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3. Efficacy and safety of glecaprevir and pibrentasvir in Japanese patients with hepatitis C virus infection aged 75 years or older

Author

Komaki, Yuri, Ozono, Yoshinori, Nakamura, Kenichi, Iwakiri, Hisayoshi, Hasuike, Satoru, Sueta, Mitsue, Miike, Tadashi, Yamamoto, Shojiro, Uto, Hirofumi, Kusumoto, Kazunori, Ochiai, Toshimasa, Kato, Junya, Komada, Naoto, Kuroki, Kazuo, Eto, Toshiharu, Shigehira, Masafumi, Hirono, Shuichi, Nagata, Kenji, and Kawakami, Hiroshi

Published
2022
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7. Mice with Calr mutations homologous to human CALR mutations only exhibit mild thrombocytosis

Author

Shide, Kotaro, Kameda, Takuro, Kamiunten, Ayako, Oji, Asami, Ozono, Yoshinori, Sekine, Masaaki, Honda, Arata, Kitanaka, Akira, Akizuki, Keiichi, Tahira, Yuki, Nakamura, Kenichi, Hidaka, Tomonori, Kubuki, Yoko, Abe, Hiroo, Miike, Tadashi, Iwakiri, Hisayoshi, Tahara, Yoshihiro, Sueta, Mitsue, Hasuike, Satoru, Yamamoto, Shojiro, Nagata, Kenji, Ikawa, Masahito, and Shimoda, Kazuya

Published
2019
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8. Inflammatory Hepatocellular Adenoma Mimicking Focal Nodular Hyperplasia that Grew during Pregnancy and Changed its Appearance on Magnetic Resonance Imaging after Delivery

Author

Hasuike, Satoru, primary, Nagata, Kenji, additional, Sasaki, Haruka, additional, Hirata, Tomoya, additional, Suzuki, Sho, additional, Komaki, Yuri, additional, Ozono, Yoshinori, additional, Nakamura, Kenichi, additional, Miike, Tadashi, additional, Iwakiri, Hisayoshi, additional, Sueta, Mitsue, additional, Yamamoto, Shojiro, additional, Maekawa, Kazuya, additional, and Kawakami, Hiroshi, additional

Published
2023
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10. Frailty Status Predicts New Long-term Care Insurance Certification in Hepatitis C Patients Receiving Antiviral Therapy

Author

NAKAMURA, KENICHI, primary, KUSUMOTO, KAZUNORI, additional, OZONO, YOSHINORI, additional, KUROKI, KAZUO, additional, MATSUURA, YUNOSUKE, additional, MUKUDA, TOSHIHIRO, additional, OCHIAI, TOSHIMASA, additional, TSUCHIMOCHI, MAI, additional, IWAKIRI, HISAYOSHI, additional, HASUIKE, SATORU, additional, SHIMODA, KAZUYA, additional, and NAGATA, KENJI, additional

Published
2021
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12. Neoplastic fibrocytes play an essential role in bone marrow fibrosis in Jak2V617F-induced primary myelofibrosis mice

Author

Ozono, Yoshinori, primary, Shide, Kotaro, additional, Kameda, Takuro, additional, Kamiunten, Ayako, additional, Tahira, Yuki, additional, Sekine, Masaaki, additional, Akizuki, Keiichi, additional, Nakamura, Kenichi, additional, Iwakiri, Hisayoshi, additional, Sueta, Mitsue, additional, Hidaka, Tomonori, additional, Kubuki, Yoko, additional, Yamamoto, Shojiro, additional, Hasuike, Satoru, additional, Sawaguchi, Akira, additional, Nagata, Kenji, additional, and Shimoda, Kazuya, additional

Published
2020
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13. Calreticulin haploinsufficiency augments stem cell activity and is required for onset of myeloproliferative neoplasms

Author

Shide, Kotaro, primary, Kameda, Takuro, primary, Kamiunten, Ayako, primary, Ozono, Yoshinori, primary, Tahira, Yuki, primary, Yokomizo-Nakano, Takako, primary, Kubota, Sho, primary, Ono, Masaya, primary, Ikeda, Kazuhiko, primary, Sekine, Masaaki, primary, Akizuki, Keiichi, primary, Nakamura, Kenichi, primary, Hidaka, Tomonori, primary, Kubuki, Yoko, primary, Iwakiri, Hisayoshi, primary, Hasuike, Satoru, primary, Nagata, Kenji, primary, Sashida, Goro, primary, and Shimoda, Kazuya, primary

