Recent eLetters

We feel Dr Markovitch (1) was over critical of Hilton et al (2). Although we agree that there was a paucity of evidence to allow them to rebut Dr Wakefield’s suggestion that MMR could in some children cause autism, we believe that they still could have been clearer in reporting the full situation. The suggestion that the MMR vaccine should be given as its separate components came, not from a scientific paper, but as an announcement by a single researcher at a press conference. Within a month of the publication of the Lancet paper, a number of authors of the paper re-emphasised the importance of the combined MMR vaccine and that they had not proven a link between it and autism (3). It is these facts that should have been more strongly communicated, thus allowing people to attach the appropriate level of credence to Dr Wakefield’s views. If editors of journals had made more of this, healthcare professionals might have been better equipped for their discussions with parents.

We agree with Dr Markovitch that “…..they [editors] should offer honest accounts of best practice couched in language that generalist health care professional readers and the non-scientists writing for the public media can understand.” However, they should include all the relevant details including a balance that is truly reflective of the scientific evidence. The individual health professional is often unable to review the evidence themselves, through lack of time or access to the relevant material, and relies on journals such as those critiqued by Hilton et al to provide the information in a full but concise manner. Although this approach may not make for earth shattering headlines, it is responsible. We don’t suggest that editors should be censorious but it behoves them to couch unsubstantiated hypotheses in an appropriately cautious manner.

1. Markovitch H. Editors should not be propagandists. Arch Dis Child 2009; 94: 827-8. 2. Hilton S, Hunt K, Langan M, Hamilton V, Petticrew M. Reporting of MMR evidence in professional publications: 1988-2007. Arch Dis Child 2009; 94: 831-3. 3. Murch S, Thompson M, Walker-Smith J. Autism, inflammatory bowel disease and MMR vaccine. Lancet 1998; 351: 908.

I was interested to read Govindaraj et al’s audit showing a fall in the number of MMR vaccines given in their hospital over the last 2 years. Unfortunately there was no data to show what happened to those children initially referred to hospital for MMR, but referred back by the outpatient sister.

A study from New Zealand suggests that children inappropriately referred for MMR in hospital can be referred back and subsequently immunised in primary care [1]. However this was not our experience in Liverpool where 22 children, who had been advised by a health professional to have MMR in the community, were still referred to hospital [2]. This request for immunisation in hospital came from both primary care staff and parents.

It is important to ensure that children referred for MMR in hospital, but referred back to primary care, are subsequently immunised. Does Dr Govindaraj have any data to reassure us that the fall in the number of MMR vaccines given in their hospital is not due to children being left unimmunised in the community?

1. Goodyear-Smith F, Wong F, Petousis-Harris H, Wilson E, Turner N. Follow-up of MMR vaccination status in children referred to a pediatric immunization clinic on account of egg allergy. Human Vaccines.2005: 1:118- 22 2. Ainsworth E, Debenham P, Carrol ED, Riordan FAI. Referrals for MMR immunisation in hospital. Arch Dis Child 2009 (in press)

We were interested to read the paper by Jones at al1 on ‘Frequent medical absences in secondary school students’. They conclude that ‘this study should prompt education departments and their NHS partners to look more critically at the problem … and to establish a system that provides more comprehensive assessment and treatment.’

Within Bolton PCT such a system has been designed in order to identify causes of frequent medical absences from school and to provide interventions aimed at supporting students to achieve an earlier and consistent return to school. Originally in Bolton (from the year 2000) referrals were made by the Education Social Work Department to a Senior Clinical Medical officer to undertake medicals on children with poor school attendance reported as due to ill health. This provided evidence to support an identified medical problem or for the LEA to issue a fixed penalties notice to the parent or carer. Since the issue of school attendance subsequently became a high priority policy concern for both the DfES and the DoH this service was re structured to develop an innovative Advanced Nursing Practitioner (with a school nursing background) led model for the evaluation of health issues for children and young people with poor school attendance. The main focus of the model was to enhance joint working between the advanced practitioner, Education Social Worker, schools and families. Changes have included a standardised threshold for referral (when attendance falls to 80%), agreed minimum information sets on referrals, agreed time frames for assessments and production of correspondence, holistic assessment, onward referrals, investigations and reintegration programmes to aide full return to school.

