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medical school in the first week of August, asking them about theirunderstanding of Homans’ sign. I received 32 replies. 2 had beentaught not to look for Homans’ sign because the test was dangerous,but all of the other 30 understood Homans’ sign to be pain in the calfon dorsiflexion of the ankle.There seems to be widespread misunderstanding of Homans’

dorsiflexion sign. Common usage may well have changed themeaning and perhaps the time has come to redefine or even renamethis clinical observation.

’

Department of Medicine,University Hospital,Queen’s Medical Centre,Nottingham NG7 2UH D. A. SANDLER

1. Archer GJ Homans’ sign. Lancet 1985; i: 8162 Sandler DA, Martin JF. Liquid crystal thermography as a screening test for deep-vein

thrombosis. Lancet 1985; i: 665-67

CALCIUM SUPPLEMENTS AND POSTMENOPAUSALOSTEOPOROSIS

SIR,-To be corrected on a point of statistics by Professor Nordin(Sept 28, p 720) is wounding indeed. It may help ifwe clarify some ofthe points raised in his letter.If we allow Nordin the validity of pooling the two prospective

studies1,2 claiming an effect of calcium, there is indeed a significantreduction in loss of metacarpal cortical width by calcium supple-mentation. Metacarpal cortical width is much less valuable thanother bone measurements because it takes no account of changes inintracortical porosity or trabecular bone resorption. However,when the forearm densitometry results are combined, we, unlikeNordin, find no significant difference between the controls and thecalcium supplemented patients (mean difference 0-Oil ±0-007

g/cm/yr; p>0-05). An even more sensitive bone measurement

technique is quantitative computerised tomographic scanning ofthe spine.3In a controlled, prospective study, Gordan and Genant4showed that 1500 mg oral calcium supplement daily has nopreventive effect whatsoever on postmenopausal bone loss over a 2year period.We did not claim that dietary calcium deficiency in animals did

not cause osteoporosis. Nor did we mention the ages of the animals.What we still question is the relevance of such studies to postmeno-pausal women.The main point of our Aug 10 letter was that, however sensible it

is as an adjuvant, dietary calcium supplementation alone cannot beregarded as an effective alternative to oestrogen/progestin hormonereplacement in the prevention of postmenopausal osteoporosis.We thank Prof M. J. R. Healy, division of medical statistics and

epidemiology, London School of Hygiene and Tropical Medicine, for hisadvice and statistical analysis.Endocrine Unit,Royal Postgraduate Medical School,Hammersmith Hospital,London W12 0HS

JOHN C. STEVENSONIAIN MACINTYRE

1. Recker RR, Saville PD, Heaney RP. Effects of estrogens and calcium carbonate onbone loss in postmenopausal women. Ann Intern Med 1977; 87: 649-55.

2 Horsman A, Gallagher JC, Simpson M, Nordin BEC. Prospective trial of oestrogeiand calcium in postmenopausal women. Br Med J 1977; ii: 789-92.

3 Cann CE, Genant HK. Precise measurement of vertebral mineral content usingcomputed tomography. J Comput Assist Tomogr 1980; 4: 493-500.

4. Gordan GS, Genant HK. The aging skeleton. Clins Geriatr Med 1985; 1: 95-118.

*t*This letter has been shown to Professor Nordin, whose replyfollows.-ED. L.

SiR,—I am pleased that Dr Stevenson and Professor MacIntyre eagree that my analysis of the metacarpal data from the two studies inquestionl,2 shows a significant effect of calcium supplementation,but cannot agree that this index is much less valuable than otherbone measurements. On the contrary, it may prove to be especiallyvaluable because of the reduced cortical bone thickness in femoralneck fracture cases.3 The intracortical resorption to which theyrefer is almost certainly closely related to endosteal resorption; ifcalcium inhibits endosteal resorption it is likely to inhibitmtracortical resorption too.

