John Adamson
AT4550
Hashimoto’s Thyroiditis: An In-Depth Look
Introduction: Hashimoto’s Thyroiditis (HT) is an autoimmune disorder that affects
the thyroid gland. It is the most prevalent autoimmune disorder of the thyroid
(Zaletel & Gaberscek, 2011). With HT, the patient’s body produces antibodies in
response to thyroid antigens (Anderson, Keith, Novak, & Elliot, 2002). These
antibodies affect thyroid peroxidase and thyroglobulin (Kakudo, Li, Hirokawa, &
Ozaki, 2011). The disease etiology and pathogenesis is not completely understood
(Zaletel & Gaberscek, 2011). However, the disease is hereditary and is more
common in woman than in men. Environmental factors are also a major
contributor. This is because even with twin studies, HT showed a concordance rate
of only 50% (Kakudo, Li, Hirokawa, & Ozaki, 2011). Environmental factors include
iodine, medications, infections, smoking, and possibly stress, with the most
established being excess dietary iodine (Kakudo, Li, Hirokawa, & Ozaki, 2011). It
happens most frequently between the ages of 30 to 50 years, but can occur at any
age (Anderson, Keith, Novak, & Elliot, 2002). The gradual destruction of they
thyroid in HT may lead to subclinical or overt hypothyroidism (Zaletel & Gaberscek,
2011). HT affects up to 2% of the general population and has no race predilection
(Kakudo, Li, Hirokawa, & Ozaki, 2011).
To better understand HT, an understanding of the functions of the thyroid
gland is necessary. The thyroid gland is located just inferior to the larynx and is
butterfly shaped. It is composed of microscopic spherical sacs called thyroid
follicles. The follicular cells produce thyroxin, or T4, and triiodothyronin, or T3.
The thyroid gland stores these secretory products in large quantities, and is the only
endocrine gland to do so (Tortora & Derrickson, 2009). The thyroid gland uses
iodide to produce these hormones.
Thyroid hormones have many important actions in our bodies. These
hormones, increase the basal metabolic rate, stimulate synthesis of additional
sodium-potassium pumps, stimulate protein synthesis and increase the use of
glucose and fatty acids for ATP production, increase lipolysis, enhance cholesterol
excretion, enhance some actions of the catecholamines, and accelerate body growth,
particularly that of the nervous and skeletal systems (Tortora & Derrickson, 2009).
Because of the many actions of the thyroid hormones, most body cells have
receptors for thyroid hormones.
The thyroid gland is controlled by the hypothalamus and anterior pituitary
glands. When there are low levels of T3 and T4 in the blood, the hypothalamus is
stimulated to release thyrotropine-releasing hormone (TRH). This flows to the
anterior pituitary gland, which stimulates thyrotrophs to secrete thyroidstimulating hormone (TSH). TSH then stimulates the thyroid follicular cells to
produce and release T3 and T4 into the blood until normal ranges are present
(Tortora & Derrickson, 2009). This is a negative feedback homeostatic loop.
Signs and Symptoms: HT does not have any unique signs or symptoms but has
signs or symptoms relative to the problems that it causes. Because of the chronic
thyroid damage, HT has signs and symptoms similar to hypothyroidism (Mayo Clinic
Staff, 2011). HT is the most frequent cause of hypothyroidism (Zaletel & Gaberscek,
2011). These are the initial manifestations in 20% of all cases (Kakudo, Li,
Hirokawa, & Ozaki, 2011). Signs and symptoms of hypothyroidism vary widely and
progress, as the condition gets worse. Because of the gradual onset, the symptoms
may barely be noticeable at first. The first symptoms are generally fatigue and
sluggishness or malaise. As HT progresses, the symptoms may become more
noticeable. These symptoms are increased sensitivity to cold, constipation, pale and
dry skin, a puffy face, hoarse voice, an elevated blood cholesterol level, unexplained
weight gain, muscle aches, tenderness, and stiffness, pain and stiffness in joints,
swelling in the knees and small joints of the hands and feet, muscle weakness,
menorrhagia, and depression. As the condition progresses without treatment, the
patient may experience forgetfulness and thought processes may become slow
(Mayo Clinic Staff, 2011). In the early stages of the disease, patients may develop
thyrotoxicosis (Kakudo, Li, Hirokawa, & Ozaki, 2011), which is hyperactivity of the
thyroid gland (Anderson, Keith, Novak, & Elliot, 2002)
Patients may also develop a goiter. These are generally firm, bumpy, and
painless, and moderate in size (Kakudo, Li, Hirokawa, & Ozaki, 2011). HT can also
cause compression of other surrounding structures such as the trachea, esophagus,
and recurrent laryngeal nerves. These symptoms should raise suspicion of thyroid
lymphoma or carcinoma (Kakudo, Li, Hirokawa, & Ozaki, 2011). About 10% of
patients have atrophic thyroid glands (Kakudo, Li, Hirokawa, & Ozaki, 2011).
