I Fresko

Istanbul University, İstanbul, Istanbul, Turkey

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Publications (43)161.26 Total impact

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    ABSTRACT: Background BCG vaccination is thought to cause false positive PPD and concomitant medications to cause false negative PPD results when screening patients before starting TNF-alpha antagonists. Moreover it is assumed that INH is difficult to tolerate in this patient group. However there is a long time between BCG vaccination and TNF-alpha antagonist use in most of the rheumatology patients; there is no consistent data to show that medications cause negative PPD results; and INH is usually well tolerated by most of our patients. Objectives To determine whether BCG vaccination causes false positive PPD, concomitant medications cause false negative PPD and whether INH is difficult to tolerate in these patients. Methods We included adult patients who were prescribed a TNF-alpha antagonist for the first time between January 2010 and December 2012 in our clinic. Patients who had a history of active tuberculosis were excluded. BCG vaccination was determined by checking for BCG scars. We used logistic regression to analyse the determinants of a positive PPD (≥5 mm). The variables were having a BCG scar, each medication, age, gender, diagnosis and disease duration. We also evaluated the frequency of being able to complete 9 months of INH treatment and the reasons for discontinuation. Results A TNF-alpha antagonist was started in 1229 patients (613 men, 616 women, mean age 39.53±13.82 years, disease duration 6.49±6.87 years). We excluded 136 patients who had previously used a TNF-alpha antagonist, 21 patients younger than age 18 and 41 patients who had previous tuberculosis treatment. Among the remaining 1031, an initial PPD test was available in 873, and QTF in 215 patients. At least one BCG scar was present in 757 patients. Multivariate regression analysis showed that BCG vaccination and male sex were associated with PPD positivity (OR=3.21, 95%CI 1.87-5.52, p<0.001; and OR=2.51, 95%CI 1.78-3.53, p<0.001 respectively), while azathioprine use was associated with a negative PPD (OR=0.50, 95%CI 0.27-0.93, p=0.029). 482/565 (85.30%) patients completed 9 months of treatment, 30 with interruptions and 34 with mild transaminase elevations not requiring interruption. 69 (12.21%) had to stop INH after 3.43±2.27 months. The reasons were hepatotoxicity in 31, non-willingness in 13, allergic dermal reactions in 6, nausea in 2, dizziness in 2, pregnancy in 1, shortness of breath in 1 and pancreatitis in 1 patient. Twelve patients stopped taking INH after their TNF-alpha therapy was stopped. Among the 31 who had to stop INH for transaminase elevation 7 were using concomitant methotrexate. None of the patients developed tuberculosis during our follow-up of up to 3 years. Conclusions BCG vaccination may still be a cause of false positive PPD in candidates for treatment with TNF-alpha antagonists. Azathioprine seems to be associated with negative PPD. INH prophylaxis is generally well tolerated despite concomitant methotrexate. Disclosure of Interest None declared
    No preview · Article · Jun 2015 · Annals of the Rheumatic Diseases
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    ABSTRACT: Background There is still controversy about the association of TNF-alpha antagonists with malignancies. Although recent meta-analyses suggest that the risk of malignancy with these agents is not increased, the suspicion still exists, at least as reflected by the current labeling information. Objectives To survey the incidence of malignancy in patients treated with TNF-alpha antagonists for up to 13 years in a single center and to compare the results with the incidence of malignancy in the general population. Methods The charts of the first consecutive 376 rheumatoid arthritis (RA) patients (307 women; 69 men; mean age 55.5±12.7 SD years) who were prescribed TNF-alpha antagonists between 2001 and 2009 were reviewed retrospectively. Information regarding the demographic and clinical features, duration of use each TNF-alpha antagonist, development time and type of malignancy and the outcomes of patients were recovered from patient charts. Patients were invited to the clinic if their current status was not known. Age and sex standardized cancer incidence rates in the general population used to calculate standardized cancer rates (SIRs) were obtained from the Turkish Ministry of Health, Public Health Institution, Department of Cancer. Results The mean duration of follow-up was 67.6±17.7 SD months from the start of the first TNF-alpha antagonist to the end of 2013. During this time, 30 (7.9%) patients had died, 132 (35.1%) were still on TNF-alpha antagonists, 67 (17.8%) were using another biologic, 138 (36.7%) were no longer using any biologics and 10 (2.6%) were lost to follow-up. The main reasons of death were cardiovascular causes in 7 patients, sepsis in 5 and malignancies in 4. In 10 (2.6%) patients cause of death was unknown. A total of 8 patients had developed malignancies (2.12% [95% CI 0.66-3.58]). These were solid cancers in 6 (breast =1, lung =1, gastric =1, rectum =1, colon =1, unknown primary=1), hematologic cancers in 2 (acute leukemia=2). Since there were patients who were lost to follow-up and those