The association between thyroid diseases (hypothyroidism and hyperthyroidism) and PH has been reported in a number of studies (127,128). In a recent prospective study using echocardiographic evaluation, more than 40% of patients with thyroid diseases had PH (129)
One instance of PVOD confirmed by histology was observed in a patient with Hashimoto thyroiditis (130).
Interestingly, a recent prospective study of 63 consecutive adult patients with PAH found a 49% prevalence of autoimmune thyroid disease, including both hypothyroidism and hyperthyroidism, suggesting that these conditions may be linked by a common immunogenetic susceptibility (131)
127 Li JH, Safford RE, Aduen JF, Heckman MG, Crook JE, Burger CD. Pulmonary hypertension and thyroid disease. Chest 2007;132:793–7
128 Ferris A, Jacobs T, Widlitz A, Barst RJ, Morse JH. Pulmonary
arterial hypertension and thyroid disease. Chest 2001;119:1980–1
129 Mercé J, Ferra ́s S, Oltra C, et al. Cardiovascular abnormalities in hyperthyroidism: a prospective Doppler echocardiographic study. Am J Med 2005;118:126–31.
130 Kokturk N, Demir N, Demircan S, et al. Pulmonary veno-occlusive disease in a patient with a history of Hashimoto’s thyroiditis. Indian J Chest Dis Allied Sci 2005;47:289–92.
131 Chu JW, Kao PN, Faul JL, Doyle RL. High prevalence of autoimmune thyroid disease in pulmonary arterial hypertension. Chest 2002;122:1668 –73
Thyrotoxicosis
Epidemiology
xx
Etiology
Inadequately-Treated Grave’s Disease
Precipitants:
Sepsis:
Medical Illness:
Iodine Load-Contrast:
Post-Thyroidal Surgery:
Post-Non-Thyroidal Surgery:
Exogenous Thyroid Intake:
Toxic Nodular Goiter:
Thyroiditis:
Thyroid Adenoma:
Thyroid Cancer:
Diagnosis
TFT’s:
TSH: decreased
Free and total T4: increased
Free and total T3: increased (usually more than serum T4)
Clinical
Neuro
Irritability:
Delirium:
Coma:
Fever:
Hyperreflexia:
Cardiac
Tachycardia:
Hypotension:
High-Output CHF:
GI
Vomiting:
Diarrhea:
Treatment
Supportive Care
Hydration:
B-complex vitamins:
Digoxin (for AF):
Therapy #1: Beta-Blockers
Propanolol is the best studied, but Esmolol is also effective
Propanolol blocks beta receptors, as well as partially inhibiting conversion of T4->T3
Relief of symptoms usually occurs within minutes
Useful if CHF is absent
Therapy #2: PTU (100 mg every 2 hours PO) or Methimazole
Effect may take weeks
Blocks T4 and T3 synthesis (within 2 hrs), as well as peripheral conversion of T4->T3
Therapy #3: Potassium Iodide (SSKI) or Lugol Solution
Works almost immediately
Give at least 1 hr after beta blockers + PTU to prevent iodine from being used as substrate by hyperfunctioning gland
Blocks hormone release and peripheral conversion
Therapy #4: Dexamethasone (2 mg IV q6 hours)
Aids decreased adrenal reserve that may be present, inhibits hormone release, and inhibits peripheral conversion from T4 to T3
Clinical Course
With treatment with PTU, iodide, and dexamethasone, T3 usually returns to normal within 24-48 hrs