SKIN ABSORPTION OF LEAD

157 SKIN ABSORPTION OF LEAD

Letters

to

the Editor

PSYCHIATRIC PROFILE OF SHOPLIFTERS

SJR,—Many lawyers, probation officers, and magistrates suspect some people charged with shoplifting have offended primarily as part of a psychiatric disturbance. One of us (G. S.) has examined more than 200 such defendants referred for psychiatric assessment over the past ten years, and has been impressed by the psychopathology demonstrated. Certain features have seemed prominent: marital disharmony (with sexual rejection by the defendant of her or his spouse); depressed mood, though not necessarily depressive illness, preceding arrest or prosecution; and phobic anxiety, which has at times prevented shopping and is distinct from a fear of being caught shoplifting. These impressions accord with anecdotal reports already published.1-5 There has, however, been little objective research into the psychiatric characteristics of legally referred shoplifters. Gibbens6,7 depended largely on probation workers’ assessments. A Canadian study8 has gone further and shown that such referred shoplifters have characteristics more in common with other psychiatric patients than with other offenders. Here we report a pilot study of such legally referred shoplifters, in which we have attempted to test these anecdotal impressions more objectively. As in other series most of our referrals were female, so to simplify matters we studied only those shoplifters who were female and still married; subjects were otherwise unselected. We used specially devised self-rating scales for marital disharmony/sexual rejection and for phobic anxiety, and a depression self-rating scale (available from G. S.). Forms were delivered and returned by post, with a return rate of just over 50%. We obtained 34 fully completed sets of scales (with ages). We ran the same tests on three comparison groups of women-namely, 42 agoraphobics (via the Phobic Society), 18 inpatients being treated for depressive illness, and 36 consecutive patients attending, for any reason, a local family practitioner health centre. that

The groups were not well matched for age, so we subdivided all groups into two by age below 38 or 38 or over. One-way analysis of variance and paired comparisons showed that the scores of the

shoplifters for marital problems (p<0’001), sexual rejection of time since last sexual intercourse (p<0’01), spouse (p < 005), depression (p < 0’001), and phobic anxiety (p < 0’001) all indicated much more disturbance than those of the family practitioner control group (except for the subgroup aged 38 or over where time since last intercourse was not significantly longer). Subdivision into subgroups seemed further justified since we could see a clear relationship between increasing age and more severe marital/sexual scores. The agoraphobic and depressive group subjects gave very significantly raised scores on the phobic and depression scales, respectively, thus validating the measures used. The agoraphobics, like the shoplifters, had raised marital/sexual dysfunction scores. We have now begun a larger study to compare non-referred shoplifters (ie, those arrested and charged but not referred for psychiatric assessment) with those who are legally referred, this time including standard scales for which there are published normative data. However, this pilot study suggests that legally referred shoplifters do have a recognisable pattern of psychiatric

SIR,-Skin absorption is not usually considered a significant mode of uptake of lead, unless the lead is present as a lipid-soluble compound such as tetraethyl lead or lead naphthenate.’ We have found that inorganic lead can be absorbed through skin and rapidly distributed throughout the body. The figure shows the appearance of raised levels of lead in sweat samples taken from the right arm, after a 25 mm diameter membrane filter, to which 60 III of 0mol/1 lead nitrate solution (6 mg Pb) had been added, was placed on the left arm, covered with a square of ’Parafilm’, wrapped firmly with plastic lunch-wrap, and left on the arm for 24 hours. Pilocarpine iontophoresis sweat samplestaken from the right arm periodically before and after the application of lead, were analysed for lead by anodic stripping voltammetry.z3 The sweat lead concentration continued to rise even after the lead was removed, and increased from the normal value of 15-30 ug/1 to over 350 Ilgjl after 2 days (figure). Similar results were obtained when 100 mesh lead metal or oxide powder were used in place of lead nitrate. Both the increase in sweat lead, and the time taken for skin transport, depended on the extent of skin sweating. If the arm was kept cool and dry, little skin transfer occurred; with profuse sweating, large increases in sweat lead occurred rapidly. These results can be explained by a diffusion model involving simultaneous diffusion of lead ions through a filled sweat duct (rapid) and through the stratum corneum (slow).’’ Although the skin absorption of lead gave rise to increased lead in sweat, similar increases in blood and urine were not observed. For the volunteer whose results are shown in the figure neither urine (2 ug/1) nor whole blood (55 ug/1) lead changed significantly from normal throughout the experiment. Saliva lead concentrations did, however, increase from 2-5 to 15 ug/1, and the increase paralleled that of lead in sweat. Since raised sweat lead values were found within 2 h of the application of lead, blood transport must be involved. However, no measurable increase in blood lead was found so the lead must be transported in plasma and rapidly concentrated into the extracellular fluid pool of sweat and saliva without significant uptake by erythrocytes, and with a very low transient concentration in the plasma. The behaviour is very different from that of ingested lead.’ Skin absorption of lead may be important in industries such as lead battery manufacture and lead smelting, where the area of a worker’s skin covered with lead dust may be orders of magnitude greater than that used in our experiments. Although face masks are usually worn when handling lead powders, few precautions are taken to prevent occupational skin exposure. A survey of workers in a lead battery factory yielded iontophoresis sweat lead values as high as 800 )g/!, even after their skin had been scrubbed with a chelating detergent and washed thoroughly before the sweat sample was