Over the last academic year 251 new referrals were received form the Education Social Work department (previously 55 a year). There were two peaks of referral (December 51, April 40). There were 120 referrals from primary schools and 131 for secondary schools. Referrals included 122 boys and 129 girls. Referrals to the service from 18 individual education social workers varied from 1 - 41 (median 14). The main causes of school absence were asthma, recurrent URTI, headache, sore throat, menstruation problems, chronic fatigue, skin problems, emotional and behavioural problems and inadequate provision for special needs within school. A variety of onward referrals were made including ENT, community paediatrics, dietetics, Young Carers, social care, occupational care, physiotherapy, CAMHs and two admissions to hospital. Support packages of care have been initiated for some together with supported reintegration plans to enable the young person to return to regular school attendance. Pathways are being devised for young people identified with ‘school phobia’ (jointly with CAMHs) and also a menstruation pathway for girls presenting with complex menstrual history.

In all cases of non attendance it is essential that preventative and early intervention should be seen as the cornerstone of multiagency working in order to ensure pupils right to education and to protect their health and well being. The redesigned service in Bolton has made good progress towards achieving these aims.

Reference 1.Jones R, Hoare P, Elton R, Dunhill Z, Sharpe M. Frequent medical absences in secondary school students: survey and case control study. Arch Dis Child 2009;94:763-767

THE TSH THRESHOLD IN NEONATAL SCREENING FOR CONGENITAL HYPOTHYROIDISM: A VARIABLE SOLUTION

Dear Editor:

In their paper on the TSH threshold in neonatal screening for congenital hypothyroidism (CH), Korada et al. (1) conclude that a threshold of 6 mIU/L for DELFIA-measured TSH in samples collected between days 5 and 8 may be preferable to the 10 mIU/L recommended by the UK Newborn Screening Programme Centre. Our laboratory instituted DELFIA measurements of TSH in 5-8—day paper-borne heelprick samples in 1985. Since 1998 we have used an accelerated AutoDELFIA(R); method – fully endorsed by the results of external quality control services (DGKL, NEQAS, AECNE) – that takes about 2 h and thus allows follow-up samples to be called for, if necessary, on the same day as the first sample is analysed. Since 2003, heelprick has been performed on day 3 in response to the desire of paediatric endocrinologists to begin the treatment of CH patients as early as possible, even though the typical physiological TSH peak on day 2 reduces the efficiency of screening thresholds; Table 1 summarizes the distribution of TSH levels in the 102,789 newborns screened during this period.

Having observed significant between-lot variation in TSH assay kits, since November 2004 we recalculate our TSH threshold for every run in the light of two factors: a) the dispersion of the calibration data in the vicinity of 10 mIU/L; and b) measurements of certified control samples with concentrations close to 10 mIU/L that are supplied by Perkin Elmer and, within its Newborn Screening Quality Assurance Program, by the CDC. Defining CV10 as the coefficient of variation of two replicate fluorescence measurements of the calibration standard nearest to 10 mIU/L, expressed as a percentage, factor (a) is assigned the value zero if CV10 < 10, and the value 0.1 x CV10 otherwise. The control samples (C1 and C2, of certified concentrations c1 and c2, respectively) are each measured once; in each case a parameter bi (i = 1,2) is assigned the value zero if the measured value mi is greater than 90% of the certified value, or the value 10 x (ci – mi)/ci otherwise; and the value of factor (b) is defined as the greater of b1 and b2. Finally, the TSH threshold is defined as (10 – j) mIU/L, where j is the larger of factors (a) and (b). This entirely empirical algorithm is displayed in flow-chart form in Fig. 1. In the 1171 runs in which the above procedure has been followed, the threshold so determined was > 9 mIU/L in 54.7%, 8 9 mIU/L in 35.3%, 7-8 mIU/L in 8.5%, and < 7 mIU/L in 1.5%. Of the 62 cases of CH that we have detected in this time, three (all with adequate weight at birth) had first-sample TSH levels lower than 10 mIU/L (see Table 2 for details).

Cristobal Colon and Jose Ramon Alonso-Fernandez. Metabolopathy Laboratory, Departament of Paediatrics, Clinical Hospital and Universiy of Santiago de Compostela (Spain).

