Array CGH (Comparative Genomic Hybridisation) tests for microdeletions, better than G-banded chromosome analysis and telomere MLPA but takes 3 months to do! So MLPA or FISH for urgent DNA test, else QF-PCR for trisomy screening (but store DNA too).
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Swimming and asthma
For competitive swimmers, note FINA doping control rules (based on the World Anti-Doping Agency regulations). Most asthma medications are on the Prohibited List including inhaled steroids and inhaled Beta2 agonists.
Therefore, elite athletes with asthma must apply for special permission to use these medications, known as the “Therapeutic Use Exemption” (TUE) program. If competing at FINA events, then you apply directly to the FINA Doping Control Review Board to have their applications considered. Lower level athletes should apply to their national anti-doping body.
Epilepsy
Historically, people with epilepsy were “considered to have unique powers, even hailed as geniuses, regarded as having a sacred disease and leading sacred lives”. But then demonisation, persecution, social rejection. “Epileptic personality” described by psychiatry in 20th century. [Sacred lives, Ian Bone]
Self control is central to our self image and the manner in which we and society believe we should behave. Epilepsy jeopardises this. Patients often conceal. Guilt, loss of confidence and low mood common after seizures.
Definition: At least 2 unprovoked (or reflex) seizures, occurring more than 24hrs apart; else one unprovoked (or reflex) seizure and probability of further seizures similar to that seen in those who have had 2 unprovoked seizures (ie at least 60%); or recognized epilepsy syndrome. Also part of the definition is that epilepsy is considered “resolved” if age dependent syndrome and past applicable age, or else those who have been seizure free for 10 years and off medication for 5 years. (ILAE 2014)
Note that “seizure” does not have any real medical meaning! Transient signs/symptoms due to excessive or synchronous neuronal activity in brain (ILAE 2017) – but implies you can tell whether caused by abnormal brain activity, which can be hard!
First assessment:
- NICE standard is that patient is seen within 2 weeks by a specialist! NICE guideline just says seen by doctor with training and expertise in epilepsy.
- First assessment should include description of event, age/timing of event, frequency of events.
- Physical examination of neurology, cardiac, mental state and development.
- Presence/absence of developmental, learning or schooling problems.
Investigations
EEG
Despite increasing sophistication, interpreting EEG remains an inexact science! Irregular background activity overlaps with detectable abnormality. Plus, only really picks up activity at surface of brain, and can miss simple partial seizures (but not tonic-clonic generalised). Review in 2000 did not find much evidence base. Requires dialogue between referrer and neurophysiologist. Diagnosis remains principally clinical – eg more than 1 tonic-clonic seizure, or multiple absences! Incidence of epileptiform activity in asymptomatic individuals appears to be about 1%, of which a few percent will develop epilepsy over the subsequent years. Abnormal activity is certainly more likely if structural abnormality, but still many will be and remain asymptomatic.<
50% of children with epilepsy have normal EEGs – so not a particularly useful test! Not only that, but in studies, at least 20% of “epileptics” were ultimately given a non-epileptic diagnosis! So request EEG with caution; should be used for confirming clinical opinion, or to guide treatment, not where symptoms are vague. Hence a firm diagnosis of epilepsy and then decisions about treatment may take some time; difficult for families to understand, but it is quite safe to be cautious esp considering the implications of a mistaken diagnosis.
If EEG is negative, then proceed to a sleep EEG (where child is woken by parents at 3am, kept awake then brought to department and allowed to fall asleep during monitoring). This has 80% sensitivity. Failing that, Medilog or Video with continous monitoring. This is good for distinguishing non-epileptic tonic-clonic seizures, but does not rule out co-existing epilepsy.
Good for:
- status in PICU patients, or non-convulsive status
- where children too young to describe their symptoms
- absences – typical absence epilepsy have 3Hz spike and wave with hyperventilation. Highly specific, although absences can be seen in complex partial seizures, which would also be obvious on EEG.
- indicating underlying brain disease (abnormal background)
- specific syndromes
- cognitive impairments that may be seizure related
Beware – an EEG finding of partial epilepsy may not have a surgical lesion! Must be used in conjunction with MRI. A generalized epilepsy may have multiple foci, so if you are unlucky to capture just one you will be misled. Similarly, if secondary generalization occurs rapidly, its partial nature may be missed.
