505

notwithstanding, streptozotocin is a valuable agent andshould be considered in the emergency treatment of patientsin crisis with malignant insulinoma, pancreatic cholera,and the Z-E svndrome. -

Kaiser Foundation Hospital,Los Angeles,

California 90027, U.S.A.

LEONARD SADOFFDONALD FRANKLIN.

DIAGNOSIS OF CŒLIAC DISEASE

SIR,-I read with interest the account (June 14, p. 1345)by Dr Challacombe and others of the problems they en-countered in diagnosing coeliac disease. In the course oftheir investigations, two intestinal biopsies were necessary,as well as a gluten challenge, which the authors agree is notwithout risk. It is likely that all this caused a hospital stayof a few weeks.

Their last two sentences state that a gluten-free dietimproved the child’s miserable mood and permitted a

satisfactory weight-gain.It strikes me that had this been the first step in investiga-

tion rather than the last, it might have obviated a numberof somewhat risky procedures and considerably shortenedthe hospital stay-with one immediate benefit, a greatsaving of money. It would also have greatly strengthenedthe presumptive diagnosis. It could indeed be argued thatthe diagnosis would not have been clinched. True: butthe child would have been effectively treated; and surelythat was the object of the exercise ?

20 West Heath Drive,London NWll 7QH. E. HINDEN.

* * We showed this letter to Dr Challacombe and hicolleagues, whose reply follows.-ED. L.

SiR,-We are unable to accept Dr Hinden’s suggestiothat gluten withdrawal from the diet of our patient shoulhave been the first step in our investigations.

In retrospect, the child described would certainly havimproved on gluten withdrawal without a biopsy, but, aDr Hinden states, " the diagnosis would hot have beeclinched ". It is essential to confirm the clinical diagnos:of coeliac disease by small-intestinal biopsy, and failure to dso may lead to the use of an unnecessary gluten-free dietSurely, the increased expenditure arising from the need 1confirm the diagnosis of cceliac disease histologically in ttcase described must be balanced against the cost of aunnecessary gluten-free diet.

Children’s Research Unit,Musgrove Park Branch,

Taunton and Somerset Hospital,Taunton, Somerset TA1 5DA.

D. N. CHALLACOMBEP. D. DAWKINSK. ROBERTSON.

EFFECT OF T.S.H. ON BROWN FAT

SiR,—Professor Doniach’s suggestion (July 26, p. 160)that thyroid-stimulating hormone (T.S.H.) stimulatesthermogenesis by brown fat may help to explain somerecent necropsy findings.There is no longer any doubt that some brown fat

persists in the normal adult. Heaton 2 studied multiple fatsamples taken from several sites at 50 necropsies at all agesand found multilocular brown fat in each subject. I havefound significant amounts of brown fat in periadrenal fatsamples in 76% of a series of 233 adult necropsies.3 Brownfat was conspicuously absent, however, in two middle-agedsubjects who had previously had a hypophysectomy withstandard hormonal replacement therapy. By contrast, a

1. Anderson, C. M., Gracey, M, Burke, V. Archs Dis. Childh. 1972,47, 292.

2. Heaton, J. M. J. Anat. 1972, 112, 35.3. Burton, P. A., Snow, M. H. Postgrad. med. J. (in the press).

young man who died of untreated thyrotoxic crisis wasfound to have extensive areas of depleted brown fat.

Another adult patient was thought clinically to haveresistant thyrotoxicosis with exophthalmos (T.S.H. beforetreatment was 2-4 pg/ml) and she had received large dosesof carbimazole for a long period. At necropsy 2 years latershe was found to have a phxochromocytoma and veryextensive lipid-depleted brown fat.

This finding may relate to the extensive catecholaminesecretion, but the observation does confirm that thyroidhormones are not essential for brown-fat stimulation, andthe presumptive iatrogenic increase in T.s.H. secretion couldhave played a part in its production. Examination of theretrobulbar fat in this patient failed to show any brown fat.

Department of Histopathology,Royal Infirmary,Bristol BS2 8HW. PATRICIA A. BURTON.

JOINT INFECTION BY PASTEURELLAMULTOCIDA

SIR,-Although Dr Griffin and Mr Barber (June 14,p. 1347) are clearly correct in asserting that joint infectionby Pasteurella multocida (Syn. septica) is rare after injuryby cats and dogs there are four relevant references not

. cited by them or by Dr Szalay (Aug. 23, p. 364).Allott et a1.l reported isolation of the organism from six

patients after cat or dog bites; one of these patients had aninterphalangeal joint infection after a cat bite, whileanother developed osteomyelitis of a terminal phalanxof a finger after a dog bite. A total of three cases of fingerinfection with joint involvement after a cat-bite woundwere described by Cooper and Moore,2 Kapel,3 andBurns et a1. 4

Allin 5 in 1942 seems to have been the first to drawattention to osteomyelitis as a complication of cat-bitewounds infected by Pasteurella multocida.

Public Health Laboratory,Glyde Path Road,Dorchester, Dorset. GEORGE TEE.

DOG COLLES

SiR,—Dr Maurer and his colleagues (Aug. 30, p. 409)describe joint infection in a patient with rheumatoid

arthritis, caused by Pasteurella multocida transmitted bya dog. Another danger from keeping dogs is the risk ofserious injury. I have seen two patients with rheumatoidarthritis on corticosteroid therapy who had fractures. Onepatient was bowled over by the exuberant animal andsustained a fractured femur and severe bruising, and theother tripped over her dog and sustained a Colles fractureof the radius with a scalp laceration. Both patients hadwidespread osteoporosis due to a combination of thedisease process and corticosteroid therapy. Gottlieb et al. 6

raised the possibility that pets might serve as a reservoirfor an infectious agent(s) capable of initiating rheumatoidarthritis, but an even greater hazard of dogs may be therisk of septic arthritis, or injury, especially for patientswith rheumatoid arthritis receiving corticosteroids.

Department of Rheumatology,King’s College Hospital,

Denmark Hill,London SE5 9RS. ANTHONY J. RICHARDS.

1. Allott, E. N., Cruickshank, R., Cyrlas-Williams, R., Glass, V.,Meyer, I. H., Straker, E. A., Tee, G. J. Path. Bact. 1944, 56, 411.

2. Cooper, T. V., Moore, B. Lancet, 1945, i, 753.3. Kapel, O. Acta chir. scand. 1947, 95, 27.4. Burns, G. C. T., Espiner, E. A., Perry, E. G. N.Z. med. J. 1959,

58, 598.5. Allin, A. E. Can. med. Ass. J. 1942, 46, 48.6. Gottlieb, N. L., Ditchek, N., Poiley, J., Kiem, I. M. Arthritis

Rheum. 1974, 17, 229.