Sternoclavicular steroid injection for treatment of pain in a patient with Osteitis condensans of the clavicle.

Osteitis condensans of the sternoclavicular joint was first described by Brower et al in 1974. It is a rare benign disorder primarily affecting women of child-bearing age. Persistent pain and swelling in the medial part of the clavicle are the most common presenting symptoms and may represent an inflammatory process in the joint among other proposed etiologies. Radiological findings include sclerosis of the medial part of the clavicle and a normal sternoclavicular joint. Diagnosis is usually confirmed by biopsy. Pain management can be challenging in these patients. Multiple treatments have been described in the past including oral NSAIDS, physical therapy, radiation, surgical resection, and oral corticosteroids but have met with limited success. This case report describes the novel utility of sternoclavicular joint steroid injections in treating a patient with Osteitis condensans of the clavicle after failed medical therapy. Based on our clinical experience, and given the limited clinical success of other reported conservative treatment measures, a sternoclavicular joint injection under fluoroscopic guidance using a local anesthetic-corticosteroid injectate should be considered as a viable treatment option for pain associated with Osteitis condensans of the clavicle.

Pentoxifylline protects against endotoxin-induced acute renal failure in mice.

Acute renal failure (ARF) in septic patients drastically increases the mortality to 50-80%. Sepsis induces several proinflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha), a major pathogenetic factor in septic ARF. Pentoxifylline has several functions including downregulation of TNF-alpha and endothelia-dependent vascular relaxation. We hypothesized that pentoxifylline may afford renal protection during endotoxemia either by downregulating TNF-alpha and/or by improving endothelial function. In wild-type mice, pentoxifylline protected against the fall in glomerular filtration rate (GFR; 105.2 +/- 6.6 vs. 50.2 +/- 6.6 microl/min, P < 0.01) at 16 h of LPS administration (2.5 mg/kg ip). This renal protective effect of pentoxifylline was associated with an inhibition of the rise in serum TNF-alpha (1.00 +/- 0.55 vs. 7.02 +/- 2.40 pg/ml, P < 0.05) and serum IL-1beta (31.3 +/- 3.6 vs. 53.3 +/- 5.9 pg/ml, P < 0.01) induced by LPS. Pentoxifylline also reversed the LPS-related increase in renal iNOS and ICAM-1 and rise in serum nitric oxide (NO). Enhanced red blood cell deformability by pentoxifylline may have increased shear rate and upregulated eNOS. Studies were therefore performed in eNOS knockout mice. The renal protection against endotoxemia with pentoxifylline was again observed as assessed by GFR (119.8 +/- 18.0 vs. 44.5 +/- 16.2 microl/min, P < 0.05) and renal blood flow (0.86 +/- 0.08 vs. 0.59 +/- 0.05 ml/min, P < 0.05). Renal vascular resistance significantly decreased with the pentoxifylline (91.0 +/- 5.8 vs. 178.0 +/- 7.6 mmHg.ml(-1).min(-1), P < 0.01). Thus pentoxifylline, an FDA-approved drug, protects against endotoxemia-related ARF and involves a decrease in serum TNF-alpha, IL-1beta, and NO as well as a decrease in renal iNOS and ICAM-1.