Advanced Erosive Gouty Arthropathy of the Knee.

A 57-year-old male, with chronic bilateral knee pain and a history of poorly controlled hyperuricemia leading to gouty attacks, underwent orthopedic assessment. Radiographic and MRI findings confirmed chronic gouty arthropathy with erosive bony defects, the most significant on the right proximal tibia. Total knee arthroplasty (TKA) was performed without any complications, addressing the bony defect with cement and a semi-constrained prosthesis. However, a gouty attack led to prolonged wound discharge and periprosthetic infection postoperatively, prompting revision surgery with debridement, antibiotics, and implant retention (DAIR). Intraoperative cultures revealed methicillin-sensitive Staphylococcus aureus (MSSA). The treatment included vancomycin and rifampicin. Two years post-surgery, the patient walked pain-free with a knee range of motion of 0-90º. This report highlights the complexity of treating gout-related knee osteoarthritis, emphasizing early intervention to mitigate risks of extensive surgical procedures and infections.

Acute Carpal Tunnel Syndrome Secondary to Gout Flare and Outcomes at 18 Months After Open Carpal Tunnel Decompression.

Acute carpal tunnel syndrome is a rare condition that requires immediate surgery. Although numerous causes have been described in the literature, only 7 reports of acute carpal tunnel syndrome secondary to gout have been reported, all with short follow-ups. We report, to our knowledge, the first case of carpal tunnel syndrome presenting with total anesthesia of the fingers innervated by the median nerve and complete recovery of the sensory and motor function after carpal tunnel decompression, with no recurrence at the 18-month follow-up. To prevent irreversible damage to the nerve, treatment should not be delayed.

Development, characterization and in vitro evaluation of single or co-loaded imatinib mesylate liposomal formulations.

Mitoxantrone-based combinations are a standard palliative treatment in hormone-refractory prostate cancer (HRPC) but with no survival benefit. Imatinib has shown preclinical activity against HRPC although minimal clinical therapeutic efficacy. Our previous in vitro studies demonstrated that simultaneous combination of imatinib with mitoxantrone yielded additive growth inhibition effects against PC-3 cell line. The main aim of the work was to develop novel liposomal formulations comprising imatinib co-encapsulated with mitoxantrone, by different loading methods and experimental conditions, in order to achieve the highest drug loading and maximum physical stability. In the optimized formulations, imatinib and mitoxantrone were actively co-loaded by means of a (NH4)2SO4 transmembrane gradient. Encapsulation efficiency, mean size diameter and drug retention in storage and in biological conditions were characterized. Our study presented for the first time an active loading method for imatinib and suggests that the optimized liposomal formulation co-encapsulates both drugs with high encapsulation efficiency (> 95%), shows enhanced drug retention under tested conditions and delivers a drug:drug ratio capable of improving tumor cell growth inhibition with a mitoxantrone dose reduction of 2.6-fold as compared to single liposomal formulation. Therefore, our nanotechnology-based drug combined platform may constitute a promising strategy in prostate cancer therapy.

Schedule treatment design and quantitative in vitro evaluation of chemotherapeutic combinations for metastatic prostate cancer therapy.

PURPOSE: Preclinical evaluation is essential for a rational design of combination chemotherapy as some agents, with known mechanisms of action and non-overlapping toxicities may increase the therapeutic index of anticancer drugs, whose clinical success is hindered by side effects and drug resistance. The present study investigated new drug combinations with potential outcome for the treatment of metastatic prostate cancer. This final clinical stage exhibits predominantly hormone-refractory prostate cancer (HRPC) cells but also a minority of hormone responsive cells. METHODS: Growth inhibition activity of simultaneous and sequential combinations was evaluated by resazurin assay. In vitro evaluation of synergism, additivity, or antagonism, against prostate cancer cell lines, was performed by the median effect analysis. The importance of dosage, exposure time, drug ratio, and type of treatment were investigated and compared. RESULTS: Most simultaneous combinations of two drugs with different mechanisms of action or of two topoisomerase II inhibitors resulted in mild antagonism of antiproliferative effects, particularly notorious at high cell death. Imatinib-mitoxantrone and ciprofloxacin-etoposide combinations were exceptions, as they yielded additivity and dose reduction index (DRI) values of 2.6 and 3.5-fold for mitoxantrone and etoposide, respectively. Sequential combinations (ciprofloxacin or imatinib pre-treatment) revealed additive growth inhibition effects, translated in much higher DRI values (from 7.0 to 15.3-fold). Moderate synergism was restricted to sequential ciprofloxacin combinations at high cell death. CONCLUSIONS: Ciprofloxacin and imatinib significantly improve growth inhibition activity of standard antineoplastic drugs in a schedule-dependent manner and, therefore, may have an important role as adjuvant therapeutic agents in a clinical setting.