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intestinal biopsy specimens. These findings lead tosome interesting conclusions. First, the fact that fatoutput could exceed intake on the very-low-fat dietconfirms the view that some faecal fat is of endogenousorigin, and the composition of this output indicatesthat it may be largely derived from desquamatedintestinal epithelium, as had previously been suggestedby indirect evidence.4 Secondly, the observation thatthe composition of the ileostomy output is greatlyinfluenced by diet shows that the fat entering thecolon has a very substantial dietary component, andthat the relative constancy of the composition ofnormal faecal fat in the face of dietary alterations isnot the result of differential absorption of individualfatty acids in the small intestine. The main changesin the composition of the unabsorbed dietary fatmust therefore occur in the colon. A clue to thenature of these changes was suggested by re-examin-ation of the data from the earlier study,8 when itwas found that the composition of the faecal fat was

11. Bolt, R. J., Napier, E. A., Jr., Howell, K. E., Pollard, H. M. Am. J.clin. Nutr. 1965, 17, 277.

not as independent of dietary fat as had been thought.Ignoring such characteristics as degree of saturation,and grouping the fatty acids by chain length alone,they found that changes in the proportion of C16 andCig fatty acids in the diet did seem to be reflectedto some extent in the composition of the fat in thefaeces. This supports the hypothesis that un-

saturated fatty acids are saturated in the colon,probably by bacterial action.

In summary, the work shows that some of thenormal faecal fat is endogenous in origin and is

probably largely derived from desquamated mucosalcells. The remainder of the fat is exogenous,representing unabsorbed fat from the diet. Both

endogenous and exogenous fat are extensivelymodified in the colon, probably by bacterial action, amajor alteration being saturation of unsaturated

fatty acids. Though some of the conclusions areonly tentative, this work represents an ingenious anddirect approach to a complex problem, which mightusefully be applied to related problems such as theorigin of faecal nitrogen.

Annotations

WHAT IS A HOME?

REMINISCING on television last week, a formerMinister of Housing and Local Government recalledthat in the early ’50s he had had to stage a military-type operation to achieve a target of 300,000 houses ayear, and expressed relief that his party’s conferencehad been restrained from committing him to an evenhigher figure. The targets may have gone up sinceHarold Macmillan’s day but the atmosphere in whichhousing is often discussed remains much the same.In its apparent simplicity and closeness to the every-day needs of people, the number of houses built orstarted has always made good hustings material, andas a straightforward measure of achievement or non-achievement it is irresistible to those engaged in thecross-play of Parliamentary debate. The Governmenthas admitted that it will not reach its current targetof 500,000 houses; (bad weather, high interest-rates,and some reassessment of need are the proferredreasons); it has announced that, over the countryas a whole, there are already many more houses thanthere are families to live in them; and, we are told,the total number of homeless is less than 20,000.All this must read rather strangely to the many peoplewho were disturbed by the tragic incongruity sym-bolised by the television play, Cathy, Come Home;and among these groups must be included thosewho by pressure and more or less militant actionare seeking to remedy the plight of individual families.The National Campaign for the Homeless (Shelter) 1does not suggest that the Government is complacentabout houses, though it naturally regrets the latestcutbacks in the programme; what it does suggest is

1. Wilson, D. (editor). Face the Facts. Obtainable from Shelter,National Campaign for the Homeless, 86 Strand, London W.C.2.2s. 6d.

that we need a redefinition of what is meant by ahome. Shelter argues, forcibly and convincingly,that one can be housed yet still homeless, and cites1966 Census figures and a large series of disturbingcase-reports to illustrate its point. The sample Censusshowed that 23,790 families of more than 3 peoplewere living in a single room and that the total numberof people living in grossly overcrowded conditions(between 3 and 10 people per room) was 390,610.The Census reports consider more than 11/2 peopleper room (including the kitchen) as evidence ofovercrowding, and the number here was 1,641,270.Many of the case-reports prepared by Shelter’sresearch-workers are of premises which, by anyinterpretation of the phrase, were unfit for humanhabitation. A common pattern runs through themall-families, often with several children, living in avery few damp, rodent and insect infested rooms,sharing lavatories and bathrooms (or having none atall), and often at risk of disease (tuberculosis, bron-chitis, and mental strain are specifically mentioned).Yet all these families, Shelter repeats, are not, officially,homeless.

