Osteochondritis dissecans of the knee occurs twice as often in males as in females. The peak incidence is about fifteen years of age, and most patients are first diagnosed before the age of eighteen. The etiology of osteochondritis dissecans is still unknown, but the most accepted theories are trauma, ischemia, abnormal ossification within the physes, constitutional or genetic predisposition, and a combination of these. Osteochondritis dissecans of the knee associated with gout was first reported by Carrabba in 1969. And no additional case has been reported. The purpose of this paper is to present an unusual case of osteochondritis dissecans of the knee associated with gout.
Female ; Genetic Predisposition to Disease ; Gout* ; Humans ; Incidence ; Ischemia ; Knee* ; Male ; Osteochondritis Dissecans* ; Osteochondritis*

Background: Lipid emulsion (LE) is effective in treating intractable cardiac depression induced by the toxicity of highly lipid-soluble drugs including local anesthetics. However, the effect of LE on chloroquine (CQ)-evoked cardiac toxicity remains unclear. This study aimed to examine the effect of Lipofundin MCT/LCT, an LE, on the cardiotoxicity caused by CQ in H9c2 rat cardiomyoblasts and elucidate the underlying cellular mechanism. Methods: The effects of CQ (1 × 10-4 M), LE, and the reactive oxygen species (ROS) scavengers mitotempo and N-acetyl-L-cysteine (NAC), alone or combined, on cell viability and migration, apoptosis, ROS production, calcium levels, mitochondrial membrane potential, and adenosine triphosphate (ATP) were examined. Additionally, the effects of LE on the activities of catalase (CAT), malondialdehyde (MDA), and superoxide dismutase (SOD) induced by CQ were assessed. Results: Pretreatment with LE, mitotempo, or NAC reversed the reduction in cell migration and viability, mitochondrial membrane potential, and ATP levels evoked by CQ, and inhibited the increase in cleaved caspase-3, ROS, and calcium concentration induced by CQ. LE inhibited the increase in Bax expression, terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells, MDA activity, and late apoptosis, and reversed the reduction in SOD and CAT activity induced by CQ. CQ did not significantly affect cleaved caspase-8 expression, and LE did not significantly affect CQ concentration. Conclusions Collectively, these results suggest that LE (Lipofundin MCT/LCT) inhibits the cardiotoxicity and late apoptosis induced by CQ toxicity via the intrinsic mitochondrial apoptotic pathway that is associated with direct inhibition of ROS production.