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the 1300 ACTG 019 participants with CD4 cell counts ofunder 500 on admission, risk of progression to AIDS orAIDS-related complex was halved in zidovudine-treatedpatients by comparison with their placebo-treatedcounterparts.

Enthusiastic US press releases at that time did notmention precise numbers of patients or patient-years ofobservation and said nothing about early vs late progression.A complete report of the trial still has not been publishedand NIAID scientists were said to be unwilling to sharetheir data with the European researchers-one reason,according to Stephen Lagakos, the Harvard statistician whoanalysed the results, was to "avoid jeopardizing publicationin a journal that has strict rules about prior publication ofresults".3 3

NIAID representatives subsequently agreed to givefurther information to the Concorde team (Data and SafetyMonitoring and Coordinating Committees) and presentedconfidential information to the European workers inLondon earlier this month. The Concorde 1 Data and

Safety Monitoring Committee reviewed the US findingstogether with the latest Concorde results, and in a pressrelease on Oct 20 said that there was no justification forterminating the Concorde 1 trial. They also thought it

important, especially for the welfare of people with HIVinfection, that "further scientific information about theeffect of long-term zidovudine treatment should beobtained" and feel that "this is unlikely to be achievable inthe USA". The Coordinating Committee believe that "thescientific data now available do not allow strictrecommendations to be made about zidovudine treatment of

asymptomatic HIV positive people based on their CD4lymphocyte counts", whether in trials or in clinical practice.Acknowledging that some physicians may not wish to

recruit into Concorde 1 patients with low CD4 counts, andmay want to give zidovudine openly to those whose countsare persistently low after entering the trial, the CoordinatingCommittee says that such a switch to open zidovudine maybe made after at least six months in the trial and should be

reported to the trial physician. They further recommendthat open treatment should be with zidovudine 1 g a day,with continuing patient follow-up in the study.

So Concorde 1 will continue, a little modified but more orless intact. If it does not undergo any further modifications itshould provide confirmation of the US results, and indicatewhether early therapy is more beneficial than deferred

therapy for symptomless HIV infection. To achieve thisgoal it is important for the patients and patient help groupsto be fully informed about the decisions and the reasons fortaking them.

AIRWAY OBSTRUCTION DURING SLEEP INCHILDREN

AIRWAY obstruction during sleep in adults was describedin The Lancet in 1877.1 Similar episodes in children wererecognised by MacKenzie in 1880 but their importance

3. Anon (J. P.). A new antiviral drug: promising or problematic? Science 1989; 246:200-87.

1. Broadbent WH. On Cheyne-Stokes respiration in cerebral haemorrhage. Lancet 1877;i: 307-08.

2. MacKenzie M. A manual of diseases of the throat and nose including the pharynx,larynx, trachea, oesophagus, nasal cavities and neck. London: J & A Churchill,1880.

was not recognised until much later.3 During normalinspiration the patency of the upper airway is maintained byphasic contraction of the muscles of the pharynx, larynx, andtongue (especially genioglossus).4 During rapid-eye-movement sleep there is inhibition of tone in all skeletalmuscles with the exception of the diaphragm,5 and in infantsthere is normally some narrowing of the oropharynx oninspiration.6 If there is any structural narrowing of the nasalairway or pharynx (eg, enlarged tonsils or adenoids, choanalstenosis, large tongue) inspiratory intrapharyngeal pressurebecomes more negative and leads to more pronouncednarrowing or to complete obstruction that may be furtherexacerbated by the presence of an upper respiratory tractinfection or by neck flexion.’-9 Tonsillar and adenoidalhypertrophy has been commonly associated withobstructive sleep apnoea (OSA) in children and severalstudies have shown improvement with tonsillectomy andadenoidectomy.3,7,8,1O Without treatment, children withOSA may get cor pulmonale or systemic hypertension ormay show growth failure or poor school performance.7-9,11,12Symptoms commonly described by parents of children

with OSA include snoring, episodes of stopping breathing,difficulty breathing when asleep, mouth breathing, restlesssleep with frequent waking, abnormal sleep positions (eg, onelbows and knees), sweating when asleep, and daytimesomnolence. Less common symptoms include nocturnalenuresis in older children, morning headaches,hyperactivity, nightmares, clumsiness, and developmentaldelay or poor school performance.8,9,11 These features arealmost always worse at the time of upper respiratoryinfection. Many of these symptoms occur in normal

children, so further investigation is essential to diagnoseOSA.11,11 Most children with OSA are 2-8 years of age at

diagnosis, but many have a history that suggests onset ofobstruction before 12 months of age.8

Guilleminault et al defined OSA in adults as the

occurrence of thirty or more episodes of apnoea lasting 10 sor more during a 7 h sleep period." The diagnosis of OSArequires a recording of respiratory activity and sleep state,together with some measure of arterial oxygen and carbondioxide.8,9,11 Such recordings have usually needed the

facilities of a specialist sleep laboratory. Southall et al14 andLong and colleagues15 have lately described more simplesystems to investigate possible OSA in children-

3. Swift AC. Upper airway obstruction, sleep disturbance and adenotonsillectomy inchildren. J Laryngol Otol 1988; 102: 419-22.

