Macrophage activation syndrome (MAS) is a complex, life-threatening, hyperinflammatory condition occurring as a form of hemophagocytic lymphohistiocytosis (HLH), commonly associated with several autoimmune and autoinflammatory diseases, and certain infections such as Parvovirus B19 (P19V). The onset of systemic lupus erythematosus (SLE) presenting as MAS during pregnancy is uncommon, posing significant diagnostic and therapeutic challenges. We present a case of a 30-year-old woman at the 12th gestational week with fever, arthralgia, rash, cervical lymphadenopathy, cytopenia, and elevated liver enzyme. Bone marrow biopsy revealing hemophagocytosis, elevated ferritin and triglycerides, high interleukin-2, fever and cytopenia, confirmed the diagnosis of HLH. Further evaluation revealed the diagnosis of SLE. Treatment was initiated with intravenous immunoglobulin and corticosteroids. Given the deterioration in the patient’s clinical condition, a decision was made to terminate the pregnancy. She continued in the following months to receive SLE treatment with corticosteroids, cyclophosphamide, hydroxychloroquine, and later with mycophenolate mofetil due to the development of Class IV of lupus nephritis. P19V IgM antibodies were initially positive, later seroconverted to IgG, indicating that infection may have acted as a trigger for the onset of SLE and MAS development during pregnancy. The overlapping clinical features of P19V infection, SLE, and MAS pose significant diagnostic and therapeutic challenges. Early recognition and comprehensive diagnostic evaluation are crucial for the management of these conditions, especially during pregnancy, where both maternal outcomes are at risk.

Background: Takayasu arteritis (TA) is a large-vessel vasculitis with an incompletely understood pathogenesis, in which genetic factors are thought to play an important role. Cytokine-mediated immune pathways, particularly those involving Th1 and Th17 responses, have been implicated in the immunopathogenesis of TA, making cytokine gene polymorphisms plausible genetic susceptibility markers. Methods: Functional single-nucleotide polymorphisms in selected cytokine- and receptor-encoding genes (IL12B, IL23R, IL6, TNF, IL10, and CSF2) were analyzed in 33 patients with TA and 486 healthy Serbian controls using TaqMan genotyping assays. Allele and genotype frequencies were compared between groups. Results: A nominally significant association was observed only for IL12B rs3212227. The T allele and TT genotype were less frequent in patients compared with controls (71.21% vs. 82.02%, p = 0.037; 48.48% vs. 66.67%, p = 0.041, respectively), suggesting a potential protective effect. No significant associations were detected for polymorphisms in IL23R, IL6, TNF, IL10, or CSF2. Conclusions: Our findings support the potential role of IL12B in genetic susceptibility to Takayasu arteritis, while other examined cytokine gene polymorphisms showed no statistically significant association. These results highlight the importance of the IL-12/IL-23 axis in disease pathogenesis and suggest possible population-specific genetic effects. Further studies in larger and independent cohorts are warranted to validate these findings.

Introduction: Patients with refractory chronic spontaneous urticaria (CSU) may pose a significant challenge to the treating physician. Although many studies have investigated the effects of omalizumab in refractory CSU, many issues remain unanswered. Aim: To describe our experience in treating refractory CSU with omalizumab in a real-life setting. Material and methods: We present a series of eight patients with refractory CSU treated with omalizumab during a 2-year period. Results: The average duration of CSU was 49.9 months (3-180). A high average 7-day Urticaria Activity Score (UAS7) of 31.3 (12-42) and a low average Urticaria Control Test (UCT) score of 4.1 (0-8) had been recorded before omalizumab therapy. Prior to omalizumab, all patients required fourfold dose of H1-anihistamines, montelukast and corticosteroids to achieve at least a partial disease control. Antimalarial was given to two patients and dapsone to three, with no response. Adverse effects of corticosteroids were noted in most patients. Patients received 150 mg or 300mg of omalizumab subcutaneously every 4 weeks, for at least 3 months. All patients responded well to omalizumab and discontinued corticosteroid therapy. There were no significant side effects during omalizumab treatment. Conclusion: Omalizumab is an effective corticosteroid sparing treatment, enabling disease control in patients with refractory CSU, even in lower doses (150 mg) and when given for a short period of time. This is especially important when the availability of the drug is determined by economic issues.