symptoms. GERALD SILVERMAN NEIL BRENER

Ealing Hospital (St Bernard’s Wing), Southall, Middlesex UB1 3EU

1. Arieff AJ, Bowie CG Some psychiatric aspects of shoplifting. Clin Exp Psychopathol 1947; 8: 565-76 2. Medlicott RW. Fifty thieves NZ Med J 1968, 67: 183-88. 3. Meyers TJ. A contribution to the psychology of shoplifting. J Forensic Sci 1970, 15: 295-310. 4. Davis H. Psychiatric aspects of shoplifting. S Afr Med 5. Gillen RS. A study of women shoplifters. S Aust Clin

J 1979; 55: 885-87 1976; ii: 173-76.

6. Gibbens TCN. Shoplifting. Med Leg J 1961, 3: 6-19 7. Gibbens TCN, Palmer C, Prince J. Mental health aspects of

shoplifting. Br Med J

1971; iii: 612-15 8. Bradford J, Balmaceda R. Shoplifting is there

1983; 28: 248-54.

a

specific syndrome? Can J Psychiatry

Lead nitrate solution placed on left arm on day 5 and removed 24 h later on day 6. Lead was measured in sweat from right arm. Horizontal line represents average background lead-in-sweat value found for this volunteer during the previous 3 months.

158 taken and when they had been away from work for several days. These men had only moderately raised lead in blood (300-400 lxgJl). Experiments with a stable lead isotope are underway to find out the fate of skin-absorbed lead and if skin exposure can add significantly to the body burden of this metal. T. M. FLORENCE S. G. LILLEY J. L. STAUBER

CSIRO Centre for Advanced Analytical Chemistry, Menai, NSW 2234, Australia 1. Waldron

HA, Soffen D. Sub-clinical lead poisoning. New York: Academic Press, 1974. 46-47. 2. Stauber JL, Florence TM. The determination of trace elements in sweat by anodic stripping voltammetry. Sci Total Envir 1987; 60: 263-71. 3. Stauber JL, Florence TM. A comparative study of copper, lead, cadmium and zinc in human sweat and blood. Sci Total Envir (in press). 4. Houk J, Guy RH. Membrane models for skin penetration studies. Chem Rev 1988; 88: 455-71. 5. Rabinowitz

MB, Wethenll GW, Kopple JD. Kinetic analysis of lead metabolism healthy humans. J Clin Invest 1976; 58: 260-70.

CIMETIDINE woman

Department of Health Care of the Elderly, University of Nottingham, Queen’s Medical Centre, Nottingham NG7 2UH

ANTHEA B. LEHMANN

CE, Besse CP, Wilson AO. Extrapyramidal and cerebellar syndrome with encephalopathy associated with cimetidine. Postgrad Med J 1982; 58: 527-28. 2. Brogden RN, Carmine AA, Heel RC, Speight TM, Avery GS. Ranitidine: a review of its pharmacology and therapeutic use in peptic ulcer disease and other allied diseases. Drugs 1982; 24: 267-303. 1. Handler

3. Gwee MCE, Cheah LS. Actions of cimetidine and ranitidine at some cholinergic sites:

implications in toxocology and anesthesia. Life Sci 1986; 39: 383-38. 4. de Silva L. Choreiform movement disorders: mechanisms and management Curr

Ther 1977; Oct: 67-79.