I much regret my mistake in calculating the t value on the pooled

densitometry data, but this does not invalidate the main thrust of mySept 28 letter. My mathematical error may be more obvious butStevenson and MacIntyre’s type II error is more fundamental. Arate of bone loss on calcium treatment which was half that in thecontrols and not significantly different from zero does not justify thestatement that the study showed no effect of calcium

supplementation-the most that can be said is that it did not show aneffect. This is a very important distinction.On present evidence, oestrogens are much more effective than

calcium, although the oestrogen action is very dose-dependent. 4-6The explanation may simply be a matter of numbers and length ofobservation, but there may be another reason. Just as bleeding is thecommonest cause of iron-deficiency anaemia, so the obligatory lossof calcium in the urine is a major factor in the pathogenesis ofosteoporosis. Correction of blood loss is a more effective cure forthis type of iron deficiency than simply feeding iron. Similarly,lowering the urine calcium with oestrogen may be more effectivethan trying to match the calcium loss by administering calcium.This may be especially true in the immediate postmenopausalperiod, and even more so if calcium absorption is impaired. Thisdoes not affect the general concept that osteoporosis is an expressionof calcium deficiency.Stevenson and MacIntyre’s reference to "a controlled,

prospective study" by Gordan and Genant is surprising. Thepaper cited is a review article in which the last illustration shows

spinal density measurement on 30 patients given extra calcium and13 given no treatment. There is no description of this "trial" and thefigure is taken, with some curious minor differences, from a paperpresented at the 1984 Copenhagen symposium8 in which the detailsof this trial were not given either. The principal investigator, DrBruce Ettinger, tells me that the patients were not randomised butthemselves chose whether to take extra calcium or not; most of themchose to do so. Nor were they given a 1500 mg calcium supplement,as stated in Stevenson and MacIntyre’s letter; their diet was madeup to 1500 mg, which is different. Although the results are

interesting, it is impossible to regard this as a controlled prospectivestudy.Stevenson and Maclntyre deny claiming that calcium deficiency

does not cause osteoporosis in animals and deny mentioning the ageof the animals, but their letter of Sept 18 says "the link betweencalcium deficiency is based on studies of growing animals". Mostreaders would take this to imply that calcium deficiency does notcause osteoporosis in mature animals, which is not correct andcannot be inferred from my review, which they cite.9 9

Department of Endocrinology,Royal Adelaide Hospital,Adelaide, South Australia 5000 B. E. C. NORDIN

1. Recker RR, Saville PD, Heaney RP. Effects of oestrogens and calcium carbonate onbone loss in postmenopausal women. Ann Intern Med 1977; 87: 649-55.

2. Horsman A, Gallagher JC, Simpson M, Nordin BEC. Prospective trial of oestrogenand calcium in postmenopausal women. Br Med J 1977; ii: 789-92

3 Horsman A, Nordin BEC, Simpson M, Speed R. Cortical and trabecular bone Status inelderly women with femoral neck fracture Clin Orthopaed Rel Res 1982; 166:143-51.

4. Horsman A, Jones M, Francis R, Nordin BEC. The effect of oestrogen dose onpostmenopausal bone loss. N Engl J Med 1983; 309: 1405-07.

5. Christiansen C, Christensen MS, Larsen NE, Transbol IB. Pathophysiologicalmechanism of oestrogen effect on bone metabolism: dose-response relationships inearly postmenopausal women. J Clin Endocrinol Metab 1982; 55: 1124-30.

6. Lindsay R, Hart DM, Clark DM. The minimum effective dose of oestrogen forprevention of postmenopausal bone loss. Obstet Gynecol 1984; 65: 759-63.

7 Gordan GS, Genant HK. The aging skeleton. Clins Geriatr Med 1985; 1: 95-118.8. Genant HK, Cann CE, Ettinger B, et al Quantitative computed tomography for spinal

mineral assessment. In: Christiansen C, Arnaud CD, Nordin BEC, Parfitt AM,Peck WA, Riggs BL, eds. Osteoporosis Proceedings of the CopenhagenInternational Symposium on Osteoporosis (Glostrup Hospital, Denmark, 1984)153-55.

