Mariusz Puszczewicz

Role of anti-citrullinated protein antibodies in diagnosis and prognosis of rheumatoid arthritis.

Antibodies to citrullinated proteins/peptides (ACPAs) are the second serological marker to have recently been included in the 2010 ACR/EULAR Rheumatoid Arthritis (RA) Classification Criteria, which are focused on early diagnosis and therapy. This review discusses their history and some clinical aspects of ACPAs, focusing on the diagnostic utility of anti-cyclic citrullinated peptide (anti-CCP) antibodies as a marker of RA as compared to the widely used rheumatoid factor (RF). Simultaneously, this review aims to raise physician awareness and interest in anti-citrullinated vimentin antibody (anti-Sa/anti-MCV), another member of the ACPA family, which appears to have a better predictive value as a marker of RA than anti-CCP or RF and correlates closely with disease activity and therapeutic response among patients with RA.

Oxidative Damage and Antioxidative Therapy in Systemic Sclerosis

Systemic sclerosis (SSc) is an autoimmune connective tissue disorder of unknown etiology. This disease is characterized by a large variety of clinical patterns, which include the fibrosis of skin and visceral organs causing a variety of clinical manifestations. Genetic and environmental factors participate in the etiology of this disease; however, recently many studies underline the oxidative background influencing the course and complications of this disease. Reactive oxygen species (ROS) synthesized in SSc can mediate extra- and intracellular oxidative processes affecting endothelial cells and fibroblasts. The estimation of prooxidative markers in the pathogenesis of SSc can enable the identification of useful markers for disease activity and, thus, may help in planning appropriate therapy focusing on the fibrotic or vascular pattern. Recently, many attempts have been made to find antioxidative molecules (nutritional and pharmacological) reducing the prooxidant state in a variety of cells—mainly in endothelium and proliferating fibroblasts. This paper presents both the background of oxidative stress processes in systemic sclerosis mediated by different mechanisms and the evidence suggesting which of the dietary and pharmacological antioxidants can be used as therapeutic targets for this disease.

Quantitative assessment of oral mucosa and labial minor salivary glands in patients with Sjögren’s syndrome using swept source OCT

Three-dimensional imaging of the mucosa of the lower lip and labial minor salivary glands is demonstrated in vivo using swept source optical coherence tomography (OCT) system at 1310 nm with modified interface. Volumetric data sets of the inner surface of the lower lip covering ~230 mm(2) field are obtained from patients with Sjögrens syndrome and a control group. OCT enables high-resolution visualization of mucosal architecture using cross-sectional images as well as en-face projection images. Comprehensive morphometry of the labial minor salivary glands is performed, and statistical significance is assessed. Statistically significant differences in morphometric parameters are found when subgroups of patients with Sjögrens syndrome are analyzed.

Co-present rheumatoid arthritis and gout successfully treated with abatacept

Dear Editor, We have read with much interest the article by Kuo et al., ‘Rare co-present rheumatoid arthritis and gout: comparison with pure rheumatoid arthritis and literature review’ [1], presenting eight new cases of concomitant rheumatoid arthritis and gout and summarizing 32 reported cases. The authors noticed that over 85% of co-present patients experienced at least one acute gout attack after continuous disease modifying antirheumatic drugs (DMARDs) and nonsteroidal anti-inflammatory drugs administration, while only one patient became totally quiescent after etanercept therapy. It is similar to our observation of a 45-year-old patient with gout and rheumatoid arthritis successfully treated with abatacept. He was admitted to our department in 2001 because of a 12-year experience of recurrent arthritis, associated with erythema, warmth, and swelling. Likemost co-present patients, he had more comorbidities [1–3], i.e., hypertension, glucose intolerance, but, interestingly, no kidney dysfunction. Laboratory tests revealed erythrocyte sedimentation rate (ESR) of 37 mm/h, C-reactive protein (CRP) of 5 mg/L, uric acid (UA) of 0.49 mmol/L, and rheumatoid factor (RF) of 1:40. There were no significant changes in X-rays of his hands and feet. While the diagnosis of gout was confirmed by the presence of monosodium urate crystals on polarized light microscopy (synovial fluid aspirated from left knee), oral colchicine and allopurinol were introduced with improvement. He was readmitted to our department in 2006 due to a 6-month history of persistent pain and swelling of joints of hands and feet, exudation in left knee, and morning stiffness lasting over 2 h. In laboratory tests, ESR revealed 72 mm/h, CRP 58.7 mg/L, UA 0.2 mmol/L, RF 1:80, and anticyclic citrullinated peptide antibodies 136 IU. In synovial fluid aspirated from left knee, not only monosodium urate crystals were found but also rheumatoid factor (1:40), which was previously negative. X-rays of feet revealed symmetrical erosive changes typical for RA with no changes in X-rays of hands and narrowing of left knee joint space. DAS28 score was 6.14. Oral methylprednisolone 6 mg was administered, and the patient was introduced to the program of abatacept therapy for early RA. He had obtained several courses of abatacapt from April 2006 to March 2008. Since the abatacept administration, no further gout attacks were observed, and DAS28 score decreased to 1.86. Both, the patient described by Kuo et al. and our patient, responded very well to biologics, etanercept and abatacept, respectively, with no gout attacks after the introduction of therapy. They were both younger than ‘average’ co-present patients and did not respond well to DMARDs (in 2001, before gout was diagnosed, our patient obtained 6 months MTX therapy, but without any improvement). This might suggest that the introduction of biologics in co-present patients may not only inhibit RA activity but also decrease the frequency of gout attacks.