4. Jeffries B, Brouillette RT, Hunt CE. EMG study of some accessory muscles ofrespiration in children with obstructive sleep apnea. Am Rev Respir Dis 1984; 129:696-702.

5. Phillipson EA. Respiratory adaptations during sleep. Am Rev Physiol 1978; 40:133-56.

6. Gunn TR, Tonkin SL. Upper airway measurements during inspiration and expirationin infants. Pediatrics 1989; 83: 73-77.

7. Brouillette RT, Fembach SK, Hunt CE. Obstructive sleep apnea in infants andchildren. J Pediatr 1982; 100: 31-40.

8. Frank Y, Kravath RE, Pollak CP, Weitzman ED. Obstructive sleep apnea and itstherapy: clinical and polysomnographic manifestations. Pediatrics 1983, 71:737-42.

9. Mark JD, Brooks JG. Sleep-associated airway problems in children Pediatr ClinNorth Am 1984; 31: 907-18.

10. Potsic WP, Pasquariello PS, Baranak CC, Marsh RR, Miller LM. Relief of upperairway obstruction by adenotonsillectomy. Otolaryngol Head Neck Surg 1986; 94:476-80.

11. Brouillette R, Hanson D, David R, et al. A diagnostic approach to suspectedobstructive sleep apnea in children. J Pediatr 1984; 105: 10-14.

12. Serratto M, Harris VJ, Carr I. Upper airway obstruction: presentation with systemichypertension. Arch Dis Child 1981; 56: 153-55.

13. Guilleminault C, Tilkian A, Dement WC. The sleep apnea syndromes. Annu Rev Med1976; 27: 465-84.

14. Southall DP, Croft CB, Stebbens VA, et al. Detection of sleep associated dysfunctionalpharyngeal obstruction m infants. Eur J Pediatr 1989; 148: 353-59.

15. Long AM, Fleming PJ, Levine MR. Polygraphic sleep studies for the investigation ofsleep related respiratory disorders. Ped Reviews Commun 1987; 1: 282.

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recordings of inductance or impedance plethysmography,pulse oximetry, and expired carbon dioxide. Such

recordings can be carried out in a children’s ward or even athome. Southall showed that partial or complete airwayobstruction during sleep, with severe hypoxaemia, can occurin children without tonsillar or adenoidal hypertrophy, andmay persist after adenotonsillectomy. Guilleminault’s

group described the use of nasal continuous positive airwaypressure (CPAP) for such children,16 and Southall andco-workersl4 have confirmed the efficacy of this treatmentand its suitability for use at home.The diagnosis of OSA is strongly suggested by a history of

frequent snoring and difficulty breathing during sleep orobstructive apnoea observed by the parents." A recording ofrespiratory movements, expired carbon dioxide, and pulseoximetry during sleep is within the capability of manypaediatric units and may confirm or refute the diagnosis.Nasal, laryngotracheal, or other abnormalities must besought by careful examination before OSA is attributed toenlarged tonsils and adenoids. The use of a flexible

fibreoptic paediatric nasopharyngoscope allows directexamination of the posterior nasopharynx, adenoids, andtonsils.9,14 Removal of hypertrophied tonsils and adenoids inchildren with OSA commonly leads to considerable

improvement.3,’,8,10 In the absence of enlarged tonsils andadenoids, nasal CPAP is the treatment of choice for childrenwith severe OSA, and in many cases can be safely used athome. Early recognition of children with such a degree ofOSA should diminish the need for temporary tracheostomyfor those severely affected.

CAMPYLOBACTER PYLORI BECOMESHELICOBACTER PYLORI

THE first successful culture of spiral or helical gram-negative bacteria from the human stomach was reported inThe Lancet in 1983.1 By light microscopy, and in the guanineplus cytosine content of their DNA, these microaerophilicorganisms resembled campylobacters, and so were namedCampylobacter pyloridis;2 the specific epithet was

grammatically incorrect and the name of the bacterium waslater changed to C pylori. However, the ultrastructure of Cpylori and its fatty acid composition were found to be verydifferent from that of campylobacters." The basic definitionof a genus rests on genomic analysis, and four studies ofrRNA sequencing have shown clearly that C pylori does notbelong in the genus Campylobacter.5-8 These studiesindicated that C pylori more closely resembles Wolinellasuccinogenes, a vibrioid microbe found in the bovine rumen,

16 Guilleminault C, Nino-Murcia G, Heldt G, Baldwin R, Hutchinson D. Alternativetreatment to tracheostomy in obstructive sleep apnea syndrome: nasal continuouspositive airway pressure in young children. Pediatrics 1986; 78: 797-802.

1. Marshall B. Unidentified curved bacilli on gastric epithelium in active chronicgastritis. Lancet 1983; i: 1273-75.

2. Marshall BJ, Royce H, Annear DI, et al. Original isolation of Campylobacter pyloridisfrom human gastric mucosa. Microbios Lett 1984; 25: 83-88.

3. Marshall BJ, Goodwin CS. Revised nomenclature of Campylobacter pyloridis fromhuman gastric mucosa. Int J Syst Bacteriol 1987; 37: 68.

