They include: nausea, vomiting, diarrhea and headache. Infrequent adverse effects (0.1–1% of patients) include: agitation, vertigo, confusion, dizziness, edema, arthralgia, sore throat, constipation, abdominal pain, rash, weakness and/or renal impairment. Rare adverse effects (<0.1% of patients) include: coma, seizures, neutropenia, leukopenia, tremor, ataxia, encephalopathy, psychotic symptoms, crystalluria, anorexia, fatigue, hepatitis, Stevens–Johnson syndrome, toxic epidermal necrolysis and/or anaphylaxis. Pharmacology
Valaciclovir is a prodrug, an esterified version of aciclovir that has greater oral bioavailability (about 55%) than aciclovir. It is converted by esterases to the active drug, aciclovir, and the amino acid valine via hepatic first-pass metabolism. Aciclovir is selectively converted into a monophosphate form by viral thymidine kinase, which is more effective (3000 times) in phosphorylation of aciclovir than cellular thymidine kinase. Subsequently, the monophosphate form is further phosphorylated into a disphosphate by cellular guanylate kinase and then into the active triphosphate form, aciclo-GTP, by cellular kinases. Mechanism of action
Aciclo-GTP, the active triphosphate metabolite of aciclovir, is a very potent inhibitor of viral DNA replication. Aciclo-GTP competitively inhibits and inactivates the viral DNA polymerase. Its monophosphate form also incorporates into the viral DNA, resulting in chain termination. It has also been shown that the viral enzymes cannot remove aciclo-GMP from the chain, which results in inhibition of further activity of DNA polymerase. Aciclo-GTP is fairly rapidly metabolized within the cell, possibly by cellular phosphatases.Aciclovir is active against most species in the herpesvirus family.
For instance, diabetes is proved to be associated with periodontitis- it is a major risk factor when glycaemic control is poor. The rate of loss of attachment and bone loss is rapid.Loss of attachment refers to the destruction of periodontium whereas the bone refers to the alveolar bone supporting the teeth. The loss can be determined by using a calibrated periodontal probe and taking radiographs of the dentition. Usually the loss of attachment is greater than 2mm per year. Aggressive periodontitis runs in the patients family.Familial aggregation of aggressive periodontitis is often discovered by taking a thorough medical history of the patient. The patient is said to have a high genetic susceptibility to aggressive periodontitis. Many studies have shown that genetic factors contribute to the pathogenesis of this disease. In this case, the manifestation of aggressive periodontitis is believed to be the result of genetic mutation, combined with environmental factors. Secondary features
Secondary features are characteristics which are frequently seen but not always present in every patient diagnosed with aggressive periodontitis. The severity of periodontal tissue destruction is out of proportion to amount of bacteria present.The amount of bacteria is often indicated by the level of dental plaque. This feature implies that when aggressive periodontitis is present, loss of attachment and bone loss tend to occur even if the plaque level is low. High levels of Aggregatibacter (or Actinobacillus) actinomycetemcomitans and, in some populations, Porphyromonas gingivalis.These gram-negative microbes are considered the chief aetiological agent of aggressive periodontitis.