HYPOTHYROIDISM ( HASHIMOTO'S THYROIDITIS)

HYPOTHYROIDISM

Is defined as a decrease of thyroxine (T4) and increase of Thyroid stimulatin hormone (TSH), accompanied by certain symptoms.

CONGENITAL HYPOTHYROIDISM

Occurs in about 1/4000 newborns, but is only diagnosed in 10% of them. As well as there are increase of TSH and T4 decrease, the main symptoms include: umbilical hernia, hypotonia, nutrional feeding problems, jaundice, enlarged of the tongue and delayed bone maturation.

AUTOIMMUNE HYPOTHYROIDISM

There are two phases: Hashimoto's thyroiditis and the atrophic thyroiditis. In the first, there are limphocityc infiltrate, a little fibrosis and coloid decrease. In the last one, there are no coloid, much fibrosis and less lymphocytic infiltrate. Is caused by auto-antibodies against Thyroperoxidase (TPO), Thyroglobuline (Tg) and TSH receptor (TSH-R). There are many evidences too, of genetic factor that may contribute to the disease, like HLA-DR and CTLA-4 mutations that can be predisposing for develope hashimoto's thyroiditis. The rubella infection is a well documented factor that can ellicit the disease, as well as the iodine excess like a risk factor.

About antibodies, TPO and Tg are in major patients and works like autoimmune markers, but can exist TSH-R antibodies that block the TSH link to receptor and ellicit hypothyrodism in 10% of patients. Rarely, can coexist TSH-R antibodies and TSI (Grave's antibodies) that bring a fluctuating situation for the patient, between hyper and hypothyroidism. Something important is that TPO and Tg antibodies don't cross the placenta, so they are not going to cause damage in the fetal thyroid. The principal warning for women who is planning be pregnant is to control her disease beacause there is a high risk for mental retard in children.

Clinical features

SYMPTOMS
The main symptoms of hypothyroidism include: weakness, tiredness, hair loss, cold sensation, hoarse voice, dispnea, constipation, weight gain despite loss of apetite, dificulty concentrating, menhorragia, paresthesia, conductive deafness, dry skin, libido lost.

SIGNS
peripheral edema, mixedema, dry skin, hair loss, nail weak, carpal tunel syndrome, serosity cavity effusions, retarded relax phase usually in the aquilian reflex, cold extremities, madarosis, heterogenous goiter.

Diagnose

The diagnose is usually performed with the hormone values mentioned above, clinical symptoms and TPO Ab + (which are positive in 90%). If there still doubt, it can proceed with FNA (fine needle aspiration) biopsy to confirm the diagnose.

Treatment

The indicated treatment is levothyroxine 1.6g/ Kg of body weight if there is no remanent of thyroid tissue. Aproximately, 100-150mg daily. If there is still thyroid tissue (e.g. graves) is recomended start with lower doses (75-125mg). The goal is reduce TSH to normal levels; this can take 3-6 months aproximately, so is very important to explain it to avoid adherence treatment lost.

Complications

Pseudotumor cerebri in children for prolonged use of levothyroxine but is too rare. Mixedema coma, is a coma induce by a crisis in which there are seizures, apnea and the patient can die, this is a very unusual complication.

SUBLINICAL HYPOTHYROIDISM

Is defined as hormones decrease but with no symptoms added. The indication of treatment is a TSH above 10mU/L, and star with only 25/50 mg. If there is TPO Ab+, the patient is in high risk of develope a overt hypothyroidism.

Another hypothyroidisms: Iatrogenic (e.g. after a thyroidectomy), excessive radioactive I therapy

References: Harrison, Internal medicine, 17 Edition.

Graves Disease

GRAVES DISEASE

The hyperthyroidism of Graves’ disease is the result of circulating IgG antibodies that bind to and activate the G-protein–coupled thyrotropin receptor.This activation stimulates follicular hypertrophy and hyperplasia, causing thyroid enlargement, as well as increases in thyroid hormone production and the fraction of triiodothyronine (T3) relative to thyroxine (T4) in thyroid secretion (from approximately 20% to as high as 30%). Thyroid-function testing in Graves’ disease typically reveals a suppressed serum thyrotropin level and elevated levels of serum T4 and T3. A suppressed serum thyrotropin level with normal serum levels of T4 and T3 is referred to as subclinical hyperthyroidism. Graves’ ophthalmopathy is clinically apparent in approximately 30 to 50% of patients with Graves’ disease, but it is detected in more than 80% of patients who undergo assessment by means of orbital imaging. Manifestations of ophthalmopathy, which vary in severity and have a course that is typically independent of the thyroid disease, can include proptosis, periorbital edema and inflammation, exposure keratitis, photophobia, extraocular muscle infiltration, and eyelid lag - Von graeffe sign (which can also occur with augmented adrenergic stimulation).

Panel A shows a man with bilateral exophthalmos and marked retraction of the upper eyelid. Panel B shows a woman with mild inflammatory signs and hypotropia in the right eye. Panel C shows a woman with marked edema and redness in the upper eyelid, redness of the conjunctiva, and severe chemosis in the left eye. Panel D shows a man with marked edema and retraction of the eyelid and exophthalmos. Panel E shows a woman with marked redness of the conjunctiva and chemosis. There is marked impairment of movement of the globes, which are unable to follow the examiner's finger; this patient had severe dysthyroid optic neuropathy, which responded dramatically to intravenous glucocorticoids (Cortesy of NEJM)

Clinical manifestations

Semiology Apart


This patient has a lot of graves signs: first et all, a big difuse goiter, probably exophtalmos, eyelid lag ( Von graeffe Sign), Pemberton sign ( yugular ingurgitation when rise up her arms due obstruction) and binocular vision impairment (Moebius sign).

The female-to-male ratio among patients with Graves’ disease is between 5:1 and 10:1. The peak incidence is between 40 and 60 years of age, although the disease can occur at any age.

Tests for Graves’ disease–associated antibodies are useful in the evaluation of some conditions, but they are not usually required for diagnosis or to monitor disease activity

IMAGING

A radioiodine-uptake study should be performed in patients in whom painless thyroiditis is considered to be a diagnostic possibility and in patients with an irregular or nodular thyroid gland.

CT is not needed for ophtalmopathy for primary care, and EKG should be performed.

THERAPY

The treatment options for Graves’ disease include antithyroid drugs (propylthiouracil and methimazole), radioiodine, and surgery.

References

- Graves DIsease Review - NEJM