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The authors prospectively investigated 155 pregnant women, without a history of rheumatic disease who visited the Department of Obstetrics and Gynecology for routine antenatal care, to evaluate the prevalences and clinical features of arthralgia and arthritis in healthy pregnant women. Mean of the 155 subjects’ ages was 31.8 ± 3.8 (years, ±SD). Arthralgia was found in 26 (16.7%) and arthritis in 15 (9.6%) pregnant women. Arthralgia or arthritis developed in the third trimester (28–40 weeks of gestation), except in one case (16 weeks of gestation). Most commonly involved joints were the proximal interphalangeal (n = 19, 12.2%). Rheumatoid factor and antinuclear antibody were negative in patients with arthritis. Ten women (6.8%) had persistent arthralgia for over 6 weeks, post-delivery. Four of them were followed up at Rheumatology Clinic and were diagnosed as having spondyloarthropathy (1), or unspecified arthralgia (3). In conclusion, arthralgia is common during pregnancy and most frequent in proximal interphalangeal joints.

Antibody activity against collagen was measured in 53 samples of serum from 48 patients with active signs of epidemic polyarthritis (EPA) following infection with Ross River virus. Activity was higher against denatured collagen than against native collagen, but was within the normal range for each. Determination of HLA phenotypes permitted a search for any relationship between HLA type and differences in collagen antibody levels within the normal range. No relationship was detected with HLA antigens predominating in EPA or with HLA antigens that are associated with high collagen-antibody levels in rheumatoid arthritis (RA), which suggests that the latter associations may represent failure to control collagen antibody levels after the onset of RA. The findings also provide evidence against a role for nonspecific enhancement of humoral immune responses in the pathogenesis of EPA, and constitute a further point of distinction between EPA and RA.

Familial Mediterranean fever (FMF) is a monogenic autoinflammatory disease characterized by fever and serositis attacks caused by mutations in the MEditerranean FeVer (MEFV) gene encoding the pyrin gene. Gain of the function mutations of the pyrin gene lead to stimulation of pro-inflammatory cytokines. Persistent pro-inflammatory situation in the course of FMF may play a role in the development of some other inflammatory diseases such as Behcet’s disease, psoriasis, and vasculitis. Multiple sclerosis (MS), as a demyelinating disorder, is also more commonly seen in FMF patients compared to the general population. There are scarcely any research reporting that these two diseases coexist in more than one person in the same family. We have discovered cases of FMF and demyelinating disorders in five members of two different families. Besides the two families we are reporting, there are only four other families reported so far. Having combined the data of all these six families, we present a case-based review in this study. We aimed to draw attention of physicians to familial co-occurence of FMF and demyelinating disorders and also to discuss possible mechanisms of the coexistence of these two diseases in light of the literature.

Familial Mediterranean fever (FMF) is an inflammatory disorder that is leading cause of secondary amyloidosis (AA). This study was designed to investigate the level of mean platelet volume (MPV) in AA. Seventy-four FMF, 29 AA patients and 180 healthy controls, were included. There was no significant difference between the cases in terms of sex and age. MPV levels were measured in all groups. In the FMF group, MPV level was significantly higher when compared to the control group. MPV level was significantly lower in AA group in comparison with the FMF and healthy control groups. In summary, our present study showed low MPV values in AA due to FMF.

The disease burden, risk factors and clinical sequelae of CMV reactivation in patients with rheumatologic conditions is poorly understood. We have described a cohort with underlying rheumatic disease and CMV, and compared a subgroup with systemic lupus erythematosus (SLE) to controls to identify potential risk factors for CMV reactivation. Adults with rheumatic disease and CMV infection from 2000–2015 were identified. SLE cases were matched 3:1 with controls based on age, sex and year of admission, and compared. Fourteen patients were included (6 SLE, 4 rheumatoid arthritis, 2 sarcoidosis, 1 psoriatic arthritis, 1 microscopic polyangiitis). Seven had viremia alone, the remainder tissue-invasive disease. Thirteen received glucocorticoids prior to CMV reactivation. Fever was the most common symptom, and coinfections were seen in eight including four with bacteremia. Thirteen received antiviral therapy (median 33 days), four died during hospitalization. Six patients with underlying SLE and CMV reactivation were compared to 18 SLE controls. Cases received more glucocorticoids prior to admission (median 36.5 vs. 2.5 mg/day, p = 0.006), had longer hospitalizations (median 47 vs. 7 days, p = 0.006) and more coinfections (67% vs. 17%, p = 0.04). There were no significant differences in symptoms at presentation. CMV reactivation occurs in patients with rheumatologic disease, can result in severe clinical sequelae, and is difficult to distinguish from a flare of the underlying disease. Patients with CMV received higher doses of glucocorticoids and developed more co-infections. CMV should be considered during the evaluation of a febrile illness in this complex patient population.

The aim of the present study was to investigate the association between Collagen 1 alpha 1 (COL1A1) polymorphism and osteoporosis in DEXA verified 349 (145 osteoporotic, 87 osteopenic and 117 normal) postmenopausal women of India, who were not taking hormone replacement therapy. Two single-nucleotide polymorphisms (SNPs), that is, −1997G/T (rs1107946) and +1245G/T (rs1800012, Sp1) of the COL1A1 gene, were analyzed. Minor allele frequencies of rs1107946 and rs1800012 were 0.15 and 0.20 in osteoporotic women, 0.18 and 0.18 in osteopenic and 0.20 and 0.17 in women having normal bone mass. An allele dose effect with BMD of lumbar spine has been exhibited by major allele G of rs1107946 (GG: 0.86 g/cm2, GT: 0.91 g/cm2 and TT: 0.93 g/cm2) and minor allele T of rs1800012 (GG: 0.91 g/cm2, GT: 0.87 g/cm2 and TT: 0.81 g/cm2). Disease association analysis revealed a haplotype GT that confers approximately threefold higher risk of osteoporosis in the carriers (OR 3.12, 95% CI 1.24–8.88, P = 0.008) after adjusting the confounding effect of age, BMI and years since menopause. These results suggest that GT haplotype of COL1A1 gene is associated with a higher risk of postmenopausal osteoporosis in Northwest Indian women.