Introduction: Scleroderma (systemic sclerosis [SSc]) is a rare autoimmune disease which manifests as fibrosis in the skin and other internal organs. Conventionally, the modified Rodnan skin score (MRSS) has been used to quantify the extent of skin fibrosis (resulting in skin tightness) in SSc. This technique, although widely validated, is limited by the requirement of a trained, experienced assessor. Recent literature suggests that utilization of the objective ultrasound-based assessment of skin fibrosis utilizing shear wave elastography (SWE) may be a more robust technique to detect early skin tightness in SSc. Methods: We evaluated the use of SWE (assessed by an experienced radiologist) in 24 patients with SSc compared with 16 healthy controls. Results: Our patients were predominantly females, with median disease duration of 1.5 years and median MRSS of 17. There was minimal intraobserver variation in the assessment of SWE. Patients with SSc had higher SWE values (mean elasticity [E_mean]) compared to healthy controls at most assessed sites for the MRSS. The E_meancorrelated significantly at all sites with the MRSS scores. At the sites where MRSS was scored as 0 (normal), the E_meanin patients with SSc was higher when compared with similarly clinical normal skin in patients with SSc, suggesting potential early involvement of these areas of the skin with fibrosis. Conclusion: SWE is a promising tool to objectively assess skin fibrosis in SSc and may be useful in detecting early, subclinical skin involvement in this disease.

Background: Enthesitis is an important feature of spondyloarthritis but may often be subclinical. Data is sparse, especially from India, on the ultrasonography (USG) detection of enthesitis in these patients. The present study aimed to find the prevalence and pattern of entheseal involvement assessed clinically and by USG. Methods: Fifty-two spondyloarthritis, 26 rheumatoid arthritis, and 26 healthy controls were evaluated for enthesitis by clinical examination and by USG using 2014 OMERACT consensus group definitions at bilateral Achilles insertion on the calcaneus, plantar fascia attachment on the calcaneus, quadriceps tendon insertion on the patella, patellar tendon origin from the inferior pole of the patella, and patellar tendon insertion on the tibial tuberosity. At least one ultrasonographic finding at any of the above sites was considered positive for enthesitis. Results: The number of entheseal sites screened in spondyloarthritis patients was 520 and 260 each in rheumatoid arthritis and healthy controls. USG (sensitivity - 94.2%) was better in detecting enthesitis than clinical examination (sensitivity - 69.2%). Clinical examination was highly specific (100%) compared to USG (55.7%) in differentiating from rheumatoid arthritis and healthy controls. USG alone without clinical findings was positive at 23.8% of sites while clinical examination alone without USG findings was positive at 5.2% of sites. Frequency of enthesitis in rheumatoid arthritis was not more than healthy controls (6.1% vs. 8.1%, respectively) and was much less than spondyloarthritis (34%). Conclusion: USG is a good screening tool for detection of enthesitis but cannot replace clinical examination completely.

Background: Immune dysregulation triggered by environmental events (including microbes) have been implicated in the etiopathogenesis of systemic sclerosis (SSc). Helicobacter pylori (H. pylori) a pathogen well known to cause gastric ulcers and has been associated with several autoimmune diseases. However, the role of H. pylori in SSc has not been widely reported. The objective of the study was to estimate the prevalence of H. pylori infection in SSc patients and analyze its clinical associations. Methods: This study comprised 55 patients who satisfied ACR/EULAR 2013 classification criteria for SSc and 25 age and sex-matched healthy controls. Demographic, clinical, laboratory, and immunological parameters were recorded. Upper gastrointestinal (GI) endoscopy was done. Anti-H. pylori IgG levels (RU/ml) were estimated by ELISA and results analyzed by SPSS. Results: Baseline characteristics were comparable in both groups. Prevalence of H. pylori infection was high in SSc patients in comparison to controls (61.8% vs. 24%). Anti-H. pylori IgG levels were high in SSc patients in comparison to controls (mean 65 RU/ml vs. 25.3RU/ml; P = 0.003). SSc patients with symptomatic GI involvement had higher anti-H. pylori IgG levels than asymptomatic patients (mean 118.3 RU/ml vs. 20.7 RU/ml; P < 0.001). Anti-H. pylori IgG levels were not significantly different between diffuse cutaneous SSc and limited cutaneous SSc (mean 72.9 RU/ml vs. 54.1RU/ml; P = 0.289). Anti-H. pylori IgG antibody levels showed no correlation with disease duration, erythrocyte sedimentation rate, C-reactive protein, interstitial lung disease, and modified Rodnan Skin Score. Conclusion: SSc patients have high seropositivity for anti-H. pylori IgG antibodies. High anti-H. pylori IgG antibody titers are associated with symptomatic upper GI dysfunction.

