South African food allergy consensus document 2014.

The prevalence of food allergy is increasing worldwide and is an important cause of anaphylaxis. There are no local South African food allergy guidelines. This document was devised by the Allergy Society of South Africa (ALLSA), the South African Gastroenterology Society (SAGES) and the Association for Dietetics in South Africa (ADSA). Subjects may have reactions to more than one food, and different types and severity of reactions to different foods may coexist in one individual. A detailed history directed at identifying the type and severity of possible reactions is essential for every food allergen under consideration. Skin-prick tests and specific immunoglobulin E (IgE) (ImmunoCAP) tests prove IgE sensitisation rather than clinical reactivity. The magnitude of sensitisation combined with the history may be sufficient to ascribe causality, but where this is not possible an incremental oral food challenge may be required to assess tolerance or clinical allergy. For milder non-IgE-mediated conditions a diagnostic elimination diet may be followed with food re-introduction at home to assess causality. The primary therapy for food allergy is strict avoidance of the offending food/s, taking into account nutritional status and provision of alternative sources of nutrients. Acute management of severe reactions requires prompt intramuscular administration of adrenaline 0.01 mg/kg and basic resuscitation. Adjunctive therapy includes antihistamines, bronchodilators and corticosteroids. Subjects with food allergy require risk assessment and those at increased risk for future severe reactions require the implementation of risk-reduction strategies, including education of the patient, families and all caregivers (including teachers), the provision of a written emergency action plan, a MedicAlert necklace or bracelet and injectable adrenaline (preferably via auto-injector) where necessary.

Effect of desloratadine on patients with allergic rhinitis and exercise-induced bronchoconstriction: a placebo controlled study.

BACKGROUND: Exercise induced broncho-constriction (EIB) is a significant problem in asthmatic patients. The link between allergic rhinitis and asthma is now well established. Patients with allergic rhinitis may have EIB. OBJECTIVE: This study compared the effects of desloratadine and placebo on EIB in a group of patients with allergic rhinitis and EIB. METHODS: This was a double blind placebo controlled, randomized, crossover study. Exercise challenge tests were performed before and after 7 days of treatment with either 5 mg desloratadine or placebo. Patients then underwent a washout period for 7 days and were crossed over to receive either 5mg desloratadine or placebo. The exercise challenge tests were repeated. RESULTS: Desloratadine had no effect on the reduction in percentage fall in FEV(1), the AUC (0-60 min) and the time to recovery. CONCLUSIONS: Desloratadine has no effect in attenuating the broncho-constriction caused by exercise in patients with allergic rhinitis and exercise induced broncho-constriction. CLINICAL IMPLICATIONS: Patients with allergic rhinitis and exercise induced broncho-constriction must be treated with either a beta(2)-agonist or LRTA for relief or prophylaxis of their EIB. CAPSULE SUMMARY: Desloratadine does not have an effect on exercise induced bronchoconstriction. Patients with allergic rhinitis with exercise induced bronchoconstriction who are on desloratadine will still require treatment with beta(2) agonist or leukotriene receptor antagonist for their symptoms.

Guideline for the management of chronic asthma in children--2009 update.

OBJECTIVE: To revise the guideline for the diagnosis and management of chronic asthma in children in view of the following considerations: the existing South African Childhood Asthma Working Group (SACAWG) guideline was produced 10 years ago; diagnosis of asthma in young children remains a challenge; evidence-based treatment is the new paradigm; new treatment approaches to achieving and maintaining control; therapeutic roles of several medications have evolved; more studies and data on treatment in young children; new medications and formulations; a change of emphasis in assessing asthma control to guide treatment changes. The main aim of the guideline is to promote a better standard of treatment based on understanding of the pathophysiology and pharmacotherapy of asthma, and encouraging uniformity in asthma management. EVIDENCE: A detailed literature review by a working group of clinicians from relevant disciplines. The strategies recommended are classified according to the evidence category in Appendix B, and denoted as Evidence A, B, C and D. RECOMMENDATIONS: These include an appropriate diagnostic approach, environmental control measures, treatment options, definition of asthma control, and strategies to achieve control. ENDORSEMENT: The guideline document was endorsed by the South African Thoracic Society (SATS), the National Asthma Education Programme (NAEP), the South African Paediatric Association (SAPA) and the South African Academy of Family Practice.

Effect of budesonide/formoterol maintenance and reliever therapy on asthma exacerbations.

