Background: Immune checkpoint inhibitors (ICIs) targeting programmed cell death protein 1 (PD-1) are used for the treatment of various cancer types. However, immune-related adverse events (irAEs) occur in patients treated with ICIs. Several small-scale studies have reported the onset of irAEs and therapeutic effects of ICIs. Here we report a large-scale retrospective study covering a wide range of cancers. We evaluated irAEs and the therapeutic effects of ICIs and determined whether irAEs could be predicted.

A combination of mixed macrovesicular and microvesicular fatty hepatocytes and the above-described findings, such as fatty liver, cholestasis, necroinflammatory reaction and iron deposition, are almost never observed in other liver diseases in infants and adults. We believe that NICCD is a disease with characteristic hepatopathological features.

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The aim of this study was to evaluate the effects of bile acid treatment and to obtain further information about the pathway of bile acid biosynthesis in a patient with 3beta-hydroxy-delta5-C27-steroid dehydrogenase/isomerase (3beta-HSD) deficiency by gas chromatography-mass spectrometry. Results showed that at 2 months of age, 3beta-hydroxy-5-cholen-24-oic acid (3.0 micromol/mmol Cr, 7.9%) was detected in the urine in essentially the same relative amount as 3beta,7alpha-dihydroxy- and 3beta,7alpha,12alpha-trihydroxy-5-cholen-24-oic acids (3.7 micromol/mmol Cr, 9.8%) during ursodeoxycholic acid treatment combined with prednisolone. As a result, diagnosis was delayed until 18 months of age. One month later with substitution of chenodeoxycholic acid treatment, urinary 3beta,7alpha-dihydroxy- and 3beta,7alpha,12alpha-trihydroxy-5-cholen-24-oic acids decreased significantly, and subsequent improvement of liver dysfunction was accelerated. Chenodeoxycholic acid treatment is useful in 3beta-HSD deficiency. However, in the diagnosis of this disease in early life, it should be noted that the acidic pathway may be the major route for bile acid biosynthesis in the neonatal period. Diagnosis of 3beta-HSD deficiency may have been delayed by administration of ursodeoxycholic acid, resulting in prolonged diagnostic investigation in this child with cholestasis. Further, use of prednisolone may have been contraindicated.