who died of unknown causes, we calculated SIRs according to three different scenarios. If we assume that none of the patients who were lost to follow-up or whose cause of death was unknown, had a malignancy, the SIR would be 0.78 (95% CI 0.34-1.42). If we assume that all of the patients who were lost to follow-up (n=10) had a malignancy, but none of the patients whose cause of death was unknown had a malignancy, the SIR would be 1.7 (95% CI 1.04-2.0). Finally if we assume all patients who were lost to follow-up or whose reason of death was unknown (n=20) had a malignancy the SIR would be 2.7 (95% CI 1.8-3.8). Conclusions Our data indicate that an increased incidence of cancer, as compared to the general population, cannot be ruled out among RA patients enrolled in a TNF – alpha antagonist registry. This uncertainty is compounded by the fact that the comparisons we make here are between the incidence in a cohort of practically cancer free patients at the time of cohort entry and a general population incidence in which no such restriction is present. Disclosure of Interest None declared
    No preview · Article · Jun 2015 · Annals of the Rheumatic Diseases
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    ABSTRACT: Background The internal and external validity of randomised controlled trials require detailed analyses of modes of patient recruitment, description of the settings and locations of the study and the individual center effects as described in the CONSORT statement (1,2). However, most of the trials published in major rheumatology journals lack this information. Objectives We surveyed the reporting of the eligibility criteria for participants, the settings and locations where the data were collected according to CONSORT and the center effects on outcomes in randomised clinical trials in major rheumatology journals. Methods A hand search was made for randomised controlled trials published in 2011 and 2012 in Ann Rheum Dis, Arthritis Rheum, Rheumatology, J Rheumatol, and Clin Exp Rheumatol. The items were separately tabulated for eligibility criteria for participants such as referral or self selection, the settings and locations of the study such as country, city; the immediate environment the study was performed in such as community, office practice, hospital clinic, inpatient unit, primary, secondary and tertiary health care and other factors related to the setting exemplified by climate, physical factors, economics, geography, social and cultural milieu (race and education), and problems with transportation. The individual center effects on outcomes in the main text were also explored. Two observers separately evaluated the papers and the disagreements were resolved by consensus. Results We evaluated 102 studies including four with childhood diseases. The following data were available for referral patterns: physician referrals (n=5), self selection (n=6) or both (n=2); locations: country (n=54), continent (n=12), and local city (n=31); settings: community (n=2), hospital clinic (n=27), inpatient unit (n=2); secondary (n=1) or tertiary health care centers (n=13); socio-economics (n=6), educational levels (n= 5), and race (n=42). No data were given for the remaining items. Multicenter differences were only reported in 1 of 24 papers in Ann Rheum Dis, 8 of 28 in Arthritis Rheum, 1 of 6 in Rheumatology, 2 of 11 in J Rheumatol, and 1of 3 in Clin Exp Rheumatol. Conclusions A few randomised controlled trials give enough information on eligibility criteria for participants and the settings and locations as well as the center effects. These cast doubt on the robustness of the results. More data are needed to apply these outcomes to other patient populations. References Disclosure of Interest None Declared
    No preview · Article · Jan 2014 · Annals of the Rheumatic Diseases
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    ABSTRACT: Behçet's syndrome (BS) is a systemic inflammatory disorder with unknown etiology. Features of both innate and adaptive immunity have been claimed in the pathogenesis of BS. To test the possible dysregulation of the NLRP3/cryopyrin (Nod-like receptor with a pyrin domain 3)inflammasome, as a result of mutation(s), we performed single-strand conformation polymorphism analyses and/ or sequencing of all the coding regions and intron–exon boundaries of NLRP3/cryopyrin and ASC (apoptosis-associated speck-like protein containing CARD) genes from Turkish BS patients and healthy controls. At the same time, we determined pro-inflammatory cytokine secretion profiles of peripheral blood cells in response to LPS treatment using ELISA. BS patients with vascular involvement showed significantly increased levels of TNF-α release at 2-, 4-and 8-h post-treatment and significantly increased IL-1β levels were detected at 2 h (P=0.005) and 4 h (P=0.025) (n=10). We identified four mutations in the NLRP3/cryopyrin gene, V200M (n=3/104) and T195M (n=1/104), in BS patients but none in control samples. No mutations were detected in the ASC gene. The effect of these NLRP3/cryopyrin mutants on ASC speck assembly and IL-1β secretion was tested and the V200M mutant was shown to induce IL-1β secretion. Thus, it is likely that certain mutations in NLRP3/cryopyrin in combination with yet unknown other factors may contribute to the pro-inflammatory cytokine profiles in BS patients.
