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health outcomes and it is manifestly in no position totry to claim increased NHS "busyness" as a measure ofprogress. Furthermore, real cuts are widespread andcan no longer be hidden, as the debate in the House ofLords last week (p 1253) again made plain. TheGovernment repeatedly promised that taxpayers’money would be used to safeguard the NHS. It shouldnow meet its obligations not only in terms of cash butalso in reasonable predictability of funding. To requirethe NHS to provide modern health care with anunpredictable as well as a meagre budget is not onlycruel, it is stupid. That message has at last got throughto some members of health authorities. Neither theynor the public are going to accept Treasury or otherGovernment attempts to confuse the issue by pointingto the gratifying and continued public respect for thework of NHS staff6 and to interpret that respect as asign of this Government’s generous stewardship of theNHS.

DUODENITIS—ANY PROGRESS?

IT is nearly 150 years since Baudin wrote his thesis onduodenitis, and we remain ignorant about its clinical

implications. The greatest hindrance to our understanding ofwhat duodenitis is, and what a diagnosis of duodenitis meansfor the patient, is confusing terminology: the term duodenitisis applied both to a macroscopic abnormality of theduodenum that is evident (in various grades) at endoscopyand to a distinct histopathological condition seen (within arange of severity) in duodenal biopsy material. Duodenitis iscommonly observed in the company of duodenal ulcers and atthe site of a recently healed ulcer; it is also seen in patients(both symptomatic and not) whose ulcers are in remission,and in "non-ulcer dyspepsia". Do endoscopic duodenitis andhistological duodenitis represent the same disease? And isduodenitis part of the spectrum of the peptic ulcer diathesis?These crucial questions were asked seven years ago and,despite much discussion,9 there are no firm answers. In theopinion of most gastroenterologists, the answer to each

question is "probably yes".The histological criteria,IO’12 both morphological and in

terms of cellular infiltrate, and the endoscopic criteria7 arewell-defined. However, it seems that histopathologists13 andendoscopists14 may have been overdiagnosing the condition;matters become clearer if the criteria are made more

stringent. The endoscopist’s patchy erythema and the

histologist’s slightly increased cellularity with normal

morphology constitute what each discipline would call themild or minimal-change grade. If these are excluded, there isan impressive concordance between the moderate and severegrades as judged by either-the endoscopist’s contact

bleeding, petechial haemorrhages, and erosions, and the

6 Halpern S. What the public thinks of the NHS. Hth Soc Serv J 1985; 702.7. Baudin JB. Essai sur la duodenite chronique. MD thesis, University of Paris, 18378. Joffe SN, Lee FD, Blumgart LH. Duodenitis. Clin Gastroenterol 1978; 7: 635-50.9. Non-ulcer dyspepsia. duodenitis Scand J Gastroenterol 1982, 17 (suppl 79): 80-103.10. Whitehead R, Roca M, Meikle DD, Skinner JM, Truelove SC. The histological

classification of duodenitis in fibreoptic biopsy specimens. Digestion 1975; 13:129-36.

11. Whitehead R. Morphological aspects of duodenitis. Scand J Gastroenterol 1982, 17(suppl 79): 80-83.

12. Hasan M, Hay R, Sircus W, Ferguson A. Nature of the inflammatory cell infiltrate induodenitis. J Clin Pathol 1983; 36: 280-88.

13. Jenkins D, Goodall A, Gillet FR, Scott BB. Defining duodenitis. quantitativehistological study of mucosal responses and their correlations J Clin Pathol 1985;38: 1119-26.

14. Joffe SN. Relevance of duodenitis to non-ulcer dyspepsia and peptic ulceration. Scand JGastroenterol 1982; 17 (suppl). 88-97

histopathologist’s morphological abnormalities combinedwith a diagnostic pattern of polymorphonuclear and

mononuclear cell infiltration.l0,12.15 In the absence of overtulceration, this "significant" duodenitis is actually quite arare finding during endoscopic examination of dyspepticpatients (less than 3% of 502 patients in one series16).Furthermore, the inclusion of patients with minimal-

change duodenitis, many of whom have associated gastric,biliary, or pancreatic disease17,18 and whose duodenitis istherefore non-specific, has tended to obscure the relationbetween duodenitis and duodenal ulcer disease. This is not to

say that erythema or a mild increased cellularity is necessarilynormal, or irrelevant either to the more severe grades or toduodenal ulceration; merely that non-specific mildduodenitis is common, and thus a poor discriminant. Onceattention is turned to moderate and severe (erosive)duodenitis, it is hard to escape the conclusion that they areindeed part of the duodenal ulcer diathesis.In over 80% of 219 cases of symptomatic duodenitis

followed for up to 3 years by Sircus, an ulcer was visible atsome time. 19 The basal and peak stimulated acid outputs induodenitis are much the same as those in duodenal ulcer; 8,20so too is the pain induced by instillation of acid into theduodenum-in contrast to the response of endoscopy-negative dyspeptic.2 Duodenitis accompanying duodenalulcer is indistinguishable from isolated duodenitis in terms ofthe extent of plasma cell infiltration.22 In the experimentalproduction and healing of duodenal ulcers in the rat, theduodenal mucosa passes through the graded stages ofduodenitis.23 Duodenitis, like duodenal ulceration, is