Not usually useful to do after multiple seizures, unless type or frequency changes significantly, in which case a new syndrome/prognosis may have developed.</p>
<p><em>”The brain is subject to maturation; there are multiple protecting and triggering factors, often unpredictable. Seizures may be rare and easy to treat for months and years, but may become more frequent and difficult to control later on. But in many children a precise syndromic diagnosis can be made, and a good final prognosis can be expected in most cases.”</em></p>
Other investigations
All children with recurrent seizures should have an ECG with calculated QTc. Children under 2 with epilepsy or with recurrent focal seizures (other than CECTS) should have an elective MRI brain scan. In most other cases the course is predictable. A normal MRI does not rule out a small dysplastic lesion, equally the finding of a lesion does not mean that it is the cause of the epilepsy. However, at least you can exclude a tumour or malformation.</p>
Focal/partial often have acquired or congenital lesions, often specific precipitating factors eg sleep, startle!</p>
Differential
- Gratification/self stimulation
- Chorea or dystonia
- Pseudo seizure – ie psychologically dependent paroxysmal event
- Syncope (cerebrovascular or cardiac/vasovagal)
- Stereotypy
Management
<p>Consider:</p>
- Drug treatment (see below) – and risk with prenatal exposure
- Education – written, peer support
- Specialist epilepsy nurse review
- Emergency medication, if appropriate
First aid advice
- <li><a href=”http://scottishpaeds.org.uk/2017/01/31/living-with-epilepsy/”>Safety advice</a></li>
<li>When/how to access health services</li>
</ul>
</div>
Treatment
Should not be started after first tonic-clonic generalized seizure. Try not to start before EEG done as may mask features.
When to start? Complex – consider:
- risk of further seizures (about 30% after first seizure if EEG normal, over 50% after second) – time interval less than 6/12, seizure during sleep, and previous febrile convulsions increase risk. Status at presentation does NOT increase risk!
- natural history of the epilepsy (if known)
- safety issues and perceived risk
- mental health and psychosocial issues
- Risk of death
- attitude to medication, lack of positive test results, etc.
The risk of accidents due to a seizure is marginal, probably because seizures mainly occur during times of reduced activity (eg somnolence, sleep, meals) rather than during intense physical or mental activity. Risk assessment should be done and documented including bathing, showering, swimming. NICE only specifically mentions with reference to epilepsy and learning disability. SIGN states that normal activities should be encouraged, but supervision requirements should be individualized taking into account type of activity and seizure activity.
“There is an old and unjustified prejudice that brain damage may result from seizures: this does not happen in the great majority, and usually only occurs in unpreventable and very special situations.” (cf severe migraine, frequent syncope).
For generalized, lamotrigine or levetiracetam. Not Valproate for girls (risk of congenital malformations) or boys (evidence of effect on fertility) unless nothing else works
Others:
- Benzodiazepines (BZP) eg clobazam good for myoclonus
- (Carbamazepine (CBZ) can exacerbate! esp childhood/juvenile absence, JME)
- Vigabatrin for infantile spasms – but ACTH and Pred better! Side effects common with all! (Lancet. 2004 Nov 13;364(9447):1773-8.)
- Ethosuximide for childhood absence.
For partial, use carbamazepine (CBZ) or lamotrigine. Else:
- Topiramate for partial lesional epilepsies
- Sulthiame for idiopathic partial epilepsies
If 6 months therapy with 2 different but appropriate drugs does not control (at adequate doses), then refer to tertiary centre for re-think on diagnosis.
Routine drug level monitoring is not required.
Consider withdrawing treatment when seizure free for 2+ years. But treatment may also be aimed at reducing cognitive effects, not just seizures: evidence for this comes from surgically treated epilepsies where rapid cognitive-behavioural improvement can be seen; and the fact that behavioural problems are more common in the months leading up to the first fit before diagnosis. For example:
- Prolonged ictal/postictal cognitive deficits in partial epilepsies. These may last for days or weeks.
- Transient cognitive impairment (TCI) without recognisable clinical seizures – may be associated with EEG discharge.
- Epileptic syndromes with cognitive/behavioural manifestation as the main or only symptom eg acquired epileptic aphasia (Landau-Kleffner syndrome)
More efficient use of known drugs (doses, slow release preparations), side effects of drugs, and new therapeutic options (treatment of acute seizures with nasal or buccal midazolam (EPISTAT) by parents at home, or in schools) can make a big difference to families.
Temporal lobe epilepsies, most often due to mesial temporal sclerosis (and often refractory to medical therapy) can be treated surgically with excellent prognosis. An increasing number of intractable focal epilepsies can now be treated surgically.