    Full-text · Dataset · Oct 2013
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    ABSTRACT: HLA-B*51 and HLA-B*52 are two close human leukocyte antigen (HLA) allele groups with minor amino acid differences. However, they are associated with two different vasculitides (HLA-B*51 in Behçet's disease and HLA-B*52 in Takayasu's arteritis (TAK)) and with major clinical and immunological differences. In this study, we aimed to screen a large cohort of TAK patients from Turkey for the presence of HLA-B*51 and HLA-B*52 as susceptibility and severity factors. TAK patients (n = 330) followed at a total of 15 centers were included in the study. The mean age of the patients was 37.8 years, and 86% were women. DNA samples from the patients and healthy controls (HC; n = 210) were isolated, and the presence of HLA-B*51 or HLA-B*52 was screened for by using PCR with sequence-specific primers. We found a significant association of HLA-B*52 with TAK (20.9% vs HC = 6.7%, P = 0.000, OR = 3.7, 95% CI = 2.02 to 6.77). The distribution of HLA-B*51 did not differ between TAK patients and HCs (22.7% vs 24.8%, OR = 0.9, 95% CI = 0.60 to 1.34). The presence of HLA-B*52 decreased in late-onset patients (> 40 years of age; 12.0%, P = 0.024, OR = 0.43, 95% CI = 0.20 to 0.91). Patients with angiographic type I disease with limited aortic involvement also had a lower presence of HLA-B*52 compared to those with all other disease subtypes (13.1% vs 26%, P = 0.005, OR = 0.43, 95% CI = 0.23 to 0.78). In this study, the previously reported association of TAK with HLA-B*52 in other populations was confirmed in patients from Turkey. The functional relevance of HLA-B*52 in TAK pathogenesis needs to be explored further.
    Full-text · Article · Feb 2012 · Arthritis research & therapy
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    ABSTRACT: Background: Arthritis in familial Mediterranean fever (FMF) is typically monoarticular, of sudden onset, self-limiting, rarely destructive, and a frequent manifestation of FMF. The mechanisms governing the initiation and resolution of this highly inflammatory disease entity are not fully understood. Therefore, to decipher the complexity of articular autoinflammation, we defined inflammatory cells and some mediators of inflammation and apoptosis in the synovial membrane of a patient with FMF. Methods: A synovial tissue sample obtained from an inflamed hip joint of a boy homozygous for mutation M694I in pyrin/marenostrin was studied by immunohistochemistry using commercially available antibodies specific for tryptase, CD68, CD3, CD20 and CD138. With the same technique, we also analyzed the expression and distribution of myeloperoxidase, lysozyme, galectin-1, galectin-3, p65 (RelA)/NF-κB, iNOS, COX-2 and activated caspase-3. Results: Abundant neutrophils, macrophages and mast cells, but also B cells were observed, which were more numerous than T lymphocytes or plasma cells. Neutrophils had no granules containing myeloperoxidase or lysozyme in their cytoplasm. Galectin-1 was found in many mononuclear cells sparse throughout the synovial tissue, whereas the expression of galectin-3 was less prominent and scattered. Neither of the galectins was detected in neutrophils. p65 (RelA)/NF-κB and iNOS were both up-regulated in most of the inflammatory cells, whereas COX-2 expression was low, and cleaved caspase-3, used as proxy to demonstrate intrinsic apoptosis, was undetectable. Conclusions: The exquisitely inflammatory, yet non-destructive character of FMF arthritis may correlate with the presence of non-pathogenic neutrophils lacking effector molecules and the preferential expression of iNOS and anti-inflammatory galectin-1 in regulatory cells of the innate immune system, most likely in macrophages. Intrinsic apoptosis seemed irrelevant for controlling synovial autoinflammation, but regulation through pyroptosis, mast cells and the adaptive immune system are possible alternatives.
