Primary antibody deficiencies (PADs) are the most common inherited primary immunodeficiencies in humans, characterized by hypogammaglobulinemia, an inability to produce specific antibodies, and recurrent infections mainly caused by encapsulated bacteria. However, it has been shown that inflammatory disorders, granulomatous lesions, lymphoproliferative diseases, cancer, and autoimmunity are associated with the various types of PAD. Both systemic and organ-specific autoimmune diseases could be attributed to B-cell defects in PAD patients. Immune thrombocytopenic purpura and autoimmune hemolytic anemia are the most common autoimmune disorders in this group of patients. The aim of this review is to describe the proposed mechanisms for autoimmunity and to review the literature with respect to the reported autoimmune disorders in each type of PAD.

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The subclavian steal syndrome (SSS), also called subclavian steal steno-occlusive disease, is defined as reversal of the vertebral artery flow secondary to significant hemodynamically ipsilateral occlusion or stenosis of the proximal subclavian artery. It is usually seen secondary to atherosclerosis and aberrant right subclavian artery (ARSA), resulting in SSS which is even less common. Aberrant right subclavian artery is a kind of vascular anomaly associated with coarctation of the aorta (CoA). It usually originates from the descending aorta distal to the site of CoA. Here, we present a young man who was a case of ARSA and CoA. He developed SSS after transcatheter aortic stenting secondary to unusual origin of ARSA from the site of CoA. Awareness of this rare anomaly helps to overcome this complication in patients undergoing interventional stenting for CoA and ARSA with anomalous origin.

Objective Placenta accreta is a pregnancy-related disorder with extreme trophoblast invasion and the adherence of the placenta to the uterine wall. This study aimed to investigate the serum level of transforming growth factor-beta 1 (TGF-β1) and interleukin (IL)-35 in patients with placenta accreta. Methods Thirty-one women with placenta accreta and 57 healthy pregnant women were enrolled. The serum levels of TGF-β1 and IL-35 were measured using the enzyme-linked immunosorbent assay method. Results The serum levels of both TGF-β and IL-35 were significantly higher in the placenta accreta group compared with the group of healthy women (1082.48 pg/mL vs 497.33 pg/mL and 4541.14 pg/mL vs 1306.04 pg/mL; P <.001, respectively). Moreover, the level of TGF-β1 positively correlated with the IL-35 level but other factors such as age, gestations, live births, and abortions did not correlate with IL-35 and TGF-β1 levels. Conclusion The serum levels of IL-35 and TGF-β1 may contribute to the pathogenesis of placenta accreta and could be considered as potential targets in clinical and diagnostic approaches.

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