virtually never seen in symptomless healthy volunteers.18Appreciation of the patchy distribution and variable severityof duodenitis is important; otherwise spurious failures ofcorrelation may result when non-targeted biopsy samplesfrom duodenal ulcer patients are examined for histologicalevidence of duodenitis. 24The evidence, then, suggests that duodenitis is a state that

lies somewhere between the normal (or, for that matter, fullyhealed) duodenal mucosa and the active duodenal ulcercrater. No longer need the endoscopist agonise over the pointat which a large erosion becomes a small ulcer. The newestideas on duodenitis and duodenal ulcer have come fromMarshall and his colleagues,25,26 champions of

Campylobacter pyloridis. Having shown the likely aetiologicalimportance of this organism in the production of antralgastritis they propose that duodenitis represents antral-typegastritis occurring in genetically susceptible individualswhose gastric/intestinal junction lies not at the pylorus but in

15. Shousha S, Spiller RC, Parkins RA The endoscopically abnormal duodenum inpatients with dyspepsia. biopsy findings in 60 cases. Histopathology 1983; 7: 23-34

16. Thomson WO, Joffe SN, Robertson AG, Lee FD, Imne CW, Blumgart LH Isduodenitis a dyspeptic myth? Lancet 1977; i: 1197-98.

17. Cheli R, Aste H. Duodenitis. Stuttgart: Georg Thieme, 1976: 69-82.18. Cheli R. Symptoms in chronic non-specific duodenitis. Scand J Gastroenterol 1982; 17

(suppl 79): 84-87.19. Sircus W. Duodenitis a clinical, endoscopic and histopathological study. Quart J Med

1985; 56: 593-600.20. Myren J. Gastric secretion in duodenitis. Scand J Gastroenterol 1982; 17 (suppl 79)

98-101.21. Joffe SN, Primrose JN. Pain provocation test in peptic ulceration. Endoscopy 1983; 29:

282-84

22. Scott BB, Goodall A, Stephenson P, Jenkins D. Duodenal bulb plasma cells induodenitis and duodenal ulceration. Gut 1985; 26: 1032-37.

23. Joffe SN, Gaskins R, Barros D’Sa AAJ, Baron JH. Secretagogue produced duodenalulcers in the rat. Br J Surg 1977; 64: 218-20.

24. Earlam RJ, Amerigo J Kakavoulis T, Pollock DJ. Histological appearances ofoesophagus, antrum and duodenum and their correlation with symptoms in patientswith a duodenal ulcer. Gut 1985; 26: 95-100.

25. Marshall BJ, Armstrong JA, McGechie DB, Glancy RJ Attempt to fulfil Koch’spostulates for pyloric campylobacter. Med J Aust 1985; 142: 436-39

26. Marshall BJ, McGechie DB, Rogers PA, Glancy RJ. Pyloric campylobacter infectionand gastroduodenal disease Med J Aust 1985; 142: 439-44.

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the duodenal bulb. They propose that gastric lesser-curve,antral, and duodenal ulcers all occur in campylobacter-damaged antral-type mucosa which harbours persistentcampylobacter infection. The time is ripe for long-term studyof both macroscopic and microscopic duodenitis in relation toulcer relapse and remission, campylobacter infection, non-ulcer dyspepsia, and symptomatic, endoscopic, and

histological response to the various treatments now on offer.Work of this kind is already underway. Even if the infectivehypothesis is correct, extermination of the pathogen may notbe curative: the inflammatory damage, once done, could bepermanent.

IRRITABILITY IN PSYCHIATRIC NOSOLOGISTS

IN the ancient world, symptoms were regarded as specificdisease entities. Not until the seventeenth century was this

approach abandoned in favour of a syndromal one in whichconstellations of related symptoms with a characteristic

prognosis were given disease status. Subsequentdevelopments in morbid anatomy, microscopy,chromosomal analysis, and electron microscopy have refinedour disease concepts. The complexity of disorders has alsobecome apparent, and many "entities"-for example,pneumonia-proved to embrace multiple syndromes.Likewise in psychiatry, diseases are no longer generallydefined by their individual symptoms, such as guilt orunhappiness, but by the syndromal approach. In the

dementias, for example, the nosology includes histologicalfindings. Nevertheless, psychiatry is still bedevilled by loosenomenclature. Exotic terms such as the Othello syndromeand the Couvade syndrome’ are still in use despite their beingbut descriptions of specific delusions. This pre-Sydenhamapproach should have no place in current psychiatricparlance.A further area of confusion lies in the inability of

psychiatrists to agree on whether the name applied to anillness refers to the aetiology, symptom pattern, or prognosis.Thus terms such as reactive and neurotic depression are usedinterchangeably, and there is continuing debate how best toconceptualise schizophrenia-whether in terms of prognosisor symptom pattern. The term puerperal psychosis, implyinga specific aetiology, is viewed with disdain by those whofavour a symptomatic approach and use the umbrella term ofschizophrenia or depressive illness.A third area of concern is that of arbitrarily assigning labels.

