PMC9065283_01
(A) Lymphocytes (red arrow), eosinophils (black arrow), and neutrophils (yellow arrow) seen in the portal duct area (HE, original magnification x 200). (B) "Rose garland" formation (HE, original magnification x 100). (C) Lymphocytes "penetrate" (HE, original magnification x 600).
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F1
A liver biopsy was performed on June 24, and pathological examinations were consistent with DILI (G3 S1) (Figure 1A). AST, 40 U/L; ALP, 204 U/L; and gamma-GT, 93 U/L. A repeat liver biopsy after 24 weeks of treatment was consistent with autoimmune-like phenomenon liver failure (G3 S3) (Figures 1B,C). A diagnosis was made according to the Roussel Uclaf Causality Assessment Method (RUCAM), and a probable diagnosis of autoimmune hepatitis was made based on 2008 International Autoimmune Hepatitis Group's (IAIHG) criteria: (1) DILI, cholestatic, acute, and RUCAM score calculated as 10 (highly likely); (2) IAIHG score 4, combined with liver pathology, the diagnosis of the teenager is drug-induced liver injury with autoimmune-like phenomenon (AL-DILI), drug-induced autoimmune hepatitis (DI-AIH) is not excluded.
(A,B) Multiple nodular soft tissue shadows were observed in both lungs. The larger one was located in the lower lobe of the right lung (15 x 23 mm).
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F2
Sputum culture revealed Candida albicans, and chest computed tomography (CT) showed multiple nodules in the lungs (Figures 2A,B).
PMC9065283_02
(A,B) Multiple nodular high-density shadows were observed in both lungs; the larger one was located in the upper lobe of the left lung (20 x 24 mm). (C,D) After 2 weeks of treatment, multiple nodular high-density shadows were observed in both lungs; the larger one was 29.4 x 28.4 mm in size, and voids were present in some lesions.
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F3
Her chest CT scan showed multiple nodules in both lungs on July 26 (Figures 3A,B), and IFI was diagnosed. However, a repeat chest CT showed an increase in the number of lung lesions and the presence of an air crescent sign (Figures 3C,D).
(A) Bridging or submass necrosis of hepatocytes and residue liver cells were arranged in a pseudolobule-like pattern, some of which had macrovesicular steatosis (<10%), and moderate to severe interfacial inflammation were noted (HE, original magnification x 40). (B) The portal duct area was obviously enlarged, interlobular bile duct hyperplasia was present, and portions of the bile ducts were slightly dilated with bile thrombosis. Infiltration of numerous mixed inflammatory cells into the interstitium, and fibrous tissue hyperplasia accompanied with partial pseudolobule formation was also noted (HE, original magnification x 100). (C) "Rose garland" formation (HE, original magnification x 40). (D) Lymphocytes "penetrate" (HE, original magnification x 200). (E,F) Slight edema and degeneration in hepatocytes, scattered with spotty necrosis. Infiltration of a small number of mixed inflammatory cells into the interstitium and fibrous tissue (HE, original magnification x 40).
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F4
S 3-4) (Figures 4A,B). She was discharged on oral voriconazole (250 mg, q12 h), methylprednisolone (4 mg, q.d.), and other medications. A second liver biopsy after 10 weeks revealed an autoimmune-like phenomena hepatitis (G 1-2 S 2-3) (Figures 4C,D). The liver histopathology indicated chronic hepatitis (G 1 S 2) (Figures 4E,F), which was significantly improved compared with the previous two.