduce inflammation and support thyroid function. It’s important to work with a healthcare provider or registered dietitian to develop an appropriate eating plan.

The Connection Between Hashimoto’s Disease and Other Autoimmune Conditions

Individuals with Hashimoto’s disease have an increased risk of developing other autoimmune disorders. This phenomenon, known as polyautoimmunity, underscores the importance of comprehensive health monitoring for those with Hashimoto’s.

Autoimmune Conditions Associated with Hashimoto’s Disease

• Celiac disease
• Rheumatoid arthritis
• Lupus
• Type 1 diabetes
• Addison’s disease
• Pernicious anemia
• Vitiligo

Why is it important to monitor for other autoimmune conditions in Hashimoto’s patients? The presence of one autoimmune disorder increases the likelihood of developing others. Early detection and management of additional autoimmune conditions can significantly improve overall health outcomes and quality of life.

Pregnancy and Hashimoto’s Disease: Special Considerations

Women with Hashimoto’s disease who are pregnant or planning to become pregnant require special attention and care. Proper management of thyroid function is crucial for both maternal and fetal health.

Thyroid Management During Pregnancy

• Increased medication needs: Thyroid hormone requirements often increase during pregnancy
• Regular monitoring: More frequent thyroid function tests are necessary
• Preconception planning: Optimize thyroid function before pregnancy when possible
• Postpartum vigilance: Monitor for postpartum thyroiditis, which can occur in women with Hashimoto’s

How does Hashimoto’s disease affect pregnancy? Untreated or poorly managed hypothyroidism during pregnancy can increase the risk of complications such as miscarriage, preterm birth, and developmental issues in the baby. Close collaboration with healthcare providers is essential to ensure proper thyroid function throughout pregnancy.

Living with Hashimoto’s Disease: Long-Term Outlook and Quality of Life

With proper treatment and management, most people with Hashimoto’s disease can lead normal, healthy lives. However, the condition requires ongoing care and monitoring to ensure optimal thyroid function and overall well-being.

Keys to Long-Term Management of Hashimoto’s Disease

• Consistent medication adherence
• Regular thyroid function tests and dose adjustments as needed
• Lifestyle modifications to support thyroid health
• Awareness of symptoms and prompt reporting of changes to healthcare providers
• Management of associated conditions or complications

Can Hashimoto’s disease go into remission? While Hashimoto’s is generally considered a lifelong condition, some individuals may experience periods of remission where antibody levels decrease and thyroid function normalizes. However, ongoing monitoring is still necessary as the disease can reactivate.

In conclusion, while Hashimoto’s disease itself is not typically fatal, it requires proper management to prevent potentially serious complications. With appropriate treatment, regular monitoring, and lifestyle adjustments, individuals with Hashimoto’s can maintain good health and quality of life. It’s crucial to work closely with healthcare providers to develop a comprehensive management plan tailored to individual needs and circumstances.

Can You Die From Hashimoto’s Disease?

Content

• Overview
• Symptoms of Hashimoto’s disease
• Diagnosis and treatment options for Hashimoto’s disease
• What happens if Hashimoto’s disease isn’t treated?
• The lowdown

Hashimoto’s disease, also known as chronic lymphocytic thyroiditis, is an autoimmune condition that affects the thyroid gland and can cause underactive thyroid or hypothyroidism. In rare cases, it can also lead to hyperthyroidism or overactive thyroid. 

Under Hashimoto’s disease, the immune system makes antibodies that attack the butterfly-shaped thyroid gland found at the bottom of the neck. 

With Hashimoto’s, vast amounts of white blood cells that form part of the immune system build up within the thyroid, affecting thyroid hormone production. Thyroid hormones regulate the metabolic activity, meaning they affect almost every organ in the body.  

The exact number¹ of people with Hashimoto’s disease is not known. However, it is the most common cause of hypothyroidism, affecting about 5 in 100 Americans.

Hashimoto’s is four to ten times more prevalent among women than men, and it might also appear in young women or teens, increasing in prevalence with age. 

Hashimoto’s disease has hereditary risks, which means you are more likely to develop the condition if a family member has genes associated with the disease. 

Additionally, an individual is more likely to have Hashimoto’s disease if they have other autoimmune disorders, such as 

• Celiac disease: which is a digestive disorder that damages the small intestine

• Lupus: a long-term, chronic disorder that can affect the whole body

• Rheumatoid arthritis: a condition that affects the joints

• Sjogren’s syndrome: usually associated with dry mouth and eyes

• Type 1 diabetes: a condition marked by high blood sugar levels

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Hashimoto’s disease usually progresses slowly for years with gradual loss of thyroid function until you notice symptoms of the disease. Most people miss the signs and symptoms during the initial stages of the disease. 

As thyroid hormone production declines, the first sign you might experience is goiter, an enlarged thyroid. Goiter is characterized by a swollen area in front of the neck, making it a challenge to swallow. 