9. Nordin BEC. Osteomalacia, osteoporosis and calcium deficiency. Clin Orthop 1960;17: 235-57.

LOCAL NERVE BLOCK AFTER STINGRAY INJURYSIR,-While scuba diving in 12 m of water off the coast of Sri

Lanka I trod on a stingray and was stung on the top of my left foot,1 cm from the web between the second and third toes.We were diving from a boat equipped for long-haul sailing and it

carried an assortment of drugs for emergencies. One of my

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companions was a general practitioner. The local people told us thatthe major effect of such stings would be pain with muscle spasm andthat anaphylaxis was unlikely. I took dihydrocodeine and

chlorpheniramine tablets but after 15 minutes this treatment wasclearly inadequate. The pain had become very severe, causingmuscle spasm of the whole leg.We decided to try blocking a deep peroneal nerve at the ankle with

1% plain lignocaine. The general practitioner, who had not used thetechnique before, did the block on my instructions. Relief wasimmediate and no other nerves were blocked. The block lasted for80 minutes and was repeated. After that the pain was far less severeand I made an uneventful recovery. Local nerve block has

advantages not only in cases of stingray injury but also for manyother forms of trauma. While at sea the patient may still be requiredto take a watch or navigate, and if systemic drugs can be avoided heor she may continue to act as a reliable member of the team. If the

patient is already seasick, heavy sedation may compromise thelaryngeal reflexes, making systemic opioids an unwise choice.Injuries on board ship are often to the hands and feet, which areespecially amenable to local nerve blocks with non"toxic doses.Our ship’s medical box carried lignocaine for suturing in

emergencies, but bupivacaine, with its longer duration of action,would have been better. Drugs with adrenaline added may give riseto other complications and are not recommended. Nerve blocksaround the ankle and wrist or of single digits can be done safely byany doctor, though a chart to remind the operator of the relevantanatomy would be helpful. 1The recommended treatment for stingray stings varies from

immersing the limb in water as hot as the patient can stand2 (thetoxin is heat sensitive) to local infiltration of anaesthetic andintravenous calcium gluconate for the muscle spasm.3 Debridementand suturing are sometimes necessary, and saline irrigation mayremove some of the venom. None of these were needed in my case.

Any seagoing doctor should carry 0 - 5% plain bupivacaine in hisemergency drug kit, not only for stingray injuries but also forsuturing and as a useful method of pain relief.Department of Anaesthetics,Hammersmith Hospital,London W12 0HS FRANCES M. DORMON

1. Eriksson E. Illustrated handbook in local anaesthesia, 2nd ed. London: Lloyd Luke,1979: 90-92, 112-15

2. Manson-Bahr P. Manson’s tropical diseases, 18th ed. London: Baillière Tindall, 1982:562.

3. Strickland T. Hunter’s tropical medicine, 6th ed. Philadelphia: WB Saunders, 1984:798

PANCREATIC POLYPEPTIDE RELEASE DURINGEMOTIONALLY INDUCED VASOVAGAL SYNCOPE

SIR,-Pancreatic polypeptide (PP) regulates exocrine pancreaticsecretion and biliary tract motility. Secretion is stimulated by foodand by low blood glucose. The PP cell in the pancreas is stimulatedthrough vagal, cholinergic mechanisms. 1-3 The PP cell is undervagal, cholinergic tone in the basal state.4 This fact has proveduseful in the investigation of suspected endocrine pancreatictumour, where an "atropine suppression test" can distinguishbetween high levels of PP due to either cholinergic tone or tumoursecretion6 In patients with autonomic neuropathy, both diabeticand idiopathic, PP can be used as an early and sensitive monitor ofthe degree of neuropathy.-9

In a study of the secretion of gastroenteropancreatic hormones inadolescents with cystic fibrosis we investigated twenty healthycontrols aged 11-20 years who, after a night’s fast, were given astandard meal. The experiment was started by the insertion of a’Venflon’ catheter in an antebrachial vein and a fasting blood samplewas drawn. One control (aged 13 years) became pale and sweaty andfelt nauseated and faint. He was laid down and his legs were raised;his blood pressure was 55/40 mm Hg and the heart rate was 72/minduring the episode. After a few minutes his blood pressure and heartrate rose to 90/60 mm Hg and 128/min, respectively. As the patientwas feeling better and insisted on going on with the experiment, thetwo remaining fasting blood samples were drawn, and the

experiment was continued. As shown in figure, the plasma PPconcentrations in this boy with typical emotional vasovagal syncope