    Full-text · Article · Feb 2011 · Rheumatology
  • Emire Seyahi · İzzet Fresko · Hasan Yazıcı
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    ABSTRACT: Endothelial dysfunction and arterial stiffness have been well documented in Behçet’s syndrome. Lipid peroxidation abnormalities also suggest a proatherogenic state. However, studies investigating carotid atherosclerosis and coronary calcification fail to show increased atherosclerosis. Similarly, a long-term outcome survey and cross-sectional clinical studies suggest that the prevalence of cardiovascular disease and its associated mortality are not increased in BS.
    No preview · Article · Jan 2010
  • S Celik · I Fresko · N Sut · N M Batumlu · H Yazici · Y Yazici
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    ABSTRACT: The concordance of patient reported outcomes in rheumatoid arthritis (RA) among different countries has not been studied in detail. We tried to determine the differences in pain and fatigue perception among a group of RA patients in the US and in Turkey who had similar disease activity and functional score in multidimensional health assessment questionnaire (MDHAQ FN). One hundred and thirty seven RA patients from Turkey and 129 from the US were studied. An MDHAQ was obtained and a DAS28 was calculated for each patient. Pain and fatigue perception was compared between the two groups after adjusting for age, sex, MDHAQ FN and DAS 28. Turkish patients had less pain than their US counterparts when adjusted for MDHAQ FN, DAS 28, age and sex (3.56 (2.24) vs. 4.35 (2.23), p=0.005) whereas there was no difference in fatigue between the two groups (3.85 (2.44) vs. 4.25 (2.45), p=0.194). When the patients with a DAS28 score of above 5.1 and below 2.6 were compared in both groups, Turkish patients had again less pain albeit less in the high disease activity group. This study suggests that Turkish patients have less pain than the US patients when controlled for age, gender and MDHAQFN and DAS28 scores. This is at odds to the conventional wisdom that pain perception is increased among the non-Western cultures.
    No preview · Article · Nov 2009 · Clinical and experimental rheumatology
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    ABSTRACT: Takayasu's arteritis (TA) is a chronic, inflammatory vasculitis affecting the aorta and its major branches. Although it is more prevalent in Far-East Asia, the distribution of the disease is worldwide with different vascular involvement patterns and clinical manifestations. The objective of this study was to evaluate the demographic, clinical, angiographic and prognostic features of TA patients in Turkey. Clinical and angiographic findings of 248 TA patients (228 female, 27 male) followed at 15 Rheumatology Centers were prospectively evaluated according to a predefined protocol. The mean age was 40.1 years (30.2 years at the clinical onset). Clinical manifestations included constitutional symptoms in 66%, absent or diminished pulses in 88%, bruits in 77%, extremity pain in 69%, claudication in 48%, hypertension in 43% and cerebrovascular accidents (CVA) in 18% of the patients. Renal artery stenosis, aortic regurgitation and pulmonary hypertension were present in 26%, 33% and 12%, respectively. According to the new angiographic classification, type V (50.8%) and Type I (32%) were the most frequent types of involvement. Corticosteroids were the main treatment in 93% of the patients alone (9%) or in combination with immunosuppressive agents (84%). Most frequently preferred immunosuppressive agents were methotrexate (63%), azathioprine (22%) and cyclophosphamide (13%). Remission was observed at least once in 94% of the patients and sustained remission in 71% during follow-up. The demographical, clinical and angiographic findings of TA patients in our series were similar to those reported from Japan, Brazil and Colombia. Combination therapies with immunosuppressive agents were the preferred choice of treatment in Turkey.