Other symptoms of Hashimoto’s disease are similar to other medical conditions, so it is critical to see a physician for a diagnosis. 

Here are some of the signs and symptoms associated with the disease:

• Metabolic: Less ability to tolerate cold, modest weight gain (due to fluid retention and decreased metabolism), hypothermia

• Neurologic: Forgetfulness, tingling, or prickling in the hands and feet

• Psychiatric: Personality changes, depression, dull facial expression, dementia or frank psychosis (myxedema madness)

• Dermatologic: Facial puffiness, myxedema (swelling of skin or tissues), sparse, coarse, and dry hair, rough, dry, scaly, and thick skin, yellowish skin hue (particularly notable on the palms and soles of feet)

• Ocular: Swollen or puffy area around the eyes, droopy eyelids

• Gynecologic: Changes in menstruation

• Cardiovascular: Slow heart rate, enlarged heart shown on examination and imaging

Unfortunately, there is no known cure for Hashimoto’s thyroiditis, but replacing hormones with medication can help manage the hormone levels and restore normal metabolism.  

Levothyroxine (Synthroid®, Levothyroid®, Levoxyl®), or T4, is the most common medication used to treat this condition.

The recommended prescription dose depends on age, weight, the severity of hypothyroidism, underlying health condition, or other medications that could interact with synthetic thyroid hormones. 

Before treatment, the physician will ensure the proper diagnosis of Hashimoto’s disease based on:

Physical exam and medical history

The physician will check the individual’s medical record and perform physical exams. Apart from exams and history, the doctor will also check your neck for goiter, a common disease symptom.

Blood tests

The doctor could also request blood tests to confirm hypothyroidism and its possible cause. Some of the tests include measuring levels of the thyroid hormones T4 (thyroxine) and T3 (triiodothyronine), thyroid-stimulating hormone (TSH), antithyroglobulin antibodies (AB), and thyroid peroxidase antibodies (TPO), a type of thyroid antibody that is present in most individuals with the disease.

Most diagnoses only need two tests (T4 and TSH/TPO) and a physical exam to confirm Hashimoto’s disease. Still, if a physician suspects you have the condition but cannot spot any antithyroid antibodies in your blood, they might request an ultrasound of your thyroid. 

The ultrasound images show the size of the thyroid and other features of Hashimoto’s disease. It is also great at ruling out other causes of an enlarged thyroid, such as small lumps in the thyroid gland (thyroid nodules).   

After diagnosis, the physician will prescribe treatment depending on whether the thyroid is damaged and causing hypothyroidism. If not currently hypothyroid, the doctor will typically check your thyroid hormone levels and symptoms regularly. 

The most commonly prescribed medication for managing Hashimoto’s disease is levothyroxine which is similar to the thyroid hormone thyroxine.    

The physician will conduct a blood test about six to eight weeks after you start taking levothyroxine and adjust the dose as needed.  

Note that you have to have a blood test every time you change the dosage. Once a perfect balanced dose is reached, the rate of blood tests slows down. 

Before stopping or increasing your dose, consult with your doctor to avoid complications. 

The issue with Hashimoto’s disease is that it has no obvious symptoms in the initial stages. Therefore, regular diagnostic testing is recommended, especially if your physician suspects you might have the condition or there is a family history of Hashimoto’s.

Over time, if Hashimoto’s disease goes untreated, it can cause several additional health problems. 

Complications

Subclinical hypothyroidism/thyroid antibodies² are linked to increased risks during pregnancy, particularly high blood pressure, miscarriage, and congenital disabilities. 

Here are more potentially severe conditions resulting from untreated Hashimoto’s disease:

• Heart disease: The condition could either lead to high blood pressure or congestive heart failure

• Kidney disease: People with hypothyroidism have a high increase in kidney dysfunction  

• Peripheral neuropathy: Untreated Hashimoto’s disease could damage your peripheral nerves because of excess pressure

• Myxedema coma: This life-threatening condition can occur when the levels of thyroid hormones get too low and symptoms get worse

• Hashimoto encephalopathy: A rare disease that involves impaired brain function

So, can you die from Hashimoto’s disease? It is possible but a rare outcome. However, Hashimoto’s is a risk factor for some severe conditions that are among the leading causes of death in America. 

Women are more likely to suffer from Hashimoto’s disease, mainly due to hormones. It’s important to seek medical attention if you develop any symptoms such as goiter or if there is a strong family history of Hashimoto’s disease.

Hashimoto’s disease – Symptoms & causes

Overview

Hashimoto’s disease is an autoimmune disorder affecting the thyroid gland. The thyroid is a butterfly-shaped gland located at the base of the neck just below the Adam’s apple. The thyroid produces hormones that help regulate many functions in the body.

