Subcutaneous cysticercosis mimicking tenosynovitis: a rare case with radiological revelation

Subcutaneous cysticercosis is a rare manifestation of cysticercosis, caused by the larval stage of Taenia solium. It presents as a swelling or a palpable cystic mass. We describe a 43-year-old female who presented with subcutaneous swelling over her right hand, gradually increasing in size over ten days. Initially, tenosynovitis was suspected clinically. However, an ultrasound of the hand revealed a well-defined, cystic lesion with eccentric echogenic foci and peripheral oedema suggestive of cysticercosis. She was treated with oral albendazole, leading to significant improvement. This case report emphasizes the importance of considering parasitic infections as a potential cause of subcutaneous swelling. It also highlights the significance of utilizing diagnostic imaging for definitive diagnosis and timely treatment

Expression of TNF-α and Related Signaling Molecules in the Peripheral Blood Mononuclear Cells of Rheumatoid Arthritis Patients

We examined the role of tumor necrosis factor (TNF-α) and its related signaling intermediates leading to apoptosis/proliferation in the peripheral blood mononuclear cells (PBMCs) of RA patients. The constitutive expression of mRNA for TNF-α receptors (TNFR-I and TNFR-II) and the adapter molecules, such as the TNF receptor-associated death domain protein (TRADD), Fas-associated death domain protein (FADD), receptor interacting protein (RIP), and TNF receptor-associated factor 2 (TRAF-2) were analyzed by reverse transcriptase-PCR (RT-PCR) in PBMCs from control and RA cases. PBMCs of RA patients showed a significant increase in TNF-α and TNFR-I expression as compared with that from control subjects along with significantly increased constitutive expression of TRADD, RIP, and TRAF-2 mRNA. There was a decrease in expression of FADD in RA patients, but the difference was not significant as compared to controls. These data suggested enhanced signaling by the TNFR-I-TRADD-RIP-TRAF-2 pathway and suppressed signaling by the TNFR-I-TRADD-FADD pathway in PBMCs of RA patients. However, the regulatory mechanisms for TNF-α induced signaling may not be explained only by these pathways