Published
2020
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14. Mice with Calr mutations homologous to human CALR mutations only exhibit mild thrombocytosis

Author

1000020468028, Shide, Kotaro, 1000030468029, Kameda, Takuro, 1000030800750, Kamiunten, Ayako, 1000050803417, Oji, Asami, 1000020839394, Ozono, Yoshinori, Sekine, Masaaki, 1000010373367, Honda, Arata, 1000070343308, Kitanaka, Akira, Akizuki, Keiichi, Tahira, Yuki, Nakamura, Kenichi, 1000040381115, Hidaka, Tomonori, 1000000284836, Kubuki, Yoko, Abe, Hiroo, Miike, Tadashi, Iwakiri, Hisayoshi, Tahara, Yoshihiro, Sueta, Mitsue, 1000050381067, Hasuike, Satoru, Yamamoto, Shojiro, 1000000372798, Nagata, Kenji, 1000020304066, Ikawa, Masahito, 1000090311844, Shimoda, Kazuya, 1000020468028, Shide, Kotaro, 1000030468029, Kameda, Takuro, 1000030800750, Kamiunten, Ayako, 1000050803417, Oji, Asami, 1000020839394, Ozono, Yoshinori, Sekine, Masaaki, 1000010373367, Honda, Arata, 1000070343308, Kitanaka, Akira, Akizuki, Keiichi, Tahira, Yuki, Nakamura, Kenichi, 1000040381115, Hidaka, Tomonori, 1000000284836, Kubuki, Yoko, Abe, Hiroo, Miike, Tadashi, Iwakiri, Hisayoshi, Tahara, Yoshihiro, Sueta, Mitsue, 1000050381067, Hasuike, Satoru, Yamamoto, Shojiro, 1000000372798, Nagata, Kenji, 1000020304066, Ikawa, Masahito, 1000090311844, and Shimoda, Kazuya

Abstract

Shide, K., Kameda, T., Kamiunten, A. et al. Mice with Calr mutations homologous to human CALR mutations only exhibit mild thrombocytosis. Blood Cancer J. 9, 42 (2019). https://doi.org/10.1038/s41408-019-0202-z, Calreticulin (CALR) exon 9 frameshift mutations, commonly detected in essential thrombocythemia (ET) and primary myelofibrosis patients, activate signal transducer and activator of transcription (STAT) proteins in the presence of Myeloproliferative Leukemia Virus (MPL) and induce ET in vivo. Loss of the KDEL motif, an endoplasmic reticulum retention signal, and generation of many positively charged amino acids (AAs) in the mutated C-terminus are thought to be important for disease induction. To test this hypothesis, we generated mice harboring a Calr frameshift mutation using the CRISPR/Cas9 system. Deletion of 19-base pairs in exon 9 (c.1099-1117del), designated the del19 mutation, induced loss of the KDEL motif and generated many positively charged AAs, similar to human mutants. Calr del19 mice exhibited mild thrombocytosis, slightly increased megakaryocytes, and mild splenomegaly. In vitro experiments revealed that the murine CALR del19 mutant had a weaker ability to combine with murine MPL than the human CALR del52 mutant. Consequently, STAT5 activation was also very weak downstream of the murine mutant and murine MPL, and may be the reason for the mild disease severity. In summary, loss of the KDEL motif and positively charged AAs in the C-terminus of CALR is insufficient for MPL binding and ET development.

Published
2019

15. Depletion of Neoplastic CD11b Positive Cells in Jak2V617F Mutant Mice Reduced Fibrocytes in Bone Marrow and Improved Myelofibrosis

Author

Ozono, Yoshinori, primary, Shide, Kotaro, primary, Kameda, Takuro, primary, Kamiunten, Ayako, primary, Tahira, Yuki, primary, Sekine, Masaaki, primary, Akizuki, Keiichi, primary, Nakamura, Kenichi, primary, Iwakiri, Hisayoshi, primary, Hidaka, Tomonori, primary, Kubuki, Yoko, primary, Hasuike, Satoru, primary, Toyoshima, Fumiyo, primary, Sawaguchi, Akira, primary, Nagata, Kenji, primary, and Shimoda, Kazuya, primary

Published
2019
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16. The Role of Calreticulin in Normal Hematopoiesis and Neoplastic Hematopoiesis of Myeloproliferative Neoplasms