References 1) KORADA SM, PEARCE M, PLATT MPW, AVIS E, TURNER S, WASTEL H, CHEETHAM T. Dificulties in selecting an appropriate Neonatal TSH screening threshold. Arch Dis Child (Online First), 12 Aug 2009. 2) ALONSO-FERNANDEZ JR. V Reunion Nacional de la Sociedad Española de Química Clínica. Santiago de Compostela 28 y 29 de abril de 1985. 3) POMBO M, ALONSO-FERNANDEZ JR, BRAVO M, FRAGA JM, PEÑA J. Diagnostico Precoz del Hipotiroidismo Congénito y de la deficiencia de Hormona del Crecimiento. An Esp Ped. 1987;27(sup.28):44-47. 4) COLON C, ALONSO-FERNANDEZ JR. Depistage de L’Hipothiroidie neonatal avec un inmuno-essai marque a l’Europeum. Etude comparative de curbes de calibrage. Proceedings of “Reunion Europeene sur le Depistage Neonatal en 1986. Evian (France). 28-30 de abril de 1986. 5) ALONSO-FERNANDEZ JR, COLON C, FRAGA JM. Neonatal Screening of Hipotiroidism: A comparative study of RIA Technique and the Non Isotopic Inmunoessay DELFIA System. In BL Therrel; Advances in Neonatal Screening pp 163-164 (1987). Excerpta Medica. 6) COLON C, ALONSO-FERNANDEZ JR, CASTIÑEIRAS DE, ROMERO ME, FRAGA JM, PEÑA J. Posible Causes of Bordeline TSH: a Summary of our experrience. In F Delange, DA Ficher, D Glinder; Research in congenital Hypothyroidism, pp 316, 1989. Plenum Press. 7) COLON C.Epidemiological study of thyroid stimulating hormone (TSH) levels in the Galician neonatal population (Estudio epidemiologico de los niveles de hormona estimuladora del tiroides (TSH) en la poblacion neonatal gallega). Microfiche ISBN 13: 978-84-8121-340-9. ISBN 10:84-8121- 340-3. Ed. Universidade de Santiago de Compostela. 1995. 8) ALONSO-FERNANDEZ JR, CASTIÑEIRAS DE, CASTIÑEIRAS C, VILLAR P. Determinacion de TSH Neonatal con el método DELFIA reduciendo a dos horas el periodo de Elucion-Incubacion, concentrando el trazador y el analito. Immunoensayo 97. La Habana (Cuba) 14-18 de septiembre de 1997.

Post date

In 1985 (2, 3) we propound the adaptation of DELFIA test for seric TSH measurement to the newborn screening sample (DBS). Once Perkin-Elmer marketed the neonatal screening TSH test, we suggested a calibrate modification, increasing from 3 to 5 points and using the interpolation with logarithmic spline instead linear regression such as made in the procedure for seric and neonatal screening TSH determination (4). It is compared with the RIA test using until then (5). In 1988 we discussed the causes of borderline results (6), one of the main reasons for recall sample. In the PhD thesis of one of us (C. Colon) in 1995 (7), we could verify that the gestational age, the birth weight, and the age of analysis, influence on the TSH values. Also was found the thyroid function alteration due to antiseptic iodine use (effect Wolff-Chaikoff).

In 1997 we presented (8) a new DELFIA test for neonatal TSH modification; reducing until 2 hours the elution-incubation time, using half buffer volume in the preparation of tracer solution and reducing to 100 microlitres the volume of this solution dispensed in the microtiter plate wells containing the DBS disc. In the next year, using the AutoDELFIA, we introduced another modification, increasing to double the content of second antibody-tracer in the immunochemistry reaction mixture, in this mixture the analyte concentration result is multiplied for 2 and Europium-labelled antibody for 4.

In the “Images in Paediatrics” section of ADC, Sept 2009 (1), I read with interest, and some alarm, Sheth et al.’s assertion that CT scan findings were of “significant value” in establishing the diagnosis of Hirschsprung’s associated enterocolitis.

As the authors themselves point out, diagnosis of enterocolitis in a child with a history of endorectal pull-through operation for Hirschsprung’s disease should be made on clinical grounds, with a plain abdominal X-ray being the investigation of choice, if required. Although it appears from the clinical history that the authors give that the CT scan was performed on their patient in order to rule out intussusception - a very reasonable intervention in the circumstances– the conclusion that the authors draw in proclaiming CT scan findings to be of significant value in establishing the diagnosis of enterocolitis surely cannot be justified. In the case they describe, the CT scan was useful in ruling out diagnosis of intussusception, not in confirming the diagnosis of enterocolitis. The message from the article may be misinterpreted by practitioners who are less clinically astute than the authors as a recommendation to use CT scan, with all its inherent risks and side- effects, as a diagnostic tool of “significant value” in children with known Hirschsprung’s disease presenting in this way.

As a general paediatrician coming across such patients in the acute setting in my practice, I would be loathe to subject my patients to the radiation, not to mention the likelihood of sedation or anaesthesia, of a CT scan which does not influence my diagnosis or management. In my non- prefessional capacity, as the parent of a 13-month old infant with Hirschsprung’s disease who has been admitted on several occasions with suspected Hirschsprung’s associated enterocolitis, I would be even more loathe to consent to such an investigation for the indications the authors seem to suggest.

References 1. Sheth et al Images in Paediatrics “CT images of Hirschsprung’s associated enterocolitis: a rare finding. ADC 2009; 94: 816

Competing Interests: None