Rheumatic diseases induced by drugs and environmental factors: the state-of-the-art – part one

The majority of rheumatic diseases belong to the group of autoimmune diseases and are associated with autoantibody production. Their etiology is not fully understood. Certain medications and environmental factors may have an influence on the occurrence of rheumatic diseases. Establishing a cause-effect relationship between a certain factor and disease induction is not always simple. It is important to administer the drug continuously or monitor exposure to a given factor in the period preceding the onset of symptoms. The lack of previously diagnosed autoimmune disease, or finally the lack of symptoms within a few weeks/months after discontinuation of the drug/cessation of exposure, is also important. The most frequently mentioned rheumatic diseases caused by drugs and environmental factors include systemic lupus erythematosus, scleroderma, systemic vasculitis, polymyositis, dermatomyositis, and Sjögrens syndrome. The objective of this study is to summarize current knowledge on rheumatic diseases induced by drugs and environmental factors.

Diagnostic value of the anti-Sa antibody compared with the anti-cyclic citrullinated peptide antibody in rheumatoid arthritis.

To evaluate the prevalence and diagnostic significance of the autoantibody against citrullinated vimentin (anti‐Sa) compared with the widely used anti‐cyclic citrullinated peptide autoantibody (anti‐CCP) in patients with rheumatoid arthritis (RA).

Botulinum toxin A in the treatment of Raynaud’s phenomenon: a systematic review

Introduction The management of Raynauds phenomenon in its most severe form is challenging, and current medical and surgical treatment methods frequently do not lead to optimal symptom control and prevention of ischemic complications. The aim of the study was to critically evaluate all existing evidence on the use of botulinum toxin A in the management of Raynauds phenomenon. Material and methods We adopted the PRISMA methodology and searched Cochrane Library, MEDLINE, SCOPUS, EULAR and ACR congresses abstract archives for Raynaud* AND botulinum toxin OR onabotulinum. All studies that contained reports of botulinum toxin A use and its outcome in Raynauds phenomenon were included in the review. Results Eleven studies met our inclusion criteria and involved a total of 125 patients. Two reviewers extracted data from the studies under review and achieved a consensus in their selection. The main outcomes measured were pain reduction and healing of digital ulcers. The level of evidence across studies was very low to moderate. Conclusions There is insufficient evidence to assess the efficacy of botulinum toxin A in Raynauds phenomenon. Despite many promising reports, further research in the form of randomized controlled trials is warranted in order to investigate this new treatment method for Raynauds phenomenon.

The influence of endogenous and exogenous sex hormones on systemic lupus erythematosus in pre- and postmenopausal women

Systemic lupus erythematosus (SLE or lupus) is a chronic inflammatory disease that occurs mainly in women. Typically, symptoms appear within the first few years of adolescence, but currently an increase can be observed in the percentage of postmenopausal women with this condition. This is possibly due to the sophisticated treatment of the disease, which significantly improves the survival curve and prognosis. Genetic and environmental factors are involved in the development of SLE. Both regulation of the immune system and the activity of this disease are influenced by a variety of hormones, including: 17β-estradiol, testosterone, prolactin, progesterone and dehydroepiandrosterone (DHEA). Early menarche, menstrual cyclicity, the total number of years characterized by ovulatory cycles and early menopause are correlated with the development of SLE. Because of the health risks, attempts are increasingly being made to evaluate the impact of exogenous hormones (especially those applied exogenously) on the course of SLE. In particular, the role of estrogens is being highlighted, either endo- or exogenous, including oral contraceptives (OC), therapy used in the treatment of infertility, and hormonal replacement therapy (HRT). The purpose of this manuscript is the revision of the literature concerning the impact of both endo- and exogenous estrogens on the development of lupus, inducement of flares and any possible complications.

Retroperitoneal fibrosis – the state-of-the-art

Retroperitoneal fibrosis (RPF) is a rare disease, hallmarked by inflammation and deposition of fibrous tissue around the abdominal aorta. This process may spread contiguously and involve adjacent structures, leading to many complications, among which the most frequent and most severe is ureteral obstruction. The condition usually has idiopathic origin (idiopathic retroperitoneal fibrosis – IRF), but can also develop secondarily to a number of factors. The etiology of the disease remains unclear. Current research suggests that about half of the cases of IRF may be a symptom of a recently discovered, clinically heterogeneous immunoglobulin G4-related disease (IgG4-RD). Corticosteroids are the first-line treatment for IRF, but effective attempts to use immunosuppressants are also made. This paper presents the current state of knowledge on the etiopathogenesis, clinical presentation, diagnosis and therapeutic possibilities in different forms of RPF. Based on the latest research, an analysis of the relationship between IRF and IgG4-RD was performed.

Subcortical gray matter atrophy is associated with cognitive deficit in multiple sclerosis but not in systemic lupus erythematosus patients

Cognitive impairment is a significant clinical problem both in multiple sclerosis (MS) and systemic lupus erythematosus (SLE) patients. In MS cognitive dysfunction has been associated with brain atrophy and total demyelinating lesion volume. In SLE cognitive impairment is much less understood, and its link to structural brain damage remains to be established. The aim of this study was to identify the relationship between subcortical gray matter volume and cognitive impairment in MS and SLE. We recruited 37 MS and 38 SLE patients matched by age, disease duration and educational level. Patients underwent magnetic resonance imaging (MRI) and a battery of psychometric tests. Severity of cognitive impairment was similar in both cohorts despite larger white matter lesion load in MS patients. Psychometric scores were associated with global and subcortical gray matter atrophy measures and lesion load in MS, but not in SLE. In SLE, the lack of a relationship between cognitive impairment and structural damage, defined either as atrophy or white matter lesions, indicates a different causal mechanism of cognitive deficit.