Category Archives: General paediatrics

MRSA

General paediatrics, Infectious disease, Microbiology

=methicillin resistant staphylococcus aureus.  Cf methicillin sensitive staph, MSSA.

Methicillin resistance equates with flucloxacillin resistance. mecA is the methicillin resistance gene, which codes for a low affinity PBP (penicillin binding protein) – ie penicillin can’t bind easily. The gene has probably crossed from coag neg staph on at least 5 occasions to create MRSA strains. As with MSSA, different strains exist, carrying a range of different pathogenic genes.

Traditionally MRSA was found in institutions and the elderly, but now can be seen frequently in the young and healthy, causing the same infections that MSSA causes eg skin/soft tissue. It can also be responsible for rarer, more severe diseases eg necrotizing fasciitis. The US Center for Disease Control details criteria for distinguishing hospital acquired and community acquired MRSA infections – community acquired strains are typically SCCmec type IV (this is the cassette that contains mecA), which are sensitive to most non-beta lactam antibiotics, but on the other hand is associated with Panton Valentine Leucocidin (PVL, a cytotoxin associated with necrotizing disease). But again, this distinction is becoming less clear with strains associated with community acquired infection becoming more frequent in hospital acquired cases, and having variable levels of non-beta lactam antibiotic resistance.

In itself, antibiotic resistance may not translate to increased virulence and pathogenicity – it may just make it harder to treat. Studies have shown that after correcting for other factors eg age and co-morbidity, mortality is not significantly different. However, one important factor is use of inappropriate antibiotics, which of course is more likely with MRSA. Furthermore, in the US many MRSA outbreaks are caused by the USA300 clone, which carries a number of genes (in common with Methicillin sensitive staphylococcus aureus) eg PVL, ACME which are associated with enhanced pathogenicity.

PVL seen in 50% of symptomatic (skin) community MRSA in the US. Now also being reported in hospital acquired MRSA. Prevalence much lower in Europe, but risk of spread. Geographical areas tend to have their own clones (eg type 80 in Europe), with occasional pandemic.

Epidemiology

  • MRSA has been shown to survive on sterile packaging for at least 6 months.Journal of hospital infection 2001;49(4):255-61.
  • Basic simple infection control like hand washing works.
  • MRSA prevalence in hospitals is associated with macrolide and 3rd generation cephalosporin use.Clinical microbiology and infection 2007;13(3):269-76.
  • Alcohol hand rub reduces its transmission and hospitals which have introduced a policy of using this between patient contacts reduce their MRSA rate.
  • Isolation and screening work but may be impracticable in emergency admissions or in hospitals with near 100% occupancy.

In the UK, most MRSA are resistant to quinolones and macrolides. Even if sensitive to quinolones, treatment is not recommended as resistance evolves rapidly. Most MRSAs are sensitive to tetracyclines (but not for use under 12yrs), rifampicin, co-trimoxazole, and linezolid, all of which can be given orally. Clindamycin can be effective but beware inducible resistance – see below. No evidence for trimethoprim alone (cf septrin); use in combination with rifampicin? Probably best not to give rifampicin or fusidic acid monotherapy anyway as resistance frequently induced.  See antibiotic classes.

In MRSA skin infections (cellulitis/abscesses), most will get better anyway, esp after I&D, but using the wrong antibiotic increases risk of treatment failure by odds ratio of 2.80 (87% success cf 95% of patients who received an active antibiotic). Topical agents will induce resistance if used for high load infections eg wounds, catheter sites so should be combined with systemic therapy.  About 12% are resistant to topical mupirocin.

For intravenous therapy, gentamicin, vancomycin and teicoplanin are effective, although vancomycin resistance has been described since 2002. Teicoplanin levels can be unpredictable, and treatment failure associated with low levels has been seen; checking levels would make sense (aiming for trough of at least 10, 20 in endocarditis) but is rarely done. In line infections, vancomycin or linezolid should be used if the infection is severe; if milder, then removal of the line and oral therapy may be sufficient.

In bone infection, linezolid is good but should be given for a maximum of 28 days. Fusidic acid and Rifampicin are good adjuncts (rifampicin has in vitro activity against biofilms). Clindamycin and co-trimoxazole have also been used for bone infections. Early surgery (eg within 2/7 of onset of symptoms) is important esp where a prosthesis is present.

