elevated (300–600 mg/l) than blood levels (10–20 mg/l).Chelation with dimercaprosuccinic acid (DMSA)(30 mg/kg daily) increased urinary excretion in allcases. Treatment was pursued 5 d to 2 mo until recoveryappeared to be complete. Three of the patients bene� tedfrom antihypertensive treatment with nicardipine. En-vironmental inquiry showed that the source of mercurywas a broken medical thermometer in the case of onefamily and small quantities of the metal brought fromthe workplace by a family member in the other case.Eradication of the source was obtained in all cases.

The purpose of this report is to demonstrate thatacrodynia can mimic the clinical and biochemicalmanifestations of pheochromocytoma and should beconsidered and excluded during the investigation ofsuspected cases. Biologically, the increase in urinarycatecholamines frequently occurs, as our four casesattest. This usually concerns norepinephrine and epi-nephrine. Cheek et al. showed that inorganic mercuryby injection can markedly increase sympathetic activityand epinephrine levels in rats, and would therefore beexpected to mimic the signs and symptoms of pheo-chromocytoma (4). In inorganic mercury poisoning, themetal combines with the sulphydryl group of S-adenosylmethionine , which acts as a co-factor forcatecholamine-o-methyltransferase (COMT). COMTinhibition leads to accumulation of catecholamines(2). This accumulation of epinephrine and norepine-phrine could explain the haemodynamic symptoms ofacrodynia (4). Although acrodynia is rare, its diagnosisshould be considered in any child with signs ofbehavioural change, skin rash and hypertension by a

single urine analysis (1, 2). There exists no correlationbetween the level of mercury and the clinical severity oreven the evolution of the disease.

We believe that mercury poisoning should beconsidered initially in any child with signs of sweating,behavioural change, skin rash, hypertension and thatpheochromocytoma might be considered in the differ-ential diagnosis. Recognition of the variable manifesta-tions of the disease and prevention of further exposureare the most important aspects of management.

References1. Velzeboer SCJM, Frenkel J, de Wolff FA. A hypertensiv e toddler.

Lancet 1997; 349: 18102. Woßmann W, Kohl M, Gruning G, Bucsky P. Mercury intoxica-

tion presenting with hypertensio n and tachycardia . Arch Dis Child1999; 80: 556–7

3. Von Muhlendahl KE. Intoxication from mercury spilled oncarpets. Lancet 1990; 336: 1578

4. Cheek DB, Bondy RK, Johnson LR. The effect of mercurouschloride (calomel) and epinephrin e (sympathetic stimulation) onrats: the importance of the � ndings to mechanisms in infantileacrodynia (pink disease). Pediatrics 1959; 23: 302–13

M Laurans, J Brouard, A Arion, D Kauffmann and JF Duhamel,Department of Pediatrics, University of Caen, France. Correspon-dence to: Muriel Laurens, Department of Pediatrics, UniversityHospital of Caen, FR-1400 Caen, France (Tel. ‡33 023 12 72 590,fax. ‡33 0231 27 2655, e-mail. t.collet@ch-bayeux.fr )

Received Sept. 4, 2000; revisions received Feb. 14, 2001; acceptedFeb. 14, 2001

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Mycoplasma pneumoniae infection associated with Kawasaki disease

Sir,Despite more than two decades of investigation, theaetiology of Kawasaki disease remains obscure (1) andnone of the proposed aetiologic theories for the diseasehave attracted independent con� rmation thus far. Thepresent report describes a young adolescent with clearevidence of mycoplasma infection complicated byKawasaki disease with coronary aneurysm.

An 11-y-old boy had suffered from intermittent feverand a cough with sneezing for about 3 wk, headache,dizziness and a skin rash developing 1 d prior toadmission. A physical examination upon admissionrevealed bilateral conjunctival congestion, lip � ssuresbut no strawberry-coloured tongue evident, and general-ized erythematous macules, papules and con� uentplaques over the face, trunk and extremities. Several

small cervical lymph nodes were palpable. Breathsounds were coarse with crackles, although no cardiacmurmur was audible. The liver was palpable 2 cmbelow the right costal margin. The limbs were mildlyindurated, distally. A complete blood count revealed ahaemoglobin level of 1.97 mmol/L, a leukocyte count of13.6 £ 109 cells/L (band 0.02, segment 0.84, monocytes0.04, lymphocytes 0.10) and a platelet count of 298 £109/L. The patient’s erythrocyte sedimentation rate was66 mm/h, and his aspartate aminotransferase (AST)level was 388 U/L (upper normal value 40 U/L) and hisalanine aminotransferase (ALT) level was 592 U/L(upper normal value 40 U/L). The boy’s alkalinephosphatase level was 366 U/L (upper normal value150 U/L) and his total bilirubin was 20 mol/L. Electro-lytes and renal function appeared to be within normal

594 Correspondenc e section ACTA PÆDIATR 90 (2001)

limits for this patient, and the results of his urineanalysis and cerebrospinal � uid examination wereunremarkable.

