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DETAILS OF SPINA BIFIDA PATIENTS WITH ANAPHYLACTIC SHOCK OR WHO WERE SYMPTOM-FREE

*By ’Phadiatop’ test (Pharmacia) NSA!D=non-stero!da! antt-inflammatory drugs; TAO = trtacetyloleandomycin.

Is this frequent sensitisation due only to repeated contacts with these substances? In over ten years’ investigation we have not observed anaesthesia-induced shock in children with repeated surgical procedures but without spina bifida.5 We suggest that this condition is correlated with a predisposition to formation of specific IgE for proteins and haptens. Although spina bifida develops in the embryo with no known anomaly of the genome, the possible existence of a link between this condition and atopy is worthy of consideration. Medicine D (Immunoallergology), Hôpital de Brabois, 54511 Vandoeuvre Nancy, France

D. A. MONERET-VAUTRIN E. MATA

Unité Inserm 308, Faculte de Medecine, Vandoeuvre Nancy

J. L. GUEANT

Centre d’Education Motrice, Grenoble

D. TURGEMAN

Department of Anaesthesia, Hôpital Central, Nancy

M. C. LAXENAIRE

1. Slater JE. Rubber anaphylaxis. N Engl J Med 1989; 320: 1126-30. 2. Turjanmaa K. Incidence of immediate allergy to latex gloves in hospital personnel. Contact Dermatiits 1987; 17: 270-75. 3. Gerber AC, Jorg W, Zbinden S, Seger RA, Dangel PH. Severe intraoperative anaphylaxis to surgical gloves: latex allergy, an unfamiliar condition. Anesthesiology 1989; 71: 800-02. 4. Leynadier F, Pecquet C, Dry J. Anaphylaxis to latex during surgery. Anaesthesia 1989; 44: 547-50. 5. Laxenaire MC, Moneret-Vautrin DA, Verdloet D. The French experience of anaphylactoid reactions. Int Anesthesiol Clin 1985; 23: 145-60.

Cyclosporin monitoring in psoriasis SIR,-Dr Bos

and

colleagues (Dec 23/30, p 1500), reporting on cyclosporin (’Sandimmun’ 3 mg/kg daily) in psoriasis, suggest monthly measurement of trough concentrations of this drug. We have evaluated cyclosporin trough levels as predictors of clinical events in 134 adults with severe disabling psoriasis who were treated with cyclosporin 2-5 mg/kg daily in two doses. The dose remained unchanged for the first month so weeks 1-4 were selected for the analysis. Cyclosporin levels were measured in whole blood by radioimmunoassay, with a monoclonal antibody specific to the parent compound and a tritium-labelled tracer (sandimmun kit). The mean of four consecutive blood level low-dose

treatment with

Reduction in PASI (panel A) and increase in serum creatinine over baseline (panel B) at week 4 by specific cyclosporin blood level.

Each circle represents 1 patient and is the value of four (at weeks 1, 2, 3, and 4). Total number of patients 134

measurements

1,2,3, and 4) was calculated and correlated efficacy and renal dysfunction at week 4. The mean cyclosporin level was 103 (SEM 5) ng/ml. Inter-individual variability was 53%. Efficacy was assessed by the percentage reduction (39 [3]%) in psoriasis activity and severity index (PASI)1 and renal dysfunction was evaluated by the percentage change in serum creatinine from baseline level (6 [1]%). As shown in the figure, no significant correlation was found between cyclosporin levels and efficacy or renal dysfunction. On the basis of experience with maintenance cyclosporin in transplantation, a cut-off of 100 ng/ml was selected for efficacy and 200 ng/ml for renal dysfunction.4 10 out of 53 patients (19%) with levels of 100 ng/ml or more had success at week 4 (75% or more reduction in PASI) compared with 5/81 (6%) with lower cyclosporin levels (p 0-040, Fisher’s exact test). The frequency of renal dysfunction (creatinine increase 30% or more above baseline) was 1/10 where the cyclosporin level was 200 ng/ml or more and 7/124 for lower levels (not significant). On the one hand, the cyclosporin level had significant but low predictive value for efficacy and no predictive value for renal

measurements (at weeks to

=

867

dysfunction in patients treated with low-dose cyclosporin for psoriasis. On the other hand, evaluating efficacy is easy since the clinical effect is rapid, simple to assess, and responds to dose titration. Renal dysfunction is infrequent with low-dose cyclosporin; it is moderate, is not sudden in onset, and is easily managed by dose adjustment based on serum creatinine. The decision to practise routine monitoring in patients with severe psoriasis on low-dose cyclosporin will have to take into account the balance between the significant but low value of the level for clinical events and the without the help of pharmacological

predicting

Clinical Research/Immunology, Sandoz Pharma Ltd, 4002 Basle, Switzerland

ease

of clinical surveillance

monitoring. G. FEUTREN D. FRIEND P. TIMONEN C. LABURTE

all children admitted to hospital with bums.2 Chlorhexidine dressings, which reduce the incidence of bum colonisation by S aureus,5 may also afford some protection against TSS. The important messages from this case are that the parents of any child with a bum should consult the treating doctor if the child becomes unwell, and that children with burns in whom systemic illness develops should be admitted to hospital. The specific treatment in suspected TSS is a parenteral anti-staphylococcal agent and transfusion of fresh blood or plasma. Departments of Plastic Surgery and Paediatric Medicine, Royal Hospital for Sick Children,

