The effect of oral acetazolamide on weight gain in children

Objective: Oral acetazolamide is a potent medical treatment for pediatric glaucoma, but ophthalmologists may have concerns that it retards weight gain in children and may choose surgical management instead.Design: Retrospective chart review.Participants: Twenty-two well children with glaucoma taking acetazolamide orally for ≥ 3 months.Methods: Abnormal weight gain was determined using downward crossing of 2 percentile lines on growth charts and change in z score for weight using a hierarchical linear model.Results: One patient with Sturge-Weber syndrome and growth failure was excluded when growth hormone deficiency was diagnosed. Two patients crossed 2 lines downward; both showed metabolic acidosis. The trend for the 2 reversed after medication was discontinued. The other 20 tracked steadily on growth curves. Eleven patients (11/22, 50%) showed a decline in z score for weight over the follow-up period, and the remainder showed an increase, for an overall estimate of slope in this sample of 0.01, which was not significant (p = 0.8).Conclusions: Oral acetazolamide may cause poor weight gain in a small subset of children on treatment. Metabolic acidosis may be a mediating factor for growth failure. Our data suggest that acetazolamide does not cause significant weight changes in cases of pediatric glaucoma. Growth parameters should be followed. Growth hormone deficiency should be considered in Sturge-Weber syndrome. Prospective study is needed.     

Dietary intake of S-(α-carboxybutyl)-dl-homocysteine induces hyperhomocysteinemia in rats

Betaine homocysteine S-methyltransferase (BHMT) catalyzes the transfer of a methyl group from betaine to homocysteine (Hcy), forming dimethylglycine and methionine. We previously showed that inhibiting BHMT in mice by intraperitoneal injection of S-(α-carboxybutyl)-dl-homocysteine (CBHcy) results in hyperhomocysteinemia. In the present study, CBHcy was fed to rats to determine whether it could be absorbed and cause hyperhomocysteinemia as observed in the intraperitoneal administration of the compound in mice. We hypothesized that dietary administered CBHcy will be absorbed and will result in the inhibition of BHMT and cause hyperhomocysteinemia. Rats were meal-fed every 8 hours an l-amino acid–defined diet either containing or devoid of CBHcy (5 mg per meal) for 3 days. The treatment decreased liver BHMT activity by 90% and had no effect on methionine synthase, methylenetetrahydrofolate reductase, phosphatidylethanolamine N-methyltransferase, and CTP:phosphocholine cytidylyltransferase activities. In contrast, cystathionine β-synthase activity and immunodetectable protein decreased (56% and 26%, respectively) and glycine N-methyltransferase activity increased (52%) in CBHcy-treated rats. Liver S-adenosylmethionine levels decreased by 25% in CBHcy-treated rats, and S-adenosylhomocysteine levels did not change. Furthermore, plasma choline decreased (22%) and plasma betaine increased (15-fold) in CBHcy-treated rats. The treatment had no effect on global DNA and CpG island methylation, liver histology, and plasma markers of liver damage. We conclude that CBHcy-mediated BHMT inhibition causes an elevation in total plasma Hcy that is not normalized by the folate-dependent conversion of Hcy to methionine. Furthermore, metabolic changes caused by BHMT inhibition affect cystathionine β-synthase and glycine N-methyltransferase activities, which further deteriorate plasma Hcy levels.     

Pharmacogenomics in oral diseases

The availability of newer technologies for identification and characterization of the human genome has enabled our understanding of the genetic variations in a majority of human diseases. Human genomic sequence varies in less than 1% among the different population group and these differences known as gene polymorphisms are the primary reasons for differences in individuals’ response to various drug therapy. Also understanding the genetic changes may enable implementation of targeted therapy, thus providing for effective treatment strategies and minimizing the adverse side effects. Pharmacogenomics is a recent development in the field of personalized medicine which focuses on the genetic determinants of drug response at the levels of entire human genome. It primarily deals with tailoring of drug therapy for every individual based on their genetic make-up and identifying new target in various diseases for drug therapy. While the application of pharmacogenomics in systemic illness is well researched, its role in oral diseases needs documentation. Identifying specific targets in periodontitis, head and neck cancer, infections and genetic disorders can be beneficial in discovery of new drugs. This editorial provides an overview of basics of pharmacogenomics, its current role in disease management and its potential role in various head and neck diseases.     

Blond hair removal using ELOS systems

Objective: The aim of this study was to test blond hair removal using the ELOS system, which is optical energy and radio‐frequency combined. Methods: Seventeen patients with blond hair were randomly selected from the Department of Lasertherapy, Medical Centre Maastricht, The Netherlands. The mean age of the patients was 57.4 years. The mean energy used per patient was 23.2?J/cm² and the mean radio‐frequency was 18.6?J/cm². Results: A mean hair reduction of 57.4% was obtained with a mean of 8.5 treatments. There was a trend found between hair removal and the number of treatments. No correlation was found between the percentage of hair removal and age. Furthermore, there was no correlation between hair removal and the device's technical data. No major side effects were observed postoperatively. Conclusions: This study showed that ELOS can effectively be used for blond hair reduction.     

Febrile Neutropenia: Outline of Management

Febrile neutropenia is a common emergency encountered in children receiving chemotherapy for a malignancy. Left untreated, it can lead to serious morbidity and mortality. Febrile neutropenia is suspected in any patient on chemotherapy who presents with fever. Prompt evaluation and management by the primary contact pediatrician is essential for a successful outcome. A detailed history and physical examination is warranted to identify source of infection, although two thirds of them may not have localizing symptoms or signs. Risk stratification is valuable in categorizing the severity and guiding therapy. Initial stabilization, prompt initiation of appropriate antibiotics and adequate supportive care are the cornerstone of treatment. Knowledge of the locally prevailing bacteriological profile and antimicrobial susceptibility data is crucial for each hospital/unit to frame and periodically modify guidelines for the choice of antimicrobials. Delay in initiating antimicrobials significantly worsens the outcome. Education of the family as well as the members of the treating unit is important in this regard. Pro-active steps must be taken to reduce incidence of hospital acquired sepsis. Diagnosis and management in relevance to the emergency room is reviewed and institutional practice is shared.