Necrotising pneumonia with MRSA post-influenza has mortality up to 75%.

For bacteraemia/endocarditis, vancomycin is the drug of choice, as treatment failures have been described with teicoplanin. Rifampicin or fusidic acid can be considered as adjuncts; there is no evidence for adding an aminoglycoside. A minimum of 14 days treatment is required (although oral treatment may be appropriate for maintenance) but should be extended if vegetations seen on trans-oesophageal echo. Infected pacemakers should be considered the same as orthopaedic prostheses.

Clindamycin resistance is sometimes only 1 mutation away from erythromycin resistance. If the bug is erythromycin sensitive, then there is no issue, and clindamycin is a good choice (and can be given orally). On the other hand, if erythromycin resistance is seen, then the D test should be done: if a D-shaped zone appears around the clindamycin disk when an erythromycin disk is placed nearby, then you have induced resistance and clindamycin should be avoided. The erm gene is responsible for erythromycin-inducible resistance; the mrsA gene also confers resistance to erythromycin but does not affect clindamycin.

Eradication

Once colonized, about 40% of patients develop persistence – commoner where skin breaks present. Vancomycin does not clear nose, throat or gut.

Eradication of S. aureus nasal colonization eg with 72 hour mupirocin has been successful. However, recolonization usually occurs within a relatively short time, and the Cochrane review did not find much evidence in favour. Use of mupirocin to prevent infection in endemic settings eg dialysis centers have shown conflicting results although metanalysis suggests benefit (but fear of mupirocin resistance). Neomycin is even less effective, but is an alternative where mupirocin resistance is seen.

Combined treatment seems sensible, and recent RCT of 2% chlorhexidine gluconate washes, 2% mupirocin ointment intranasally, oral rifampin and doxycycline for 7 days vs no treatment confirms. At 3 months of follow-up, 74% cf 32% had cleared. Still significant benefit at 8 months (54% of those treated culture negative). On multivariable analysis, having a mupirocin-resistant isolate increased the risk of treatment failure nearly 10 fold. Mupirocin resistance emerged in only 5% of follow-up isolates. Clin Infect Dis. 2007 Jan 15;44(2):178-85.

Other control measures include a combination of active surveillance cultures of high risk patients, improved health care worker hand hygiene, consistent use of contact precautions for colonized/infected patients, and directed treatment of health care workers implicated in transmission. PIDJ January 2005 pp 79-80

Screening patients seems to reduce hospital acquired infection in the Netherlands, but not in Switzerland. UK guidelines say do for high risk only eg previous carriers, transfers, ICU. Standard infection control procedures alone seem to have worked in UK although what do you compare with? Rapid test (PCR) did not help (in crossover trial) except in reducing inappropriate isolation. 3-4x as expensive.

[UK guidelines, J antimicro chemo 2006 PMID 16507559]

 

 

Benign transient hyperphosphatasaemia

Common, General paediatrics

Common, typically young children with minor infections.

Due to decreased clearance, probably, carbohydrate side chains changed, affecting recognition – characteristic iso enzyme pattern on electrophoresis (ie not usual bone/liver forms).

Can be as high as 50x normal upper limit viz 10 000+!  Can last up to 6 months.

Just show that other liver function tests normal, normal calcium/phosphate and no suspicion of myositis, rickets.

Asthma

Common, General paediatrics, OPD, Respiratory

See BTS/SIGN/NICE 2025 guidance on asthma,  asthma prevention, asthma and obesity

FeNO is expensive and available in only a minority of GP practices and hospital services.  Requiring it means GPs can no longer make diagnosis themselves.

Spirometry results in most primary care patients with asthma are normal!

Spacer best for everyone! Orange aerochamber is small mask, up to 18 months, yellow is 1-5yrs. Green is 5+, blue is adult. You can get blue with mask, not green.

200 doses in an MDI.   2 puffs BD exhausts an MDI in 50 days. Multidosing 5 puffs 4hrly will exhaust it in 6 days.

Growth Restriction

Children who use inhaled steroids for asthma grow slower than their peers in the first year of taking the medication, by about half a centimetre per year. Metanalysis of 25 trials, various types of steroid.  Seems to be most obvious in initial year of treatment.  Only 1 study followed children into adulthood – budesonide, used for average of 4 years – reduction in final height of  1.2cm (Kelly, PMID 22938716).