HT in children and adolescents has a much larger effect than that of adults.
HT in children and adolescents may cause retardation in growth and development,
resulting in a short stature, decline in school performance, and anemia. The most
common complaint of HT in children and adolescents is swelling in the neck,
nervousness, dermatological problems, and hair loss(Ozen, Berk, Simsek, & Darcan,
2011).
Referral: A patient needs to see a doctor if he/she is experiencing any of the
symptoms associated with HT, especially fatigue with no apparent reason, dry skin,
pale, puffy face, constipation, and a hoarse voice. HT may also be considered with
high blood cholesterol (Mayo Clinic Staff, 2011). A primary care physician can take
care of all of the necessary blood work and treatment of HT, but may refer a patient
to an endocrinologist for further testing.
Diagnostic Tests: In order to confirm a diagnosis of HT, the practitioner
needs to do laboratory tests that include a hormone test and an antibody test (Mayo
Clinic Staff, 2011). The hormones tested are a serum concentration of thyroxine
hormone and TSH (Kakudo, Li, Hirokawa, & Ozaki, 2011). In HT the TSH levels are
higher than reference ranges, while the thyroxine hormones generally are inside of
reference ranges. This is due to the pituitary gland attempting to increase the
amount of thyroid production in the failing thyroid gland (Kakudo, Li, Hirokawa, &
Ozaki, 2011). The reference range for the TSH test is 0.4-4.0 mlU/L (A.D.A.M., Inc.,
2012). The reference range for the thyroxine test is 4.5-11.2 mcg/dL (A.D.A.M.,
2012). The hallmark of HT is the presence of thyroid specific antibodies in the
blood. The antibody in the case of HT is thyroid peroxidase autoantibodies.
Another diagnostic test that a practitioner may do is to check for thyroglobulin
antibodies. However, there is some debate over the clinical utility in diagnosing HT
because of presence of thyroglobulin antibodies in patients without HT (Kakudo, Li,
Hirokawa, & Ozaki, 2011).
Another means of diagnosing HT is through the use of ultrasonography.
While the laboratory findings are sufficient to diagnose HT, ultrasonography is
useful for monitoring thyroid size, monitoring size change after therapy, assessing
thyroid echotexture, and confirming the presence of thyroid nodules. The
sonographic findings, coupled with the results from laboratory values are a good
indicator of the severity of the HT in a patient (Kakudo, Li, Hirokawa, & Ozaki,
2011).
Differential Diagnosis: There are many different differential diagnoses for HT.
They are all in the thyroiditis category. Subacute lymphocytic thyroiditis generally
occurs postpartum but can also appear sporadically. It is broken up into two
subtypes, postpartum thyroiditis and painless sporadic thyroiditis. Antithyroid
peroxidase antibodies are present in nearly all patients. Subacute lymphocytic
thyroiditis starts with a hyperthyroidism episode, followed by hypothyroidism,
followed by a euthyroid state. This type of thyroiditis accounts for 29 to 50 percent
of thyroiditis cases (Slatosky, Shipton, & Wahba, 2000).