Archives of Disease in Childhood 2005;90:5-10, T Deonna
SIGN guideline 81
Refer to tertiary if –
- child fails to respond to two AEDs appropriate to the epilepsy in adequate dosages over a period of 6 months (SIGN), or 3 over 12 months (NICE)
- children less than 2 years with epilepsy as defined
SPEN network has pathways for first seizure, new diagnosis, continuing seizures.
See also Living with Epilepsy
Caldicott 2
Dame Fiona Caldicott’s review of original 1997
information governance recommendations – response to perceived
reluctance to share info appropriately.
Appropriate sharing should be the rule, not the exception. Given need for informed consent, concludes that patients should be better informed as to how their
information is used. Needs system for recording consent applicable
across all NHS and care systems. Sharing info with a private
organisation or local authority should be equally straightforward, if
data protection principles are applied.
Confidentiality
For information to be confidential in law it must:
- not be common knowledge among lots of people, for example, the
content of a discussion between a patient and a health professional; - and be useful and not irrelevant or trivial
Explicit consent is not required for the following purposes:
- Where patient information is used for the routine clinical care of that patient – for example between health professionals and intra NHS multidisciplinary teams
- Where patient information is used for administration and management purposes, for example, waiting list management.
- Child protection purposes (see below)
Most patients understand that their information must be shared within
the healthcare team. However, patients do not expect this to be shared
with others who will not be involved in their care.
Aggregated and management information is used to plan and monitor
progress of the organisation in its delivery of services. This is
generally outside the scope of the Data Protection Act 1998 on the
basis that a living individual could not be identified from such data.
Anonymized/coded information would normally fall outside the scope of
the Data Protection Act 1998, but care must be taken with all coded
and anonymised information as it may still be possible to identify
individuals, e.g. with rare diseases, drug treatments or statistical
analyses within a small population.
For other uses, it is your responsibility to make sure that patients
are aware of the wider uses of their information and to get their
permission. It is your responsibility to make sure that you provide
versions in any community languages or meet other accessibility
requirements.
You should:
* make clear to patients when information is or may be disclosed
(shared) to others involved in their health care;
* make sure that patients are aware of the choices that are available
to them on how their information may be disclosed and used;
* check with patients to make sure that they have no concerns or
questions about how their information will be disclosed and may be
used;
* answer any questions personally or direct patients to others who can
answer their questions; and
* respect the rights of patients and help them to access their health
records if they have asked to do this.
Intra NHS Information Sharing NHS Scotland policy
3rd party info eg family history or info coming from an identifiable
family member – may itself be confidential, even if in patient’s
record, so 3rd parties should be told if their identity might be
revealed, and given opportunity to decline.
Beware use of automated reports for insurance etc, where only minimum
necessary info is appropriate, and would be wrong to disclose more
than that.
Option to opt out of data analysis emphasized – not clear how this
would be done.
Training seen as tick box rather than education.
£100 000 fine for Aberdeen city council for a home worker accidentally uploading files regarding vulnerable children to an online file store. A fine has never been issued for formal sharing of information. “Blagging” is also an issue, where a 3rd party obtains information by ostensibly acting as a healthcare professional or family member.
Guidance from 2003 still applies – obtain confirmation of identity (or
phone number etc) from second source. If breach occurs, individual
should be informed.
See also Data Protection for Caldicott principles etc.
Child Protection
Scottish Government’s Sharing Information about Children at Risk: A Guide to Good Practice (2003) states:-
“If there is reasonable concern that a child may be at risk of harm this will always override a professional or agency requirement to keep information confidential. All professionals and service providers have a responsibility to act to make sure that a child whose safety or welfare may be at risk is protected from harm.”
The National Guidance for Child Protection in Scotland (2014) states:
‟Harm‟ means the ill treatment or the impairment of the health or development of the child, including, for example, impairment suffered as a result of seeing or hearing the ill treatment of another. In this context, ‟development‟ can mean physical, intellectual, emotional, social or behavioural development and ‟health‟ can mean physical or mental health.”
Recent advice has also been received from the Scottish Government, having consulted with the Information Commissioner’s Office, regarding the impact of GDPR and the Data Protection Act 2018 in this area. The Information Commissioner’s Officer has confirmed:
“It is important that those whose work brings them into contact with children and young people continue to share child protection concerns in the same way as they did previously. Child protection matters at the significant harm level equate to sharing/processing being necessary to protect the vital interests of the child where reliance on consent may be prejudicial to that purpose. The same lawful purposes are provided for in Articles 6:1(b) and 9:2(c) of the GDPR for personal and special category data so nothing has changed at that level”.