Author

Shide, Kotaro, primary, Kameda, Takuro, primary, Kamiunten, Ayako, primary, Ozono, Yoshinori, primary, Tahira, Yuki, primary, Sekine, Masaaki, primary, Ono, Masaya, primary, Yokomizo, Takako, primary, Kubota, Sho, primary, Akizuki, Keiichi, primary, Kubuki, Yoko, primary, Hidaka, Tomonori, primary, Sashida, Goro, primary, and Shimoda, Kazuya, primary

Published
2019
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17. Acute Liver Failure Due to Severe Hepatic Metastasis of Small-cell Lung Cancer Producing Adrenocorticotropic Hormone Complicating Ectopic Cushing Syndrome

Author

Kamijo, Sonoko, primary, Hasuike, Satoru, additional, Nakamura, Kenichi, additional, Takaishi, Yuuka, additional, Yamada, Yuri, additional, Ozono, Yoshinori, additional, Tsuchimochi, Mai, additional, Sueta, Mitsue, additional, Kusumoto, Kazunori, additional, Iwakiri, Hisayoshi, additional, Akaki, Mayumi, additional, Tanaka, Hiroyuki, additional, Kataoka, Hiroaki, additional, Shimoda, Kazuya, additional, and Nagata, Kenji, additional

Published
2019
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18. Haploinsufficiency of CALR Confers Hematopoietic Stem Cells (HSCs) with a Clonal Advantage over Wild-Type Cells, and, in Setting of Myeloproliferative Neoplasms, Compensates for the Functions of HSCs Impaired By the Calr Mutation

Author

Shide, Kotaro, primary, Kameda, Takuro, additional, Kamiunten, Ayako, additional, Sekine, Masaaki, additional, Ozono, Yoshinori, additional, Yokomizo, Takako, additional, Akizuki, Keiichi, additional, Tahira, Yuki, additional, Kubuki, Yoko, additional, Hidaka, Tomonori, additional, Sashida, Goro, additional, and Shimoda, Kazuya, additional

Published
2018
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19. Efficacy and safety of sofosbuvir and ledipasvir in Japanese patients aged 75 years or over with hepatitis C genotype 1

Author

Ozono, Yoshinori, primary, Nagata, Kenji, additional, Hasuike, Satoru, additional, Iwakiri, Hisayoshi, additional, Nakamura, Kenichi, additional, Tsuchimochi, Mai, additional, Yamada, Yuri, additional, Takaishi, Yuka, additional, Sueta, Mitsue, additional, Miike, Tadashi, additional, Tahara, Yoshihiro, additional, Yamamoto, Shojiro, additional, Shide, Kotaro, additional, Hidaka, Tomonori, additional, Kubuki, Yoko, additional, Kusumoto, Kazunori, additional, Ochiai, Toshimasa, additional, Kato, Junya, additional, Komada, Naoto, additional, Hirono, Shuichi, additional, Kuroki, Kazuo, additional, Shigehira, Masafumi, additional, and Shimoda, Kazuya, additional

Published
2017
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20. Prediction of Sustained Virological Response to Telaprevir/Simeprevir-Based Triple Therapy in Patients with Genotype 1 Hepatitis C Virus Using Super-Early Viral Response within 2 Weeks

Author

Ozono, Yoshinori, primary, Takaishi, Yuka, additional, Tsuchimochi, Mai, additional, Nakamura, Kenichi, additional, Abe, Hiroo, additional, Miike, Tadashi, additional, Kusumoto, Kazunori, additional, Iwakiri, Hisayoshi, additional, Sueta, Mitsue, additional, Tahara, Yoshihiro, additional, Yamamoto, Shojiro, additional, Hasuike, Satoru, additional, Nagata, Kenji, additional, and Shimoda, Kazuya, additional

Published
2017
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21. Reactivation of hepatitis B virus in a hepatitis B surface antigen-negative patient with membranous nephropathy treated with immunosuppression

Author

Ozono, Yoshinori, primary, Hasuike, Satoru, additional, Nagata, Kenji, additional, Yamada, Yuri, additional, Tsuchimochi, Mai, additional, Nakamura, Kenichi, additional, Shirado, Akemi, additional, Kusumoto, Kazunori, additional, Iwakiri, Hisayoshi, additional, Sato, Yuji, additional, Fujimoto, Syoichi, additional, Kitamura, Kazuo, additional, Samejima, Naoki, additional, and Shimoda, Kazuya, additional