The patient’s chest roentgenogram (CXR) revealedincreased lung markings bilaterally in the lower lung� elds and blurring of the left costophrenic angle.Mycoplasma pneumonia complicated by Kawasakidisease was suspected, although echocardiographydemonstrated normal coronary artery size and noapparent cardiac disturbance. Erythromycin (40 mg/kg/d) was given initially for 1 d and was replaced byAzithromycin (10 mg/kg/d) for the subsequent 5 d,although the spiking fever persisted. The titre ofMycoplasma pneumoniae IgM antibody, as found bythe complement-� xation test on the second day ofhospitalization, was 1:256. The titre of M. pneumoniaeantibody in an agglutination test (Fujir Myco II) on the� rst day of hospitalization was 1:2560, and 1:5120 onday 12. The Widal test, Weil-Felix test and additionalserological investigations testing for Epstein-Barr virus,cytomegalovirus, hepatitis B, and hepatitis C virus allproved negative. Throat and rectal swabs failed toproduce any viral isolates. The anti-streptolysin-O titrewas less than 25 Todd units. The complement compo-nents (C3, C4) and anti-nuclear antibody appearednormal. Distal membranous desquamation of thepatient’s limbs was observed on day 7. Follow-upechocardiography indicated aneurysm of the left cor-onary artery (size: 0.69 cm) on day 7. Intravenousimmunoglobulin (IVIG) (2 g/kg) and aspirin (80 mg/kg/day) were administered. The clinical symptoms de-clined steadily with IVIG treatment and the boy’s fevereventually subsided. The patient was discharged on day14, with oral aspirin (5 mg/kg/d) and dipyridamole(5 mg/kg/d). The platelet count had increased to558,000/mm3. The patient was symptom-free, withechocardiography indicating a persisting aneurysm ofthe left coronary artery at his 2-mo follow-up.

Respiratory and non-respiratory sites are involved inM. pneumoniae infections, but the lower respiratorytract tends to be the primary site (2). The clinicalmanifestations such as cough with sneezing, relevantchest X-ray � ndings, and serological investigations for

this 11-y-old boy were suggestive of M. pneumoniaeinfection. The diagnosis of Kawasaki disease in thispatient was also based on the clinical history andphysical � ndings, although most patients with Kawasa-ki disease are aged 5 y or less. A con� dent diagnosis ofKawasaki disease for this young adolescent might haveproved dif� cult, had it not been for the detectedcoronary aneurysm, which constitutes one of the mostsigni� cant � ndings for Kawasaki disease, typicallydeveloping within 1 to 3 wk of disease onset. Thisanomaly could explain the echocardiographic evidencefor coronary artery changes noted for this patient.

Although the causative agent for Kawasaki disease is,as yet, unidenti� ed, to the best of our knowledge therehas been only one literature-cited case report ofmycoplasma infection complicated by Kawasaki dis-ease without coronary involvement and the super-antigenic pathogenesis has been proposed (3). In thepresent case, the patient’s clinical presentation alongwith coronary-artery aneurysm strongly supported adiagnosis of Kawasaki disease associated with myco-plasma infection. We therefore speculate that myco-plasma infection might be an unrecognized precipitantof Kawasaki disease.

References1. Laupland KB, Davies HD. Epidemiology, etiology, and manage-

ment of Kawasaki disease: state of the art. Pediatr Cardiol 1999;20: 177–83

2. Cimolai N. Mycoplasma pneumoniae respiratory infection. PediatrRev 1998; 19: 327–31

3. Leen C, Ling S. Mycoplasma infection and Kawasaki disease.Arch Dis Child 1996; 75: 266–7

JN Wang1, SM Wang2, CC Liu1 and JM Wu1, Department ofPediatrics 1 and Emergency Medicine2, National Cheng KungUniversity Hospital, Tainan, Taiwan. Correspondence to: Jing-MingWu, Department of Pediatrics, National Cheng Kung UniversityHospital, 138 Sheng Li Road, Tainan, 70428, Taiwan (Tel. ‡886 62353 535 exit 5641, fax. ‡886 6 2753 083, e-mail: jingming@-mail.ncku.edu.tw)

Received Oct. 10, 2000; accepted Jan. 16, 2001

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Further evidence that � broblast growth factor receptor 2 mutationscause Antley-Bixler syndromeSir,Recent progress in the elucidation of the genetic basis ofcraniosynostosis syndromes has demonstrated that the� broblast growth factor receptors (FGFRs) play a

signi� cant role in limb and craniofacial development.Mutations in the FGFR2 gene may manifest in over-lapping and variable phenotypes designated as Crouzon,Pfeiffer and Apert syndromes (1–3).

ACTA PÆDIATR 90 (2001) Correspondenc e section 595