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Case Reports
. 2022 May 4;9(5):e00774.
doi: 10.14309/crj.0000000000000774. eCollection 2022 May.

Statin-Induced Rhabdomyolysis Associated With Transjugular Intrahepatic Portosystemic Shunt Placement

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Case Reports

Statin-Induced Rhabdomyolysis Associated With Transjugular Intrahepatic Portosystemic Shunt Placement

Eric C Swei et al. ACG Case Rep J. .

Abstract

Rhabdomyolysis is a known rare and potentially lethal complication of statin use. This toxic effect is potentiated by alterations in hepatic physiology in patients with cirrhosis. Transjugular intrahepatic portosystemic shunt placement has the potential to further compound this effect; yet, examples of this have not previously been described in the literature. We present a case of a patient who experienced statin-induced rhabdomyolysis likely as a direct consequence of transjugular intrahepatic portosystemic shunt placement.

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Figures

Figure 1.
Figure 1.
(A) Before TIPS placement, portal vein injection shows flow to the intrahepatic portal vein branches (open arrow). Incidental note is made of hepatofugal flow in the inferior mesenteric vein (solid arrow). (B) After TIPS placement, portal vein injection shows absent intrahepatic portal flow, with nearly all flow going through the TIPS (open arrow) and into the right atrium. Minimal flow is seen in the left portal vein (solid arrow). TIPS, transjugular intrahepatic portosystemic shunt.
Figure 2.
Figure 2.
(A) Precontrast and (B) postcontrast axial T1 fat-saturated image of the right thigh. There is minimal change in the intrinsic signal of the musculature from precontrast to postcontrast images, indicative of poor enhancement. (C) Axial T2 fat-saturated image of the same thigh showing diffuse high-intensity signal, most substantially involving the distal adductor and proximal vastus muscles, indicative of intramuscular edema. Together, these changes are consistent with an inflammatory myositis.
Figure 3.
Figure 3.
Photomicrographs of the rectus femoris muscle. (A) Hematoxylin and eosin (H&E) stain shows active myopathic damage, necrosis, and myofiber atrophy without significant inflammation, inclusion bodies, or evidence of vasculitis (10× objective). Inset with special stain trichrome shows no significant fibrosis (20× objective) nor were other signs of chronicity seen, indicating the changes were acute. (B) Higher magnification of H&E confirms the above findings (20× objective).

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