    Full-text · Article · Jan 2009 · Clinical and experimental rheumatology
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    ABSTRACT: To assess the association of polymorphisms of the IL-6 receptor gene (+24013A/G:Ala31Ala; +48892 A/C:Asp358Ala), the IL-8 receptor gene (+2607G/C:Ser/Thr IL-8RA), and TNF-alpha 238 (G/A) single nucleotide polymorphism (SNP) with Behçet's disease in patients of German or Turkish origin. DNA was extracted from blood samples taken from patients in Germany (n=93) and Turkey (n=28), as well as from 51 German and 20 Turkish healthy controls. The polymorphisms were analysed by PCR with the LightCycler system. No significant association was found between TNF-alpha 238, +2607 IL-8RA, +48892 IL-6R or +24013 IL-6R- polymorphisms and nationality or disease. Statistically there was no difference between the patients and controls (TNF-alpha 238: p = 0.86; +2607 IL-8RA: p=0.23; +48892 IL-6R: p=0.087; +24013 IL-6R: p = 0.80) nor between Germans and Turks (TNF-alpha 238: p=0.13; +2607 IL-8RA: p=0.68; +48892 IL-6R: p=0.32; +24013 IL-6R: p=0.65). The single nucleotide polymorphisms of the IL-6 and IL-8 receptor genes and the TNF-alpha gene analysed here do not appear to be associated with Behçet's disease.
    Preview · Article · Jul 2008 · Clinical and experimental rheumatology
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    ABSTRACT: Takayasu's arteritis (TA) is a chronic, rare granulomatous panarteritis of unknown aetiology involving mainly the aorta and its major branches. In this study, genetic susceptibility to TA has been investigated by screening the functional single nucleotide polymorphism (SNP) of PTPN22 gene encoding the lymphoid-specific protein tyrosine phosphatase. Totally, 181 patients with TA and 177 healthy controls are genotyped by PCR-RFLP method for the SNP rs2476601 (A/G) of PTPN22 gene. Polymorphic region was amplified by PCR and digested with Xcm I enzyme. Detected frequencies of heterozygous genotype (AG) were 5.1% (9/177) in control group and 3.8% (7/181) in TA group (P = 0.61, odds ratio: 0.75, 95% CI: 0.3, 2.0). No association with angiographic type, vascular involvement or prognosis of TA was observed either. The distribution of PTPN22 polymorphism did not reveal any association with TA in Turkey.
    Full-text · Article · Jun 2008 · Rheumatology (Oxford, England)

  • No preview · Article · Jan 2008 · Clinical and experimental rheumatology
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    ABSTRACT: To investigate the role of shared epitope (SE) alleles in the short-term clinical response to leflunomide for the treatment of active RA. In an open-label, multi-centre study of 16-weeks duration, 93 patients (82% female) fulfilling ARA 1987 RA criteria were treated with leflunomide (100 mg loading dose for 3 days, then 20 mg/day as the maintenance dose). The primary efficacy criterion was the response status according to the European League Against Rheumatism (EULAR) response criteria using Disease Activity Score-28 (DAS28) activity measure. SE determinations have been undertaken by polymerase chain reaction and sequence-specific oligonucleotide genotyping methods. The mean (s.d.) Disease Activity Score-28 (DAS28) was 5.1 (1.3) before the treatment, which was significantly decreased after 16 weeks [3.0 (1.1), P < 0.001]. According to the EULAR response criteria, 55 patients (59.1%) were classified as good responders. SE was positive in 51 (54.8%) of the patients, with 13 (13.9%) having SE homozygosity or carrying any two SE alleles. Among SE-positive patients, 68.6% (35/51) were good responders, compared with 47.6% (20/42) in SE negatives (P = 0.04). No difference was present according to SE hetero- or homozygosity (68.4 vs 69.2%). RF was also present significantly more frequently in the SE-positive group compared with negatives (78.4 vs 57.1%, P = 0.03). However, no significant difference was observed in the prevalence of RF positivity in patients with a good clinical response (72.7 vs 63.2%, P = 0.32). The results suggest that HLA-DRB1 SE presence may favourably affect the outcome of leflunomide monotherapy in an unselected group of RA patients with an active disease and naive to leflunomide.