It is important to be open and transparent and make people aware that we will share information when we suspect a child or young person is at risk of harm. It is also important to record any decision to share or not to share information and reasons for doing so.
Relevant Acts/Policies
* Human Rights Act 1998
* Freedom of Information (Scotland) Act 2002
* NHSS Code of Practice on Protecting Patient Confidentiality.
* NHSS Information Governance standards 2005
Note that Scotland leads patient data protection with Fairwarning software.
VZV encephalitis
VZV encephalitis presentation not different from usual, viz fever, headache, altered consciousness, etc. But can be subacute onset.
The more common neuro manifestation of VZV in young children is post-infectious cerebellitis – usually mild and self limiting, child not unwell but risk of secondary
hydrocephalus in more severe cases.
There is also a well recognized association in childhood between VZV infection and stroke, usually presents after the rash has cleared – typically 3 months [London study, Miravet & Danchaivijitr 2007). Post-VZV thromboembolism also seen rarely eg lower limb DVT.
Encephalitis can present early, even before rash (which may
not be very obvious either). PCR for VZV DNA in the CSF is positive in around a third of patients; VZV specific IgG seen in 90% in CSF. Compare levels to serum as a way
of confirming CNS involvement.
Usually (not for cerebellitis), steroids given eg 60-80 mg of prednisolone daily for 3 to 5 days) is given (Gilden & Kleinschmidt-DeMasters 2000) esp where MRI evidence of vasculitis.
[encephalitis article, source?]
Chickenpox (Varicella Zoster virus)
A systemic viral illness characterised by widespread vesicles. Like other herpesviruses, it retains the ability to lie dormant in ganglions after initial infection, possibly reactivating in the future as Herpes Zoster (= shingles).
Age and immunodeficiency are the most important predictors of severity, with adults and infants having more severe disease. Cellular rather than humoral immunodeficiency is associated with more severe disease. Nonetheless, most cases of severe disease (and 90% of the deaths) occur in previously healthy people.
Average age is falling, now under 5 (presumably increased day care) cf underdeveloped countries, where average age is older eg teens. Peak incidence March to May.
There are 3 genotypes but they are virtually identical, and only 1 circulates in Europe; it remains theoretically possible, therefore, to get chickenpox twice! But more likely is that one or more episodes were due to another virus eg enterovirus.
Clinical
Starts as small spots, spreading over the trunk within 24 hr. There is usually no prodrome in children, can be 1-2 days in adults. Within 24-48 hours the classic vesicles, followed by pustules, develop. Burst to leave a scab which falls off after 4-5 days. There may be several crops of these blisters which follow the same pattern. The classical distribution is on the trunk but lesions can be widespread and can affect the mouth, the eyes and the urethra.
Onset of the rash is often associated with fever and other systemic symptoms. The disease can however be subclinical (or at least unrecognized) in some cases. Secondary cases in a household on the other hand tend to be more severe, probably due to increased viral load.
In the immunocompromised, there may be a prodrome ie symptoms at the time of initial viraemia, around day 7 of the incubation period. The classic prodrome is of abdominal symptoms and/or hyponatraemia, and can precede the classic vesicular rash by several days (up to 3 weeks). Abdominal manifestations include severe pain, diarrhoea, or vomiting which are explained by hepatitis, gastritis, oesophagitis, pancreatitis, and paralytic ileus owing to viral spreading from the posterior nerve roots that supply abdominal organs. The mechanism of hyponatraemia is presumed to be SIADH.
See Congenital varicella for infection in pregnancy and neonatal period.
Diagnosis
Usually clinical. If in doubt, PCR and culture can be done on skin scrapings (particularly from the base of lesions, but potentially also from the crust) or from other sites eg CSF.
IgM can be positive from as early as 1-2 days after appearance of the rash. But serology is not 100% sensitive. Antibodies persist lifelong and are useful for indicating previous exposure and hence immunity; they may however be passed on passively through transfusion. Not very good for confirming response to vaccination, as levels are 10 times lower than after disease.
Complications of varicella occur in the immunocompetent, as well as the immunocompromised :
- Bacterial superinfection of the rash, potentially cellulitis, even necrotizing fasciitis. Streptococcal infections are more common after chickenpox, and not just in the skin.
- Pneumonitis
- Meningoencephalitis – usually after onset of rash but may present before. High mortality.
- Hepatitis
- Glomerulonephritis
- Haemorrhagic disease (purpura fulminans) – with shock, DIC
- Post varicella cerebellar ataxia – sudden onset but 2-3 weeks later (immune)
See also Congenital varicella.