Another differential diagnosis is subacute granulomatous thyroiditis or de
Quervain’s disease. This is the most common cause of a painful thyroid gland. It is
generally caused by a viral infection and is usually preceded by an upper respiratory
tract infection. Etiologic agents that have been implicated in subacute
granulomatous thyroiditis include mumps, echovirus, coxsackievirus, Epstein-Barr
virus, influenza, and adenovirus. This type of thyroiditis is generally geographical
and seasonal, happening most often in the summer and fall (Slatosky, Shipton, &
Wahba, 2000).
Microbial inflammatory thyroiditis is caused by the presence of grampositive bacteria in the thyroid gland. While there have been other infectious agents
implicated in this type of thyroiditis, staphylococcus aureus is the most common.
This disorder is rare because the thyroid is resistant to infections. Patients usually
have a preexisting thyroid disorder. It presents as pain and tenderness in the
anterior neck that gets worse with swallowing. The patient may have a fever or
pharyngitis (Slatosky, Shipton, & Wahba, 2000).
Invasive fibrous thyroiditis is the most rare type of thyroiditis. The thyroid
gland develops a dense fibrosis, which can extend into extracervical sites. A stonehard or woody mass that extends from the thyroid is common and can develop
gradually or suddenly. This can result in dyspnea, dysphagia, and occasionally
stridor (Slatosky, Shipton, & Wahba, 2000).
Treatment: Treatment is dependent on the symptoms and whether the patient is
displays hypothyroidism or not. If there is no hormone deficiency, a doctor may
decide not to use medication. Medication for the treatment of HT is a synthetic
hormone called levothyroxine. The trade names for levothyroxine are Levothroid,
Levoxyl, and Synthroid. Levothyroxine is identical to the thyroxine produced in the
body. This is used to restore normal levels of thyroid hormone in the body and
reverse the symptoms of hypothyroidism (Mayo Clinic Staff, 2011). Levothyroxine
helps to reduce fatigue lower blood cholesterol, and reverse weight gain. The
patient is generally on levothyroxine for life but needs frequent monitoring to adjust
the dosage. It is important to monitor the dosage because excessive amounts of
levothyroxine can cause bone loss, osteoporosis, and irregular heart rhythm
disorders. Levothyroxine has no side effects and is relatively inexpensive. It is
important to continue taking the correct dosage even if you start to feel better
because symptoms will gradually return upon cessation of taking the medicine
(Mayo Clinic Staff, 2011).
There is an alternative medicine treatment for HT as well. These natural
extracts contain the thyroid hormone derived from the thyroid gland of a pig. One
such product is called Armour Thyroid. These products contain both levothyroxine
and T3 hormone. Doctors, however, have concerns about treating HT with Armour
Thyroid. One concern is that the balance between T3 and T4 hormones in pigs is
different than the balance of T3 and T4 hormones in humans. Another concern is
that the amount of hormone in each batch varies, which can lead to unpredictable
amounts of hormone in your blood. Current research suggests that adding the T3
hormone has no added advantages to just having thyroxine (Mayo Clinic Staff,
2011).
Another treatment for HT is a thyroidectomy, however, these are only
performed with certain indications. Current indications for a thyroidectomy include
suspicion of malignancy, tracheal/esophageal compression, and pain.
Thyroidectomies may also be considered for cosmetic reasons such as an enlarged
goiter, difficulty swallowing without dysphagia, and sensation of tightness in the
neck. This method of treatment can cause hypocalcemia, hypoparathyroidism, and
recurrent pharyngeal nerve paralysis. People who do choose surgical intervention
often feel relief of their symptoms (Pradeep, Ragavan, Ramakrishna, Jayasree, &
Skanda, 2011).
There are no generally accepted treatment guidelines for HT in children and
adolescents even though symptoms during this age can be worse than those in
adults. Many endocrinologists, however, recommend treatment during childhood
even though the number of studies on this subject are limited. Ozen et al performed
a study on the effect of using levothyroxine in pediatric HT. They concluded that
levothyroxine treatment may be beneficial on the clinical course of the disease but
should be closely monitored (Ozen, Berk, Simsek, & Darcan, 2011).