Should therefore be prescribed at the lowest effective dose. Cochrane 2014 found significant difference between low dosing (50-100 Clenil equivalent) and medium dosing  of 0.2cm per year but noted that the  majority of trials did not report height data.

However, the small effect on growth needs to be weighed against the proven benefits of these drugs in controlling asthma, and ensuring children’s lungs grow to their full capacity.   Undertreated asthma is much more likely to have a harmful effect on a child’s development than a small reduction in growth.

Newer Therapies

Xolair=Omalizumab, monoclonal vs IgE. Subcut, 2-4 weekly, for age 6+ where conventional therapy not working.  Other criteria are total igE >30, positive tests for aeroallergens, FEV1<80%.

Airsonett is evidence based, temperature controlled laminar flow system for bedroom. Noisy!

Management

See National review of asthma deaths.  Recommendations include:

  • Refer specialist if >=2 courses oral steroids within 12 month period
  • Follow up after every ED/OOH attendance
  • Hospital follow up after every hospital attendance
  • Annual inhaler technique check
  • Personal asthma plan for everyone

See MyLungsMyLife.org website for self management.

Depigmentation

Dermatology

Generalized

  • Oculocutaneous Albinism is most common. Non-type 1more subtle – in fair skinned families, may only be obvious in comparison with family members.
  • Griscelli, Elejalde and Chediak–Higashi syndromes have been termed “silvery hair syndromes” – generalized, but eyes spared. Griscelli and Elejalde include severe neurological defects, as well as immunological. Immunodeficiency severe in Chediak-Higashi.
  • Menkes is X-linked copper defect, progressive CNS degeneration and death in early childhood.
  • Selenium deficiency? Only really in malnutrition.
  • In later life, homocystinuria.
  • Post inflammatory – pityriasis alba –  ill-defined macules or plaques, typically circular or oval, often with mild scaling. Can be itchy. Usually found on the face, arms, and upper trunk,

Localized syndromes

  • Ocular albinism – light coloured eyes mostly rather than pink.  Associated with poor visual development. Heterochromia (different coloured eyes) that develops or worsens soon after birth can be seen with congenital Horner’s syndrome (with neuroblastoma) – also part of Waardenburg’s (below).
  • Piebaldism looks like vitiligo but is congenital and permanent. Usually affects forehead causing patch of white hair (“forelock”), with or without eyelash and eyebrow involvement.  Autosomal dominant. Can occur in tuberosclerosis. Becomes more obvious when surrounding skin becomes tanned.
  • Waardenburg syndrome includes piebaldism, but also heterochromia irides (different coloured eyes, or else different colours of same iris, or just pale blue eyes).  Subtypes have hypertelorism (increased space between eyes), limb defects, Hirschsprungs, deafness.
  • Single depigmented patch: naevus anemicus (vascular, Woods light neg), ash leaf macule of tuberosclerosis (usually multiple) or naevus depigmentosus (identical but single, less likely to be leaf like).
  • In later life, vitiligo (autoimmune), post inflammatory (eg eczema, pityriasis), lichen sclerosus and morphoea.

[Hong Liang Tey, Acta Dermato-Venereologica online]

Autosomal dominant polycystic kidney disease

General paediatrics, Genetics, Renal

ADPKD – previously Adult PCKD but now recognized as having manifestations in childhood.  Cf Autosomal recessive disease, severe, renal failure in infancy.

1 in 400 to 1,000 live births, making it the most common monogenic cause of renal failure. The typical age of onset is in middle life, but the range is from infancy to 80 years.  Associated with liver cysts (asymptomatic) and intracranial aneurysms. 10-25% do not have family history (de novo mutations, missing records or mosaicism).

Possible presenting symptoms of renal disease in children with ADPKD are frequency, nocturia and/or, hematuria, urinary tract infection(s) and back, flank or abdominal pain. Often, the earliest symptoms are polyuria and polydipsia, from decreased urinary concentrating ability.

Extrarenal manifestations seen esp hypertension (renin angiotensin system, sodium retention, endothelial dysfunction), also liver cysts (asymptomatic), intracranial cysts and valvular defects but these are only seen in adults. 25% of children are hypertensive by the time they reach adolescence.  (GFR stays stable until around 40yrs, then rapid decline, about 50% have ESRF by 60yrs).

