Treatment of ankylosing spondylitis with TNFα inhibitors does not affect serum levels of tryptophan metabolites.

The imbalance between the kynurenine and serotonin pathways can have serious consequences, e.g., depression. One of the factors leading to the imbalance between the pathways of tryptophan metabolism is inflammation. The aim of our study was to assess the impact of treatment with tumor necrosis factor-alpha (TNFα)-inhibitors on tryptophan metabolism in patients with ankylosing spondylitis (AS). Forty patients with AS (twenty-eight males, twelve females; mean age 40 ± 11 years), qualified to receive anti-TNF-α treatment, were prospectively assessed. As a control group, 20 healthy volunteers (7 males and 13 females, mean age 38 ± 5 years) were recruited from the general population. Patients underwent full clinical and biochemical assessment before and after 6 months of therapy. Disease activity was assessed by the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI). The presence of depressive disorders was assessed with Beck's Depression Inventory (BDI) scale. Serum concentrations of tryptophan, serotonin, kynurenine, and quinolinic acid were measured. The predominance of the kynurenine pathway in AS patients (compared to the control group) was demonstrated (p < 0.001). Surprisingly, no significant changes in serum levels of tryptophan and its metabolites in AS patients after treatment were found, despite clinical improvement. Moreover, the components of tryptophan metabolism did not correlate significantly with the clinical activity of AS, depression nor laboratory inflammatory markers. Probably some other factors influence the pathways of tryptophan metabolism in patients with ankylosing spondylitis.

Relationship between changes observed in nailfold capillaroscopy and serological profile, lung fibrosis, and elevated risk of pulmonary hypertension in patients with systemic sclerosis and mixed connective tissue disease.

Introduction: Microvascular changes play a significant role in systemic sclerosis (SSc) and mixed connective tissue disease (MCTD). The most serious complications of SSc and MCTD are lung fibrosis (LF) and pulmonary hypertension (PH). Aim: To determine the relationship of the changes observed in capillaries with the serological profile, LF, PH, and finger ulcerations in patients with SSc and MCTD. Material and methods: The tested group comprised 80 persons (61 SSc, 19 MCTD); mean age 53.6 ±13.6 years. Patients were qualified to the LF group based on HRCT. Likelihood of PH was determined using echocardiography. The presence of antinuclear antibodies (ANA) was assessed using indirect immunofluorescence, while ANA profile, and sclerosis profile were assessed using EUROIMMUN kits, and antiphospholipid antibodies (aPL) using the ELISA method. Capillaroscopy was performed using the Nikon CPS 160 optical microscope. Results: The following were found: a relationship between occurrence of anti-SS-A (p = 0.006) and anti-centromere B antibodies (p = 0.012) and ramified vessels, between anti-SS-B and capillary haemorrhages (p = 0.019), a positive correlation between NOR90 antibodies and winding loops (p = 0.021), PM-Scl 100 antibodies and enlarged vessels (p = 0.033), a negative correlation between Scl-70 antibodies and winding loops (p = 0.033), and a relationship between aCL and winding loops (p = 0.002). No relationship between the capillaroscopy image and PH risk was found. A positive correlation was found between avascularisation areas and LF and between giant capillaries and finger ulcerations. A negative correlation was found between U1-RNP antibodies and finger ulcerations (p = 0.009), and a positive correlation between antibodies to fibrillarin and ulcerations (p = 0.028). Conclusions: SS-A, SS-B and anti-centromere antibodies are associated with the late phase of sclerodermic microangiopathy. Avascularisation areas significantly correlate with a higher prevalence of LF. U1-RNP antibodies have a protective role, while anti-fibrillarin antibodies are the risk factor for finger ulcerations.

The importance of homocysteine in the development of cardiovascular complications in patients with rheumatoid arthritis.

Rheumatoid arthritis (RA) not only leads to disability due to joint changes, but also significantly shortens the life expectancy of patients, mainly due to more frequent occurrence of heart attacks and strokes. Accelerated atherosclerosis in these patients is caused, among other factors, by high homocysteine (HCY) concentration in blood. Numerous studies have shown that treatment with vitamin B significantly reduces the concentration of HCY in blood, but does not reduce the risk of heart diseases. Recent studies have shown, however, that folic acid (FA) administration reduces the risk of stroke by 10-20%. Due to the fact that in patients with RA strokes are more frequent than in the general population and hyperhomocysteinemia (HHCY) is often found, determination of HCY concentration in blood is advisable, and in persons with HHCY it is recommended to use FA in primary and secondary stroke prevention.

The concentration of tumor necrosis factor in the blood serum and in the urine and selected early organ damages in patients with primary systemic arterial hypertension.