PP concentrations in plasma in normal child who experiencedemotional vasovagal syncope after first blood sampling.All twenty controls given standard meal (bar). 0 = affected child;. =other

nineteen controls (mean and SEM).

rose sharply from 50 to 220 pmol/l, whereas no change was observedin the fasting PP levels of the nineteen other controls. The presenceof a possible "vagal episode" during the fasting period in this boywas suggested by the "blind" measurer of PP and confirmed by theclinician.The observation of a striking release of PP during emotionally

induced vasovagal syncope corroborates with experiments on PPrelease during hypovolaemia induced vasovagal shock, also charac-terised by bradycardia. Previously, we demonstrated increased PPrelease during hypotensive central hypovolaemia and bradycardiaelicited by head-up tilting in fasting subjects Furthermore, in aseries of twenty consecutive patients in reversible, haemorrhagicshock, bradycardia was observed, and this was accompanied by PPplasma concentrations (unpublished) similar to those seen duringthe emotionally induced vasovagal syncope reported here. Thesesupport the notion that the vasovagal reaction contributes to thedevelopment of haemorrhagic shock, even when it is still reversible.

Department of Medical Physiology C,Panum Institute;and Departments of Paediatricsand Clinical Chemistry,

Rigshospitalet,University of Copenhagen,DK-2100 Copenhagen, Denmark

K. SANDER-JENSENS. GARNET. W. SCHWARTZ

1. Schwartz TW. Pancreatic polypeptide: a hormone under vagal control. Gastro-

enterology 1983; 85: 1411-25.2. Schwartz TW, Rehfeld JF, Stadil F, Larsson L-I, Moon N, Chance RE. Pancreatic

polypeptide response to food in duodenal ulcer patients before and after truncalvagotomy Lancet 1976; i: 1102-05.

3. Schwartz TW, Holst JJ, Fahrenkrug J, et al, Vagal, cholinergic regulation of pancreatic-polypeptide secretion. J Clin Invest 1978; 61: 781-89.

4 Schwartz TW, Stenquist B, Olbe L, Stadil F. Synchronous oscillations in the basalsecretion of pancreatic-polypeptide and gastric acid: Depression by cholinergicblockade of pancreatic-polypeptide concentrations in plasma. Gastroenterology1979; 76: 14-19.

5. Schwartz TW Atropine suppression test for pancreatic polypeptide. Lancet 1978; ii:42-43.

6. Adrian TE, Bloom SR. Clinical application of the atropine test for diagnosis ofpancreatic PP-omas. 4th International Symposium on GastroentetologicalHormones, 1982 33 (abstr).

7. Krarup T, Schwartz TW, Hilsted J, Madsbad S, Verlaege O, Sestoft L. Impairedresponse of pancreatic polypeptide to hypoglycemia: an early sign of autonomicneuropathy in diabetics. Br Med J 1979; ii: 1544-46.

8. Levitt NS, Vinik AI, Sive AA, Van Tonder S, Lund A. Impaired pancreatic polypeptideresponse to insulin induced hypoglycemia in diabetic autonomic neuropathy J ClinEndocrinol Metab 1980, 50: 445-49

9. Polinsky RJ, Taylor IL, Chen P, Weise V, Kopin IJ Pancreatic polypeptide responsesto hypoglycemia in chronic autonomic failure. J Clin Endocrinol Metab 1982, 54:48-52.

10. Bie P, Secher NH, Sander-Jensen K, Warberg J, Christensen NJ, Giese J. Endocrineresponses to hypotensive gravitational stress catecholammes, pancreatic poly-peptide and vasopressin. Life Sci Res Space 1984, 2: 193-95.