Published
2013
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22. Portal Vein Thrombosis during Eltrombopag Treatment for Immune Thrombocytopenic Purpura in a Patient with Liver Cirrhosis due to Hepatitis C Viral Infection

Author

Kawano, Noriaki, primary, Hasuike, Satoru, additional, Iwakiri, Hisayoshi, additional, Nakamura, Kenichi, additional, Ozono, Yoshinori, additional, Kusumoto, Hisanori, additional, Nagata, Kenji, additional, Kikuchi, Ikuko, additional, Yoshida, Shuro, additional, Kuriyama, Takuro, additional, Yamashita, Kiyoshi, additional, Muranaka, Takahiro, additional, Kawaguchi, Takumi, additional, Sata, Michio, additional, Okamura, Takashi, additional, Ueda, Akira, additional, and Shimoda, Kazuya, additional

Published
2013
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23. Mice with Calr mutations homologous to human CALR mutations only exhibit mild thrombocytosis

Author

Shide, Kotaro, Kameda, Takuro, Kamiunten, Ayako, Oji, Asami, Ozono, Yoshinori, Sekine, Masaaki, Honda, Arata, Kitanaka, Akira, Akizuki, Keiichi, Tahira, Yuki, Nakamura, Kenichi, Hidaka, Tomonori, Kubuki, Yoko, Abe, Hiroo, Miike, Tadashi, Iwakiri, Hisayoshi, Tahara, Yoshihiro, Sueta, Mitsue, Hasuike, Satoru, Yamamoto, Shojiro, Nagata, Kenji, Ikawa, Masahito, Shimoda, Kazuya, Shide, Kotaro, Kameda, Takuro, Kamiunten, Ayako, Oji, Asami, Ozono, Yoshinori, Sekine, Masaaki, Honda, Arata, Kitanaka, Akira, Akizuki, Keiichi, Tahira, Yuki, Nakamura, Kenichi, Hidaka, Tomonori, Kubuki, Yoko, Abe, Hiroo, Miike, Tadashi, Iwakiri, Hisayoshi, Tahara, Yoshihiro, Sueta, Mitsue, Hasuike, Satoru, Yamamoto, Shojiro, Nagata, Kenji, Ikawa, Masahito, and Shimoda, Kazuya

Abstract

Calreticulin (CALR) exon 9 frameshift mutations, commonly detected in essential thrombocythemia (ET) and primary myelofibrosis patients, activate signal transducer and activator of transcription (STAT) proteins in the presence of Myeloproliferative Leukemia Virus (MPL) and induce ET in vivo. Loss of the KDEL motif, an endoplasmic reticulum retention signal, and generation of many positively charged amino acids (AAs) in the mutated C-terminus are thought to be important for disease induction. To test this hypothesis, we generated mice harboring a Calr frameshift mutation using the CRISPR/Cas9 system. Deletion of 19-base pairs in exon 9 (c.1099-1117del), designated the del19 mutation, induced loss of the KDEL motif and generated many positively charged AAs, similar to human mutants. Calr del19 mice exhibited mild thrombocytosis, slightly increased megakaryocytes, and mild splenomegaly. In vitro experiments revealed that the murine CALR del19 mutant had a weaker ability to combine with murine MPL than the human CALR del52 mutant. Consequently, STAT5 activation was also very weak downstream of the murine mutant and murine MPL, and may be the reason for the mild disease severity. In summary, loss of the KDEL motif and positively charged AAs in the C-terminus of CALR is insufficient for MPL binding and ET development., Shide, K., Kameda, T., Kamiunten, A. et al. Mice with Calr mutations homologous to human CALR mutations only exhibit mild thrombocytosis. Blood Cancer J. 9, 42 (2019). https://doi.org/10.1038/s41408-019-0202-z