    Full-text · Article · Dec 2007 · Rheumatology (Oxford, England)
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    Full-text · Article · Aug 2007 · Rheumatology
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    ABSTRACT: Takayasu's arteritis (TA) is a chronic arterial inflammation of unknown etiology involving mainly the aorta and its major branches. Genetic polymorphisms of cytokines are screened as susceptibility factors for TA in Turkey. A total of 94 patients with TA were investigated for the genetic polymorphisms of the interleukin genes IL12, IL2,and IL6 and were compared with 108 healthy control subjects using polymerase chain reaction-sequence-specific primer method. The frequencies of IL12B 1188 C allele (p = 0.03, OR = 1.7) and CC genotype (p = 0.007, OR = 3.7) were both higher in TA patients than in control subjects. TT genotype at IL2-330 (p = 0.006, OR = 2.4) and GG genotype at IL6-174 (p = 0.04, OR = 1.9) were more frequent in TA patients. Lower prevalence of GT genotype at IL2-330 (p = 0.005, OR = 0.4), CG genotype at IL6-174 (p = 0.001, OR = 0.4), and AG genotypes at IL6-598 (p = 0.01, OR = 0.4) were also detected. The polymorphism of IL-12 as well as IL-6 and IL-2 genes may contribute to susceptibility and pathogenesis of TA by altering cytokine production and inducing inflammation.
    No preview · Article · Oct 2006 · Human Immunology
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    C Mat · S Yurdakul · S Uysal · F Gogus · Y Ozyazgan · O Uysal · I Fresko · H Yazici
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    ABSTRACT: Corticosteroids are widely used in Behçet's syndrome despite the absence of controlled studies. We assessed the effect of depot corticosteroids primarily for genital ulcers and secondarily for the other mucocutaneous manifestations of Behçet's syndrome. We randomized 86 patients who had active disease with genital ulcers to receive either intramuscular corticosteroid injections (40 mg methylprednisolone acetate) or placebo every 3 weeks for 27 weeks. Seventy-six patients (88%) completed the treatment. There were no significant differences in the mean number of genital and oral ulcers, or folliculitis between groups. The mean number of erythema nodosum lesions was less in the corticosteroid group as a whole (P = 0.0046); subgroup analyses revealed that this was significant for females (P = 0.0148) but not for males (P = 0.1). Low-dose depot corticosteroids did not have any beneficial effect on genital ulcers. However, it was useful in controlling erythema nodosum lesions, especially among the females.
    Full-text · Article · Apr 2006 · Rheumatology
  • E Seyahi · N Seyahi · I Fresko · M Kuyumcu · H Yazici
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    ABSTRACT: It is widely appreciated that patients with systemic lupus erythematosus (SLE) get thinner and shorter hair. However little work has been done to quantitate this. We assessed hair thickness of SLE patients and compared this to that of patients with rheumatoid arthritis (RA) and healthy controls (HC). Fifty-seven female patients with SLE (mean age: 32 +/- 8 years) and 77 female patients with RA (mean age: 50 +/- 12 years) were studied along with 75 healthy women (mean age: 27 +/- 6 years). Five strands of hair were taken from each subset and mounted on glass slides. Two independent observers, blind to the sources of the hair, measured the hair strands under a light microscope, using a micrometer. Finally, the mean hair thickness between each of the three groups was calculated. The hair in both SLE and RA patients was found to be thinner than that of HC by both observers (P < 0.001). Age adjusted analysis between SLE and HC showed similar results. However, there was no significant difference in hair thickness between SLE and RA. SLE patients have thinner hair compared to HC. More studies are needed to investigate the effect of disease activity, therapy and other factors on hair diameter.
