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vol. 58
Letter to the Editor

Liver involvement in polymyalgia rheumatica and giant cell arteritis

Elvis Hysa
Alberto Castagna
Ciro Manzo

Research Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, San Martino Policlinic Hospital, Genoa, Italy
Azienda Sanitaria Provinciale Catanzaro, Geriatric Medicine Department, Fragility Outpatient Clinic, Casa della Salute di Chiaravalle Centrale, Catanzaro, Italy
Internal and Geriatric Medicine Department, Azienda Sanitaria Locale Napoli 3 sud, Rheumatologic Outpatient Clinic Hospital “Mariano Lauro”, Sant’Agnello, Naples, Italy
Reumatologia 2020; 58, 6: 444–445
Online publish date: 2020/12/23
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JabRef, Mendeley
Papers, Reference Manager, RefWorks, Zotero
Dear Editor,
We read with great interest the review paper entitled “Liver involvement in rheumatic diseases” [1]. In this letter, our aim is to add a brief focus about the hepatic manifestations related to polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) according to the evidences of literature. Polymyalgia rheumatica is estimated to be one of the most common inflammatory rheumatic diseases affecting older adults [2]. At least 10–16% of PMR patients have also manifestations of GCA, whereas 40–60% of GCA patients have also manifestations of PMR. Glucocorticosteroids (GCs) are the cornerstone of their treatment [3].
Liver involvement is a recognized association in PMR and GCA, but it has not been commonly reported in published literature. Multiple studies have reported an increase of serum alkaline phosphatase (AP), with a confirm of the hepatic isoenzyme, in about 30–60% of newly diagnosed PMR and GCA patients [4–6]. Less frequent is a cytolytic pattern with elevation of alanine (ALT) and aspartate (AST) transaminases without raised ALP and gamma-glutamyltranspeptidase (gGT) – it occurred in 18% of PMR patients [6].
Other causes of liver dysfunction such as alcoholism, exposure to drugs and hepatotoxic agents, viral hepatitis were excluded for these subjects. Besides, liver enzymes correlated with systemic symptoms and with higher values of the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) concentrations. In most cases, they normalized after GCs therapy and increased during disease relapses. A limited number of biopsies have been performed in these patients documenting different histological pictures from a normal liver architecture to fatty infiltration of hepatocytes, widening of bile canali-culi, immune infiltrates of lymphocytes and plasma cells in the peri-sinusoidal spaces and, more rarely, granulomatous lesions or vasculitis in the hepatic artery and in portal-tract arteries [7]. Interestingly, these alterations reversed with GCs treatment. It has been also speculated whether liver damage could have immune-mediated origins. In fact, some authors observed an increase of anti-mitochondrial autoantibodies (AMA) in up to 30% of PMR patients. However, no correlation was detected between AMA titers and inflammatory indexes, clinical state or biopsy specimens [8]. It would be interesting to understand if PMR/GCA patients are more likely to develop a primary biliary cholangitis (PBC) compared with general...

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