24. Mice with Calr mutations homologous to human CALR mutations only exhibit mild thrombocytosis

Author

Shide, Kotaro, Kameda, Takuro, Kamiunten, Ayako, Oji, Asami, Ozono, Yoshinori, Sekine, Masaaki, Honda, Arata, Kitanaka, Akira, Akizuki, Keiichi, Tahira, Yuki, Nakamura, Kenichi, Hidaka, Tomonori, Kubuki, Yoko, Abe, Hiroo, Miike, Tadashi, Iwakiri, Hisayoshi, Tahara, Yoshihiro, Sueta, Mitsue, Hasuike, Satoru, Yamamoto, Shojiro, Nagata, Kenji, Ikawa, Masahito, Shimoda, Kazuya, Shide, Kotaro, Kameda, Takuro, Kamiunten, Ayako, Oji, Asami, Ozono, Yoshinori, Sekine, Masaaki, Honda, Arata, Kitanaka, Akira, Akizuki, Keiichi, Tahira, Yuki, Nakamura, Kenichi, Hidaka, Tomonori, Kubuki, Yoko, Abe, Hiroo, Miike, Tadashi, Iwakiri, Hisayoshi, Tahara, Yoshihiro, Sueta, Mitsue, Hasuike, Satoru, Yamamoto, Shojiro, Nagata, Kenji, Ikawa, Masahito, and Shimoda, Kazuya

Abstract

Calreticulin (CALR) exon 9 frameshift mutations, commonly detected in essential thrombocythemia (ET) and primary myelofibrosis patients, activate signal transducer and activator of transcription (STAT) proteins in the presence of Myeloproliferative Leukemia Virus (MPL) and induce ET in vivo. Loss of the KDEL motif, an endoplasmic reticulum retention signal, and generation of many positively charged amino acids (AAs) in the mutated C-terminus are thought to be important for disease induction. To test this hypothesis, we generated mice harboring a Calr frameshift mutation using the CRISPR/Cas9 system. Deletion of 19-base pairs in exon 9 (c.1099-1117del), designated the del19 mutation, induced loss of the KDEL motif and generated many positively charged AAs, similar to human mutants. Calr del19 mice exhibited mild thrombocytosis, slightly increased megakaryocytes, and mild splenomegaly. In vitro experiments revealed that the murine CALR del19 mutant had a weaker ability to combine with murine MPL than the human CALR del52 mutant. Consequently, STAT5 activation was also very weak downstream of the murine mutant and murine MPL, and may be the reason for the mild disease severity. In summary, loss of the KDEL motif and positively charged AAs in the C-terminus of CALR is insufficient for MPL binding and ET development., Shide, K., Kameda, T., Kamiunten, A. et al. Mice with Calr mutations homologous to human CALR mutations only exhibit mild thrombocytosis. Blood Cancer J. 9, 42 (2019). https://doi.org/10.1038/s41408-019-0202-z

25. Haploinsufficiency of CALRConfers Hematopoietic Stem Cells (HSCs) with a Clonal Advantage over Wild-Type Cells, and, in Setting of Myeloproliferative Neoplasms, Compensates for the Functions of HSCs Impaired By the CalrMutation

Author

Shide, Kotaro, Kameda, Takuro, Kamiunten, Ayako, Sekine, Masaaki, Ozono, Yoshinori, Yokomizo, Takako, Akizuki, Keiichi, Tahira, Yuki, Kubuki, Yoko, Hidaka, Tomonori, Sashida, Goro, and Shimoda, Kazuya

Abstract

CALRexon9 frameshift mutations function as driver mutations in essential thrombocythemia (ET) and primary myelofibrosis patients with non-mutated JAK2or MPL. The mutations augment signal transducer and activator of transcription activity in the presence of MPL, induce increased cell proliferation and growth factor independence in cell lines, and cause ET-like myeloproliferative neoplasms (MPN) in mice.

Published
2018
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26. An autopsy case of an adult woman with Rapid-Onset Obesity with Hypoventilation, Hypothalamic, Autonomic Dysregulation, and Neuroendocrine Tumors (ROHHAD(NET)) syndrome developing nonalcoholic steatohepatitis and hepatocellular carcinoma: A case report.

Author

Hasuike S, Ozono Y, Uchida K, Ogawa S, Tamura H, Uchiyama N, Hatada H, Komaki Y, Nakamura K, Iwakiri H, Sueta M, Nagata K, Nishimura T, Matsuyama M, Sawada H, Oguri T, Sato Y, and Kawakami H

Subjects
Humans, Female, Obesity complications, Neuroendocrine Tumors complications, Neuroendocrine Tumors pathology, Neuroendocrine Tumors therapy, Fatal Outcome, Young Adult, Autonomic Nervous System Diseases etiology, Syndrome, Liver Neoplasms pathology, Liver Neoplasms complications, Liver Neoplasms therapy, Carcinoma, Hepatocellular pathology, Carcinoma, Hepatocellular complications, Carcinoma, Hepatocellular therapy, Hypoventilation etiology, Hypoventilation complications, Non-alcoholic Fatty Liver Disease complications, Non-alcoholic Fatty Liver Disease pathology, Autopsy, Hypothalamic Diseases complications, Hypothalamic Diseases diagnosis
Abstract