An autoimmune disorder is an illness caused by the immune system attacking healthy tissues. In Hashimoto’s disease, immune-system cells lead to the death of the thyroid’s hormone-producing cells. The disease usually results in a decline in hormone production (hypothyroidism).

Although anyone can develop Hashimoto’s disease, it’s most common among middle-aged women. The primary treatment is thyroid hormone replacement.

Hashimoto’s disease is also known as Hashimoto’s thyroiditis, chronic lymphocytic thyroiditis and chronic autoimmune thyroiditis.

Thyroid gland

The thyroid gland is located at the base of the neck, just below the Adam’s apple.

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Symptoms

Hashimoto’s disease progresses slowly over the years. You may not notice signs or symptoms of the disease. Eventually, the decline in thyroid hormone production can result in any of the following:

• Fatigue and sluggishness
• Increased sensitivity to cold
• Increased sleepiness
• Dry skin
• Constipation
• Muscle weakness
• Muscle aches, tenderness and stiffness
• Joint pain and stiffness
• Irregular or excessive menstrual bleeding
• Depression
• Problems with memory or concentration
• Swelling of the thyroid (goiter)
• A puffy face
• Brittle nails
• Hair loss
• Enlargement of the tongue

When to see a doctor

Signs and symptoms of Hashimoto’s disease vary widely and are not specific to the disorder. Because these symptoms could result from any number of disorders, it’s important to see your health care provider as soon as possible for a timely and accurate diagnosis.

Causes

Hashimoto’s disease is an autoimmune disorder. The immune system creates antibodies that attack thyroid cells as if they were bacteria, viruses or some other foreign body. The immune system wrongly enlists disease-fighting agents that damage cells and lead to cell death.

What causes the immune system to attack thyroid cells is not clear. The onset of disease may be related to:

• Genetic factors
• Environmental triggers, such as infection, stress or radiation exposure
• Interactions between environmental and genetic factors

Risk factors

The following factors are associated with an increased risk of Hashimoto’s disease:

• Sex. Women are much more likely to get Hashimoto’s disease.
• Age. Hashimoto’s disease can occur at any age but more commonly occurs during middle age.
• Other autoimmune disease. Having another autoimmune disease — such as rheumatoid arthritis, type 1 diabetes or lupus — increases your risk of developing Hashimoto’s disease.
• Genetics and family history. You’re at higher risk for Hashimoto’s disease if others in your family have thyroid disorders or other autoimmune diseases.
• Pregnancy. Typical changes in immune function during pregnancy may be a factor in Hashimoto’s disease that begins after pregnancy.
• Excessive iodine intake. Too much iodine in the diet may function as a trigger among people already at risk for Hashimoto’s disease.
• Radiation exposure. People exposed to excessive levels of environmental radiation are more prone to Hashimoto’s disease.

Complications

Thyroid hormones are essential for the healthy function of many body systems. Therefore, when Hashimoto’s disease and hypothyroidism are left untreated, many complications can occur. These include:

• Goiter. A goiter is enlargement of the thyroid. As thyroid hormone production declines due to Hashimoto’s disease, the thyroid receives signals from the pituitary gland to make more. This cycle may result in a goiter. It’s generally not uncomfortable, but a large goiter can affect your appearance and may interfere with swallowing or breathing.
• Heart problems. Hypothyroidism can result in poor heart function, an enlarged heart and irregular heartbeats. It can also result in high levels of low-density lipoprotein (LDL) cholesterol — the “bad” cholesterol — that is a risk factor for cardiovascular disease and heart failure.
• Mental health issues. Depression or other mental health disorders may occur early in Hashimoto’s disease and may become more severe over time.
• Sexual and reproductive dysfunction. In women, hypothyroidism can result in a reduced sexual desire (libido), an inability to ovulate, and irregular and excessive menstrual bleeding. Men with hypothyroidism may have a reduced libido, erectile dysfunction and a lowered sperm count.
• Poor pregnancy outcomes. Hypothyroidism during pregnancy may increase the risk of a miscarriage or preterm birth. Babies born to women with untreated hypothyroidism are at risk for decreased intellectual abilities, autism, speech delays and other developmental disorders.
• Myxedema (miks-uh-DEE-muh). This rare, life-threatening condition can develop due to long-term, severe, untreated hypothyroidism. Its signs and symptoms include drowsiness followed by profound lethargy and unconsciousness. A myxedema coma may be triggered by exposure to cold, sedatives, infection or other stress on your body. Myxedema requires immediate emergency medical treatment.

Hashimoto’s Encephalopathy

Hashimoto’s Encephalopathy (HE) is an autoimmune inflammatory brain disease associated with the production of antithyroid antibodies. This disease is traditionally classified as rare, with a prevalence of more than 2 cases per 100,000 population [10].