4. Goodwin CS, McCulloch RK, Armstrong JA, Wee SH. Unusual cellular fatty acidsand distinctive ultrastructure in a new spiral bacterium (Campylobacter pyloridis)from the human gastric mucosa. J Med Microbiol 1985; 19: 257-67.

5. Romaniuk PJ, Doltowaska B, Trust TJ, et al. Campylobacter pylori, the spiralbacterium associated with human gastritis, is not a true Campylobacter spp.J Bacteriol 1987; 169: 2137-41.

6. Lau PP, DeBrunner-Vossbrinck B, Dunn B, et al. Phylogenetic diversity and positionof the genus Campylobacter. Syst Appl Microbiol 1987; 9: 231-38.

7 Thompson LM, Smibert RM, Johnson JL, Krieg N. Phylogenetic study of the genusCampylobacter. Int J Syst Bacteriol 1988; 38: 190-200.

and the type species of Wolinella, but two of the studiesnoted sufficient differences between W succinogenes and Cpylori to justify separate general.5,6 Owen9 identified fourteenphenotypic differences between C pylori and W succinogenes,and has argued cogently that these species should be inseparate genera. Detailed analysis of five major groups oftaxonomic features of these bacteria (ultrastructuralfeatures, cellular fatty acid profiles, respiratory quinones,growth characteristics, and enzyme capabilities) has nowrevealed pronounced phenotypic differences between Cpylori and W succinogenes.10 Thus a new genus name isrequired and, because of the medical importance of C pylori,the sooner the better.

Earlier this month, in the International Journal ofSystematic Bacteriology, the new name Helicobacter pyloriwas proposed for C pylori,1O and with publication in thatjournal it is now the validated name. Similarly, the gastricspiral organism from the ferret has been renamedHelicobacter mustelae.1O The genus name reflects the twomorphological appearances of the organism, helical in vivobut often rodlike in vitro (bacter, a staff). From a species ofmacaque monkey, M nemestrina, two different gastric spiral,urease-positive organisms have been isolated; type B seemsto have a unique fatty acid composition." This organismcould represent a third species in the genus Helicobacter.

Physicians may be understandably irritated when

microbiological considerations reveal the need for a changein name of an organism. However, the new genus name willalso avoid existing confusion about "campylobacterinfections"-ie, usually a reference to diarrhoea due toC jejuni and allied campylobacters and not to stomachsymptoms due to H pylori. H pylori has burst onto thegastroenterological scene, and its aetiological role in gastritis(type B) has been accepted." (Type A gastritis is associatedwith pernicious anaemia, but type B is by far the commonesttype of chronic gastritis.) In 0-3% of patients with gastritis along "corkscrew" organism is present. This organismoccurs much more commonly in monkeys, cats, and dogs;although it has not been cultured, the name "Gastrospirillumhominis" has been suggested,13 but not yet validated. Theaetiology of duodenal ulcer (DU) is obviously multifactorial,with acid and pepsin as the preciptating causes. However, ifduodenitis is a precursor of DU, and H pylori is largelyresponsible for duodenitis, then H pylori is the majorpredisposing cause of DU. 14--16 In a double-blind study ofantibiotic treatment of DU, some patients from whom Hpylori was eradicated still smoked, and did not have a relapseof their DU; among patients in whom H pylori was not

8. Paster BJ, Dewhirst FE. Phylogeny of campylobacters, wolinellas, Bacteroides gracilis,and Bacteroides ureolyticus by 16S ribosomal ribonucleic acid sequencing Int J SystBacteriol 1988; 38: 56-62.

9. Owen JR. Taxonomy of Campylobacter pylori. In: Rathbone BJ, Heatley RV, eds.Campylobacter pylori and gastroduodenal disease. Oxford: Blackwell, 1989: 12-23.

10. Goodwin CS, Armstrong JA, Chilvers T, et al. Transfer of Campylobacter pylori andCampylobacter mustelae to Helicobacter gen nov as Helicobacter pylon comb nov andHelicobacter mustelae comb nov, respectively. Int J Syst Bacteriol 1989; 39:397-405.

11. Goodwin CS, McConnell W, McCulloch RK, et al. Cellular fatty acid composition ofCampylobacter pylori from primates and ferrets compared with those of othercampylobacters. J Clin Microbiol 1989; 27: 938-43.

12. Dooley CP, Cohen H. The clinical significance of Campylobacter pylori. Ann InternMed 1988; 108: 70-79.

13. McNulty CAM, Dent JC, Curry A, et al. New spiral bacterium in gastric mucosa.J Clin Pathol 1989; 42: 585-91.

14. Goodwin CS. Duodenal ulcer, Campylobacter pylori, and the "leaking roof" concept.Lancet 1988; ii: 1467-69.

15. Graham DY. Campylobacter pylori and peptic ulcer disease. Gastroenterol 1989; 96:615-25.

16. Wyatt JI. Relationship of C pylori to duodenal ulcer disease. In: Blaser MJ, ed.Campylobacter pylori in gastritis and peptic ulcer disease. New York: Igaku-Shoin,1989· 90-114.