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Key Clinical Message: In ankylosing spondylitis cases, axonal-type sensory-motor polyneuropathy is a rare manifestation and should be considered an underlying etiology in patients with unexplained neuropathy. Abstract: This case report discusses a 45-year-old male diagnosed with ankylosing spondylitis (AS), a chronic inflammatory disorder affecting the axial skeleton and peripheral joints. The patient presented with polyneuropathy, characterized by tingling and numbness in the upper and lower limbs, which is an uncommon manifestation of AS. After undergoing various tests, including CT scans and EMG-NCV, no secondary cause for the neuropathy was identified; AS was considered the etiology of the patient's axonal-type sensory-motor polyneuropathy.

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BACKGROUND: Ankylosing spondylitis (AS) is an inflammatory rheumatic disease that leads to a progressive ankylosis of vertebras and ossification of paravertebral ligaments. Bone loss and osteoporosis are amongst the important complications of AS, treatment of which is a challenging issue. OBJECTIVES: This study aimed to clarify the effect of alendronate on the prevention of bone loss in patients with early AS. PATIENTS AND METHODS: In a randomized, double-blind, placebo-controlled study, 24 patients with early stages of AS were recruited in Emam Reza Hospital, Tabriz University of Medical Sciences. The diagnostic criteria of early AS were Schober's index ≥ 5, normal hip joint in pelvic radiography, and absence or rarity of syndesmophytes in spine radiography (Taylor index ≤ 1). The participants were randomly allocated to the treatment and control groups and received 70 mg/week of alendronate and the same dose of placebo, respectively, for 12 months. Before and 12 months after the intervention, bone densitometry was performed from lumbar and pelvic region using the dual-energy X-ray absorptiometry (DEXA) method with Hologic QDR model instrument. Patients, physicians who prescribed the medications and those who interpreted the outcomes, and densitometry technicians were unaware of the assigned medication to each patient. Both groups received supplemental calcium (1000 mg/day) and vitamin D (400 mg/day). RESULTS: After 12 months of treatment, hip and lumbar bone mineral density differences were not statistically significant between study groups (P = 0.061 and P = 0.112, respectively). No case of clinically apparent vertebral and nonvertebral fracture were observed in the treatment and control groups. CONCLUSIONS: Our results suggested that applying alendronate was ineffective in preventing bone loss in patients with early stages of AS.

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AIM: The objective of this study was to compare the efficacy and safety of dexamethasone and methylprednisolone for pulse therapy of rheumatoid arthritis flare-up. METHODS: This randomized double-blind controlled study was performed in the Emam Reza Educational Hospital of Tabriz University of Medical Sciences, Tabriz, Iran. Thirty rheumatoid arthritis patients who had severely active disease were recruited to the dexamethasone and methylprednisolone pulse groups. Disease activity of all the patients was measured by the Disease Activity Score in 28 joints (DAS28) at baseline, and days 4 and 30. RESULTS: The differences in the DAS28 at days 4 and 30, and the number of patients whose DAS28 obtained less than 3.2 and 2.6 in the dexamethasone and methylprednisolone groups were non-significant. There was not any significant difference between the adverse effects of the treatments in the two groups. CONCLUSIONS: The results of the study suggest that dexamethasone pulse therapy is a safe and effective treatment for severe rheumatoid arthritis flare-up.

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BACKGROUND: The familial clustering of rheumatoid arthritis (RA) in first and second degree relatives of patients supports the role of genetic factors. The proportion of heredity in its development is roughly 60%; however, most individuals closely related to someone with RA do not get the disease. Considering the lack of sufficient data on the familial aggregation of RA in Iran, we designed this study for clarifying the familial prevalence of RA. OBJECTIVE: To determine the prevalence of RA among relatives of patients with RA and to evaluate the mean disease onset age in relatives. METHODS: In a longitudinal study from July 2008 to July 2010, we followed 210 unrelated patients with RA and their first and second degree relatives (FDR+ and SDR+), by interviewing and physical examination of those with symptoms, to ascertain prevalence. Familial RA was defined by presence of at least two siblings fulfilling the 1987 ACR criteria for RA. RESULTS: We demonstrated that 17.6% of patients have at least one affected relative. The prevalence of RA in the family of studied patients was 0.83% (42 people). Thirty-two in FDR+ and 10 people in SDR+ (2.53% and 0.26% of all family), also 1.12% in female relatives and 0.39% in male relatives had RA. The odds ratio for FDR/SDR was 2.52. The mean age at disease onset in relatives was 42.30 ± 1.51 years in FDR+ and 34.40 ± 2.10 years in the SDR+ group (0.03). CONCLUSION: The risk of RA is greatest in FDR+ and is likely to be due to a combination of inherited and environmental factors.

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Genetic factors that predispose individuals to Behcet's disease (BD) are considered to play an important role in the development of the disease. The serum level of tumor necrosis factor (TNF) is elevated in patients with BD, and a dramatic response to anti-TNF-alpha antibody treatment further supports the role of TNF in BD. We investigated the distribution of TNF-alpha promoter -1031T/C and -308G/A polymorphisms in 53 BD patients of Iranian Azeri Turks and 79 matched healthy controls, via the PCR-RFLP technique. The frequency of the TNF-alpha -1031C allele was significantly higher in Behcet's patients than in healthy controls (p < 0.0001, OR = 3.08; 95% CI = 1.73-5.47), whereas the frequency of the TNF-alpha -308A allele was similar in the two compared groups. The frequency of CG haplotype was significantly higher (p < 0.0001, OR = 3.42; 95% CI = 1.89-6.18), and that of the TA haplotype was significantly lower in BD patients than in healthy controls. These results suggest that TNF-alpha is a susceptibility gene for BD in patients from Iranian Azeri Turk ethnic group.

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