Long-Term Azathioprine Use and the Development of Non-Cirrhotic Portal Hypertension

Manfready, Richard A.; Husney, Jack; Golfeyz, Shmuel; Thung, Swan N.; Weisberg, Ilan

doi:10.14309/00000434-201810001-02249

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“…There is evidence from myasthenia gravis (MG) case reports that MG patients on azathioprine [21] and MG patients not on azathioprine are both prone to PSVD, with the implication that immunologic mechanisms intrinsic to MG may have contributed to the pathogenesis in the latter case [16]. Likewise, inherent immune dysfunction in our patient with Crohn's disease [22] may have played a role in the absence of immunosuppressive therapy [1]. Additionally, portal hypertension in our patient is unlikely to be attributable to PSC; a small percentage (3.3%) of patients in one PSC transplant study had portal hypertension without cirrhosis due to NRH or obliterative venopathy [23].…”

Section: Discussionmentioning

confidence: 67%

Porto-Sinusoidal Vascular Disease with Obliterative Portal Venopathy Associated with Long-Term Azathioprine for Crohn’s Disease

Manfready¹,

Husney²,

Thung³

et al. 2020

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Patients receiving immunosuppressive therapy for inflammatory bowel disease may be susceptible to non-cirrhotic portal hypertension, now referred to as porto-sinusoidal vascular disease. Here we describe a patient treated with long-term azathioprine for Crohn's disease who developed porto-sinusoidal vascular disease with obliterative portal venopathy without nodular regenerative hyperplasia on histology. Specific signs of portal hypertension were present, including porto-systemic collaterals on imaging. Histopathologic findings of porto-sinusoidal vascular disease support the hypothesis of endothelial cell injury induced by 6-thioguanine secondary to azathioprine use.

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