This randomised, double-blind, 6-month study compared budesonide/formoterol for maintenance and relief with salmeterol/fluticasone and a fixed maintenance dose of budesonide/formoterol, both with terbutaline for relief. Following a 2-week run-in, 3335 symptomatic adults and adolescents (mean FEV1 73% predicted, mean inhaled corticosteroid dose 745 microg/day) received budesonide/formoterol 160/4.5 microg one inhalation bid plus additional inhalations as needed, salmeterol/fluticasone 25/125 microg two inhalations bid plus as-needed terbutaline or budesonide/formoterol 320/9 microg one inhalation bid plus as-needed terbutaline. Budesonide/formoterol for maintenance and relief prolonged the time to first severe exacerbation requiring hospitalisation, emergency room treatment or oral steroids (primary variable) vs. fixed-dose salmeterol/fluticasone and budesonide/formoterol (p=0.0034 and p=0.023 respectively; log-rank test). Exacerbation rates were 19, 16 and 12 events/100 patients/6 months for salmeterol/fluticasone, fixed-dose budesonide/formoterol and budesonide/formoterol for maintenance and relief, respectively, [rate reduction vs. fixed-dose salmeterol/fluticasone (0.61; 95% CI 0.49-0.76, p<0.001) and vs. fixed-dose budesonide/formoterol (0.72; 95% CI 0.57-0.90, p=0.0048)]. Budesonide/formoterol maintenance and relief patients used less inhaled corticosteroid vs. salmeterol/fluticasone and fixed-dose budesonide/formoterol patients. All treatments provided similar marked improvements in lung function, asthma control days and asthma-related quality of life. Budesonide/formoterol for maintenance and relief reduces asthma exacerbations and maintains similar daily asthma control at a lower overall drug load compared with fixed-dose salmeterol/fluticasone and budesonide/formoterol.

Efficacy of nebulized fluticasone propionate compared with oral prednisolone in children with an acute exacerbation of asthma.

The aim of the present study was to investigate the efficacy and safety of nebulized fluticasone propionate (FP Nebules) compared with oral soluble prednisolone in children with an acute exacerbation of asthma. The study used an international, multi-centre, randomized, double-blind, parallel group design. Three hundred and twenty-one patients, aged 4-16 years old, who presented with an acute exacerbation of asthma, were randomly allocated to either nebulized FP (1 mg b.d.) or oral prednisolone (2 mg kg(-1) day(-1) for 4 days then 1 mg kg(-1) day(-1) for 3 days) for 7 days. Patients in the FP group showed a significantly greater increase in diary card morning peak expiratory flow (PEF) over 7 days compared with patients in the prednisolone group (difference = 9.51 min(-1), CI = 2.1, 16.8, P = 0.034). Similar increases for both treatments were shown for evening PEF. Clinic PEF improved with both treatments, but was significantly greater in patients taking FP after 7 days (difference = 11.41 min(-1), CI = 2.8, 20.0, P = 0.029). Both treatments reduced symptom scores to a similar extent. The two treatments were well tolerated, and there was no difference in the incidence of adverse events. The present study demonstrated that nebulized FP is at least as effective as oral prednisolone in the treatment of children presenting with an acute exacerbation of asthma.

Accumulation of house-dust mite (Der-p-1) levels on mattress covers.

Mattresses serve as a large reservoir for house-dust mite antigens and harbour the highest mite levels within the household. Mite reduction measures have previously been shown to be unsuccessful. The effect of mattress covers and acaracides on Der-p-1 levels in the mattresses of 60 patients with mite-allergic asthma was studied. Der-p-1 levels were measured using monoclonal antibodies (ELISA method). Baseline levels were recorded and re-assessed at 8-week intervals over a 6-month period. Patients were randomised into three equal groups. In group A mattresses were treated with Metsan (Snowchem) and benzylbenzoate only; group C had their mattresses covered with mattress covers (Allergy Control Products). Group B was the control group. We were unable to demonstrate any reduction of mite levels in the beds of all 3 groups. In fact all 3 groups demonstrated an increase in Der-p-1 levels over the study period, viz. group A (mean pre: 14.28, post: 34.18 micrograms/g dust); group C (mean pre: 8.26, post: 20.80 micrograms/g dust) and group B (mean pre: 18.21, post 38.47 micrograms/g dust). However, 12 patients in group C had their mattress covers washed in hot water at weekly intervals over a 5-week period at the end of the study. The results demonstrated a significant reduction in mite levels (mean pre: 41.95, post: 26.2 micrograms/g dust; P = 0.027). We therefore conclude that the use of mattress covers per se does not reduce Der-p-1 levels. The regular application of benzylbenzoate and Metsan does not prevent the accumulation of Der-p-1 on mattresses either.(ABSTRACT TRUNCATED AT 250 WORDS)

Fatal neonatal meningitis and ventriculitis caused by multiresistant Achromobacter xylosoxidans. A case report.

Meningitis and ventriculitis in a 6-day-old neonate caused by a Gram-negative glucose-non-fermenting organism, Achromobacter xylosoxidans, was resistant to most antibiotics except ceftazidime and imipenem. The organism became resistant after 28 days treatment with ceftazidime. When the infant was 7 weeks old, imipenem became available but, in spite of 3 days of intravenous treatment, the organism was still recovered from ventricular cerebrospinal fluid and the child died. This would appear to be only the second report of neonatal meningitis caused by this organism.