目的:探讨阿昔洛韦+醋酸泼尼松片、丙氧鸟苷+醋酸泼尼松片+阿司匹林两种给药方案治疗急性视网膜坏死综合征的临床疗效。 方法:采用随机数字表法将我院急性视网膜坏死综合征患者30例40眼分为 A、B 两组,其中 A 组采用阿昔洛韦+醋酸泼尼松片的给药方案,B 组采用丙氧鸟苷+醋酸泼尼松片+阿司匹林的给药方案,观察并比较两组患者治疗后的临床效果。 结果:经过治疗后,B 组总有效率(90%)明显高于 A 组(70%),两种给药方案均有效,差异无统计学意义( P>0.05);两组患者在治疗前视力情况差异无统计学意义(P>0.05);经不同给药方案治疗后,A 组视力≥0.5者9眼,视力0.1~<0.5者3眼,视力0.02~<0.1者6眼,无感光者2眼,B 组视力≥0.5者12眼,视力0.1~<0.5者4眼,视力0.02~<0.1者3眼,无感光者1眼, B 组患者视力恢复情况优于 A 组,差异有统计学意义(P<0.05);B组患者视网膜裂孔、疱疹、口腔溃疡、水痘、病毒性脑炎及中枢神经病变等并发症的发生率(10%)明显低于 A 组(35%),差异有统计学意义(P<0.05)。 结论:阿昔洛韦+醋酸泼尼松片、丙氧鸟苷+醋酸泼尼松片+阿司匹林两种给药方案都具有较为肯定的治疗效果,但后者对患者视力的恢复及并发症发生率的降低具有更好的优势。 相似文献
The development of antiviral‐resistant cytomegalovirus (CMV) infection complicates the management of transplant recipients. We describe the case of a 65‐year‐old male who developed CMV disease on valganciclovir prophylaxis (donor CMV IgG positive, recipient CMV IgG indeterminate) 30 days after combined liver–kidney transplantation for alcoholic cirrhosis and hepato‐renal syndrome. After an initial complete response to treatment dose oral valganciclovir, he developed recurrent CMV viraemia. Resistance testing revealed a UL97 mutation with in‐frame deletions of codons 595‐596. He was treated successfully with foscarnet and reduction in immunosuppression. This mutation has not been described previously and was suspected to confer ganciclovir resistance. Ganciclovir resistance occurs most commonly due to mutations in the UL97 or UL54 genes, which encode a protein kinase and a DNA polymerase, respectively. The UL97‐encoded protein kinase phosphorylates ganciclovir to ganciclovir triphosphate, which competitively inhibits viral replication. Mutations in the UL97 gene are typically point mutations or deletions. We describe a new mutation, del595‐596 in the CMV UL97 gene, occurring in the context of clinical treatment failure with standard and double‐dose ganciclovir, and successful virological control achieved with foscarnet. This mutation is likely to result in ganciclovir resistance, although recombinant phenotyping is required for confirmation. 相似文献
High grade gliomas in adults are devastating diseases, with very poor survival despite their lack of distant metastases. Local treatments, such as surgical resection and stereotactic radiosurgery, have been most successful, whereas systemic therapy (for example, chemotherapy and immunotherapy) have been rather disappointing. Several gene therapy systems have been successful in controlling or eradicating these tumours in animal models and are now being tested as a logical addition to current clinical management. This review describes the gene therapy clinical protocols that have been completed or that are ongoing for human gliomas. These include the prodrug activating system, herpes simplex thymidine kinase (HSVtk)/ganciclovir (GCV), utilising either retrovirus vector producer cells or adenovirus vectors; adenovirus mediated p53 gene transfer; adenovirus mediated IFN-β gene transfer and oncolytic herpes virus and adenovirus vectors. To date, all of the clinical studies have used direct injection of the vector into the glioma. The Phase I clinical studies have demonstrated low to moderate toxicity and variable levels of gene transfer and in some cases anti-tumour effect. Future directions will rely upon improvements in gene delivery as well as gene therapies and combinations of gene therapy with other treatment modalities. 相似文献