Hyperbilirubinemia Maintained by Chronic Supplementation of Unconjugated Bilirubin Improves the Clinical Course of Experimental Autoimmune Arthritis.

Rheumatoid arthritis (RA) is a chronic multisystem disease, therapy of which remains a challenge for basic research. The present work examined the effect of unconjugated bilirubin (UCB) administration in adjuvant-induced arthritis (AIA)-an experimental model, in which oxidative stress (OS), inflammation and inadequate immune response are often similar to RA. Male Lewis rats were randomized into groups: CO-control, AIA-untreated adjuvant-induced arthritis, AIA-BIL-adjuvant-induced arthritis administrated UCB, CO-BIL-control with administrated UCB. UCB was administered intraperitoneally 200 mg/kg of body weight daily from 14th day of the experiment, when clinical signs of the disease are fully manifested, to 28th day, the end of the experiment. AIA was induced by a single intradermal immunization at the base of the tail with suspension of Mycobacterium butyricum in incomplete Freund's adjuvant. Clinical, hematologic, biochemical and histologic examinations were performed. UCB administration to animals with AIA lead to a significant decrease in hind paws volume, plasma levels of C-reactive protein (CRP) and ceruloplasmin, drop of leukocytes, lymphocytes, erythrocytes, hemoglobin and an increase in platelet count. UCB administration caused significantly lowered oxidative damage to DNA in arthritic animals, whereas in healthy controls it induced considerable oxidative damage to DNA. UCB administration also induced atrophy of the spleen and thymus in AIA and CO animals comparing to untreated animals. Histological signs of joint damage assessed by neutrophils infiltration and deposition of fibrin were significantly reduced by UCB administration. The effects of exogenously administered UCB to the animals with adjuvant-induced arthritis might be identified as therapeutic, in contrast to the effects of UCB administration in healthy animals rather classified as toxic.

Left Ventricle Outflow Obstruction by Reverse-Oriented Tricuspid Semilunar Valve-Like Endocardial Duplicatures.

A 57-year-old female had a history of hypertension disease, and one year before her death, her ECG showed signs of left ventricle hypertrophy. She died with signs of heart failure with pulmonary edema development. At autopsy, there was left ventricle hypertrophy (wall thickness: 21 mm). In the left ventricle outflow channel, 15 mm below the aortic valve on the muscular wall, there were three white 1-1.5 mm thick membranous semilunar valve-like structures with the sizes of 9, 7, and 5 mm, with concavities opened into the left ventricle, reducing the outflow area by 21.5%. These structures were hanging on the regular muscular ventricular wall, without any visible fibrous anchoring structure and without formation of commissures, and were composed of fine collagen and elastic fibers. Gross anatomy as well as histological structure was different from the subaortic membrane. The reported accessory reverse-oriented tricuspid semilunar valve-like structure is an unusual finding of a structure in the left ventricular outflow tract, to which we could not find an analogy in the available literature.