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Background Immunoglobulin G4 (IgG4)-related disease is a chronic inflammatory disease that was recognized in 2011. Pleuritis associated with IgG4-related disease is rare and can be difficult to diagnose. Although there have been previous reports on pleuritis associated with IgG4-related disease by thoracoscopic findings, this is the first to observe pleuritis with IgG4-related disease from normal pleural thoracoscopic findings. Case presentation A 70-year-old Japanese female treated for breast cancer 33 years ago was referred to our hospital complaining of dyspnea on exertion. Chest computed tomography (CT) revealed left pleural effusion that was exudative and predominant with lymphocytes, elevated adenosine deaminase (ADA) and Class III cytology (malignancy suspected). Subsequently, thoracoscopic pleural biopsy was performed for definitive diagnosis. Although pleural macroscopic findings appeared normal, we performed pleural biopsy at random sites. This patient was negative for mycobacterium tuberculosis, and neither granulomas nor malignant cells were found in the collected specimens. An infiltration of inflammatory cells, mainly plasma cells and lymphocytes, was observed. Immunostaining revealed the number of IgG4-positive plasma cells was 102/high power field (HPF), and the percentage of IgG4 positive/immunoglobulin G (IgG)-positive cells was 41.4%. Since IgG4 serum levels were high and IgG4-related submandibular sialadenitis was also observed, a definitive diagnose of pleuritis associated with IgG4-related disease was confirmed. Conclusions We diagnosed pleuritis associated with IgG4-related disease by thoracoscopic pleural biopsy samples taken from a visually normal pleura. Although exudative pleural effusion with high ADA and lymphocyte predominance is a characteristic of tuberculous pleuritis, other diseases might be present. Since thoracoscopy can increase the diagnostic yield, pleural biopsy should be considered even if thoracoscopic pleural findings are deemed normal.

The possible protection of cultured human cells from acute dioxin injury by antioxidants was investigated. The most potent dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), caused vacuolization of the smooth endoplasmic reticulum and Golgi apparatus in cultured human conjunctival epithelial cells and cervical cancer cells. Subsequent nuclear damage included a deep irregular indentation resulting in cell death. A dosage of 30-40 ng/mL TCDD induced maximal intracellular production of H2O2 at 30 minutes and led to severe cell death (0-31% survival) at two hours. A dose of 1.7 mM alpha-tocopherol or 1 mM L-dehydroascorbic acid significantly protected human cells against acute TCDD injuries (78-97% survivals), but vitamin C did not provide this protection. These results indicate that accidental exposure to fatal doses of TCDD causes cytoplasmic free radical production within the smooth endoplasmic reticular systems, resulting in severe cytotoxicity, and that vitamin E and dehydroascorbic acid can protect against TCDD-induced cell damage.

Occasionally, over-anticoagulation with warfarin induces acute kidney injury (AKI) characterized by glomerular hemorrhage with tubular obstruction by red blood cell casts, which is widely acknowledged as warfarin-related nephropathy. Owing to extensive use of direct oral anticoagulants, similar AKI cases have been reported among patients treated with dabigatran. Dabigatran is primarily excreted by the kidneys; thus, renal impairment is one of the risk factors for dabigatran-induced bleeding complications. Nevertheless, risk factors for dabigatran-induced anticoagulant-related nephropathy (ARN) remain partially clarified. Here, we report a histologically established case of dabigatran-induced ARN with undiagnosed IgA nephropathy in a patient with normal baseline renal function. In addition, we summarize previously published cases of biopsyproven, dabigatran-related ARN. A 67-year-old female with normal preexisting renal function developed macrohematuria and AKI. She had been treated with dabigatran for deep vein thrombosis. A renal biopsy diagnosed ARN with inactive IgA nephropathy. After dabigatran withdrawal, her macrohematuria and renal function improved. This report demonstrates that ARN could occur in patients with normal baseline renal function. Our case and prior reports suggest that IgA nephropathy could be a risk factor for dabigatran-induced ARN.