DRUG-INDUCED LUNG DISEASE

No matter how drugs are given, they may reach thelungs by the venous return; and adverse respiratoryreactions to drugs may follow administration by themost unlikely routes. Davies gives examples of severeiodism affecting the whole respiratory tract after theinstillation of iodised talc into the pleural space toproduce pleurodesis; oil embolism of the lungs aftermyelography using a radio-opaque oil 2; and eosino-philic infiltration of the lung after the application of asulphonamide-containing cream to the vagina.3

1. Davies, P. D. B. Br. J. Dis. Chest, 1969, 63, 57.2. Todd, E. M., Gardner, W. T. J. Neurosurg. 1957, 14, 230.3. Klinghoffer, J. F. Ann. intern. Med. 1954, 40, 343.

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Drugs may induce specific respiratory reactions; orthe lungs may be affected as part of a generalised.res-ponse. Hexamethonium lung 4 has no counterpart inother viscera; and nitrofurantoin may produce pul-monary eosinophilia with no systemic component otherthan occasional fever. In contrast, the pulmonary andpleural changes that may be associated with hydralla-zine 6 are part of a generalised systemic-lupus-erythematosus-like reaction; and the large atypicalcells seen in the alveoli in busulphan lung are part ofwidespread cellular changes.Though the mechanisms of most drug-induced lung

diseases are poorly understood, an exception is pitui-tary-snuff-takers’ lung, for which understanding of thereaction is virtually complete and of great interest:this syndrome includes alveolitis (type ill hyper-sensitivity), asthma (type ill and type i), and rhinitis(type 1).8 Iodism 9 and aspirin-induced asthma 10 havesome clinical resemblance to allergic reactions, butthey also have important features apparently incom-patible with a basis of hypersensitivity. The increas-

ingly recognised toxic effects of high concentrations ofoxygen 11,12 on the lung are not only surprising butquite mysterious. In some cases the evidence thatreactions in the lung are drug-induced is circumstantialonly-for instance, the appearance of pulmonarypolyarteritis after the administration of drugs.13New drug-induced respiratory syndromes are con-

stantly appearing. The lipoid granulomas which maycomplicate the use of oily contrast media for broncho-graphy have been known for many years.14 More

recently, oil embolism has been described as a sequelto their use in lymphangiography.15-18 Bacterial pneu-monias and pulmonary tuberculosis are well recognisedas complications of corticosteroids; and, with increasinguse of immunosuppression, opportunistic infections ofthe lung with fungi (such as aspergillus), actinomycetes(such as nocardia), protozoa (such as Pneumocystiscarinii), and viruses (such as cytomegalovirus) are nowbeing seen.19 Suppurative pneumonia and the forma-tion of lung abscess are common in " mainline " drugaddicts 20; and to these must be added pulmonaryoedema after an overdose of opiates, particularly heroin,and cor pulmonale as the result of pulmonary vascularobstruction caused by repeated intravenous injectionof drugs in particulate form.21 The association of pul-4. Heard, B. E. J. Path. Bact. 1962, 83, 159.5. Nicklaus, T. M., Snyder, A. B. Archs intern. Med. 1968, 121, 151.6. Lee, S. L., Siegel, M. Drug Induced Diseases (edited by L. Meyler

and H. M. Seck); vol. III, p. 239. Amsterdam, 1968.7. Heard, B. E., Cooke, R. A. Thorax, 1968, 23, 187.8. Pepys, J., Jenkins, P. A., Lackmann, P. J., Mahon, W. C. Clin.

exp. Immun. 1966, 1, 377.9. Mann, M. R. Proc. R. Soc. Med. 1961, 54, 473.

10. Samter, M., Beers, R. F. Ann. intern. Med. 1968, 68, 975.11. Nash, G., Blennerhassett, J. B., Pontoppidan, H. New. Engl. J.