Importantly, children who were diagnosed in utero or within their first 18 months of life, the so-called VEO group, represent a particularly high-risk group of ADPKD patients and should be managed accordingly.  Diagnostic imaging criteria not validated under 15yrs, genetic testing also challenging.

Recommendation from Kidney Disease Improving Global Outcomes (KDIGO) Consortium against screening children for APCKD.  [Also highlight variety of different cystic disorders in children, so recommend thorough clinical assessment for extrarenal manifestations in case syndrome eg Von Hippel Lindau, USS of parents and/or grandparents if negative family history, and USS to look for dysplastic kidneys, glomerulocystic disease, and tuberous sclerosis complex].[Kidney international 2015]

Increasing evidence that hypertension, left ventricular hypertrophy (even between 75th and 95th centile for BP) and increased kidney volume predates symptoms in affected children.  A study of early use of ACE inhibitor halted progression of LVH and fall in renal function.  Adding pravastatin reduced progression of structural kidney disease.  Disease modifying drugs in development.  [BMJ 2016;353:i2957 Editorial, GOS, Birmingham, Evelina].  “We propose an urgent national debate on an improved inclusive approach involving patients and their families and a range of clinicians, ethicists, and commissioners. A few pounds spent now on screening and early intervention could save many thousands later by delaying hypertensive complications and chronic kidney disease.”

Potential for pre-implantation genetic diagnosis.  See Ethics.

Only one drug known to have moderate effect on disease progression in adult ADPKD patients, vasopressin V2 receptor antagonist tolvaptan (recent Cochrane review).  But timing of use unclear.

Psychological impact of having genetic disease that can be passed on to children very common in adult patients.  But a benefit of diagnosis is potential to target modifiable risk factors  – children with normal BP have slower cyst growth.  And knowledge can give sense of control over life decisions, esp reproductive decisions.

Penis problems

Clinical, General paediatrics, OPD, Surgical

The foreskin cannot, and should not, be retracted in newborn babies.  It should gradually begin to separate in the first few years of life. Sometimes it takes until puberty.

Retraction should lead to a pouting appearance of the foreskin. Technically this is not phimosis, which implies an abnormality. Some ballooning with micturition is seen, and is not an indication for surgery.

Can try application of topical steroid cream to speed up separation eg 0.025% betamethasone (1 in 4, or RD) cream twice daily for 2 to 4 weeks.  Gently retract foreskin without causing any discomfort and apply a thick layer of cream to the tightest part of the foreskin.  Steroid creams of higher potency may be tried if this fails.

Inflammation of the foreskin (posthitis), glans (balanitis) responds usually just to hygiene measures – bathing, cleaning, drying. Antibiotics might be needed if spreads on to shaft. Topical steroids can help.

Circumcision if significant phimosis and steroid creams fail.

Smegma pearls

Retained smegma can accumulate into substantial but painless lumps down the shaft of the penis.  Can be ignored.

Balanitis Xerotica Obliterans

A form of lichen sclerosus affecting the tip of the penis. No pouting of foreskin seen on retraction. Can be white, crinkly thickening. Can be bleeding, discomfort. No good evidence for topical steroids, usually surgical treatment.

House dust mite allergy

Allergy, General paediatrics

People assume they are allergic to dust – more likely is that they are allergic to dust mites (HDM).  These are microscopic, and tend to reside in fabrics in the home esp bedding, carpets, sofas.  So your house can be spotless but still be full of mites!

There are a number of different house dust mite species – most are Dermatophagoides (“skin eating”…), D. farinae is the American type, D. pteronyssinus is the European one.

HDM allergy is common in atopic individuals, contributing to eczema, rhinoconjunctivitis and asthma. Eczema usually comes first, but sensitisation (usually develops in young children) seems to predict development of asthma persisting into school age!

Although common, it doesn’t tend to cause immediate reactions, the way cat/dog does, probably because mites don’t fly – so exposure only caused when surfaces disturbed or if skin/nose/mouth/eyes in direct contact. But inflammation may be chronic, from brief, low quantity, frequent exposure. So even with avoidance/ reduction measures, it can take months to see the benefit…

There is cross-sensitivity with shellfish allergy but not fish allergy.

In some parts of the world, mouse and cockroach allergies more of an issue.

