Anti-Varicella zoster virus Monoclonal antibody, Clone 482

There are a number of medications which can serve as catalysts for drug-induced immune thrombocytopenia (DIPT). A minimum of six different mechanisms have been put forward as the means by which drug-induced antibodies can encourage platelet destruction, thus emphasising the complexity of the pathogenesis of DITP. Acyclovir, has been widely used because of its highly potent prohibitive properties for infections caused by HSV and VZV. The common adverse effects of this drug are well known, the severe adverse reactions are mostly related to high dose intravenous administrations. The immune thrombocytopenia induced by acyclovir is unusual. The authors present a rare clinical case of acyclovir-induced immune thrombocytopenia in a 72-year-old female patient with typical herpes zoster treated with acyclovir. The clinical and laboratory findings, taken together with the transitory relationship between acycolvir and the start of thrombocytopenia, combined with the elimination of the other know sources of thrombocytopenia, allowed us to reach the diagnosis of acyclovir-induced immune thrombocytopenia. An international database search was employed to complete an extensive review of the current literature. Contemporary information on acyclovir-induced immune thrombocytopenia was collected by the analysis of present day review articles and accessible case reports. The authors found five published cases of acyclovir-induced immune thrombocytopenia. Analyzing these articles it was concluded that immune thrombocytopenia induced by acyclovir is rare, and an unusual side effect, with good prognosis. Prompt diagnosis is vital to appropriate management, therefore clinicians need to be cognisant of this rare potential adverse reaction.

There are no surrogate markers for the development of postherpetic neuralgia (PHN) in patients with herpes zoster (HZ). All patients with HZ were prospectively enrolled to evaluate the associations of saliva varicella zoster virus (VZV) DNA persistence and VZV-specific cell-mediated immunity (CMI) with the development of PHN. Slow clearers were defined if salivary VZV DNA persisted after day 15. Salivary VZV was detected in 60 (85.7%) of a total of 70 patients with HZ on initial presentation. Of 38 patients for whom follow-up saliva samples were available, 26 (68.4%) were classified as rapid clearers and 12 (31.6%) as slow cleares. Initial VZV-specific CMI was lower in slow clearers than rapid clearers (median 45 vs 158 spot forming cells/10(6) cells, P = .02). Of the 70 patients with HZ, 22 (31.4%) eventually developed PHN. Multivariate analysis showed that slow clearers (OR, 15.7, P = .01) and lower initial VZV-specific CMI (OR, 13.8, P = .04) were independent predictors of the development of PHN, after adjustment for age and immunocompromised status. Initial low VZV CMI response and persistence of VZV DNA in saliva may be associated with the development of PHN.