ABSTRACT
Background: Two recognized antibodies, Rheumatoid Factor (RF) and Anti-Citrullinated Peptide Antibody (ACPA), are produced in rheumatoid arthritis to target common autoantigens that are expressed in and around the joints. Tobacco and microorganisms, as well as the relationship between genetics and environment, play a critical role in the progression of the illness (e.g. Porphyromonas gingivalis). Rheumatoid arthritis is visualized as a Th1 and Th17 illness in the first stages of the disease. There is a significant role for inflammatory cytokines in the hierarchy of RA processes. Additionally, RA-related joint degradation is mediated by the Wnt system and osteoprotegerin抯 impact on osteoclasts, as well as the matrix synthesis dysregulation that causes cartilage degeneration. Rheumatoid arthritis is a disease in which both innate and adaptive immunity have been shown to play a key role, thanks to the development of effective therapies for TNF-, IL-6 receptor, IL-1, CD20 B cells, and T-cell/Dendritic cell interactions.
ABSTRACT
Splenic abscess is a rare clinical condition and yet rarer is a tubercular splenic abscess. Here we report a case of tubercular splenic abscess. A forty years old male patient was admitted in Medicine unit of Mymensingh Medical College Hospital (MMCH) on 09-08-2006 with the complaints of Left upper quadrant abdominal pain and fever for 15 days and Respiratory difficulty for 2 days. Two days after admission he developed generalized abdominal pain and distension. Pain was not associated with vomiting. Patient was transferred to surgical unit for features of peritonitis. Ultrasonogram of whole abdomen revealed moderately enlarged spleen showing 8.8 x 9.7 cm semicystic mass, which may represent an abscess. There was mild free fluid collection in the lower abdomen. X-ray chest P/A view showed bilateral pleural effusion. On laparotomy huge amount of free pus was found in the peritoneal cavity and the spleen was hugely enlarged with a burst abscess cavity in it. Splenectomy and thorough peritoneal toileting was done. Postoperative recovery was uneventful except few stitch infections. Pus culture revealed no growth but histopathology of spleen confirmed Tubercular Splenic Abscess. Patient was given an antitubercular regimen with Rifampicin, Isoniazid, Ethambutol and Pyrazinamide for initial two month which to be followed by Rifampicin and Isoniazid for another ten months.