Med. 1967, 276, 368.12. Case Records of the Massachusetts General Hospital. ibid. p. 401.13. Rose, G. A., Spencer, H. Q. Jl Med. 1957, 26, 43.14. Spencer, H. Pathology of the Lung; p. 479. Oxford, 1968.15. Gough, J. H., Gough, M. H., Thomas, M. L. Br. J. Radiol. 1964,

37, 416.16. Fraimow, W., Wallace, S., Lewis, P., Greening, R. R., Cathcart,

R. T. Radiology, 1965, 85, 231.17. Hamilton, R. W., Hustead, R. F., Peltier, L. F., Kuenzig, M. C.,

Stradinark, J. F., Rosenbaum, S. M. Surgery, St. Louis, 1964,56, 53.

18. Bron, K. M., Baum, S., Abrams, H. L. Radiology, 1963, 80, 194.19. Symmers, W. St. C. Proc. R. Soc. Med. 1965, 58, 341.20. Briggs, J. H., McKerron, C. G., Souhami, R. L., Taylor, D. J. E.,

Andrews, H. Lancet, 1967, ii, 1227.21. Silber, R., Clerkin, E. P. Am. J. Med. 1959, 27, 187.

monary thromboembolism with the taking of contra-ceptive pills is now established beyond doubt.22 Thepossibility has been raised of an association betweencertain appetite suppressants and the development ofpulmonary hypertension; a number of drugs of thistype have been withdrawn from the European market;and doctors in the United Kingdom have been askedto notify cases of this kind to the Committee on Safetyof Drugs.23

TOPICAL TREATMENT OF BURNS

THE mortality from extensive burns is still high, anda leading cause is overwhelming local infection goingon to septicaemia. The increasing importance of gram-negative bacteria associated with this invasive infectionafter burns is again illustrated by a review 24 of 84 casesof proven septicxmia among 1059 admissions to theCincinnati General Hospital and the Shriners BurnsInstitute between 1960 and 1968. Only 7 of these caseshad coagulase-positive staphylococcal septicaemia, com-pared with 76 due to gram-negative organisms.Candida albicans was held responsible in 1 case.

Systemic antibiotics and other agents are unable tocontrol sepsis in the burn wound, so local treatmenthas been more widely used. Moncrief 25 has definedsome of the characteristics required of the ideal com-pound for topical use. It must be effective against themajor pathogens concerned; it must be able to pene-trate the wound in effective concentrations; it must notbe toxic either to the local viable tissue or systemically;it must be rapidly excreted or detoxicated if absorbed;it should have no significant harmful side-effects; andit should be easy to use and inexpensive. In a compar-ison of silver nitrate (0-5% in distilled water) andp-aminomethylbenzenesulphonamide (mafenide) (10%in a water-miscible cream), Moncrief found that bothcompounds reduced the septic complications and in-creased the survival-rates in patients with extensiveburns, particularly children. Both compounds hadside-effects, but they could be controlled. Gentamicin,an aminoglycoside antibiotic which has also been usedlocally in severe burns, is effective systemically againsta wide spectrum of organisms including pseudomo-nas.26 Although Moncrief was unable to come to anyconclusion about its value in topical treatment ofburns, MacMillan,24 in a randomly selected group of161 patients, found that gentamicin in 0-1% ointmentwas more effective than mafenide 10% or silver nitrate0-5%, although all three agents reduced the mortality-rate from major burns. Gentamicin has toxic effects,particularly on the auditory nerve, but MacMillan 24recommends that topical and systemic gentamicinshould be used to treat thermal burns covering 20%or more of the total body-surface. Stone 27 found that291 out of 1721 patients with major burns treated inthe Grady Memorial Hospital, Atlanta, Georgia in1958-67 had pseudomonas infection of the wounds

22. Vessey, M. P., Doll, R. Br. med. J. 1969, ii, 651.23. Cahal, D. A. Lancet, 1969, i, 947.24. MacMillan, B. G. J. infect. Dis. 1969. 119, 492.25. Moncrief, J. A. Clin. Pharmac. Ther. 1969, 10, 439.26. International Symposium on Gentamicin. J. infect. Dis. 1969, 119,

341.27. Stone, H. H. ibid. p. 504.