This is particularly true in the sphere of personality disorderwhere nosological entities are frequently regarded as if theywere specific disorders. The Diagnostic and StatisticalManual (DSM)2 added five new types of abnormal

personality in the third edition: borderline, schizotypal,narcissistic, avoidant, and dependent. Although these weredefined operationally, in the hope of improving the reliabilityand limiting the arbitrariness of psychiatric diagnosis, someworkers have rashly accorded them the status of diseaseentities. Lately, more diffuse disturbances have beenembraced by epithets such as irritability neurosis,3 mixedanxiety/depression,4 the general neurotic syndrome,51. Enoch MD, Trethowan WH, Banker JC. Uncommon psychiatric syndromes, 2nd ed.

Bristol: John Wright, 1980.2 American Psychiatric Association Committee on Nomenclature and Statistics.

Diagnostic and statistical manual of mental disorders, 3rd ed. Washington DC:American Psychiatric Association, 1981.

3 Snaith RP, Taylor CM. Irritability: definition, assessment and associated factors. Br JPsychiatry 1985, 147: 129-36.

4 Eastwood MR. Screening for paychiatric disorder. Psychol Med 1971; 1: 197-208.5 Tyrer P Neurosis divisible. Lancet 1985; i: 685-88.6 Gunderson JG, Colb JE Discriminating features of borderline patients. Am J

Psychiatry 1978; 135: 792-96.7 Miller D, Green J, Farmer K, Carroll G. "A pseudo-AIDS" syndrome following from

fear of aids. Br J Psychiatry 1985; 146: 550-51.

borderline personaÍity,6 and (inevitably) a "pseudo AIDS"syndrome.’

Psychiatric nosology remains utterly confused. Those whotry to define what constitutes psychiatric illness-whether interms of failure of social functioning,8 of numbers of

symptoms, or of operational criteria9-will unite in thedespair of the whimsical shibboleths in current psychiatricwriting.

EXPATRIATE VOLUNTEERS IN AFRICA

EARLIER this year British television viewers were gratifiedby the sight of a young midwife emerging in fair health from aBristol hospital after recovery from near-fatal Lassa fever.For two months she had been nursed there in an isolator, aftertransport (also in strict isolation) by the Royal Air Force fromSierra Leone. A triumph of logistics and technology, it

seemed; but the article on p 1227 records that this was not thewhole story. Before transit, her life had been saved by theconcentrated efforts of nursing and medical colleagues on thespot, working under difficult conditions and protected onlyby barrier nursing. Furthermore, the article hints that partsof the British end of the operation were something less than atriumph.

Firstly, difficulties were experienced in arranging earlyrepatriation. Expert opinion in Sierra Leone, since endorsedby a World Health Organisation workshop, was that in Lassafever the safety of attending personnel can be assured bybarrier nursing-in other words, she might have been takenhome by commercial flight. Only two weeks after her

evacuation, it seems, a German medical student with

suspected Lassa fever returned to Germany by air withoutuse of an isolator. Yet the British authorities insisted on strictisolation. Paradoxically, the consequent delay in arrangingtransport to Britain may have been to this young woman’s

advantage, since the close care she eventually required mightwell have been hampered by the physical constraints of anisolator system, even in a British infectious diseases unit.Future victims, however, may not be so lucky in their localcolleagues.Secondly, there is the observation that some British

volunteers working in Eastern Province, Sierra Leone, hadnot been briefed on Lassa fever. We have inquired furtherinto this matter. In Sierra Leone, American Peace Corpsvolunteers are made fully aware of the hazards of this diseaseand of the necessary precautions; and so too are expatriatesworking in British Methodist mission hospitals. By contrast,British personnel who are sent out by the Government-linkedcharity Voluntary Service Overseas acquire their knowledgeof Lassa fever from other workers, if at all. Some (like thepatient reported this week) are serving in hospitals withnumerous Lassa patients. That VSO is less assiduous in

caring for these volunteers is further suggested by the factthat they are not routinely offered vaccination- againsthepatitis B or rabies, both of which are endemic.There is no reason why Western volunteers should not

work in places such as Sierra Leone; there is a great need fortheir services. But they should be told how to protectthemselves against local diseases, should be offeredimmunisation with the safe and effective vaccines that exist,and should be assured of prompt repatriation if the medicalneed arises.

8. Ingham JG. Neurosis: disease or distress. In: Wing JK, Bebbington P, Robins LN, eds."What is a case?" The problem of definition in psychiatric community surveysLondon: Grant McIntyre, 1981.

9. Spitzer RL, Endicott J, Robins E. Research diagnostic criteria: rationale and reliability.Arch Gen Psychiatry 1978; 35: 773-82.