Can you die from hashimoto disease: Can You Die From Hashimoto’s Disease?

29.07.202307.07.2023 by alexxlab

Содержание

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.

Death by unnatural causes, mainly suicide, is increased in patients with Hashimoto’s thyroiditis. A nationwide Danish register study

. 2019 Sep;65(3):616-622.

doi: 10.1007/s12020-019-01946-5.

Epub 2019 May 7.

Thomas Heiberg Brix¹, Charlotte Ferløv-Schwensen¹, Marianne Thvilum², Laszlo Hegedüs¹

Affiliations

¹ Department of Endocrinology and Metabolism, Odense University Hospital, Kløvervænget 6, DK-5000, Odense, Denmark.
² Department of Endocrinology and Metabolism, Odense University Hospital, Kløvervænget 6, DK-5000, Odense, Denmark. [email protected].

PMID:
31065912
DOI:
10.1007/s12020-019-01946-5

Thomas Heiberg Brix et al.

Endocrine.

2019 Sep.

. 2019 Sep;65(3):616-622.

doi: 10.1007/s12020-019-01946-5.

Epub 2019 May 7.

Authors

Thomas Heiberg Brix¹, Charlotte Ferløv-Schwensen¹, Marianne Thvilum², Laszlo Hegedüs¹

Affiliations

¹ Department of Endocrinology and Metabolism, Odense University Hospital, Kløvervænget 6, DK-5000, Odense, Denmark.
² Department of Endocrinology and Metabolism, Odense University Hospital, Kløvervænget 6, DK-5000, Odense, Denmark. [email protected].

PMID:
31065912
DOI:
10.1007/s12020-019-01946-5

Abstract

Purpose:

Hashimoto’s thyroiditis (HT) is associated with excess psychiatric in addition to reduced quality of life. However, little is known about risk of unnatural manners of death in HT. We investigated the risk of death by accidents, suicide, violence/homicide, and unknown causes in patients with HT, compared to a matched control population.

Methods:

Register study covering all adult Danes diagnosed with HT during 1995-2012. In total, 111,565 HT cases were identified and matched for age and sex with four euthyroid controls. The hazard ratios (HR) for mortality were calculated using Cox regression analyses, adjusted for pre-existing morbidity. Median follow-up time was 5.9 years (range 0-17.5).

Results:

Compared to controls, HT patients had an increased frequency of death by suicide (0.10% vs 0.07%, p < 0.001) and unknown manners (0.05% vs 0.02%, p < 0.001). There were no significant differences between controls and HT patients in risk of death by accidents (0.36% vs 0.37%, p = 0.384) or violence (0.004% vs 0.005%, p = 0.749). After adjustment for pre-existing somatic and psychiatric morbidity HT patients still had an increased risk of suicide and death by unknown causes, whereas risk of death caused by accidents was reduced.

Conclusions:

Mortality due to suicide and unknown causes, but not accidents and violence, was increased in HT. This indicates that HT may have a significant role in the pathophysiological mechanisms of suicidal behavior. This suggests that physicians caring for HT patients should be vigilant when facing expressions of suicidal ideation or signs and symptoms of self-harm as a first step towards prevention.

Keywords:

Hashimoto’s thyroiditis; Hypothyroidism; Mortality; Population-based; Suicide; Unnatural death.

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Nat Rev Endocrinol. 2022 Apr;18(4):230-242. doi: 10.1038/s41574-021-00625-8. Epub 2022 Jan 18.
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Toloza FJK, et al.
Medicina (Kaunas). 2021 Jul 15;57(7):714. doi: 10.3390/medicina57070714.
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MeSH terms

Autoimmune thyroiditis of the thyroid gland

Many are sure that the cause of fatigue and chronic fatigue syndrome is in “malfunctions” with the thyroid gland. Namely – in chronic inflammation of the tissues of the thyroid gland (autoimmune thyroiditis). But is it?

Doctor’s consultation

You can get the consultation of the necessary specialist online in the Doctis application

Laboratory

You can undergo a comprehensive examination of all major body systems

Signs of autoimmune thyroiditis?
Autoimmune thyroiditis – as a cause of chronic fatigue
Diagnosis of autoimmune thyroiditis
Causes of autoimmune thyroiditis
Treatment of autoimmune thyroiditis

Autoimmune thyroiditis accounts for 20-30% of all thyroid diseases. Occurs in women
10-20 times more often than in men. What you need to know about this disease – signs
autoimmune thyroiditis and possible consequences?