    No preview · Article · Feb 2006 · Lupus
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    ABSTRACT: In order to evaluate the role of human parvovirus B19 in the etiopathogenesis of autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), synovial fluid and blood specimens were collected at 1-month intervals from 20 patients with early synovitis (ES) and 31 with RA. Blood specimens were also collected from 25 patients with SLE, 25 with osteoarthritis (OA) as the diseased control group, and 50 healthy blood donors (HBD) as the healthy control group. Detection of B19 IgM and B19 IgG were performed by enzyme-linked immunosorbent assay from serum specimens, and B19 DNA was detected by polymerase chain reaction from synovial fluid samples. B19 IgM, B19 IgG, and B19 DNA were found in the three patients of the ES group. Subsequently, two of them were diagnosed with RA and one with SLE. B19 DNA was also detected in the synovial fluid of eight patients in the RA group. Of them, all were positive for B19 IgG and half were positive for B19 IgM. B19 IgM was not detected in either of the control groups. To define the role of B19 in the etiopathogenesis and prognosis of undiagnosed arthritis and other chronic inflammatory diseases such as RA and SLE, we need broader serial and prospective studies based on clinical and laboratory collaboration. In conjunction with case reports, these studies would also serve to detect other possible factors in the etiopathogenesis of chronic inflammatory diseases.
    No preview · Article · Dec 2005 · Rheumatology International
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    ABSTRACT: Anti-Saccharomyces cerevisiae antibodies (ASCA) are found in 50-60% of patients with Crohn's disease. Increased as well as normal levels have been reported in Behçet's syndrome (BS). We reassessed the level of IgG and IgA ASCA antibodies in BS and in a group of diseased and healthy controls. Eighty-five patients with BS were studied along with 20 patients with ankylosing spondylitis (AS), 24 with Crohn's disease (CD), 25 with ulcerative colitis (UC) and 21 healthy volunteers. A commercial ELISA kit was used (Inova Diagnostics). It was only the patients with CD who had significantly higher levels of antibodies compared with the rest of the group (ANOVA: ASCA IgG, p = 0.0001; ASCA IgA, p = 0.0001). 42% of CD, 4% of BS, 4% of UC and 15% of AS patients had a positive IgG+IgA ASCA. There was a significant trend for patients with gastrointestinal (GI) involvement with BS (n = 8) to be more positive for IgG and IgG+IgA ASCA compared to the rest of the patients with BS (n = 77) (Chi-square, IgG, p = 0.02, IgG+IgA, p = 0.001). The rate of positivity of ASCA in BS is comparable to that observed among patients with UC and AS. Patients with BS who have GI involvement may have higher levels of ASCA and this needs to be further studied.
    Full-text · Article · Jul 2005 · Clinical and experimental rheumatology
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    ABSTRACT: An erythematous response to intradermal injection of monosodium urate crystals (MSU) has been demonstrated in Behçet's syndrome (BS). To further elucidate the pathogenesis of this response, the effects of MSU on in vitro oxidative burst reaction of neutrophils and monocytes were investigated. Peripheral blood mononuclear cells from patients with Behçet's syndrome (BS), rheumatoid arthritis (RA), familial Mediterranean fever (FMF) and healthy controls (HC) were incubated with 100 ng/ml phorbol myristate acetate (PMA) and MSU at different dosages (25-500 microg/ml). Oxidative burst reaction was evaluated in neutrophils and monocytes by flow cytometry. In patients with BS, oxidative burst of neutrophils was significantly increased compared to HC at 125 microg/ml and 250 microg/ml dosages of MSU (p < or = 0.001 and 0.004 respectively). In patients with FMF; there was also an increased oxidative burst reaction at 75 microg/ml, 250 g/ml and 500 microg/ml (p < or = 0.007; 0.001 and 0.004 respectively). In patients with BS, oxidative burst of monocytes was increased only at 125 g/ml dosage of MSU (p < or = 0.002). However, in patients with FMF monocyte burst response was increased at 25 microg/ml, 75 microg/ml and 125 g/ml (p < or = 0.004; < 0.0001; < 0.0001 and 0.002 respectively). In RA group, stimulation with PMA resulted in a higher oxidative burst reaction than FMF and BS (p < or = 0.000 and p < or = 0.008). No correlation was observed between oxidative burst of neutrophils or monocytes and intradermal responses to MSU crystals. Oxidative burst reaction with MSU is augmented in neutrophils and monocytes of BS. However, the response is not specific and is unassociated with skin dermal test which has a high specificity for BS.
    Preview · Article · Jul 2005 · Clinical and experimental rheumatology