Spread
Incubation period is 10-21 days, typically 14 days. Longer in some situations (eg post ZIG). Infectivity (by aerosol spread) begins up to 48 hours before onset of the rash and persists until all lesions have dried (crusted), usually 1-2 weeks but may be longer in the immunocompromised. In theory transmission from a moist spot can occur but infection is generally by respiratory route.
Infectious or isolation period is until all lesions crusted, or else 5 days after the last spot appears. UK HPA guidance is available on exclusion periods from school or nursery on health grounds. Infectivity can persist in the immunocompromised for up to several weeks. Note also that after VZIG administration, incubation period is prolonged.
Treatment
Chickenpox can be treated with aciclovir or the like. Oral aciclovir in the healthy child reduces fever by 1 day and symptoms by 15-30%; not clear if complications are reduced. NEJM 1991;325(22):1539-44. Not standard practice, however! Adolescents and adults should be offered it.
Oral aciclovir only works if given in first 24 hours; IV most effective if given within 72 hours of onset of the rash.
A variety of topical products are available eg calamine. Antihistamines.
Various studies have found an association between severe soft tissue infection and use of ibuprofen (in children, anyway – rate ratio 4.9 [Br J Clin Pharmacol. 2008 Feb;65(2):203-9. doi: 10.1111/j.1365-2125.2007.02997.x]). Likely to be confounding, but in absence of prospective studies, NICE recommends avoiding non-steroidal anti-inflammatories in varicella [https://cks.nice.org.uk/chickenpox#!scenario].
Prevention
See Vaccines for details on live attenuated vaccine.
Post-exposure prophylaxis (PEP) is required for at risk groups who have had significant exposure. This includes:
- pregnant women,
- immunodeficient (except those receiving regular normal immunoglobulin),
- susceptible neonates exposed up to 7 days after birth (which includes mum developing chickenpox up to 7 days before or after birth), or any neonate (susceptible or otherwise) that require intensive or prolonged special care).
Specific Varicella Zoster Immunoglobulin (VZIG) is effective at reducing the likelihood of disease, and where disease occurs it tends to be less severe. It is given intramuscularly. Should be given within 10 days of exposure. Protection lasts 3 weeks, after which a further dose should be considered if re-exposure occurs and antibody has not persisted. Can prolong period of infectivity though. See Greenbook for more details.
Aciclovir can also be used for PEP.
Varivax vaccine is also licensed for this indication, but of course contraindicated in the type of patient who might need it: 18% of healthy contacts developed varicella compared with 78% who did not get vaccine. Of the vaccine recipients who nonetheless developed varicella, the majority only had mild disease (with less than 50 skin lesions). Evidence only really supports PEP within three days following exposure.
Congenital varicella
If a pregnant woman is infected during the first trimester (risk extends to 20th week), a fetus has a 1% chance of developing widespread scarring, hypoplastic limbs, cataracts and brain lesions (congenital varicella). Affected infants have a poor neurodevelopmental outlook.
Risk of neonatal VZV (severe, disseminated disease in newborn) if chickenpox is contracted by the mother 4 days before birth, to 2 days after (risk 20%). Before that, good chance that maternal immune response will protect baby, after that the dose of infection transmitted to the baby via the umbilical cord is likely to be small (although will still be exposed to droplets).
See Maternal for advice on varicella exposure in pregnancy and in neonates.
Varicella Zoster Virus vaccine
Following varicella vaccine introduction in Australia, coverage of greater than 80% at 2 years of age was achieved, with varicella hospitalizations reduced by almost 70%. 40% of hospitalized children were immunocompromised. Of hospitalized children age-eligible for varicella vaccine, 80% were unimmunized, including all cases (3) requiring intensive care. No deaths.
[Pediatric Infectious Disease Journal. , 17 December 2012]
Eczema
NICE (CG57, 2007) diagnostic criteria: itchy skin plus 3+ :
- visible flexural dermatitis (or visible dermatitis on the cheeks and/or extensor areas in children <18/12) – can look like dirt where darkened esp neck
- personal history of flexural dermatitis (or dermatitis on the cheeks and/or extensor areas in children <18/12)
- personal history of dry skin (xerosis) in the last 12 months
- personal history of asthma or allergic rhinitis (or history of atopic disease in a first-degree relative of children aged <4yr)
- onset of signs and symptoms under the age of 2 years (do not use this criterion in children under 4 years).