Prognosis: Prognosis for those with HT is good. With treatment, symptoms will
generally subside. Medication is generally taken throughout the lifetime of the
individual and requires frequent monitoring to adjust the dosage. A high dosage of
malignancy has been reported with patients with HT (Pradeep, Ragavan,
Ramakrishna, Jayasree, & Skanda, 2011). A rare complication of HT is thyroid
lymphoma (Slatosky, Shipton, & Wahba, 2000). HT has also been linked to other
autoimmune diseases including systemic lupus erythematosus, rheumatoid
arthritis, pernicious anemia, diabetes mellitus, Sjogren’s syndrome.
Children and adolescents with HT may experience growth problems both
mentally and physically. This is because of the thyroid’s effect on many different
body systems. Untreated HT in the pediatric population can lead to retardation of
growth and development, leading to short stature, decline in school performance
and anemia (Ozen, Berk, Simsek, & Darcan, 2011).
Prevention: HT has a strong genetic component so prevention strategies are very
limited. It is inherited as a dominant trait (Slatosky, Shipton, & Wahba, 2000).
There are, however, some environmental factors that may cause HT. These factors
include iodine, medications, infections, smoking, and possibly stress. The most
established of the environmental factors is excess amount of iodine in a patient’s
diet (Kakudo, Li, Hirokawa, & Ozaki, 2011). The cases of HT has risen dramatically
in the past 50 years, which may be related to an increased iodine content in the
North American diet (Slatosky, Shipton, & Wahba, 2000).
Case Study: Patient is a 25 year-old male student at Weber State University.
Patient presented to the student health center in the spring of 2011. Primary
complaints were malaise, fatigue, headaches, and sluggishness. Patient was in
general good health and all routine exams were normal including palpation of the
thyroid cartilage. Patient was sent to do lab work. The tests ordered were a
comprehensive metabolic panel, lipid profile, testosterone, TSH reflex, free T4, and
CBC with differential. Patient had lab work done on May 11, 2011. Results were
within normal limits for the metabolic panel, testosterone, free T4, and CBC with
differential. The TSH reflex test was out of range at 6.54 mIU/mL. HDL cholesterol
was low at 28 mg/dL but LDL was within normal limits. The cholesterol HDL ratio
showed an average risk with a reading of 4.9. Doctor diagnosed as hypothyroidism
and explained that this could be causing the symptoms. Doctor referred the patient
to an endocrinologist for further lab test and to rule out HT. Doctor prescribed
levothyroxine at 50 mcg, once a day.
Patient went to an endocrinologist on June 28, 2011 where he saw a nurse
practitioner. The nurse practitioner ordered lab work for the patient to rule out HT
and any problems with the pituitary or hypothalamus glands due to the headaches
the patient was experiencing. Tests performed were TSH, T3, T4, thyroid
peroxidase antibodies, testosterone, prolactin, luteinizing hormone, and follicle
stimulating hormone. The testosterone, prolactin, luteinizing hormone, and folliclestimulating hormone all came back within normal limits, showing that there wasn’t
a problem with the pituitary or hypothalamus glands. TSH was within normal limits
at 3.48 showing that the hormone replacement therapy had been effective at
establishing normal levels. Thyroid peroxidase antibodies were elevated at 332.6
confirming a diagnosis of HT. The nurse practitioner increased the dosage of
levothyroxine by a half a tablet to further optimized thyroid function.
Patient continued to monitor thyroid hormone levels for one year after the
initial diagnosis of HT. The patient’s symptoms resolved with hormone therapy
after the first month. After the patient’s symptoms resolved, patient discontinued
use of medication. Because of the discontinuation of hormone therapy, the patient’s
symptoms returned, prompting a follow-up visit to the student health center. Lab
work was done which showed that the TSH levels had slightly elevated, but were
within normal limits at 3.79 mIU/mL. The doctor refilled the prescription and the
patient resumed hormone therapy. The doctor informed the patient that hormone
therapy would be required for the rest of his life and that frequent monitoring of
thyroid function would be necessary.
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