European journal of gastroenterology & hepatology · 2021
"Hepatotoxicity in inflammatory bowel disease: mesalazine, the forgotten drug".
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Garrido Isabel, Santos Ana Luísa, Lopes Joanne, Lopes Susana, Macedo Guilherme
Аннотация
INTRODUCTION: Mesalazine is a widely prescribed drug, used for the treatment of ulcerative colitis to both induce and maintain remissions in disease. Mesalazine therapy has been associated with a low rate of serum enzyme elevations and a with rare instances of clinically apparent acute liver injury.
CASE PRESENTATION: A 51-year-old Caucasian woman with ulcerative colitis was treated with mesalazine. Two weeks later, the patient presented severe liver cholestatic injury. No symptoms of generalized hypersensitivity were seen. She had no history of liver disease and was known to have normal routine liver tests before starting treatment. The liver biopsy revealed mild periportal necroinflammatory lesions with no fibrosis, suggestive of drug-induced liver injury. The patient's symptoms were resolved by discontinuing the mesalazine treatment; within 6 months, all her liver panels returned to normal. After extensively excluding other potential causes of liver injury and with clinical and lab resolution after discontinuing the drug, we assumed mesalazine as the cause of hepatic toxicity.
CONCLUSION: We describe a patient with ulcerative colitis who developed severe but fully reversible liver cholestatic injury following the prescription of mesalazine. This case reinforces the possibility of a causal relationship between mesalazine therapy and toxic hepatic injury without systemic hypersensitivity. Although it is a usually well-tolerated drug, clinicians should be alert and discontinue therapy when liver dysfunction occurs to avoid the development of chronic hepatitis and liver fibrosis.
CASE PRESENTATION: A 51-year-old Caucasian woman with ulcerative colitis was treated with mesalazine. Two weeks later, the patient presented severe liver cholestatic injury. No symptoms of generalized hypersensitivity were seen. She had no history of liver disease and was known to have normal routine liver tests before starting treatment. The liver biopsy revealed mild periportal necroinflammatory lesions with no fibrosis, suggestive of drug-induced liver injury. The patient's symptoms were resolved by discontinuing the mesalazine treatment; within 6 months, all her liver panels returned to normal. After extensively excluding other potential causes of liver injury and with clinical and lab resolution after discontinuing the drug, we assumed mesalazine as the cause of hepatic toxicity.
CONCLUSION: We describe a patient with ulcerative colitis who developed severe but fully reversible liver cholestatic injury following the prescription of mesalazine. This case reinforces the possibility of a causal relationship between mesalazine therapy and toxic hepatic injury without systemic hypersensitivity. Although it is a usually well-tolerated drug, clinicians should be alert and discontinue therapy when liver dysfunction occurs to avoid the development of chronic hepatitis and liver fibrosis.