According to the literature, the age range of patients with EC ranges from 8 to 78 years, the number of diseased women is 4 times higher than the number of men. The duration of the disease varies from 2 to 25 years [20, 24].

Since the first description of EC by the eminent English neurologist L. Brain et al. in 1966 [5] and until 2010, there were 52 publications in the literature describing only 130 cases of the disease [9]. However, the increased number of publications in recent years describing not individual cases, but small series of observations suggests that HE occurs much more often than it is diagnosed.

The first descriptions of the symptoms of the disease appeared in the late 40s of the last century. They were erroneously associated with metabolic brain damage in hypothyroidism and were referred to as “myxedematous madness” [1, 13, 18]. Only a few decades later it was established that encephalopathy is not a neurological complication of hypothyroidism or Hashimoto’s thyroiditis, but a kind of “parallel” disorder, which, like thyroiditis, has an autoimmune nature. In this regard, the term “Hashimoto’s encephalopathy” seems to be not quite correct, since the Japanese surgeon H. Hashimoto, working in Berlin, described in 1912 years (exactly 100 years ago) thyroiditis, later named after him, and not encephalopathy at all. Nevertheless, the name has taken root, and it would hardly be right to change it.

This article describes a clinical observation of EC, illustrating the variety of clinical manifestations of the disease that can mimic various neurological and psychiatric disorders, the difficulties of diagnosis and the importance of timely diagnosis of this severe but curable disease.

Patient , 64 years old, was admitted with acutely developed right-sided hemiparesis, hemihypesthesia, and speech disorders of the type of sensory aphasia, followed by a significant regression of symptoms, which were regarded as manifestations of acute cerebrovascular accident, which was also indicated by a zone of low density in the left posterior temporal region, detected on CT.

After 2 months the patient’s condition worsened: there were episodes of confusion, behavioral disorders, aggression, delusional interpretation of events, severe emotional lability, postural instability with frequent falls. Repeated CT revealed a hypodense focus of the same location and size. Routine examination methods (clinical and biochemical blood tests, urinalysis, ECG, examination by an ophthalmologist, ultrasound of the brachiocephalic arteries) did not reveal any deviations. The condition was regarded as a “psycho-organic syndrome” against the background of the consequences of an ischemic stroke.

In the next 3 months there was an increase in mental symptoms – periods of inappropriate behavior with psychomotor agitation lengthened and became more frequent. The patient ceased to serve herself, did not get out of bed, did not control her pelvic functions, and ceased to understand the speech addressed to her.

5 months after the onset of the disease, the patient developed an epileptiform convulsive episode with loss of consciousness, bilateral but asymmetric convulsions and subsequent deep sleep for 20 hours. The condition was regarded as the consequences of ischemic stroke with psychotic manifestations and epileptic syndrome. Conducted a course of treatment with vascular drugs. Anticonvulsants were prescribed.

Over the next year, there was an undulating course of the disease with periods of deterioration, and during periods of deterioration, in addition to confusion, visual and auditory hallucinations were noted, which are realistic images of people who live side by side, as if in a parallel world and communicate with each other without noticing the patient. A persistent hallucinatory syndrome forced psychiatrists who repeatedly examined the patient to make assumptions about schizophrenia. At the same time, psychotic disorders were combined with a generalized convulsive syndrome, increasing postural disorders, and the appearance of myoclonus of the fingers and chin.

According to the neuropsychological examination, both fronto-subcortical and parietal-temporal defects were determined with impaired memory, attention, regulatory functions, aphasic and apraxic disorders.

MRI showed no additional structural changes in the brain. Blood and urine tests also did not have any features. The EEG showed nonspecific changes in the form of a slowdown in the main rhythm. Ultrasound of the thyroid gland revealed diffuse changes in its parenchyma, corresponding to chronic thyroiditis. Thyroid hormone and TSH levels were within normal limits.

In this period, the patient’s condition continued to be regarded as a progressive discirculatory encephalopathy against the background of the consequences of acute cerebrovascular accident in the left hemisphere with an epileptic syndrome, atactic disorders and a pronounced psychoorganic syndrome.

17 months after the onset of the disease, with another deterioration after a series of epipileptic seizures, the patient was hospitalized in the intensive care unit of the Moscow City Clinical Hospital. Botkin. The state is confused, with the phenomena of catatonia and akinetic mutism. The tone in the extremities was increased according to the extrapyramidal type, multifocal myoclonus was observed in the extremities and face; Peculiar paroxysms lasting from 2 to 10 minutes developed 2-3 times a day in the form of high-amplitude myoclonic twitches in the proximal limbs and face (more pronounced on the right than on the left), accompanied by the release of foam from the mouth, which imitated an epileptic attack. However, during the entire attack the patient was conscious. Neurological examination, which was possible in brief minutes of relative “enlightenment” of consciousness, revealed bilateral dysmetria when performing coordinating tests, the absence of anisoreflexia, pathological hand and foot signs. The patient was disoriented and indifferent to her surroundings.

