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      Nonalcoholic fatty liver disease with prolactin-secreting pituitary adenoma in an adolescent : A case report

      , MD, , MD, PhD , , MD, PhD, , MD, , MD, PhD, , MD, PhD


      Wolters Kluwer Health

      amenorrhea, cabergoline, children, nonalcoholic fatty liver disease, prolactinoma

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          Nonalcoholic fatty liver disease (NAFLD), among the commonest chronic liver disorders in children and adolescents, is considered a reflection of the current obesity epidemic in children and adults. This liver disease has been linked with various metabolic disorders, but not with prolactinoma (PRLoma).

          Patient concerns:

          A 13-year-old Japanese girl manifested obesity, serum transaminase and γ-glutamyltransferase elevations, and amenorrhea. Abdominal ultrasonography showed fatty liver. Her serum prolactin concentration was elevated, and cranial magnetic resonance imaging showed a pituitary mass consistent with macroadenoma.


          NAFLD and PRLoma.

          Interventions and outcomes:

          After the patient's NAFLD failed to respond to diet and exercise, cabergoline treatment of the PRLoma decreased body weight, serum transaminase and γ-glutamyltransferase elevations, and ultrasonographic fatty liver grade as the tumor became smaller.


          Physicians should consider the possibility of PRLoma when diet and exercise fail to improve fatty liver disease in a patient with endocrine symptoms such as amenorrhea.

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          Most cited references 14

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          Global epidemiology of nonalcoholic fatty liver disease-Meta-analytic assessment of prevalence, incidence, and outcomes.

          Nonalcoholic fatty liver disease (NAFLD) is a major cause of liver disease worldwide. We estimated the global prevalence, incidence, progression, and outcomes of NAFLD and nonalcoholic steatohepatitis (NASH). PubMed/MEDLINE were searched from 1989 to 2015 for terms involving epidemiology and progression of NAFLD. Exclusions included selected groups (studies that exclusively enrolled morbidly obese or diabetics or pediatric) and no data on alcohol consumption or other liver diseases. Incidence of hepatocellular carcinoma (HCC), cirrhosis, overall mortality, and liver-related mortality were determined. NASH required histological diagnosis. All studies were reviewed by three independent investigators. Analysis was stratified by region, diagnostic technique, biopsy indication, and study population. We used random-effects models to provide point estimates (95% confidence interval [CI]) of prevalence, incidence, mortality and incidence rate ratios, and metaregression with subgroup analysis to account for heterogeneity. Of 729 studies, 86 were included with a sample size of 8,515,431 from 22 countries. Global prevalence of NAFLD is 25.24% (95% CI: 22.10-28.65) with highest prevalence in the Middle East and South America and lowest in Africa. Metabolic comorbidities associated with NAFLD included obesity (51.34%; 95% CI: 41.38-61.20), type 2 diabetes (22.51%; 95% CI: 17.92-27.89), hyperlipidemia (69.16%; 95% CI: 49.91-83.46%), hypertension (39.34%; 95% CI: 33.15-45.88), and metabolic syndrome (42.54%; 95% CI: 30.06-56.05). Fibrosis progression proportion, and mean annual rate of progression in NASH were 40.76% (95% CI: 34.69-47.13) and 0.09 (95% CI: 0.06-0.12). HCC incidence among NAFLD patients was 0.44 per 1,000 person-years (range, 0.29-0.66). Liver-specific mortality and overall mortality among NAFLD and NASH were 0.77 per 1,000 (range, 0.33-1.77) and 11.77 per 1,000 person-years (range, 7.10-19.53) and 15.44 per 1,000 (range, 11.72-20.34) and 25.56 per 1,000 person-years (range, 6.29-103.80). Incidence risk ratios for liver-specific and overall mortality for NAFLD were 1.94 (range, 1.28-2.92) and 1.05 (range, 0.70-1.56).
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            The diagnosis and management of non-alcoholic fatty liver disease: practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association.

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              The utility of radiological imaging in nonalcoholic fatty liver disease.

              This prospective study evaluates the role of radiological modalities in establishing the diagnosis of nonalcoholic steatohepatitis (NASH). Consecutive patients with biopsy-proven nonalcoholic fatty liver disease (NAFLD) were enrolled (2000-2001). Patients with other liver diseases and significant alcohol consumption (>20 g/day) were excluded. Clinicodemographic data were gathered at the time of liver biopsy. Each biopsy specimen was assessed by a hepatopathologist. Each patient underwent a limited abdominal ultrasonography (US), computerized tomography (CT), and magnetic resonance imaging (MRI). Films were interpreted by a radiologist who used a predetermined radiological protocol. Each radiological study was reread by the same radiologist and a second radiologist. Patients with NASH had greater aspartate aminotransferase levels (P = 0.03), greater ferritin levels (P = 0.05), more hepatocyte ballooning (P 33% fat on liver biopsy was optimal for detecting steatosis on radiological imaging. Differences between NASH and nonprogressive NAFLD were not apparent with any radiological modality. Of the pathologic features important for establishing the diagnosis of NASH, only the severity of steatosis was reflected in these radiological modalities. Good intraobserver agreement was evident for each modality (US, CT, and MRI) that was superior to interobserver agreement.

                Author and article information

                Department of Pediatrics and Child Health, Kurume University School of Medicine, Kurume, Japan.
                Author notes
                []Correspondence: Tatsuki Mizuochi, Department of Pediatrics and Child Health, Kurume University School of Medicine, 67 Asahi-machi, Kurume 830-0011, Japan (e-mail: mizuochi_tatsuki@ )
                Medicine (Baltimore)
                Medicine (Baltimore)
                Wolters Kluwer Health
                October 2018
                19 October 2018
                : 97
                : 42
                30335007 6211884 MD-D-18-04303 10.1097/MD.0000000000012879 12879
                Copyright © 2018 the Author(s). Published by Wolters Kluwer Health, Inc.

                This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial License 4.0 (CCBY-NC), where it is permissible to download, share, remix, transform, and buildup the work provided it is properly cited. The work cannot be used commercially without permission from the journal.

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