Arterial hypertension is considered to be an inflammatory condition with low intensity. Therefore, an elevated concentration of inflammatory cytokines can be expected in patients with systemic arterial hypertension, including tumor necrosis factor (TNF).The study included a group of 96 persons aged 18 to 65 years: 76 patients with primary arterial hypertension and 20 healthy individuals (control group). Blood pressure was measured in all individuals using the office and ambulatory blood pressure monitoring (ABPM) measurement, blood was collected for laboratory tests [tumor necrosis factor (TNF), tumor necrosis factor receptor 1 (TNFR1)], and 24-hour urine collection was performed in which albuminuria and TNF concentration were assessed. Moreover, assessment of the intima-media thickness (IMT) in ultrasonography and left ventricular mass index (LVMI) in echocardiography were carried out.Statistically elevated TNF concentration in the blood serum (P = .0001) and in the 24-hour urine collection (P = .0087) was determined in patients with hypertension in comparison with the control group. The TNF and TNFR1 concentration in the serum and TNF in the 24-hour urine in the group of patients with arterial hypertension and organ damages and without such complications did not differ statistically significantly.We observed a positive and statistically significant correlation between TNFR1 concentration in the serum and TNF urine excretion in patients with hypertension (r = 0.369, P < .05)Patients with arterial hypertension are characterized by higher TNF concentrations in blood serum and higher TNF excretion in 24-hour urine than healthy persons.TNF and TNFR1 concentration in blood serum and TNF excretion in 24-hour urine in patients with early organ damages due to arterial hypertension do not differ significantly from those parameters in patients with arterial hypertension without organ complications.There is a positive correlation between TNFR1 concentration in the serum and TNF urine excretion in patients with hypertension.

Prevalence of pulmonary hypertension in patients with systemic sclerosis and mixed connective tissue disease.

Systemic sclerosis (SSc) and mixed connective tissue disease (MCTD) are 2 conditions in which pulmonary hypertension (PH) can develop.We retrospectively analyzed the probability of PH in case of 83 patients (69 SSc and 14 MCTD). The European Society of Cardiology/European Respiratory Society (ESC/ERS) echocardiographic guidelines of 2015 were used for the evaluation.On the basis of an echocardiography, the patients were divided into 2 subgroups: patients with elevated probability of PH (EP) (n = 16) versus the group with a low probability of PH (LP) (n = 67). Of the 16 patients in the EP group, 15 were SSc patients and 1 was an MCTD patient, respectively, that is, 21.7% and 7.1% of all patients. Of the 16 patients with EP, 10 with SSc had right-heart catheterization, which excluded PH in 7 patients; hence, PH was estimated to be 11.6% in the SSc group. The distribution of the individual causes of PH was arterial PH 2.9%, PH associated with interstitial lung disease 4.3%, PH associated with left ventricular disease 1.5%, and PH of unknown origin 2.9%. Further, there was a significant difference between EP and LP in the incidence of the right bundle branch block in standard electrocardiography, left atrial and right ventricular dimension, tricuspid annular plane systolic excursion, and Doppler-derived tricuspid lateral annular systolic velocity (S') in echocardiography.Echocardiography, particularly those evaluating the parameters included in the ESC/ERS guidelines of 2015, appears to be a useful tool in the detection of patients with a high PH probability. Additional tissue Doppler echocardiography seems to be a good option.

Chikungunya virus: a rheumatologist's perspective.

Chikungunya virus (CHIKV) is an arthropod-borne alphavirus, transmitted by Aedes aegypti and Aedes albopictus mosquitoes. It is responsible for a febrile illness, typically accompanied by maculopapular rash and severe, incapacitating arthralgia. The disease, although generally self-limiting, frequently evolves into a long-lasting, debilitating rheumatic disorder, which shares many clinical features with rheumatoid arthritis (RA). The underlying mechanism by which CHIKV induces persistent arthritis remains under investigation, however, currently, attention is drawn to the fact, that chronic chikungunya (CHIK) and RA have many common cellular and cytokine pathways involved in their pathogenesis. Over the past decades, the virus has dispersed unexpectedly from tropical and subtropical regions of Africa and Asia, affecting millions of people worldwide. No licensed vaccine, nor antiviral drug against CHIKV is yet available. Treatment of acute CHIK is symptomatic, whereas in chronic stages, different disease-modifying anti-rheumatic drugs (DMARDs) have been used with variable success. Hence, chronic CHIK is an emerging rheumatic condition that rheumatologists have to deal with. This review provides brief insights into the epidemiology, pathogenesis, clinical features and management of Chikungunya disease, with special regard to post-chikungunya rheumatic disorder and its relationship with RA.

Rheumatic diseases induced by drugs and environmental factors: the state-of-the-art - part two.

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 early 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 (SLE), scleroderma, systemic vasculitis, polymyositis, dermatomyositis, and Sjögren's syndrome. The objective of this study is to summarize current knowledge on rheumatic diseases induced by drugs and environmental factors.

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 Sjögren's syndrome. The objective of this study is to summarize current knowledge on rheumatic diseases induced by drugs and environmental factors.

[Eosinophilic fasciitis]. / Eozynofilowe zapalenie powiezi.

Eosinophilic fasciitis is a rare connective tissue disease with unclear etiology and pathogenesis. It is classified as a scleroderma-like syndrome. The disease is characterized by fibrosis of the skin and subcutaneous tissues with significant thickening of fascia. Visceral involvement is rare. Characteristic feature in laboratory tests is peripheral blood eosinophilia. Differential diagnosis should be performed, including ruling out systemic sclerosis, nephrogenic systemic fibrosis, eosinophilia-myalgia syndrome, scleromyxedema, hypereosinophilic syndrome or Churg-Strauss syndrome. Final diagnosis is confirmed by histopathological examination. In treatment of the disease corticosteroids and/or immunosuppressive drugs are used. Some other drugs showed activity in this disease e.g. dapsone, infiximab or rituximab. Prognosis is rather good but sometimes a long-term treatment is necessary. In this paper we summarized the current knowledge on eosinophilic fasciitis.