Osamu Arisaka, Satomi Koyama, George Imataka, Junko Naganuma, Takahiro Arisaka, Sei Akatsuka
{"title":"意外发现一名 47 岁男子因肝硬化引发食管静脉曲张,他在童年时曾接受生长激素治疗。","authors":"Osamu Arisaka, Satomi Koyama, George Imataka, Junko Naganuma, Takahiro Arisaka, Sei Akatsuka","doi":"10.3390/diseases12100251","DOIUrl":null,"url":null,"abstract":"<p><p><i>Background:</i> We report a rare case highlighting the progression of liver disease in a male patient with idiopathic childhood-onset growth hormone (GH) deficiency. <i>Case presentation:</i> The patient was diagnosed with hypopituitarism at six years old and was treated with thyroxine therapy and GH for his short stature, with testosterone added at the age of 15. GH therapy was discontinued when the patient was 18 years old, but thyroid and testosterone treatments continued. The patient had been taking medication for hyperlipidemia until the age of 30 and was noted to have impaired glucose tolerance at the age of 40, but HbA1c levels remained normal. At the age of 47, esophageal varices were incidentally discovered via endoscopy, revealing liver cirrhosis. Laboratory tests showed liver dysfunction and abnormal lipid levels, and hepatitis viral markers were absent. The patient had no history of drinking alcohol or smoking, and no family history of diabetes. <i>Results:</i> Ultimately, this case demonstrates that metabolic dysfunction-associated steatotic liver disease (MASLD/metabolic dysfunction-associated steatohepatitis (MASH)) is under-recognized in GH deficiency cases and can progress to liver cirrhosis. <i>Conclusions:</i> Therefore, careful evaluation of MASLD/MASH in childhood-onset GH deficiency is necessary, and GH replacement therapy should continue into adulthood, if possible.</p>","PeriodicalId":72832,"journal":{"name":"Diseases (Basel, Switzerland)","volume":null,"pages":null},"PeriodicalIF":2.9000,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11507581/pdf/","citationCount":"0","resultStr":"{\"title\":\"The Unexpected Detection of Esophageal Varices Caused by Liver Cirrhosis in a 47-Year-Old Man Treated with a Growth Hormone in Childhood.\",\"authors\":\"Osamu Arisaka, Satomi Koyama, George Imataka, Junko Naganuma, Takahiro Arisaka, Sei Akatsuka\",\"doi\":\"10.3390/diseases12100251\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p><i>Background:</i> We report a rare case highlighting the progression of liver disease in a male patient with idiopathic childhood-onset growth hormone (GH) deficiency. <i>Case presentation:</i> The patient was diagnosed with hypopituitarism at six years old and was treated with thyroxine therapy and GH for his short stature, with testosterone added at the age of 15. GH therapy was discontinued when the patient was 18 years old, but thyroid and testosterone treatments continued. The patient had been taking medication for hyperlipidemia until the age of 30 and was noted to have impaired glucose tolerance at the age of 40, but HbA1c levels remained normal. At the age of 47, esophageal varices were incidentally discovered via endoscopy, revealing liver cirrhosis. Laboratory tests showed liver dysfunction and abnormal lipid levels, and hepatitis viral markers were absent. The patient had no history of drinking alcohol or smoking, and no family history of diabetes. <i>Results:</i> Ultimately, this case demonstrates that metabolic dysfunction-associated steatotic liver disease (MASLD/metabolic dysfunction-associated steatohepatitis (MASH)) is under-recognized in GH deficiency cases and can progress to liver cirrhosis. <i>Conclusions:</i> Therefore, careful evaluation of MASLD/MASH in childhood-onset GH deficiency is necessary, and GH replacement therapy should continue into adulthood, if possible.</p>\",\"PeriodicalId\":72832,\"journal\":{\"name\":\"Diseases (Basel, Switzerland)\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2024-10-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11507581/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Diseases (Basel, Switzerland)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3390/diseases12100251\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Diseases (Basel, Switzerland)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3390/diseases12100251","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
The Unexpected Detection of Esophageal Varices Caused by Liver Cirrhosis in a 47-Year-Old Man Treated with a Growth Hormone in Childhood.
Background: We report a rare case highlighting the progression of liver disease in a male patient with idiopathic childhood-onset growth hormone (GH) deficiency. Case presentation: The patient was diagnosed with hypopituitarism at six years old and was treated with thyroxine therapy and GH for his short stature, with testosterone added at the age of 15. GH therapy was discontinued when the patient was 18 years old, but thyroid and testosterone treatments continued. The patient had been taking medication for hyperlipidemia until the age of 30 and was noted to have impaired glucose tolerance at the age of 40, but HbA1c levels remained normal. At the age of 47, esophageal varices were incidentally discovered via endoscopy, revealing liver cirrhosis. Laboratory tests showed liver dysfunction and abnormal lipid levels, and hepatitis viral markers were absent. The patient had no history of drinking alcohol or smoking, and no family history of diabetes. Results: Ultimately, this case demonstrates that metabolic dysfunction-associated steatotic liver disease (MASLD/metabolic dysfunction-associated steatohepatitis (MASH)) is under-recognized in GH deficiency cases and can progress to liver cirrhosis. Conclusions: Therefore, careful evaluation of MASLD/MASH in childhood-onset GH deficiency is necessary, and GH replacement therapy should continue into adulthood, if possible.