Symptomatic therapy was carried out, however, the condition continued to worsen, and due to the increase in respiratory failure, artificial ventilation of the lungs in the auxiliary mode was required. Clinical and biochemical analyzes still showed no pathology. Clinical examination of cerebrospinal fluid (CSF) showed no abnormalities. Given the typical set of clinical manifestations and the rapid progression of the disease, the patient is suspected of Creutzfeldt-Jakob disease.

The decision was made to exclude curable brain diseases characterized by multifocal cortical-subcortical lesions and rapid progression. Serological markers of viral infections in the blood and CSF were not detected. MRI of the brain revealed nonspecific diffuse changes in the white matter in the form of moderate but uneven bilateral bands of leukoaraiosis in the periventricular region. The EEG showed diffuse slow-wave activity without periodic complexes and epileptiform discharges.

A blood test for thyroid hormones did not reveal any deviations from the norm, however, the titers of antibodies to thyroperoxidase (TPO) and thyroglobulin (TG) exceeded the norm by more than 10 times. Given the peculiarity of clinical manifestations, the fluctuating course of the disease, the presence of signs of thyroiditis and a high level of antibodies to TPO and TG, as well as the absence of undoubted signs of other diseases, a presumptive diagnosis was made: subacute inflammatory EC.

Trial of high-dose corticosteroid treatment (methylprednisolone 1 g daily for 5 days) was initiated followed by a switch to oral prednisolone 60 mg followed by gradual dose reduction over 2 months. A significant improvement was noted already after the second infusion of methylprednisolone: ​​the respiratory function returned to normal, paroxysmal phenomena completely regressed. By the end of the 1st month there was a complete regression of psychotic symptoms, by the middle of the 2nd month – almost complete normalization of the neuropsychological status, including the regression of aphasic disorders. Movement disorders were more resistant. By the 3rd month postural instability and coordinating disturbances decreased. The patient began to sit independently and moved with support within the ward, and then the corridor. Follow-up was followed up for 4 years. During this period, short courses of corticosteroid therapy had to be carried out twice – with a significant (at least threefold) increase in the titer of antithyroid antibodies, accompanied by clinical deterioration. The neuropsychological status remains normal. A moderate motor deficit in the lower extremities persists, which partially decreases with the use of levodopa.

EC has a wide range of mental and neurological manifestations, including cognitive impairment, affective and psychotic disorders, extrapyramidal symptoms (both akinetic-rigid syndrome and generalized choreiform hyperkinesia), multifocal myoclonus, opsoclonus, epileptic seizures, stroke-like episodes, myelopathy, ataxia [4, 11, 16, 19, 20, 23]. Symptoms do not depend on age [9].

In this case, the leading manifestations of the disease were a stroke-like episode followed by the development of progressive cognitive decline, hallucinatory-delusional syndrome, akinetic-rigid syndrome, and multifocal myoclonus mimicking epileptic seizures.

Symptoms can occur acutely, which was observed in our case, or subacutely and have a relapsing-remitting course. Sometimes there is a slower progression of symptoms, which presents significant difficulties in the aspect of differential diagnosis with neurodegenerative diseases.

2 clinical types of HE have been identified [6]. Vasculitic type debuts with stroke-like episodes (with or without cognitive impairment or altered consciousness). Diffuse progressive type is characterized by a subacute debut and a progressive course with a predominance of cognitive decline up to the development of dementia, akinetic mutism, lethargy, coma. Tremor, myoclonus, epileptic seizures, and extrapyramidal disorders may be present in both types of disease development, but are more characteristic in the second [23]. Clinical data show that this classification is arbitrary, since a combination of syndromes involving different parts of the brain is often observed in one patient [23]. According to some authors [6, 15], cognitive and behavioral disorders are detected in 100% of patients; in this case, they also dominated throughout the disease.

Symptoms fluctuate, which is based not only on the patterns of the course of an autoimmune inflammatory disease, but also on the cyclical dynamics of the hormonal background, which was noted in women of reproductive age [2].

Currently, the diagnosis of EC is facilitated by the presence of clear criteria, which include the following points [6, 20]: 1. Signs of encephalopathy, including obligate cognitive impairment. 2. At least one of the following symptoms: hallucinations; rave; myoclonus; generalized tonic-clonic or partial epileptic seizures; focal neurological symptoms. 3. High titer of antithyroid antibodies in blood serum. 4. The absence of severe thyroid dysfunction that can explain the development of encephalopathy. 5. The absence of a structural brain lesion of a different nature (according to neuroimaging), which can better explain the clinical picture. 6. Full or partial recovery after pathogenetic (immunotropic) treatment.

