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      Rheumatoid Arthritis, Kartagener's Syndrome, and Hyperprolactinemia: Who Started It?

      case-report
      Author(s): * ,
      Publication date (Electronic):
      Journal: Case Reports in Rheumatology
      Publisher: Hindawi Publishing Corporation

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          Abstract

          We report a case of an 18-year-old girl who presented to our hospital with history of recurrent respiratory infections, amenorrhea, and symmetric polyarthritis. She was diagnosed with rheumatoid arthritis (RA), Kartagener's syndrome (KS), and hyperprolactinemia. There have been very few case reports in the literature of RA occurring in the setting of KS, theoretically proposed to be due to chronic stimulation of the immune system by recurrent infections. Furthermore, hyperprolactinemia has been hypothesized to mirror RA disease activity and case reports of treatment with dopamine agonists have led to the speculation of whether or not they represent a new line of experimental treatment in the future. Our patient was found to have both KS and hyperprolactinemia together in the setting of RA, and based on our literature search, this is the first reported case of such a combination. This strikes a very intriguing question: are these three conditions interlinked by a yet to be defined association? And treatment of which condition leads to the resolution of the other?

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          Prolactin promotes cartilage survival and attenuates inflammation in inflammatory arthritis.

          I Perales, Carmen Clapp, Isabel Méndez … (2013)
          Chondrocytes are the only cells in cartilage, and their death by apoptosis contributes to cartilage loss in inflammatory joint diseases, such as rheumatoid arthritis (RA). A putative therapeutic intervention for RA is the inhibition of apoptosis-mediated cartilage degradation. The hormone prolactin (PRL) frequently increases in the circulation of patients with RA, but the role of hyperprolactinemia in disease activity is unclear. Here, we demonstrate that PRL inhibits the apoptosis of cultured chondrocytes in response to a mixture of proinflammatory cytokines (TNF-α, IL-1β, and IFN-γ) by preventing the induction of p53 and decreasing the BAX/BCL-2 ratio through a NO-independent, JAK2/STAT3-dependent pathway. Local treatment with PRL or increasing PRL circulating levels also prevented chondrocyte apoptosis evoked by injecting cytokines into the knee joints of rats, whereas the proapoptotic effect of cytokines was enhanced in PRL receptor-null (Prlr(-/-)) mice. Moreover, eliciting hyperprolactinemia in rats before or after inducing the adjuvant model of inflammatory arthritis reduced chondrocyte apoptosis, proinflammatory cytokine expression, pannus formation, bone erosion, joint swelling, and pain. These results reveal the protective effect of PRL against inflammation-induced chondrocyte apoptosis and the therapeutic potential of hyperprolactinemia to reduce permanent joint damage and inflammation in RA.
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            The role of Toll-like receptor signalling in the pathogenesis of arthritis.

            Fabia Brentano, Steffen Gay, Renate Gay … (2005)
            Recent evidence highlighted the role of Toll-like receptors (TLRs) as key recognition structures of the innate immune system. The activation of TLRs initiates the production of inflammatory cytokines, chemokines, tissue destructive enzymes, and type I interferons. In addition, TLR signalling plays an important role in the activation and direction of the adaptive immune system by the upregulation of costimulatory molecules of antigen presenting cells. Considering the important role of TLR signalling as a critical link between innate and adaptive immunity it has been proposed that a dysregulation in TLR signalling might be associated with autoimmunity. In this review, recent studies on TLR signal transduction pathways activated by corresponding ligands are summarized and evidence for a possible role of TLR signalling in the pathogenesis of rheumatoid arthritis is discussed.
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              Rheumatoid arthritis.

              June Spector (1990)
              RA is a common disease with a worldwide prevalence of about 1% with an annual incidence of about 3/10,000 adults. It is two to three times more common in women. There is some evidence that over the last few decades the disease is declining in incidence or severity. Patients with RA have a reduced life expectancy and a one in three chance of becoming disabled, depending on the severity of the disease at onset. The cause of the disease is unknown, although genetic factors account for up to 30% of disease susceptibility. The most important genetic factors are related to HLA-DR4 and DR1, which may have identical regions conferring the risk of disease. Many infectious agents have also been implicated in the etiology of RA, although there is no good epidemiologic evidence to support the laboratory findings. Hormonal and reproductive factors are known to play a major role in disease pathogenesis. Both pregnancy and the oral contraceptive pill are believed to be protective against development of the disease, although they may act by delaying or modifying the course of the disease rather than conferring "immunity".
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                Author and article information

                Journal
                Journal ID (nlm-ta): Case Rep Rheumatol
                Journal ID (iso-abbrev): Case Rep Rheumatol
                Journal ID (publisher-id): CRIRH
                Title: Case Reports in Rheumatology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-6889
                ISSN (Electronic): 2090-6897
                Publication date (Print): 2016
                Publication date (Electronic): 20 January 2016
                Volume: 2016
                Electronic Location Identifier: 7367232
                Affiliations
                King Faisal Specialist Hospital & Research Center, P.O. Box 40047, Jeddah 21499, Saudi Arabia
                Author notes

                Academic Editor: Shigeko Inokuma

                Author information
                http://orcid.org/0000-0003-2879-2890
                Article
                DOI: 10.1155/2016/7367232
                PMC ID: 4745912
                PubMed ID: 26904347
                SO-VID: ce669151-a768-46c0-a505-8663d5c6b9d3
                Copyright © Copyright © 2016 H. Halabi and I. Mulla.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 24 October 2015
                Date accepted : 3 January 2016
                Categories
                Subject: Case Report

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