On examination, may also see lichenification (increased skin markings due to chronic rubbing), excoriations caused by scratching, and hyperlinear palms (look at thenar eminence).
Babies tend to get eczema on the face. Older infants get it on extensor surfaces. From walking age, antecubital and popliteal fossae. In children of Asian, black Caribbean and black African ethnic groups, extensor surfaces tend to be affected rather than flexures, and discoid or follicular patterns may be more common.
Severe (NICE criteria): widespread areas of dry skin, incessant itching, redness (with or without excoriation, extensive skin thickening, bleeding, oozing, cracking and alteration of pigmentation).
Cf Moderate: frequent itching, redness (with or without excoriation and localised skin thickening)
Risk factors
Eczema (or atopic dermatitis, same thing) associated with parental allergies (OR 1.94), parent-reported infection after birth (OR 1.45), parent-reported jaundice (OR 1.27). Being a migrant (OR 0.63) and keeping a dog (OR 0.78) are protective. Prenatal probiotics did not reduce risk (Lactobacillus rhamnosus GG, LGG). Respiratory viral infections in pregnancy associated with wheezing illness in infants (mothers with asthma) and eczema. [Australia, Ped All Imm 2014:25:151]. Febrile and gynae infections in pregnancy associated with eczema in child (Italy, Ped All Imm 2014:25:159]. Children of Japanese mothers with higher anxiety scores during pregnancy were more likely to be affected by eczema!
Immunology
Many roads lead to Rome! Can be seen as combination of impaired innate and distorted adaptive immunity, interacting in framework of cutaneous immune system with suboptimal barrier function. Epidermal barrier can be genetically disturbed, but gene expression (eg of filaggrin) is also influenced by microenvironment eg Th2 cells. Some genetic structural abnormalities can be seen to induce nonspecific inflammatory reaction (eg SPINK5 defects). And almost certainly, epigenetic regulation will affect gene expression in both keratinocytes and immune cells.
Facilitated antigen presentation mediated by IgE bound to high affinity IgE receptor FcEpsilonRI, on dendritic cells, is an important part of it. Vitamin D plays a key roll, stimulates Toll like receptors, increasing pro-inflammatory cytokines but studies equivocal whether low (or indeed high) levels increase risk.
Eczema can exist without IgE against aeroallergens and food allergens, so is primarily a non IgE mediated disease, although both IgE and non-IgE hypersensitivity can co-exist, particularly in babies.
Still not understood how eczema and Staph aureus interact. Colonization appears to amplify local inflammatory reaction, but also increases IgE against a large spectrum of other things (possibly including self proteins). It is as if there is something specifically different about how immune cells handle Staph. Toll like receptors esp TLR-2 recognize Staph aureus cell wall. Overgrowth of staph during flares is associated (preceded?) by loss of diversity of skin microbiome.
Unmasking of the HSV entry receptor Nectin-1 in adherence junctions, among other things, contribute to eczema herpeticum. See Flares, below.
Atopy patch test (using intact protein allergens) can prove type IV reactions. Correlates with oral food challenge. Hyper IgE syndromes are important differential for AD, STAT3 mutations, skin (and other) abscesses, recurrent pneumonia (and pneumatocoele), connective tissue and skeletal abnormalities, mucocutaneous candidiasis. DOCK8 type Hyper IgE syndrome show sensitization predominantly against food allergens, which is a clue (STAT3 and AD show predominantly sensitization to aeroallergens).
Normal looking skin is not immunobiologically normal! Invisible inflammation, hence still needs treatment. Pimecrolimus and betamethasone both normalize expression of filaggrin, the later is perhaps a better anti-inflammatory but steroids reduce expression of enzymes for lipid and protein synthesis, so may impair skin barrier restoration.
Triggers
Stress, humidity, extremes of temperature can cause flares of atopic eczema. But what causes a flare in some can apparently help in others! Any factors causing flares should be avoided where possible.
UVB causes sunburn. UVA (longer wavelength) more relevant to photosensitivity reactions. Both cause long term skin damage. EU commission recommends UVA protection making up at least 1/3 of total suncream SPF. A few available on prescription for photodermatosis (incl vitiligo) but not for eczema per se. Lipscreen (Uvistat) available for chronic/rec HSV labialis. Sunsense is lotion.
Avoid wool in contact with skin. No evidence that bio detergent or fabric softener a major problem. Avoiding excessive product and not overloading machine (so disperses fully) prob more important.
Management
See eczema management.
Parental support
National eczema society, British Association of Dermatologists, Eczema Outreach Scotland.