Chronic tonsillitis, tonsillectomy and sickle cell crises

A study of the effect of tonsillectomy on the frequency of sickle cell pain crises was carried out on 15 patients with sickle cell disease (Hb SS) who presented with complaints of frequent pain crises and were found to have chronic tonsillitis. They comprised 9 females and 6 males and ranged in age from 6 to 35 years, with a mean of 15 years. Tonsillectomy was performed under general anaesthesia. The mean number of pain crises in the one-year period after tonsillectomy was 1.5 and was significantly less than the mean number 4.7 in the one year preceding the operation (p less than 0.001). Four patients failed to show a reduced number of crises and these were those whose tonsils at operation showed no pus in their tonsillar crypts. It is thus observed that chronic tonsillitis, symptoms of which may not be volunteered at examination, is a potent inductor of sickle cell pain crisis and that tonsillectomy is an effective mode of treatment, especially when the tonsillar crypts contain pus.     

The effect of cimetidine on anesthetic metabolism and toxicity

Because the H2-receptor antagonist cimetidine has been shown to inhibit drug metabolism, the effects of cimetidine on anesthetic metabolism and toxicity were investigated in a rat model. Cimetidine decreased inorganic plasma fluoride production after methoxyflurane administration both in 21% oxygen (P less than 0.001) and in 100% oxygen (P less than 0.001). Phenobarbital produces an increased fluoride formation after methoxyflurane anesthesia, and this fluoride formation is also reduced by cimetidine (P less than 0.005). There was no significant difference between the plasma fluoride levels in rats anesthetized with halothane or enflurane. Although cimetidine inhibited the in vivo defluorination of methoxyflurane, fluoride levels were still within the nephrotoxic range, and cimetidine is not likely to play a role as part of a preanesthetic regimen that would permit the increased clinical use of methoxyflurane. Cimetidine also inhibited the oxidative metabolism of halothane; cimetidine decreased (P less than 0.05) trifluoroacetic acid concentrations after halothane anesthesia in 21% oxygen and in 100% oxygen and decreased (P less than 0.05) bromide concentrations after halothane anesthesia in 100% oxygen. Trifluoroacetic acid levels were less (P less than 0.02) after halothane anesthesia in 14% oxygen as compared with 100% oxygen, indicating a reduction in oxidative metabolism under hypoxic conditions. However, bromide concentrations were maximal after halothane anesthesia in 21% oxygen, and significantly (P less than 0.001) less after halothane anesthesia in 14% and 100% oxygen. Bromide production, therefore, seems to be inhibited by both hypoxia and hyperoxia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of transtympanally applied lidocaine on the cochleovestibular function

Twenty-two patients with recurring attacks of tinnitus, hearing loss and dizziness were treated with transtympanally injected lidocaine. The tinnitus improved in 19, and the pure tone and speech audiometric thresholds decreased in 15 cases. The dizziness and latent spontaneous nystagmus disappeared in all subjects where these symptoms were manifest before treatment.     

IS VECURONIUM A LONG-ACTING NEUROMUSCULAR BLOCKING AGENT IN NEONATES AND INFANTS?

Vecuronium was used as the only neuromuscular blocking agentin 81 paediatric patients (neonates to adolescents) during fentanyland nitrous oxide anaesthesia. The thenar electromyogram wasused to monitor neuromuscular blockade. Neonates and infantshad a mean requirement of vecuronium 105 µg kg^–1during the first 1 h of anaesthesia, to establish and maintain90–98% neuromuscular blockade, compared with a mean requirementof 217 µg kg^–1 for children aged 3–10 yr (P< 0.05). Vecuronium 100 and 150 µg kg^–1 maintainedneuromuscular blockade > 90% for 59 and 110 min, respectively,in neonates and infants, but only for 18 and 38 min in childrenand for 37 and 68 min in adolescents (P < 0.05). Vecuroniummay be regarded as a long-acting neuromuscular blocking agentin patients aged less than 1 yr. Present address: Department of Anaesthesia, Royal Children'sHospital, Flemington Road, Parkville, Victoria 3052, Australia.     

Evaluation of anti-C1q capture assay for detecting circulating immune complexes and comparison with polyethylene glycol-immunoglobulin G, C1q-binding, and Raji cell methods.

An anti-C1q capture method kit (C1q-immunoglobulin G [IgG]) (Ortho Diagnostics, Inc., Raritan, N.J.) for measuring circulating immune complexes (CIC) was evaluated. The kit showed poor diagnostic sensitivity (P less than 0.005) for identifying CIC in patients with systemic lupus, rheumatoid arthritis, and bacterial endocarditis, as compared with polyethylene glycol-IgG and Raji cell tests (12, 24, and 24 positive, respectively, of 31 patients). Of the patients who were positive with the C1q-IgG test, 25% showed discrepancies when their results were compared with the polyethylene glycol-IgG and C1q-binding test results. Gel filtration chromatography of two of these discrepant sera showed the only peak of C1q-IgG activity to be associated with monomeric IgG (molecular weight, less than 200,000). We concluded that the kit method may be measuring substances other than CIC in some sera, because molecules of C1q attached to IgG should exhibit a molecular weight of greater than 500,000.     

Lectin histochemistry of embryonal carcinoma

Histological tissue sections of human testicular embryonal carcinoma from 13 patients and of a xenograft tumour in nude mice, as well as cell lines of human embryonal carcinoma, were investigated with eight different lectins to characterize the distribution of glycoconjugates in embryonal carcinoma. In all cases the malignant cells showed binding with Con A, WGA and RCA I conjugates, whereas other lectins were bound to some, but never to all, tumour cells in each group, revealing the heterogeneity of the malignant cells. A polarization of cancer cells was shown particularly with WGA and RCA I labelling, which was most intense on the luminal borders of the carcinoma cells, where pseudotubular structures were formed. The sugar staining properties were retained in cell culture and in the xenograft tumour. Regardless of the germ cell origin, embryonal carcinoma cells differed from normal germ cells. The distribution of glycoconjugates was also different from that of testicular carcinoma-in-situ germ cells, which share morphological features and the pattern of glycosylation with seminoma cells. However, the similarities in lectin binding pattern of seminomas and embryonal carcinomas suggest the close relationship between the two types of testicular malignancy, without excluding the possibility that embryonal carcinomas were derived from seminomas. Although lectins seem to be less important for differential diagnostic use in testicular cancer, our findings showed the usefulness of lectin histochemistry for characterization of embryonal carcinoma.