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A 58-year-old woman with a history of Sjogren’s syndrome was admitted to our hospital with cough, decreased right lung breath sounds and arthralgia in both thumbs. Chest computed tomography showed consolidation with air bronchogram in the right lung. Levels of anti-cyclic citrullinated peptide antibody and rheumatoid factor levels were significantly elevated. She was diagnosed with rheumatoid arthritis induced by bacterial organizing pneumonia. Treatment with salazosulfapyridine was added for rheumatoid arthritis and arthralgia gradually improved. This case highlights that respiratory infections could lead to anti-cyclic citrullinated peptide antibody-positive rheumatoid arthritis in patients with Sjogren’s syndrome.

We herein report the first case of lupus-related protein-losing enteropathy associated with pseudo-pseudo Meigs’ syndrome. Lupus-related protein-losing enteropathy and pseudo-pseudo Meigs’ syndrome are extremely rare complications in patients with systemic lupus erythematosus, Both have a similar clinical course characterized by producing marked ascites, and respond to steroids in typical cases. However, in our case, steroid monotherapy was inadequate and the addition of hydroxychloroquine was effective for their treatment. Furthermore, no reports have previously confirmed elevated CA 125 levels with lupus-related protein-losing enteropathy or increased 99mTc-HSA activity with pseudo-pseudo Meigs’ syndrome. In addition, we are the first to report an evaluation of the histopathology of lupus-related protein-losing enteropathy. Previously reported cases have been described as being caused by either pseudo-Meigs’s syndrome or lupus-related protein-losing enteropathy as the cause of the rare pathology that causes marked pleural effusion and ascites in patients with systemic lupus erythematosus, but it has not been evaluated whether the other is co-occurring. Our case highlights that there is a potential case of overlapping lupus-related protein-losing enteropathy and pseudo-Pseudo-Meigs’s syndrome. Furthermore, it is possible that patients with marked ascites with elevated CA 125 levels were mistakenly diagnosed with Meigs’s syndrome or pseudo-Meigs’s syndrome associated with malignant or benign ovarian tumors and underwent surgery. Clinicians should not forget SLE with pseudo-Pseudo-Meigs’s syndrome as one of the differential diagnoses for marked ascites with elevated CA 125 levels.

The histomorphological features of normal kidneys in cats and dogs have been revealed despite the high susceptibility of cats to tubulointerstitial damage. Herein, the histological characteristics of the two species were compared. Cytoplasmic lipid droplets (LDs) were abundant in the proximal convoluted tubules (PCTs) of cats aged 23–27 months but scarce in dogs aged 24–27 months. LDs were rarely observed in the distal tubules (DTs) and collecting ducts (CDs) of either species, as visualized by the expression of Tamm–Horsfall protein 1, calbindin-D28K, and aquaporin 2. The occupational area ratio of proximal tubules (PTs) in the renal cortex was higher, but that of DTs or CDs was significantly lower in adult cats than in dogs. Single PT epithelial cells were larger, but PCT, DT, and CD lumens were significantly narrower in adult cats than in dogs. Unlike adults, young cats at 6 months exhibited significantly abundant cytoplasmic LDs in proximal straight tubules, indicating lipid metabolism-related development. Histochemistry of the 21 lectins also revealed variations in glycosylation across different renal tubules and CDs in both species. Sodium-glucose cotransporter 2 was expressed only in PTs, excluding the proximal straight tubules with few LDs in adult cats or the PCTs of young cats and adult dogs. These findings are crucial for understanding species-specific characteristics of renal histomorphology and pathogenesis. [ABSTRACT FROM AUTHOR]

Introduction. Although type 1 diabetes mellitus is largely associated with autoimmune thyroid disease and this entity has been recently referred to as autoimmune polyglandular syndrome type 3 variant, the autoimmune polyglandular syndrome type 3 variant in patients with rheumatoid arthritis has not been reported so far. We herein describe the first case of rheumatoid arthritis that was associated with autoimmune polyglandular syndrome type 3 variant.

Kikuchi-Fujimoto disease (KFD), also known as histiocytic necrotizing lymphadenitis, is a rare, benign, self-limiting disease characterized by cervical lymphadenopathy and fever. Since KFD was first reported in 1972, the validity of this clinical entity has been controversial and its aetiology remains unknown. Herein, we report a case of a patient with KFD, which was believed to be associated with systemic lupus erythematosus.

Macrophage activation syndrome (MAS), a variant of secondary hemophagocyticlymphohistiocytosis, is a potentially life-threatening complication of inflammatory and autoimmune diseases. We present a case of MAS as a rare manifestation of systemic lupus erythematosus. Although initial treatment with corticosteroid, with or without cyclosporine A, is justified in patients with MAS, evidence regarding the effectiveness of this treatment protocol remains to be clarified. Our patient was successfully treated with a combination of intravenous immunoglobulin therapy and intravenous methyl predonisolone pulse therapy, which was followed by a course of oral prednisolone and oral tacrolimus. Based on our experience, we propose tacrolimus to provide a more useful adjuvant treatment to corticosteroid therapy than cyclosporine A.