Background: Nonalcoholic steatohepatitis (NASH) is an important etiology of hepatocellular carcinoma (HCC), and there is no established therapy for this syndrome. Rapid-onset obesity with hypothalamic dysfunction, hypoventilation, autonomic dysregulation, and neural crest tumor (ROHHAD(NET)) is an extremely rare syndrome considered to be life-threatening, with death occurring around 10 years of age. We present the oldest known autopsy case of this syndrome that developed HCC. This case provided important information on not only improving the course of this syndrome, but also understanding the natural history and therapeutic modalities of NASH and HCC., Methods: The patient was diagnosed with ROHHAD(NET) syndrome in childhood, and liver cirrhosis due to NASH was diagnosed at age 17. HCC was detected at age 20, and embolization and irradiation were performed. At age 21, she died from accidental acute pancreatitis and subsequent liver failure and pulmonary hemorrhage., Results: Rapid onset of obesity, hypoventilation, and hypothalamic disturbance appeared in childhood and was diagnosed as this syndrome. At age 17, liver cirrhosis due to NASH was diagnosed by liver biopsy, and at age 20, HCC was diagnosed by imaging. Transarterial chemoembolization and irradiation were performed, and the HCC was well controlled for a year., Conclusion: At age 21, she died from accidental acute pancreatitis, subsequent liver failure and pulmonary hemorrhage. Autopsy revealed that the HCC was mostly necrotized. This case was valuable not only for other ROHHAD(NET) syndrome cases, but also in improving our understanding of the natural history of NASH and HCC., Competing Interests: The authors have no funding and conflicts of interest to disclose., (Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.)

Published
2024
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27. [A case of invasive liver abscess syndrome caused by Klebsiella pneumoniae causing endophthalmitis-induced blindness].

Author

Tamura H, Ozono Y, Uchiyama N, Hatada H, Nakamura K, Iwakiri H, Hasuike S, Nagata K, and Kawakami H

Subjects
Female, Humans, Aged, 80 and over, Klebsiella pneumoniae, Blindness, Endophthalmitis drug therapy, Endophthalmitis etiology, Liver Abscess complications, Liver Abscess diagnostic imaging
Abstract

An 82-year-old female patient was admitted to our hospital for visual acuity loss in both eyes. The patient was diagnosed with invasive liver abscess syndrome and bilateral endophthalmitis due to Klebsiella pneumoniae 4 days after the onset of ocular symptoms. The liver abscess improved by broad-spectrum antibiotics and intravitreal injection, but bilateral blindness occurred. Most literature reported fever as the first symptom of invasive abscess syndrome, but this case had no fever at the onset of ocular symptoms. Delayed invasive liver abscess syndrome diagnosis might cause poor visual acuity prognosis.

Published
2023
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28. Hematochezia Due to Panitumumab-induced Colitis with Vitamin K Deficiency.

Author

Tamura H, Nakashima K, Uchiyama N, Ogawa S, Hatada H, Yoshida N, Uchida K, Ozono Y, Tanaka H, Yamamto K, and Kawakami H

Subjects
Antibodies, Monoclonal adverse effects, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Gastrointestinal Hemorrhage etiology, Humans, Male, Middle Aged, Mutation, Neoplasm Recurrence, Local drug therapy, Panitumumab adverse effects, Proto-Oncogene Proteins p21(ras) metabolism, Antineoplastic Agents adverse effects, Colitis drug therapy, Colorectal Neoplasms drug therapy, Short Bowel Syndrome drug therapy, Vitamin K Deficiency chemically induced, Vitamin K Deficiency drug therapy
Abstract

Panitumumab, a fully human anti-epidermal growth factor receptor (EGFR) monoclonal antibody, has been shown to be useful in treating either advanced or recurrent KRAS/NRAS/BRAF wild-type colorectal cancer. We herein report the case of a 60-year-old man with short bowel syndrome who developed hematochezia due to panitumumab-induced colitis with vitamin K deficiency during third-line chemotherapy. The cause of vitamin K deficiency was the lack of intravenous vitamin K supplementation following a change from central venous nutrition to peripheral venous nutrition. We advise clinicians to carefully check for colitis and manage the infusions of chemotherapy patients with short bowel syndrome.

Published
2022
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