1 Fredriksson

Toxic shock syndrome in child with burn

only 2%

SiR,—Bums rarely prove fatal if less than 5% of total body surface is affected, unless the patient is very old.l We describe a serious complication of a very small burn. A 2-year-old boy was burned by hot tea spilling onto his chest, resulting in a 2% burn. Accident department staff judged the burn to be mainly superficial and of partial thickness, and the boy was treated with a proprietary gauze dressing which may have been impregnated with plain paraffin, chlorhexidine, or framycetin sulphate (the notes do not record which). He was then taken home. After 24 hours he had a fever with cough, diarrhoea, and vomiting. A general practitioner prescribed paracetamol and erythromycin. At 48 hours he had convulsions and was admitted to hospital drowsy, pale, and mildly dehydrated, with a temperature of 393°C (later rising to 41 °C), pulse 170/min, blood pressure 100/70 mm Hg, and respiratory rate 37/min. There was no lymphadenopathy, neck stiffness, or focal neurological deficit, and his optic fundi were normal. The burn looked clean and there was area

no

cellulitis. The white cell count was 4200/ul and rose to 18

800/ltl

days later; his platelet count fell from 248 000/ul to 96 000/ltl; clotting times were prolonged; and he had raised levels of fibrinogen-degradation products. He had uraemia, hyponatraemia, hypokalaemia, hypocalcaemia, low serum osmolality, and low albumin and total protein. He had another convulsion and became shocked, with cold, cyanosed extremities and a core/peripheral temperature difference of 14°C. His condition improved after an infusion of plasma protein, 2

and treatment with intravenous cefotaxime and flucloxacillin was started. After 7 days a widespread pink maculopapular rash and mild generalised lymphadenopathy developed. The rash resolved without desquamation. He was discharged home after 10 days and has remained well. Culture of a wound swab grew Staphylococcus aureus, later shown to produce toxic shock syndrome toxin (TSST-1). This toxin was also identified in serum. The diagnosis was toxic shock syndrome (TSS), which was suspected after the episode of shock. Frame et al2 described seven cases of TSS in children with burns; four of the children died. Single cases have also been described. Most of these burns were more than 10%, although one child had a 5% burn3 and another 4%.2 All were already in hospital when they became ill. TSS is caused by an exotoxin known as TSST-1, a glycoprotein that diffuses into the blood, causing illness in the absence of tissue invasion by staphylococci. Antibiotics are recommended to eradicate the S aureus but are of no avail against the toxin. S aureus has been isolated from 12% of small burns within 24 hours of injury.4 Routine antibiotic prophylaxis has been recommended for

IFK, Barclay TL, Settle JAD. Burns and their treatment, 3rd ed. London: Butterworths, 1987. Frame JD, Eve MD, Hackett MEJ, et al. The toxic shock syndrome in burned children. Burns 1985; 11: 234-41. Egan WC, Clark WR. The toxic shock syndrome in a burn victim. Burns 1988; 14:

1. Muir

2.

T, Pettersson U. Severe psoriasis-oral therapy with a new retinoid. Dermatologia 1978; 157: 238-44. 2 Dieterle A, Abeywickrama K, von Graffenned B. Nephrotoxicity and hypertension in patients with autoimmune disease treated with cyclosporine. Transplant Proc 1988; 20 (suppl 4): 349-55. 3 Feutren G. Functional consequences and nsk factors of chronic cyclosporine nephrotoxicity in type I diabetes trials. Transplant Proc 1988; 20 (suppl 4): 356-66. 4. Critical issues in cyclosporine monitoring: report of the task force on cyclosporine monitoring. Clin Chem 1987; 33: 1269-88.

A. J. HEYWOOD S. AL-ESSA

Edinburgh EH9 1 LF, UK

3.

135-38. 4. Lawrence JC. The bacteriology of burns. J Hosp Infect 1985; 6 (suppl B): 3-17. 5. Lawrence JC. The treatment of small burns with a chlorhexidine-medicated tulle gras.

Burns 1977; 3: 239-44.

Chrysotherapy provoking exacerbation of contact hypersensitivity to nickel SiR,—The most common side-effect of parenteral gold therapy in rheumatoid arthritis is cutaneous eruptions.1 At this university hospital, consecutive patients with recently diagnosed rheumatoid arthritis who had not previously been treated with second-line antirheumatic drugs were asked to participate in a long-term prospective open study in which treatment by different rheumatologists was monitored by a research nurse. Parenteral gold was started in 47 of the 148 patients. During chrysotherapy 14 patients had a dermatitis severe enough for the dose to be reduced or for gold to be discontinued. 2 patients had dyshidrotic eczema,1 had papular prurigo, and 1 had mycosis; a close resemblance to contact dermatitis was noticed in 3 patients; and in the other 7 "gold dermatitis" was diagnosed by exclusion (table). The patients with a contact-dermatitis-like rash were all female, and 2 had previously been sensitised to nickel; the time to recovery after discontinuation of chrysotherapy was shorter in these patients than in those with gold dermatitis. 1 patient who had a reaction compatible with contact dermatitis is described below in more detail. We propose that chrysotherapy can provoke an exacerbation of, or may even induce, contact hypersensitivity to nickel. A 71-year-old woman with seronegative rheumatoid arthritis had been on nonsteroidal anti-inflammatory drugs and hydroxychloroquine. After 5 months the hydroxychloroquine was replaced by intramuscular aurothioglucose 50 mg weekly and 10 mg CHARACTERISTICS OFTEN PATIENTS WITH CONTACT DERMATITIS OR GOLD DERMATITIS

*After discontinuation of chrysotherapy NA= not

applicable.

Cyclosporin monitoring in psoriasis.

866 DETAILS OF SPINA BIFIDA PATIENTS WITH ANAPHYLACTIC SHOCK OR WHO WERE SYMPTOM-FREE *By ’Phadiatop’ test (Pharmacia) NSA!D=non-stero!da! antt-infl...
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