Hurry up!
: : Get The Offer
Unlimited Access Step ( one, two and three ).
Priority Access To New Features.
Free Lifetime Updates Facility.
Dedicated Support.
1
Question:

A 28-year-old woman, gravida 1 para 1, comes to the office for a follow-up appointment 4 months after giving birth to a healthy boy.  For the past 3 weeks the patient has had progressive fatigue associated with loss of interest in day-to-day activities, irritability, and poor concentration.  In the 2 weeks prior to the onset of fatigue, she experienced excessive sweating and palpitations.  Blood pressure is 140/74 mm Hg and pulse is 60/min.  The thyroid gland is firm, diffusely enlarged, and nontender.  Laboratory results show elevated serum TSH and low free T4.  Which of the following pathological processes is likely responsible for this patient's condition?

Hurry up!
: : Get The Offer
Unlimited Access Step ( one, two and three ).
Priority Access To New Features.
Free Lifetime Updates Facility.
Dedicated Support.


Explanation:

There are many explanatory sources, such as pictures, videos, and audio clips to explain these explanations and questions and explain the answers, but you must subscribe first so that you can enjoy all these advantages. We have many subscription plans at the lowest prices. Don't miss today's offer. Subscribe

This patient has primary hypothyroidism, presenting with a low serum thyroxine level and elevated TSH, associated with fatigue and neurocognitive symptoms.  Immediately preceding this, she had symptoms suggesting hyperthyroidism (ie, palpitation, diaphoresis).  In light of her recent childbirth, this phasic pattern of thyroid dysfunction is most consistent with postpartum thyroiditis.

Postpartum thyroiditis occurs within 12 months of pregnancy and is characterized by autoimmune destruction of thyroid follicles similar to that seen in chronic lymphocytic (Hashimoto) thyroiditis.  It typically begins with a hyperthyroid phase due to release of preformed thyroid hormone, followed by a transient hypothyroid phase due to depletion of thyroid hormone and an eventual return to a euthyroid state.

Postpartum thyroiditis is associated with high titers of antithyroid peroxidase and antithyroglobulin autoantibodies, which activate complement in thyroid follicles and stimulate NK cells.  Histologic inspection demonstrates lymphocytic infiltration, sometimes with formation of germinal centers.  Breakdown of follicle margins and loss of colloid may also be seen.

(Choice A)  Riedel thyroiditis is a rare disorder characterized by extensive fibrosis of the thyroid that extends into surrounding tissues.  The thyroid gland is hard and fixed.  Hypothyroidism is common but is not typically preceded by a hyperthyroid phase.

(Choices B and E)  Granulomatous inflammation in the pituitary can occur as a primary phenomenon or secondary to systemic granulomatous disorders (eg, sarcoidosis, tuberculosis).  Lymphocytic hypophysitis is an uncommon disorder that also occurs with increased frequency in postpartum women.  Both of these disorders can cause secondary/central hypothyroidism due to loss of pituitary thyrotrophs, which leads to low (not elevated) TSH.

(Choice C)  Like postpartum thyroiditis, subacute (postviral, granulomatous, De Quervain) thyroiditis also follows a phasic course with initial hyperthyroidism due to release of preformed hormone followed by a hypothyroid phase.  However, the thyroid is painful and tender, and fever is common because it is believed to be a postviral inflammatory process.

Educational objective:
Postpartum thyroiditis occurs within 12 months of pregnancy and is characterized by autoimmune destruction of thyroid follicles.  It begins with a hyperthyroid phase due to release of preformed thyroid hormone, followed by a transient hypothyroid phase due to depletion of thyroid hormone.  Histologic inspection demonstrates lymphocytic infiltration, sometimes with formation of germinal centers.