Lots of different allergens identified.  der p 1 and 2 are major allergens in mite faeces, in kids with eczema various other allergens found in mite bodies also important. Mite faeces are the most important cause of sensitisation. Composition of skin prick solutions seems to vary…

Avoidance/reduction

Allergy UK has an advice leaflet with different measures for reducing levels of HDM in the home.  Evidence however is that this is difficult to do and rarely seems to have any significant clinical effect!  So no point in doing piecemeal, certainly.

Dust mites need high humidity to get water, so high altitude and air conditioning suppresses them.  They also like temperatures over 20deg. They are photophobic so hide deep in fabrics.

Get rid of carpets, curtains, excess cushions/pillow/throws, move soft toys off bed.

Wash bedding at 60, or tumble dry! Soft toys go in the freezer overnight once a month (in a bag, obviously, to avoid collecting smells). Protective covers for mattresses and hypoallergenic bedding materials.

Some vacuum cleaners are better than others (in theory) eg with HEPMA filter.  Allergy UK approves products (but only if company pay, of course). But the mechanical action of cleaning (plus moving furniture, changing beds etc) can whip particles up into the air (as can emptying the contents of the cleaner) so best done when kids are out, and wait 20 minutes before letting them back in…  Cleaning and replacing filters important too esp if bagless design.

Vacuuming alone resulted in a significant reduction in carpet house dust mite allergen concentration and load. Levels approached pretreatment values by 4 weeks posttreatment in the intensive vacuuming group, whereas combination of dry steam cleaning plus vacuuming lasted up to 8 weeks. 

You can also use a steam cleaner on a mattress!

Evidence for air purifiers is mixed.  If placed on carpet, they can actually disturb more allergen than they remove! You need to close doors and windows of course. Unfortunately the best ones tend to be big, expensive and noisy, and price does not mean good quality. Plus you have to remember to replace the filters. The cheapest Which? recommended one (the Electriq EAP500HC) costs over £200.

In PAXAMA study in the NW England (kids with a history of wheeze requiring a visit to hospital), impermeable covers (blinded!) halved risk of having an emergency hospital attendance over the next year. [Murray 2017] Maximum benefit was seen in under 11yrs, mono-sensitized to mite, living in nonsmoking households, and requiring more ICS.  

[JACI 2018]

Immunotherapy

Systematic review found good evidence of benefit for eczema with immunotherapy against house dust mite, with subcut immunotherapy superior to sublingual. [Journal of Allergy & Clinical Immunology. 151(1):147-158, 2023 PMID 36191689]

Evidence for immunotherapy for allergic rhinitis, at least in adults… Treatment effect from 14 weeks, so not rapid…

No evidence for asthma but given as indication… although research into whether HDM immunotherapy might prevent.

NICE approved Acarizax for moderate to severe HDM rhinitis from age 12 in the NHS in England in January 2025. Acarizax is sublingual therapy (derived from D pteronyssinus and D farinae), indicated in adolescents (12-17 years) as well as adults diagnosed by clinical history and a positive test of house dust mite sensitisation (skin prick test and/or specific IgE) with persistent moderate to severe house dust mite allergic rhinitis despite use of symptom-relieving medication.

NICE appraisal also comments that avoidance/reduction of HDM burden in home is almost impossible and if problems persist, it can induce strong feelings of guilt in parents/carers.

Also, many patients would prefer not to be using regular, large doses of steroids, even if effective.

£80 a month on NHS, has not been submitted to Scottish Medicines Consortium so currently not recommended.

International treatment guidelines refer to a treatment period of 3 years for allergy immunotherapy to achieve disease modification. Efficacy data is available for 18 months of treatment with ACARIZAX in adults; no data is available for 3 years of treatment. If no benefit in first year, no indication to continue.

First dose should be observed and the patient monitored for at least 30 minutes.

Place under the tongue, avoid swallowing for 1 minute, avoid food/drink for 5 minutes.

Contraindications are FEV1 <70% of predicted value despite treatment, or severe asthma exacerbation within the last 3 months.

If oral ulceration, postpone treatment.

Eosinophilic oesophagitis has been reported.

Accidental Adrenaline self-injection

Allergy, Emergency medicine, General paediatrics, Surgical

eg with Epipen or Emerade.

Causes vasoconstriction with potential for gangrene.