Objective: The objective of this study was to appraise the correlation and agreement of RAPID 3 with DAS 28 and CDAI in terms of measuring disease activity/severity and for monitoring response to treatment at 2 and 4 month follow up. Methods: 105 adult literate persons having rheumatoid arthritis according to the 2010 ACR EULAR revised criteria were included. They were evaluated for disease activity by DAS 28, CDAI, and RAPID 3 scores. Response to treatment at 2 month and 4 month follow up was measured by these scores. Achievement of treatment target was defined as conversion from high/moderate disease activity at initial visit to low activity/remission at follow up visit. Result: The mean DAS 28 (0-10), CDAI (0-76) , RAPID 3 (0-30) were 4.73 , 16.72, 10.72 respectively. There was substantial agreement between DAS 28 and RAPID 3 severity categories (kappa = 0.959, P < 0.0001) and also between CDAI and RAPID 3. Conclusion: In a busy clinical setting, our study has shown usefulness of RAPID3 compared to the two most commonly used indices to assess disease activity in RA, both in terms of measuring quantitative disease activity as well as monitoring of treatment response at follow up visits.

Background: Systemic lupus erythematosus (SLE), a systemic autoimmune disease, occurs due to disruption of immune homeostasis against self-antigens. The etiology of SLE is complex and multiple genetic factors contribute to disease susceptibility and clinical phenotypes. Protein tyrosine phosphatase, nonreceptor type 22 (PTPN22) is a lymphoid-specific phosphatase that negatively regulates T-cell receptor signaling and is responsible for the maintenance of T-cell homeostasis. Genetic aberrations affecting the function of PTPN22 result in the proliferation of autoreactive T-cells and development of autoimmune diseases. Methods: We carried out a case–control genetic study to analyze the association of PTPN22 R620W polymorphism (rs2476601) with disease susceptibility and clinical and autoantibody profile in Indian Tamils with SLE. Three hundred SLE patients satisfying the 1997 revised American College of Rheumatology classification criteria for SLE were enrolled in the study. Disease activity was measured using the SLE Disease Activity Index. We recruited 460 age-, sex-, and ethnicity-matched individuals without a family history of autoimmune diseases as control population. Genomic DNA was extracted from the blood sample by salting-out method. The PTPN22-1858C->T (rs2476601) polymorphism was screened by polymerase chain reaction-restriction fragment length polymorphism. Results: The frequency of the ancestral allele “C” was similar in both cases and controls (99.3% and 99.8%, respectively) and the mutant allele “T” was less frequent in South Indian Tamil population; it did not influence clinical or serological phenotypes. Conclusion: Our findings suggest that the PTPN22 (rs2476601) polymorphism is less frequent and did not confer a risk for lupus or its associated clinical or serological phenotypes in South Indian Tamils.

Vitamin D and its deficiency are becoming a subject of great interest in recent years. In addition to the well-known role of vitamin D in maintaining bone health, evidence from recent years are accumulating in favor of its importance in the functioning of the immune system. The association between vitamin D deficiency and autoimmune diseases has been supported by epidemiological studies, demonstrating higher prevalence of vitamin D deficiency among autoimmune patients, in comparison to the general population. Vitamin D was also associated to various autoimmune diseases in both molecular and interventional studies; among the associated diseases are: systemic lupus erythematosus, type 1 diabetes mellitus, multiple sclerosis and others. In this review, relevant literature on the association between autoimmunity and vitamin D deficiency will be reviewed and discussed, as well as a summary of important recommendations for vitamin D supplementations in autoimmune patients.