Introduction:Livedoid vasculopathy is a chronic noninflammatory skin disease secondary to hypercoagulable states.No therapeutic guideline has yet been established for livedoid vasculopathy.We herein report a case of l...Introduction:Livedoid vasculopathy is a chronic noninflammatory skin disease secondary to hypercoagulable states.No therapeutic guideline has yet been established for livedoid vasculopathy.We herein report a case of livedoid vasculopathy secondary to protein C deficiency that was successfully treated with rivaroxaban.Case presentation:A 31-year-old Thai woman who had been diagnosed with livedoid vasculopathy 10 years previously presented with a 2-month history of worsening leg ulcers and failure to respond to aspirin,colchicine,and pentoxifylline.Further investigations confirmed protein C deficiency.Rivaroxaban was initiated,and clinical improvement was achieved in 8 weeks.Discussion:When livedoid vasculopathy is confirmed by skin biopsy,additional investigations for hypercoagulable states should be performed to exclude secondary causes.Identification of the causes of livedoid vasculopathy can direct physicians to therapeutic options based on previously reported cases of successful treatment.Our patient,whose livedoid vasculopathy was caused by protein C deficiency,responded well to rivaroxaban.Conclusion:Protein C deficiency results in a hypercoagulable state,and affected patients can present with livedoid vasculopathy.The anticoagulant rivaroxaban has been beneficial in the treatment of livedoid vasculopathy.展开更多
Helicobacter pylori (H. pylori) infection is well known to be associated with the development of precancerous lesions such as chronic atrophic gastritis (AG), or gastric intestinal metaplasia (GIM), and cancer. Variou...Helicobacter pylori (H. pylori) infection is well known to be associated with the development of precancerous lesions such as chronic atrophic gastritis (AG), or gastric intestinal metaplasia (GIM), and cancer. Various molecular alterations are identified not only in gastric cancer (GC) but also in precancerous lesions. H. pylori treatment seems to improve AG and GIM, but still remains controversial. In contrast, many studies, including meta-analysis, show that H. pylori eradication reduces GC. Molecular markers detected by genetic and epigenetic alterations related to carcinogenesis reverse following H. pylori eradication. This indicates that these changes may be an important factor in the identification of high risk patients for cancer development. Patients who underwent endoscopic treatment of GC are at high risk for development of metachronous GC. A randomized controlled trial from Japan concluded that prophylactic eradication of H. pylori after endoscopic resection should be used to prevent the development of metachronous GC, but recent retrospective studies did not show the tendency. Patients with precancerous lesions (molecular alterations) that do not reverse after H. pylori treatment, represent the “point of no return” and may be at high risk for the development of GC. Therefore, earlier H. pylori eradication should be considered for preventing GC development prior to the appearance of precancerous lesions.展开更多
文摘Introduction:Livedoid vasculopathy is a chronic noninflammatory skin disease secondary to hypercoagulable states.No therapeutic guideline has yet been established for livedoid vasculopathy.We herein report a case of livedoid vasculopathy secondary to protein C deficiency that was successfully treated with rivaroxaban.Case presentation:A 31-year-old Thai woman who had been diagnosed with livedoid vasculopathy 10 years previously presented with a 2-month history of worsening leg ulcers and failure to respond to aspirin,colchicine,and pentoxifylline.Further investigations confirmed protein C deficiency.Rivaroxaban was initiated,and clinical improvement was achieved in 8 weeks.Discussion:When livedoid vasculopathy is confirmed by skin biopsy,additional investigations for hypercoagulable states should be performed to exclude secondary causes.Identification of the causes of livedoid vasculopathy can direct physicians to therapeutic options based on previously reported cases of successful treatment.Our patient,whose livedoid vasculopathy was caused by protein C deficiency,responded well to rivaroxaban.Conclusion:Protein C deficiency results in a hypercoagulable state,and affected patients can present with livedoid vasculopathy.The anticoagulant rivaroxaban has been beneficial in the treatment of livedoid vasculopathy.
基金Supported by Grant,NIDDK,RO1DK63618 to KMD from the National Institutes of Health,Bethesda,MD
文摘Helicobacter pylori (H. pylori) infection is well known to be associated with the development of precancerous lesions such as chronic atrophic gastritis (AG), or gastric intestinal metaplasia (GIM), and cancer. Various molecular alterations are identified not only in gastric cancer (GC) but also in precancerous lesions. H. pylori treatment seems to improve AG and GIM, but still remains controversial. In contrast, many studies, including meta-analysis, show that H. pylori eradication reduces GC. Molecular markers detected by genetic and epigenetic alterations related to carcinogenesis reverse following H. pylori eradication. This indicates that these changes may be an important factor in the identification of high risk patients for cancer development. Patients who underwent endoscopic treatment of GC are at high risk for development of metachronous GC. A randomized controlled trial from Japan concluded that prophylactic eradication of H. pylori after endoscopic resection should be used to prevent the development of metachronous GC, but recent retrospective studies did not show the tendency. Patients with precancerous lesions (molecular alterations) that do not reverse after H. pylori treatment, represent the “point of no return” and may be at high risk for the development of GC. Therefore, earlier H. pylori eradication should be considered for preventing GC development prior to the appearance of precancerous lesions.
