Refractory hepatic encephalopathy in a patient with hypothyroidism: Another element in ammonia metabolism

Fernando Díaz-Fontenla; Marta Castillo-Pradillo; Arantxa Díaz-Gómez; Luis Ibañez-Samaniego; Pilar Gancedo; Juan Adan Guzmán-de-Villoria; Pilar Fernández-García; Rafael Bañares-Cañizares; Rita García-Martínez

doi:10.3748/wjg.v23.i28.5246

Refractory hepatic encephalopathy in a patient with hypothyroidism: Another element in ammonia metabolism

World J Gastroenterol. 2017 Jul 28;23(28):5246-5252. doi: 10.3748/wjg.v23.i28.5246.

Authors

Fernando Díaz-Fontenla¹, Marta Castillo-Pradillo¹, Arantxa Díaz-Gómez¹, Luis Ibañez-Samaniego¹, Pilar Gancedo¹, Juan Adan Guzmán-de-Villoria¹, Pilar Fernández-García¹, Rafael Bañares-Cañizares¹, Rita García-Martínez¹

Affiliation

¹ Fernando Díaz-Fontenla, Marta Castillo-Pradillo, Arantxa Díaz-Gómez, Luis Ibañez-Samaniego, Rafael Bañares-Cañizares, Rita García-Martínez, Unidad de Hepatología, Servicio de Aparato Digestivo, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.

Abstract

Hepatic encephalopathy (HE) remains a diagnosis of exclusion due to the lack of specific signs and symptoms. Refractory HE is an uncommon but serious condition that requires the search of hidden precipitating events (i.e., portosystemic shunt) and alternative diagnosis. Hypothyroidism shares clinical manifestations with HE and is usually considered within the differential diagnosis of HE. Here, we describe a patient with refractory HE who presented a large portosystemic shunt and post-ablative hypothyroidism. Her cognitive impairment, hyperammonaemia, electroencephalograph alterations, impaired neuropsychological performance, and magnetic resonance imaging and spectroscopy disturbances were highly suggestive of HE, paralleled the course of hypothyroidism and normalized after thyroid hormone replacement. There was no need for intervention over the portosystemic shunt. The case findings support that hypothyroidism may precipitate HE in cirrhotic patients by inducing hyperammonaemia and/or enhancing ammonia brain toxicity. This case led us to consider hypothyroidism not only in the differential diagnosis but also as a precipitating factor of HE.

Keywords: Cirrhosis; Cognitive impairment; Hepatic encephalopathy; Hypothyroidism; Magnetic resonance spectroscopy; Portosystemic shunt.

Publication types

Case Reports

MeSH terms

Adrenergic beta-Antagonists / therapeutic use
Alcoholism / complications
Ammonia / blood
Ammonia / metabolism*
Antithyroid Agents / therapeutic use
Brain / diagnostic imaging
Carbimazole / therapeutic use
Diagnosis, Differential
Disorders of Excessive Somnolence / blood
Disorders of Excessive Somnolence / diagnostic imaging
Disorders of Excessive Somnolence / etiology
Drug Resistance*
Dysarthria / blood
Dysarthria / diagnostic imaging
Dysarthria / etiology
Electroencephalography
Embolization, Therapeutic
Female
Goiter, Nodular / blood
Goiter, Nodular / complications
Goiter, Nodular / drug therapy
Goiter, Nodular / metabolism
Hepatic Encephalopathy / blood
Hepatic Encephalopathy / diagnosis
Hepatic Encephalopathy / drug therapy*
Hepatic Encephalopathy / metabolism
Humans
Hyperammonemia / blood*
Hyperammonemia / complications
Hypothyroidism / blood
Hypothyroidism / diagnosis
Hypothyroidism / drug therapy
Hypothyroidism / metabolism*
Liver Cirrhosis, Alcoholic / blood
Liver Cirrhosis, Alcoholic / complications*
Magnetic Resonance Imaging
Middle Aged
Portal Vein / abnormalities
Portal Vein / diagnostic imaging
Portasystemic Shunt, Transjugular Intrahepatic
Propranolol / therapeutic use
Renal Veins / abnormalities
Renal Veins / diagnostic imaging
Thyrotropin / blood
Thyroxine / therapeutic use
Tomography, X-Ray Computed
Vascular Malformations / blood
Vascular Malformations / complications
Vascular Malformations / therapy

Substances

Adrenergic beta-Antagonists
Antithyroid Agents
Ammonia
Carbimazole
Thyrotropin
Propranolol
Thyroxine