RESUMO
CASES: Two women presented with newly growing callosities beneath the first and second metatarsal heads, initially believed to reflect gastrocnemius tightness and plantar plate pathology. In another man, swelling at the posterolateral aspect of the heel was mistaken for a Haglund deformity. Subsequent imaging of each patient led to delayed diagnosis of extraskeletal osteochondroma (ESO). Surgical excision resolved symptoms in all 3 with no recurrence over 12 months later. CONCLUSIONS: Whenever bony prominences newly develop in soft tissues of the foot, ESO should be suspected and appropriate imaging obtained. We describe physical features to help differentiate ESO from other common causes of foot overload.
Assuntos
Neoplasias Ósseas , Condroma , Osteocondroma , Neoplasias de Tecidos Moles , Erros de Diagnóstico , Feminino , Pé/patologia , Humanos , Masculino , Osteocondroma/diagnóstico por imagem , Osteocondroma/cirurgia , Neoplasias de Tecidos Moles/patologiaRESUMO
Ca2+ signaling plays crucial role in ischemia and reperfusion (I/R) injury. Although blockade of L-type Ca2+ channels by amlodipine (AML) has been shown to suppress hepatic I/R injury in several animal models, information is still needed regarding the hepatoprotective effects of the dual L/N-type Ca2+ channel blockers, cilnidipine (CIL). We examined the effect of pretreatment with AML or CIL (100 µg/kg i.p.) 45 min before induction of 60 min of liver ischemia followed by reperfusion, on oxidative stress markers, liver enzymes, serum tumor necrosis factor-α, interleukin-1ß, apoptosis markers, and nuclear factor KB after 6 and 24 h of hepatic reperfusion. Both drugs significantly ameliorated biochemical and histological markers of hepatic I/R injury, but protection with CIL was more significant at the 6-h time point where protection with AML outlasted that of CIL. Both drugs offered significant protection against hepatic I/R damage, but the protection with CIL seemed more potent but of shorter duration than that observed with AML possibly due to the shorter half-life of CIL.