The clinical case described in this publication fully meets the criteria for diagnosing EC, while the following are of key diagnostic importance: acute / subacute development of the disease with subsequent fluctuating course and a tendency to rapid progression; cognitive decline with the development of dementia; a bizarre combination of symptoms of “loss” and “irritation”, the latter can include not only myoclonus and epileptiform paroxysms, but also psychotic disorders; high titer of serum antithyroid antibodies; no signs of other diseases; typical positive response to corticosteroid therapy.

Additional research methods for suspected EC should include the determination of antibody titers to TG and TPO, the determination of the level of thyroid hormones and TSH, the study of CSF, EEG, ultrasound of the thyroid gland, MRI of the brain. The results of additional research methods can be very variable. Nevertheless, a typical patient with EC has a high titer of antibodies to TG and/or TPO, signs of subclinical hypothyroidism, a moderate increase in the protein level in the CSF, and nonspecific EEG changes in the absence of neuroimaging abnormalities [2]. In the described case, a moderate increase in protein in the CSF, a diffuse change in the bioelectrical activity of the brain according to EEG data, and diffuse changes in the white matter were detected.

The state of thyroid function can be very variable, however, this most often does not have a significant effect on the clinical picture [10]. A large number (42%) of patients have euthyroidism, overt (25%) or subclinical (12%) hypothyroidism [23]. Latent or clinically obvious thyrotoxicosis is observed only in 19% of cases. Enlargement of the thyroid gland is noted in 62% of patients.

Caution against possible overdiagnosis of HE based solely on laboratory testing of antithyroid antibody levels. In the general population, antithyroid antibodies are detected in 11% of the population, predominantly in women, and do not always have clinical significance. The diagnosis of HE should be based primarily on clinical data. However, in EC, anti-TPO antibodies are detected in 86-95%, and to TG – in 48-75% of cases. It is important to emphasize that these antibodies themselves do not have a pathogenic effect, but are indicators (markers) of the disease.

In the study of CSF in 72% of cases, at least a moderate increase in protein levels is detected with normal cytosis or slight pleocytosis. ⅓ patients in the CSF are determined by oligoclonal antibodies.

EEG changes are also very polymorphic. In almost all cases, a diffuse slowdown in the bioelectrical activity of the brain is recorded, sometimes there are intermittent d-waves in the frontal lead, triphasic waves, focal slowing of the rhythm, epileptiform discharges, etc. [7-9, 20]. MRI can reveal nonspecific focal or diffuse changes in the subcortical white matter, cerebral atrophy, and focal cortical changes of an inflammatory nature [2, 20, 23]. Single-photon emission computed tomography in most cases reveals focal hypoperfusion in the temporal areas, less often – diffuse hypoperfusion [2, 20-22].

Diagnosis of EC can be difficult. Most often, a differential diagnosis has to be made with viral encephalitis, Creutzfeldt-Jakob disease and other rapidly progressive degenerative dementias, as well as schizophrenia [3]. In Creutzfeldt-Jakob disease, the symptoms may indeed resemble those of HE, however, the progression of the first disease, as a rule, is faster (patients most often die within 1 year), in addition, EEG and MRI patterns are typical in Creutzfeldt-Jakob disease, a positive test for protein 14-3-3 in CSF. The duration of the disease does not exceed 1 year. There may be an increase in the signal from the thalamus on T2-weighted images. Difficult differential diagnosis and with dementia with Lewy bodies (LTB). A characteristic neuropsychological profile and the absence of antithyroid antibodies with similar symptoms would be in favor of DTL.

Since the criteria for the disease include psychotic disorders (delusions, hallucinations), it becomes necessary to differentiate EC from schizophrenia, more precisely from its paranoid form, which is characterized by the presence of anergy, thought disorders, delirium and behavior determined by it, psychomotor agitation and / or depression . If there is a hallucinatory-delusional syndrome, then it is characterized by imperative voices, delusions of influence, etc.), usually transforming into the Kandinsky-Clerambault syndrome. Extrapyramidal symptoms in this disease usually appear as a complication of antipsychotic therapy.

EC should also be differentiated from dysmetabolic encephalopathy developed as a result of hypothyroidism, however, this diagnostic problem is usually resolved by determining the level of thyroxin in the blood and the success of its correction [2]. Severe hypothyroidism is rarely detected in HE, the degree of which could explain the resulting cognitive and motor impairment.

The pathophysiology of EC remains poorly understood. The fluctuating course of the disease, the possibility of simultaneous involvement of various parts of the central nervous system, the dramatic effect of steroid therapy testify in favor of the autoimmune inflammatory nature of the disease. Antithyroid antibodies are markers of the current autoimmune process; they are found not only in the blood, but also in the CSF, but their concentration does not correlate with the course of the disease and the effectiveness of therapy. Thus, a high level of antithyroid antibodies in the CSF may be an additional diagnostic criterion, but its dynamics does not indicate the effectiveness of the treatment.