Try:

  • warm water immersion
  • local nitroglycerin paste
  • subcut infiltration with a mixture of 1.5mg of phentolamine, 1mL of 2% lidocaine (at site and along course of digital arteries)

[advised by National Poisons Information Service]

n=365 adrenaline injections to hand, 213 to digit.  No cases with clinically apparent systemic effects, only a few patients had ischemia. No patient was admitted or had surgery. [Annals of Emergency Medicine. 56(3):270-4, 2010 Sep. PMID: 20346537]

Familial Hypercholesterolaemia

Cardiology, General paediatrics

Usually LDL receptor gene mutations (on liver, for removing lipids from blood). One Apo-B mutation (on LDL) identified.  Least common is PCSK9 mutation – higher degradation of receptor, most severe.

If normal BMI, elevated LDL, autosomal dom inheritance, normal TFTs then 95% LDL receptor defect.

If one sibling has a LDL double that of another sibling, 99.8% LDL receptor mutation.

Highly heterogeneous in UK, over a 1000 mutations.

Estimated 1/500 in most countries [but in Denmark found 1/137, Holland has found 1 in 232].  So prob only 12% of cases identified in UK, even less in young individuals!

DNA screening cf lipid testing cost effective (and enhances cascade screening).  Using LDL only, 8-15% false neg and pos, due to overlapping of ranges.  Gene scoring (using SNPs) for mutation neg clinical cases helps to find polygenic cases. But 40% less risk of disease so cascade testing less effective.

American college of med genetics have recommended that familial hypercholesterolaemia (FH) mutations detected on whole genome should be reported to patient.

Cases of sudden cardiac death in 4-6yr olds reported in homozygous.  Heterozygous cases still important – 100X coronary risk age 20-40yrs…

Diagnosis

Diagnosis in childhood could save 50 healthy life years!!!  Dutch cascade screening since 1994 stopped last year. Only 1/3 of known paed cases came clinically, hence big gap in case finding.

Simon Broome criteria – (else use Dutch system) distinguishes Definite FH vs Possible.

  • Definite = DNA pos for known mutation, else tendon xanthomata (personal or 1st or 2nd deg relative) plus cholesterol as below.
  • Possible = cholesterol concentrations as below PLUS:
    • Family history of myocardial infarction: aged younger than 50 years in second-degree relative or aged younger than 60 years in first-degree relative.
    • Family history of raised total cholesterol: greater than 7.5 mmol/l in adult first- or second-degree relative or greater than 6.7 mmol/l in child, brother or sister aged younger than 16 years.

Cholesterol cut offs for Simon Broome

Total cholesterol LDL-C
Child/young person > 6.7 mmol/l > 4.0 mmol/l
Adults > 7.5 mmol/l > 4.9 mmol/l

Refer both definite and possible cases for DNA testing. Plus there are age/sex specific cholesterol cut offs for relative of a known case where DNA is negative.  NICE standard is that children with possible FH should be offered diagnostic tests by age 10.

Given how prevalent use of statins is now, it’s harder to get a positive family history! So history of grandparents more important! 10% have no family history

Only 4% of heterozygotes have xanthomas (can be in buttock cleft, but only look if found elsewhere!). Arcus at 6 oclock in children, all round in adults. Palpable in Achilles tendon rather than seen? Pain in achilles often reported! Resolve with treatment.

Management

NL guidelines – 5-7yr diet etc only.  Diet with plant sterols can drop LDL by 7%

Over 10yrs, treatment (high dose, low dose, combination) depends on mutation and LDL. Most experience with pravastatin.

LDL apheresis as treatment.

Excellent safety and tolerance of statins. Significant reduction within 2 years.

Like any regular medication, compare it to toothbrushing.  Do both at the same time!

Most cardiologists don’t consider FH when high cholesterol found. Nurses? Via labs?

Check growth, puberty, healthy lifestyle. Update family pedigree, contraception.

Smoking confers massive additional risk.  Albert Wiegman has had a 5yr old admitting to smoking…

Treating from age 6.

Outcome

10yr follow up submitted – mean age 24yrs. 7 already older than the age their parent had event. LDL still higher than sibs.

 

Boys have higher risk of cardiac death then girls, but smoking gives girls worse risk than boys.

Intima media thickness – increases year on year, so earlier treatment the better?  Even before age 8 significantly different from non FH.

