A multicentre study of loratadine, clemastine and placebo in patients with perennial allergic rhinitis.

This multicentre, double-blind, randomized parallel-group study compared 3 weeks' treatment with either loratadine (Clarityn) 10 mg once daily, or clemastine (Tavegyl) 1 mg twice daily, and placebo in outpatients with active perennial allergic rhinitis. 155 patients were evaluated for efficacy and safety. Grading of four nasal and three non-nasal symptoms, rhinoscopy signs, and therapeutic response was performed on treatment days 6, 13, and 20. Patients recorded daily symptoms and possible adverse experiences in a diary, also indicating when symptoms of active rhinitis were relieved. Loratadine and clemastine were statistically significantly superior to placebo throughout the study (P less than 0.05), based on assessment of patients' nasal and eye symptoms, patients' diary scores, rhinoscopy signs of symptoms, and onset of relief. The loratadine group showed a statistically significantly (P less than 0.05) faster onset of relief of symptoms compared with the group treated with clemastine. Concerning nasal stuffiness, loratadine was significantly (P less than 0.05) superior to clemastine after 1 week's treatment. Reports of adverse reactions showed that significantly (P less than 0.05) more patients complained of sedation in the clemastine than in the loratadine group. Regarding other adverse experiences and laboratory tests, the three treatment groups were statistically comparable (P less than 0.05). The study showed that compared with placebo both loratadine and clemastine were effective in relieving nasal and eye symptoms in patients with perennial allergic rhinitis. Loratadine was safe and well tolerated and was significantly less sedative than clemastine; loratadine may therefore possess an advantage in clinical use in the treatment of perennial allergic rhinitis.

Viral infection as a cause of acute peripheral facial palsy.

Among 51 patients with acute peripheral facial palsy, varicella-zoster virus was isolated from the cerebrospinal fluid (CSF) in one case, and Herpesvirus hominis from the nasopharynx in two cases. In 12 other cases, complement-fixing antibody or hemagglutination inhibition tests indicated a recent viral infection (varicella-zoster, seven; herpes simplex, one; cytomegalovirus, one; influenza type B virus, two; and mumps virus, one). One additional patient had clinical signs of herpes zoster oticus. About one third of these 16 virus-positive patients, but also one third of the remaining group, had increased levels of alpha 1-antitrypsin, orosomucoid, haptoglobin, and immunoglobulins. Evidently, an inflammatory reaction preceded or coincided with the facial palsy in both groups. In CSF, an increase of total proteins and gamma-globulins was frequently found among all 20 patients examined (eight were virus-positive).

The role of viral infection in acute peripheral facial palsy.

Thirty-three patients with acute non-traumatic peripheral facial palsy were studied. In one patient, varicella-zoster virus was isolated from CSF. Antibody against the same virus was present in CSF, and rising titre was demonstrated in serum. In two cases, herpes virus hominis was isolated from the nasopharynx. CF-antibody tests indicated recent viral infection in 7 other cases. One additional patient had clinical signs of herpes zoster oticus. In most of these 11 patients, but also in the majority of the remaining 22 patients, an acute phase reaction was present, and serum and CSF immunoglobulins were increased. Thus, an active or recent infection (probably viral) seemed to precede or coincide with the facial palsy in most cases in both groups.