In favor of the autoimmune nature of HE is also an increased frequency of other autoimmune pathologies: type 1 diabetes mellitus, systemic lupus erythematosus, Crohn’s disease [6]. Biopsy data and pathomorphological examination of the brain indicate T- and B-cell infiltration of the parenchyma. In some patients, lymphocytic infiltration of the walls of arterioles and venules, as well as perivascular lymphocytic infiltration, were found, indicating the role of vasculitis in brain tissue damage.

Aminoterminal (propto) enolase antigen may play an important role in initiating the development of EC. This cross-reactive antigen has been found in both brain and thyroid tissue and is highly specific for EC. Moreover, an elevated level of α-enolase may indicate the role of cerebral vasculitis in HE, since this antigen is detected in autoimmune vasculitis and is present in high concentrations in the endothelium [12, 23, 25]. Currently, studies are ongoing to study the mechanisms of development of an autoimmune reaction in response to dimethylarginase-1 and aldehyde reductase-1 [3, 14].

Rapid response to high doses of corticosteroids may serve as the most important criterion for the diagnosis of EC (hence one of the synonyms for EC – “steroid-sensitive encephalopathy associated with autoimmune thyroiditis”). Currently, treatment is most often started with intravenous infusions of methylprednisolone (1 g per day for 3-7 days). In 90% of patients, this leads to a significant improvement within 1 week. Then, for 2–4 months, patients continue to take oral prednisolone daily, initially at a dose of 1–2 mg/kg, then the dose is gradually reduced [20]. With premature withdrawal of corticosteroids, the likelihood of a relapse of the disease is high.

In case of unsatisfactory effect or poor tolerance of hormones in some patients, it is possible to use cytostatics (azathioprine, cyclophosphamide or methotrexate), as well as the course administration of immunoglobulin or a course of plasmapheresis [6]. In rare cases, preparations of monoclonal antibodies are used [17]. Along with the main treatment, correction of thyroid dysfunction is carried out. Epileptic and hyperkinetic manifestations usually regress with corticosteroid treatment, and antiepileptic drugs are usually not required [20].

The variety of the clinical picture of HE, which mimics the manifestations of other, more common diseases, along with a fluctuating course, often leads the clinician down the wrong path. As a result, the patient’s condition may deteriorate rapidly and require placement in the intensive care unit. In this situation, patients may seem to the doctor “incurable” and “unpromising”. And this despite the fact that just one test for antithyroid antibodies, as shown by the above clinical case, can indicate the right direction of the diagnostic search and become a salvation for the patient.

Autoimmune thyroiditis – causes, symptoms and diagnosis, indications for visiting a doctor

A typical representative of a large group of autoimmune diseases is autoimmune thyroiditis. This is an inflammation of the thyroid gland that occurs from the destruction of its cells by the immune system. It proceeds for a long time, often becomes chronic, therefore it is also found under the wording Hashimoto’s thyroiditis (Hashimoto) in honor of the scientist who studied and described the disease in 1912, and as “chronic thyroiditis” (although there is another form of chronic inflammation – Riedel’s thyroiditis). This is the most common type of inflammation in the thyroid gland, among the four main forms of pathologies. Let’s take a closer look at what causes inflammation, how to diagnose, treat, and avoid it.

What is Hashimoto’s thyroiditis

This is inflammation that results from damage or destruction of thyroid follicles by cells of the immune system (T-lymphocytes). At the same time, infiltrates appear in the gland, and the activity of the gland and the amount of thyroid hormones in the body decrease. Hypothyroidism develops slowly.

The disease is diagnosed in 3% of all thyroid pathologies. Most of the patients are women. In them, this diagnosis occurs 10-20 times more often than in men. There is also a dependence on age – Hashimoto’s thyroiditis rarely occurs in people under thirty years of age. Most patients are middle-aged women (30-50 years).

Symptoms of autoimmune thyroiditis of the thyroid gland

The clinical picture largely depends on the form of the disease. In autoimmune thyroiditis, they distinguish:

• Atrophic course – the gland retains its former dimensions, but as the cells die, the glandular tissue is replaced by fibrous tissue.
• Hypertrophic – a dense goiter is formed.

This is a slowly progressive inflammation, which is rarely characterized by exacerbations and signs of damage to the body as a whole (fever, increased ESR).

A typical picture at the beginning of the inflammatory process is implicit. Usually there are no symptoms.

Approximately 10% of women and 5% of men are carriers of antibodies to TPO or TG, while thyroid dysfunction may develop in 3-6%. Later, the production of TSH increases, the diagnosis is made according to the results of the tests. A sign of the next stage is hypothyroidism – the growth of the gland and a significant decrease in the hormones T3 and T4. As a result of the inflammatory process in the thyroid gland, it is destroyed and it stops producing hormones.