Daly MJ, Humphray JM, Stables R. Some in vitro and in vivo actions of the new H2-receptor antagonist, ranitidine. Br J Pharmacol 1981; 72: 49. 6. Davies WA. Mental confusion associated with ranitidine. Med J Aust 1983; ii: 478. 7. Pujadas R, Femandez-Monras F, Argimon J, Gago MJ, Costa I, Galera JG, Jane J. Trastornos neurologicos por cimitidina y ranitidina. A proposito de un caso. Rev Exp Enferm Apar Dig 1986; 70: 377-79. 8. Langman MJS. Central nervous system adverse drug reactions with H2 blockers. In: Dukes MNG, ed. Side effects of drugs annual 8. Amsterdam: Elsevier, 1984 5.

in

REVERSIBLE CHOREA DUE TO RANITIDINE AND

SIR,-A 76-year-old

cimetidine on separate occasions in the same patient,6.7 would suggest that chorea (and acute confusion) may be induced by action on systems other than cholinergic, dopaminergic or adrenergic. H2-receptors in the brain8 may be implicated.

admitted with She had no history of

(weight 66 kg) was

iron-deficiency anaemia and epigastric pain. central-nervous-system symptoms, chorea, thyroid disease, or any serious illnesses other than a possible transient ischaemic attack 2 years previously. Endoscopy revealed a duodenal ulcer and she was started on oral ranitidine and ferrous sulphate. After 1 week she was discharged well. On review one month later, her epigastric pain persisted and it transpired that she had stopped taking the ranitidine

tablets because she found them difficult to swallow. She was, therefore, given dispersible ranitidine, which she took for one month at a dose of 150 mg twice daily. She was then seen in the outpatient clinic and bilateral choreiform movements of the face, mouth, neck, and arms were noted. ’De-Nol’ (tripotassium dicitratobismuthate) was substituted for ranitidine and blood tests checked. 1 month later no involuntary movements were seen. Blood tests, including glucose, renal, liver, and thyroid functions, haemoglobin, erythrocyte sedimentation rate, and autoantibody screen, were normal at both outpatient visits. The patient herself was not aware of the movements and could not put a date to their onset or cessation. 1 month later she was admitted urgently to another unit with a recurrence of anaemia, at which time she was empirically started on cimetidine 400 mg twice daily pending further investigations (which subsequently revealed blood loss from an area of colonic diverticulosis). She had received cimetidine for 5 days when chorea similar in distribution to the previous episode but with larger movements recurred. Cimetidine was stopped and within 3 days the chorea had resolved. At no time did she experience any impairment of cognition. She remains well and free of involuntary movements 6 months later. Cimetidine has previously been reported to cause extrapyramidal problems, predominantly parkinsonism, facial twitching and dyskinesia,! but in the only two previous case-reports of chorea developing in patients taking ranitidine the chorea was attributed to coexisting systemic lupus erythematosus or aggravation of previous choreoathetosis due to septicaemia (Brogden et al,2 and personal communication, from Glaxo and the Committee on Safety of Medicines). H2-receptor blockers can enter the CNS, despite early reports to the contrary, and CNS side-effects have been reported. The risk of extrapyramidal symptoms developing in patients taking such drugs is likely to be small, but this case may contribute to our understanding of the pharmacology of chorea. In their report on cimetidine Handler et all suggested that the extrapyramidal syndrome may have been produced by action on cholinergic or dopaminergic CNS receptors. An action on cholinergic receptors since seems unlikely H2-receptor antagonists have anticholinesterase activity on the brain at therapeutic blood levels,33 which would tend to reduce rather than cause choreiform movements,4 Animal studies suggest that these drugs have no action on dopaminergic or adrenergic receptors.’ The case described here and two previous cases of acute confusion due to ranitidine and

333-40.

TREATMENT OF BUDD-CHIARI SYNDROME BY PERCUTANEOUS TRANSLUMINAL ANGIOPLASTY

SIR,-Budd-Chiari syndrome is a rare condition with a poor prognosis. We report a case treated by hepatic vein angioplasty. A 48-year-old man presented with a 2 week history of abdominal pain and distention. 10 years previously he had a resection for ileocaecal Crohn’s disease, subsequently requiring vitamin B12 injections. There was marked ascites, but no abdominal masses. Paracentesis yielded a transudate with an albumin of 13 g/1. Liver function tests were mildly abnormal. His haemoglobin was 77 g/dl and he had signs of iron deficiency. Clinically he was thought to have portal hypertension with some hypersplenism. Ultrasound examination, after drainage of ascites, revealed some residual fluid and demonstrated patent splenic and portal veins. Only a dilated right hepatic vein was visible with narrowing at its point of entry into the inferior vena cava, which appeared narrowed due to compression by an enlarged caudate lobe. These findings are typical of Budd-Chiari syndrome. Inflammatory bowel disease has been associated with this syndrome.1

Fig 1-Inferior vena cavagram demonstrating narrowing by extrinsic compression of inferior vena cava and right hepatic vein orifice.