Frontiers in medicine · 2026
Case Report: A case of drug-induced pancreatitis caused by paroxetine with a literature review.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Wu Yangpeng, Lv DongFeng, Liu Lihua, Liu YaDong
Аннотация
BACKGROUND: Acute pancreatitis (AP) incidence is ~76.2 per 100,000. Drug-induced pancreatitis (DIP) accounts for <2%, yet >500 drugs are implicated. Evidence linking the SSRI paroxetine to AP remains sparse.
CASE PRESENTATION: A 28-year-old woman with severe depression self-initiated paroxetine 20 mg once daily; within 24 h she developed persistent epigastric pain and bloating. After brief relief with intravenous fluids she re-administered the same dose, and symptoms recurred within 24 h. Labs showed elevated pancreatic enzymes and CRP. CT revealed mild pancreatitis. No alcohol, hyperlipidemia or other classic risk factors were identified. Paroxetine was immediately discontinued; supportive care led to symptom and enzyme normalization within 72 h. She was discharged on trazodone and remains recurrence-free.
DISCUSSION: Population studies have not established a significant SSRI-AP association, probably because of the extreme rarity of such events (<0.01%). The positive rechallenge observed here provides robust individual-level evidence of causality, supported by formal probability scales and international criteria. SSRIs may precipitate AP through serotonin-mediated β-cell dysfunction, oxidative stress, or idiosyncratic hypersensitivity. Early recognition is critical because DIP is usually reversible after drug withdrawal.
CONCLUSION: This case suggests that paroxetine may induce AP even at standard doses. Clinicians should consider DIP in patients lacking traditional risk factors, especially after self-rechallenge. Early recognition, immediate drug cessation and supportive therapy ensure excellent recovery.
CASE PRESENTATION: A 28-year-old woman with severe depression self-initiated paroxetine 20 mg once daily; within 24 h she developed persistent epigastric pain and bloating. After brief relief with intravenous fluids she re-administered the same dose, and symptoms recurred within 24 h. Labs showed elevated pancreatic enzymes and CRP. CT revealed mild pancreatitis. No alcohol, hyperlipidemia or other classic risk factors were identified. Paroxetine was immediately discontinued; supportive care led to symptom and enzyme normalization within 72 h. She was discharged on trazodone and remains recurrence-free.
DISCUSSION: Population studies have not established a significant SSRI-AP association, probably because of the extreme rarity of such events (<0.01%). The positive rechallenge observed here provides robust individual-level evidence of causality, supported by formal probability scales and international criteria. SSRIs may precipitate AP through serotonin-mediated β-cell dysfunction, oxidative stress, or idiosyncratic hypersensitivity. Early recognition is critical because DIP is usually reversible after drug withdrawal.
CONCLUSION: This case suggests that paroxetine may induce AP even at standard doses. Clinicians should consider DIP in patients lacking traditional risk factors, especially after self-rechallenge. Early recognition, immediate drug cessation and supportive therapy ensure excellent recovery.