In an acute form of inflammation or as the disease develops, symptoms of destructive thyroiditis appear – palpitations, trembling in the hands, sweating.
This process usually takes 3 to 6 months. Subsequently, it turns into hypofunction of the thyroid gland, which is characterized by:

• The induration on the neck is rather firm in structure, but painless on palpation and pressure (only 10% of patients complain of pain on palpation). Over time, iron, on the contrary, significantly decreases in volume.
• As the gland grows, adjacent structures of the neck are compressed, there is a feeling of a foreign body in the throat, lack of air, hoarseness of the voice.
• Pain in the joints, rarely in the muscles.
• General weakness.
• Weight gain.
• Constipation or indigestion.
• Loss of hair, including on the eyebrows.
• Dryness, unhealthy pallor of the skin, brittle nails.
• Mental disorders of depressive type.
• Frequent feeling of cold, chilliness.
• Deterioration of memory and attention.
• Edema of the face.
• Bradycardia.
• Decreased sex drive.

Many of the symptoms are associated not so much with inflammation, but with already developing hypothyroidism.

The characteristic symptoms of autoimmune thyroiditis in women are: irregular menstruation, prolonged absence of pregnancy with regular sexual activity, spontaneous miscarriages.

Causes of autoimmune thyroiditis

The disease occurs due to a malfunction of the immune system, which leads to the fact that the cells of the gland are mistakenly perceived as foreign organisms. Why such a failure occurs is not exactly established. But there are a number of factors that can be considered risk factors and causes of autoimmune thyroiditis of the thyroid gland:

• Hereditary predisposition at the gene level – dependence is confirmed by the fact that often the disease is familial and occurs in representatives of several generations. In such patients, often thyroiditis is complemented by such diseases as: vitiligo, rheumatism and others.
• Infections of the nasopharynx, tonsils and oral cavity: laryngitis, pharyngitis and others, as well as untreated caries. The most dangerous are chronic diseases or acute forms of infection with complications in neighboring organs.
• Severe or chronic stressful situations.
• Polluted ecology (for example, excess chlorine in water, air).
• An excess of iodine in the body for a long time.
• Radiation exposure or a course of radiation therapy in the treatment of oncology.
• Thyroid tumors of a benign nature (eg endemic goiter).
• UV exposure, frequent and long exposure to the sun without protection during the hours when it is most active.
• Uncontrolled or on the recommendation of a doctor (if necessary) intake of immunomodulators (for example, Interferon).
• Long-term treatment with certain drugs.
• Blood diseases.

Complications

The main complications of thyroiditis include hypothyroidism and thyrotoxicosis.

Thyroid dysfunction may adversely affect:

• Nervous, digestive, respiratory and cardiovascular systems.
• Kidneys.
• Skin and its appendages – nails and hair.
• Musculoskeletal system.
• Organs of the reproductive system.
• Disorders of growth and mental development.
• Metabolism.

Diagnosis

If you suspect thyroiditis or other pathologies of the thyroid gland, you should contact an endocrinologist. It is this doctor who prescribes examinations, finds out the possible causes of thyroid dysfunction and decides how to treat the patient. At the appointment, the doctor will examine the patient and assess the condition of his skin, enlargement and soreness of the thyroid gland, learn about complaints, family history, concomitant diseases. Depending on the clinical picture, certain examinations may be prescribed.

Help with diagnosis:

• Blood test – general, for TSH, T3, T4 hormones and antibodies to them.
• Ultrasound is an affordable, quick and informative examination to assess the condition of the gland, its size, uniformity of structure, the presence of nodes, seals, fibrous areas and other pathologies.
• Scintigraphy will help distinguish thyroiditis with thyrotoxicosis from other diseases with similar signs. It is based on the property of the affected gland not to accumulate a contrast agent in large quantities.

After the diagnosis is clarified by the endocrinologist, the method of therapy is selected.

Treatment

In the early stages, when there are no disorders in the thyroid gland, no specific treatment is required. The doctor will recommend leading a healthy lifestyle, normalizing nutrition, giving up bad habits and monitoring your well-being. Regular annual consultations and examinations are necessary in order not to miss the further development of the disease.

If the function of the gland is already impaired, then in most cases hormone replacement therapy is prescribed.

Against the background of maintenance therapy, it is recommended to undergo periodic examinations to monitor the dynamics of changes and, if necessary, change the dosage of the drug.

It is not recommended to self-medicate, use folk remedies, take vitamins on your own or increase the dose of iodine in the diet. Autoimmune thyroiditis is not associated with its deficiency, and an excess of micronutrients can worsen the situation.

Hashimoto’s chronic thyroiditis is a disease with a relatively favorable prognosis. The quality of life of the patient can be maintained almost unchanged, even if hormone therapy remains forever.

The key to competent treatment and preservation of health is the qualification of doctors.