PGY2 Justine Ko presented a case of a 73 y/o F with history of HTN, Afib and HLD presents with weakness x 1month and RUQ/R flank pain x2-3 days. She has had recent weight loss but also started a new diet per instructions by her PMD. Home medications include Amiodarone, amlodipine, benazepril, citalopram, eliquis, ezetimibe, and hydrochlorothiazide. Patient was born in El Salvador and denies any history of ETOH/tobacco/drug use. Physical exam significant for bradycardia to 56, BP to 155/54, scleral icterus and jaundiced skin. Chest was clear to auscultation and no b/l lower extremity edema or tremors noted.
CBC: WBC 6.1>Hb 15.7/Hct 45.1<Plt 190
Na 112/K 4.2/Cl 79/HCO3 19/BUN 13/Cr 0.78 <Glucose 157
ALP 130>T.protein 6.8/Albumin 4.1/AST 762/ALT 680/Tbili 13.6/Dbili 9
- Sosm 248 mOsm/kg (normal: 275-295)
- Uosm 259 mOsm/kg
- UNa <20 mmol/L
- Uchloride <22 mmol/L
- Serum uric acid 1.9 mg/dL (normal: 2.7-6.4)
- UA with negative protein, glucose or nitrite, small leuks (4-10/HPF)
- Trop <0.01
- Pro-BNP 228 pg/mL (normal <125)
- TTE showed normal EF of 60-65%, normal wall motion, no significant valvular disease
- Acute Hepatitis panel (A, B, C, E): all non-reactive
- Actin Ab IgG <20 units
- ANA 1:1280, nuclear, centromere
- RUQ US showed cholelithiasis and gallbladder wall thickening. No pericholecystic fluid. No biliary ductal dilatation. Hepatic steatosis
The thyroid function tests were sent:
- TSH 0.09 uIU/mL (normal: 0.27-4.2)
- Free T4 4.34 ng/dL (normal: 0.93-1.70)
- Free T3 1.6 pg/mL (normal: 2.5-4.3)
CT Soft Tissue Neck showed R sided thyroid nodules measuring up to 1.6cm
Treatment: Patient was treated for hypovolemic hyponatremia with nephrology consult on board. Hepatology and endocrine consulted with Amiodarone held given concern for Amiodarone induced thyrotoxicosis with plans for weekly thyroid function tests and consider initiation of tapazole (less hepatocellular damage vs PTU).
Take home points:
- Hy’s Law = patient is at a higher risk of fatal drug induced liver injury (DILI) if the drug causes hepatocellular injury with jaundice than if the drug causes hepatobiliary injury with jaundice.
- Thyrotoxicosis affects 5% of patients taking Amiodarone and can happen any time during or up to 9 months AFTER treatment.
- Type 1 Amiodarone induced thyrotoxicosis = occurs in people with underlying multinodular goiter or latent Graves disease and you will see increased vascularity on Doppler. Cessation of Amiodarone is more important in type 1 than 2.
- Type 2 Amiodarone induced thyrotoxicosis = affects patients without thyroid disease, not associated with increased vascularity on Doppler.
Methimazole is most effect in type 1 amiodarone induced thyrotoxicosis and prednisone is the preferred treatment for type 2 amiodarone induced thyrotoxicosis. If there is cardiovascular compromise, treat with methimazole and steroids.