Arthritis Prediction of Advanced Hepatic Fibrosis in HFE Hemochromatosis |
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Institution: | 1. Department of Gastroenterology and Hepatology, Fiona Stanley Fremantle Hospital Group, Murdoch, Western Australia, Australia;2. Faculty of Medicine, The University of Queensland, Herston, Brisbane, Queensland, Australia;3. Hepatic Fibrosis Group, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia;4. School of Medical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australia;1. Division of Cardiovascular Medicine, University of Toledo Medical Center, Toledo, OH;2. Division of Medicine, Forrest General Hospital, Hattiesburg, MS;3. Department of Cardiology, Reading Hospital–Tower Health System, West Reading, PA;4. Section of Cardiology, Baylor College of Medicine, Houston, TX;1. Stanford Children’s Health, Stanford, CA, USA;2. Stanford University School of Medicine, Stanford, CA, USA;3. Vanderbilt Center for Patient and Professional Advocacy, Vanderbilt University Medical Center, Nashville, TN, USA;4. Tribeca Companies, San Francisco, CA, USA;1. Keele Cardiovascular Research Group, School of Medicine, Keele University, Stoke-on-Trent, UK;2. Department of Cardiology, Royal Stoke University Hospital, Stoke-on-Trent, UK;3. Population Health Research Institute, Hamilton, Ontario, Canada;4. Department of Medicine and Department of Health Research, Evidence, and Impact, McMaster University, Hamilton, Ontario, Canada;5. Division of Cardiology, William Beaumont Hospital, Royal Oak, MI, USA;6. Division of Cardiology, Department of Medicine, Loma Linda University Health, Loma Linda, CA, USA;7. Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, MD, USA;8. Deborah Heart and Lung Center, Browns Mill, NJ, USA;9. Division of Cardiology, Rush Medical College, Rush University, Chicago, IL, USA;10. Department of Medicine, Thomas Jefferson University, Philadelphia, PA, USA;1. Department of Medicine, Albert Einstein Medical Center, Philadelphia, PA, USA;2. Division of Cardiology, Henry Ford Hospital, Detroit, MI, USA;3. Section of Cardiology, Baylor College of Medicine, Houston, TX, USA;4. Department of Medicine, Ascension Macomb-Oakland Hospital, Warren, MI, USA;5. Division of Cardiology, Massachusetts General Hospital, Boston, MA, USA;6. Division of Cardiology, University of Arizona-College of Medicine, Phoenix, AZ, USA;7. Division of Cardiovascular Medicine, Gill Heart Institute, University of Kentucky, Lexington, KY, USA |
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Abstract: | ObjectiveTo evaluate whether arthritis predicts the likelihood of advanced hepatic fibrosis in HFE hemochromatosis.Patients and MethodsWe conducted a retrospective, cross-sectional analysis of 112 well-characterized patients with HFE hemochromatosis and liver biopsy–validated fibrosis staging recruited between January 1, 1983, and December 31, 2013. Complete clinical, biochemical, hematologic, and noninvasive serum biochemical indices (aspartate aminotransferase to platelet ratio index APRI] and fibrosis 4 index FIB4]) were available. Scheuer fibrosis stages 3 and 4, APRI greater than 0.44, or FIB4 greater than 1.1 were used to define advanced hepatic fibrosis. Comparisons between groups were performed using categorical analysis, unpaired or paired t test.ResultsMale (n=76) and female (n=36) patients were similar in age. Nineteen patients had advanced hepatic fibrosis, and 47 had hemochromatosis arthritis. Arthritis was significantly associated with the presence of advanced hepatic fibrosis as determined by liver biopsy (sensitivity, 84%, 95% CI, 62% to 95%]; negative predictive value, 95% 95% CI, 87% to 99%]; relative risk, 7.4 95% CI, 2.5 to 23]; P<.001), APRI (sensitivity, 75% 95% CI, 55% to 88%]; negative predictive value, 91% 95% CI, 81% to 96%]; relative risk, 4.5 95% CI, 2.0 to 10.2]; P<.001), or FIB4 (sensitivity, 61% 95% CI, 41% to 78%]; negative predictive value, 67% 95% CI, 68% to 90%]; relative risk, 2.2 95% CI, 1.1 to 4.6]; P=.03). Mean cell volume values were significantly higher pretreatment in patients with F3-4 fibrosis (96.7±1.1 fL) compared with F0-2 fibrosis (93.4±0.5 fL; P=.004) and declined following treatment (F3-4, 93.2±0.9 fL, P=.01; F0-2, 91.7±0.6 fL, P=.01).ConclusionAdvanced hepatic fibrosis is strongly associated with arthritis in HFE hemochromatosis. The absence of arthritis predicts a low likelihood of advanced hepatic fibrosis, supporting its use as a clinical marker for advanced hepatic fibrosis in HFE hemochromatosis. |
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Keywords: | APRI"} {"#name":"keyword" "$":{"id":"kwrd0015"} "$$":[{"#name":"text" "_":"aspartate aminotransferase to platelet ratio index FIB4"} {"#name":"keyword" "$":{"id":"kwrd0025"} "$$":[{"#name":"text" "_":"fibrosis 4 index HH"} {"#name":"keyword" "$":{"id":"kwrd0035"} "$$":[{"#name":"text" "$$":[{"#name":"italic" "_":"HFE"} {"#name":"__text__" "_":" hemochromatosis HIC"} {"#name":"keyword" "$":{"id":"kwrd0045"} "$$":[{"#name":"text" "_":"hepatic iron concentration MCV"} {"#name":"keyword" "$":{"id":"kwrd0055"} "$$":[{"#name":"text" "_":"mean cell volume NPV"} {"#name":"keyword" "$":{"id":"kwrd0065"} "$$":[{"#name":"text" "_":"negative predictive value PPV"} {"#name":"keyword" "$":{"id":"kwrd0075"} "$$":[{"#name":"text" "_":"positive predictive value SENS"} {"#name":"keyword" "$":{"id":"kwrd0085"} "$$":[{"#name":"text" "_":"sensitivity SPEC"} {"#name":"keyword" "$":{"id":"kwrd0095"} "$$":[{"#name":"text" "_":"specificity |
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