Symptoms of autoimmune thyroiditis

What are the signs of autoimmune thyroiditis? Is it true that at the first stage the disease proceeds
no symptoms?

In fact, autoimmune thyroiditis is not one, but several diseases that are united by
inflammation in the thyroid gland. The classic variant is chronic autoimmune thyroiditis, or thyroiditis.
Hashimoto. It can lead to a persistent decrease in thyroid function – hypothyroidism.
I emphasize – maybe. But not always.

Autoimmune thyroiditis itself does not have any clinical
signs. Manifestations can only be in violation of the function of the thyroid gland. And then not immediately. Usually,
chronic thyroiditis leads to hypothyroidism years later, often even decades later.

Diagnosis of chronic fatigue syndrome

It is believed that autoimmune thyroiditis is the cause of rapid fatigue, weakness, syndrome
chronic fatigue.

Is it so?

Since autoimmune thyroiditis does not manifest itself in any way with intact thyroid function, let’s immediately
talk about its possible consequence – hypothyroidism. Hypothyroidism can indeed be accompanied
asthenia-like symptoms. Symptoms such as menstrual irregularities, constipation,
anemia, increased
cholesterol levels. However, similar manifestations occur in many diseases. That’s the problem
diagnosis of hypothyroidism, since even at advanced stages it does not have
specific signs.

Fatigue, weakness and drowsiness in some cases may be
associated with decreased thyroid function. But they can be a trail of other chronic diseases. And what
As for chronic fatigue syndrome, this is a beautiful, but not quite definite concept.

What tests to take to confirm (or rule out) autoimmune thyroiditis?

Search for autoimmune thyroiditis, in most cases, does not make much sense. A person can live a lifetime with
signs of autoimmune thyroiditis and die from another disease. But hypothyroidism is really
should not be ignored, since thyroid hormones (thyroxine and triiodothyronine) regulate
supply of oxygen to cells. With a deficiency of thyroid hormones, all cells without exception function.
in power saving mode. They seem to run out of batteries. They cannot adequately exercise their
functions.

Accurate and simple test for diagnosing hypothyroidism – TSH (thyroid stimulating hormone) level determination
in blood. With a decrease in thyroid function, it rises.

Why does autoimmune thyroiditis develop? I read that there are many provoking factors. For example,
pregnancy, lack of iodine in food.

A question for the Nobel Prize – no less! We do not know exactly the root causes of autoimmune diseases.
Even when it comes to the most common autoimmune disease – autoimmune thyroiditis. For some reason
cause, in predisposed persons, the normal functioning of the immune system is disrupted, and it attacks its own
cells. In this case, thyroid cells. Any autoimmune disease in general
significantly more common in women than in men. Sometimes – 10-20 times.

Pregnancy can indeed be a provoking factor. And more precisely –
period. The fact is that during pregnancy, the activity of the immune system is suppressed (this is necessary,
to carry an immunologically foreign fetus), and after childbirth is activated. Sometimes – excessively, causing autoimmune
processes.

Dietary iodine deficiency does not lead to autoimmune thyroiditis. And in general, you shouldn’t
associate thyroid disease only with iodine deficiency. Dozens of diseases have been described
thyroid gland – completely different in causes, course and prognosis – and only
some of them are directly or indirectly related to iodine deficiency.

Treatment of autoimmune thyroiditis

Is it true that hypothyroidism is the only indication for treatment
autoimmune thyroiditis, and in other cases, treatment is not required?

When it comes to chronic
autoimmune thyroiditis – absolutely right. Specifically affect the autoimmune process
modern medicine, alas, does not yet know how. Moreover, autoimmune thyroiditis, as already noted, is far from always
has an adverse effect on the body. Its only significant consequence is a decrease in function
thyroid gland.

And hypothyroidism is fairly easy to control. Replacement therapy for hypothyroidism involves taking daily
levothyroxine tablets. The dose is selected and
supervised by an endocrinologist
when determining the level of TSH. Any restrictions compensated patients with hypothyroidism,
usually do not experience.

The author of the article: Valentin Viktorovich Fadeev

Doctor’s consultation

You can get the consultation of the necessary specialist online

Laboratory

You can undergo a comprehensive examination of all major body systems

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].

Can you die from hashimoto disease: Can You Die From Hashimoto’s Disease?

Can You Die From Hashimoto’s Disease?

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Have you considered clinical trials for Hashimoto’s disease?