Background：Galectin-3 （Gal-3） plays a role in the mechanisms underlying ocular venous malformation.We conducted this study to investigate the effect of pingyangmycin pretreatment on the Gal-3 expressions and biolog...Background：Galectin-3 （Gal-3） plays a role in the mechanisms underlying ocular venous malformation.We conducted this study to investigate the effect of pingyangmycin pretreatment on the Gal-3 expressions and biological behavior of ocular venous malformation.Methods：Tissue samples were collected from 136 patients with ocular venous malformation.Patients were randomly divided into pingyangmycin （n =69） and nonpingyangmycin group （n 67）.Patients in the pingyangmycin group received a local injection of 0.02% pingyangmycin once every 2 days for 2 weeks （7 doses） before removal surgery,whereas patients in the nonpingyangmycin group underwent removal surgery without local injection.The protein and messenger RNA （mRNA） expression of Gal-3 were detected by using immunohistochemistry and in situ hybridization.Results：Gal-3 protein was expressed in 35 （52%） of 67 samples in the nonpingyangmycin group and in 19 （28%） of 69 samples in the pingyangmycin group （P 〈 0.05）.Gal-3 mRNA expression was detected in 39 （58%） of 67 samples in the nonpingyangmycin group and 22 （32%） of 69 samples in the pingyangmycin group （P 〈 0.05）.The higher Gal-3 expressions were detected in samples with deeper invasiveness than those with superficial invasiveness before （χ^2=12.720 and 13.369,respectively,both P 〈 0.05） and after pingyangmycin treatment （χ^2=8.429 and 4.590,respectively,both P 〈 0.05）.It was more frequently detected in mesh-like lesions with unclear boundary than round lesions with clear boundary before （χ^2= =30.291 and 41.466,respectively,both P 〈 0.05） and after pingyangmycin treatment （χ^2= =14.619 and 15.130,respectively,both P 〈 0.05）.Pingyangmycin treatment led to a significant difference in Gal-3 expressions at both protein and mRNA levels （χ^2==8.664 and 9.524,respectively,both P 〈 0.05）.Conclusions：Gal-3 expression may be involved in the development and invasiveness of ocular venous malformation,and pingyangmycin can inhibit Gal-3 expression,indicating a role of pingyangmycin treatment before the removal of ocular venous malformation.展开更多
According to a new international classification of vascular lesions, venous vascular malformation has become the most common type of congenital vascular malformation. A characteristic of this disease is its life-long ...According to a new international classification of vascular lesions, venous vascular malformation has become the most common type of congenital vascular malformation. A characteristic of this disease is its life-long progressive development, which is the main cause of harm to health and is different from hemangioma. Severe hemangioma with thrombocytopenia （Kasabach-Merritt syndrome） is often encountered in children, especially in infants younger than 1 year old. Coagulation abnormalities in Kasabach-Merritt syndrome are mainly caused by increased platelet destruction. Whereas, severe venous malformation-associated coagulopathy is attributed to the depletion of coagulation substances and extensive intravenous coagulation, and it occurs in adults. In principle, surgery is required.展开更多
文摘Background：Galectin-3 （Gal-3） plays a role in the mechanisms underlying ocular venous malformation.We conducted this study to investigate the effect of pingyangmycin pretreatment on the Gal-3 expressions and biological behavior of ocular venous malformation.Methods：Tissue samples were collected from 136 patients with ocular venous malformation.Patients were randomly divided into pingyangmycin （n =69） and nonpingyangmycin group （n 67）.Patients in the pingyangmycin group received a local injection of 0.02% pingyangmycin once every 2 days for 2 weeks （7 doses） before removal surgery,whereas patients in the nonpingyangmycin group underwent removal surgery without local injection.The protein and messenger RNA （mRNA） expression of Gal-3 were detected by using immunohistochemistry and in situ hybridization.Results：Gal-3 protein was expressed in 35 （52%） of 67 samples in the nonpingyangmycin group and in 19 （28%） of 69 samples in the pingyangmycin group （P 〈 0.05）.Gal-3 mRNA expression was detected in 39 （58%） of 67 samples in the nonpingyangmycin group and 22 （32%） of 69 samples in the pingyangmycin group （P 〈 0.05）.The higher Gal-3 expressions were detected in samples with deeper invasiveness than those with superficial invasiveness before （χ^2=12.720 and 13.369,respectively,both P 〈 0.05） and after pingyangmycin treatment （χ^2=8.429 and 4.590,respectively,both P 〈 0.05）.It was more frequently detected in mesh-like lesions with unclear boundary than round lesions with clear boundary before （χ^2= =30.291 and 41.466,respectively,both P 〈 0.05） and after pingyangmycin treatment （χ^2= =14.619 and 15.130,respectively,both P 〈 0.05）.Pingyangmycin treatment led to a significant difference in Gal-3 expressions at both protein and mRNA levels （χ^2==8.664 and 9.524,respectively,both P 〈 0.05）.Conclusions：Gal-3 expression may be involved in the development and invasiveness of ocular venous malformation,and pingyangmycin can inhibit Gal-3 expression,indicating a role of pingyangmycin treatment before the removal of ocular venous malformation.
文摘According to a new international classification of vascular lesions, venous vascular malformation has become the most common type of congenital vascular malformation. A characteristic of this disease is its life-long progressive development, which is the main cause of harm to health and is different from hemangioma. Severe hemangioma with thrombocytopenia （Kasabach-Merritt syndrome） is often encountered in children, especially in infants younger than 1 year old. Coagulation abnormalities in Kasabach-Merritt syndrome are mainly caused by increased platelet destruction. Whereas, severe venous malformation-associated coagulopathy is attributed to the depletion of coagulation substances and extensive intravenous coagulation, and it occurs in adults. In principle, surgery is required.