 

In NICE audit, majority of children not on treatment, and being seen in adult lipid clinics.

No evidence that low fat diets etc are affecting growth (limited numbers so far).

Homozygous FH being recommended as rare disease, so deserving of national specialist service.

 

 

 

Peanut allergy

Allergy, General paediatrics

See also Prevention, pregnancy, EAT/LEAP studies and immunotherapy.

One of the most common food allergies, and a frequent cause of anaphylaxis.  Peanut is technically a legume, although there is cross-reactivity with tree nuts so often included when people talk about “nuts”.  Always consider if there are potentially other allergies to lentils, sesame, tree nuts eg cashew etc.

Also known as groundnut or monkey nut.

[Gary Stiefel, Leicester Royal, BSACI guideline peanut allergy]

Diagnosis

Wide range of potential peanut proteins.  In US study, vast majority were Ara h1/2 positive, but European more diverse. h1, h2, h3 most common for systemic reactions.  You would think testing with whole peanut would be more sensitive but component testing probably more sensitive and specific than total IgE – but not better than skin prick testing.

peanut allergy diagnosis BSACI 2017With a decent history, SPT >3mm or IgE >0.35 sufficient.

Before proceeding to a hospital challenge, footnote suggests either 2 negatives, or else both IgE and SPT negative.

Distinguish Pollen Food Syndrome – ie older, rhinitis, oral allergy symptoms with nuts/fruit. These kids will have a milder allergy.  Hazelnut mostly (Cor a1) but almond, walnut too. But can coexist with more severe allergy! Doing grass/birch pollen would support diagnosis, doing components might help assess prognosis. If history unclear, but positive IgE/Skin prick test then do components h2 and h8 (list of different cut offs for different commercial products given, with related specificity/sensitivity, just says positive/negative in flow chart). Footnote suggests adding Ara h 1, 3 and 9 as also suggest primary peanut allergy even if Ara h 2 neg.

Sibling risk 5-9%. Too low to justify routinely screening.  If family likely to just avoid forever, living in fear, then consider SPT to encourage home challenge!?

Prognosis

Up to 20% will outgrow, usually before age 8. Review may not be necessary if PFS only.  Follow up is essentially about education.  Testing can be done periodically, depending on resources.

In a study of adults coming to allergy clinics, 10% of peanut allergic turned out not to be.  Partly this would have been because the diagnosis was wrong (many had never actually reacted to peanut in the past).  Having eczema meant you were more likely to still be positive on testing.  Having asthma and being male made it half as likely you would not be allergic anymore.  But many of the cases described were not formally challenged so these results are of limited value.  [Poster at AAI 2021, Rima Rachid]

Avoidance

Difficult, as often used in biscuits, chocolate, ethnic foods eg satay.

As for any food allergy:

Peanut needs to be specified on food labels under UK/EU law.

Precautionary labels – impossible to eliminate risk. Often these “may contain” warnings and similar just say “nuts” without specifying whether the risk is from peanut or a tree nut (the company may be able to give further information if you enquire directly). 

Snack foods with precautionary labels are higher risk eg biscuits, cakes [Helen Brough].

Balance between convenience and risk (probably a very small risk, as many families ignore these warnings to some degree).  Stratify risk according to type of food, previous reactions, threshold, asthma, illness, time of day, location etc. Crossing the road metaphor – choose a safe place!

Should you avoid all nuts?  Some kids will be allergic to other (tree) nuts, but not all.  Andrew Clark reports v low rate of accidental reactions, 3%, with avoidance of all nuts. But increases quality of life to be allowed other nuts!  Risk assessment for each individual person!

Peanut oil

Probability of any reaction to refined peanut oil is remote (Blom et al, 2017). Little evidence that anyone has ever reacted to refined peanut oil. Code of practice is that presence of UNREFINED peanut oil should be declared on bottles of oil (UK and Europe).

But peanut oil, even if refined, still has to be declared on food labels.  Beware unrefined oil in ethnic foods.  Peanut oil also found in some medicines eg vitamins, antibiotic creams.

Some suspicion that peanut oil in cosmetics and pharmaceuticals might lead to sensitization and subsequent peanut allergy, even if not enough peanut protein to cause a reaction in an allergic person. So advice is avoid if you have a strong family history of allergy.

Immunotherapy

See Peanut immunotherapy.