Eczema genes and exposure to cats

Behind the Headlines

Tuesday June 24 2008

The FLG mutation has been estimated to account for about 11% of eczema cases

“Own a cat and run the risk of eczema”, warns the Daily Mail today. They say that a study looking at 800 British and Danish babies has found that “those with mutations in a certain skin protein gene were twice as likely to get eczema in their first year. If they lived with a cat they were almost certain to develop it”. The article quoted the author of the research, Dr Hans Bisgaard, as saying, “If you haven't got the mutation, it doesn't matter if you have a cat. But if you have the mutation, a cat has an effect.”

This study looked at the interaction of genes and environment in the development of eczema in the first year of life. Limitations to the methods of the study, including its small size, means that this research should be considered as preliminary. Further studies will be required to confirm these findings and quantify this possible risk.

In addition, the FLG mutation has been estimated to account for about 11% of cases of eczema. Therefore, these findings will not apply to the majority of people with eczema.

Where did the story come from?

Dr Hans Bisgaard and colleagues from the Danish Paediatric Asthma Centre, and universities in the UK carried out the research. The research article was based on two cohort studies, the Copenhagen Study on Asthma in Childhood (COPSAC) and the Manchester Asthma and Allergy Study (MAAS). COPSAC was funded by the Lundbeck Foundation, the Pharmacy Foundation of 1991, the Augustinus Foundation, and the Danish Medical Research Council. MAAS was funded by the Moulton Charitable Trust and Asthma UK. The study was published in the peer-reviewed open-access medical journal PLoS Medicine.

What kind of scientific study was this?

The study used data from two cohort (group) studies to look at the interaction of genes and environment in the development of eczema. The two group studies were from Denmark and the UK, and were called the Copenhagen Study on Asthma in Childhood, and the Manchester Asthma and Allergy Study.

In the Copenhagen study, the researchers obtained blood samples from 379 one-month-old babies, who were considered to be at high risk of developing eczema because their mothers had asthma. The children were tested to see whether they had one of two mutations known to increase the risk of developing eczema, in either copy of the Filaggrin (FLG) gene. The FLG gene encodes a protein that helps the skin form barriers against water loss and exposure to the environment. The children’s mothers were asked whether there was a pet in the home when the child was born. The parents also took vacuum samples from the children’s beds at one year to test for dust mites, and cat and dog allergens (substances that can provoke an immune reaction). The children were examined by a clinician at one month, and at six-month intervals afterwards to determine whether they had eczema.

In the Manchester study, the researchers enrolled 503 children before birth, and followed them up until age five. These children did not have any particular risk factors for developing eczema. This study collected similar information to the Copenhagen study, but the dust samples were collected from the living room (presumably by the parents) rather than the children’s beds, and eczema was assessed by a validated parental questionnaire rather than by clinical examination of the child.

In both groups, the researchers looked at the risk of developing eczema among children with and without the FLG gene, with and without the different environmental exposures, and with or without various combinations of these factors. Because of differences in study design, the researchers did not pool data from the two studies.

What were the results of the study?

Of the 379 children in the Copenhagen study, 105 (28%) developed eczema before their first birthday. Information about pets present in the home at time of birth showed that 265 homes (75%) did not have a pet, 38 (11%) had a cat, 37 (11%) had a dog, and 11 (3%) had both. Information on pet ownership was not available for 28 children.

The blood samples showed that 38 children (10%) had mutations in the FLG gene and had provided information about pet ownership. Babies with an FLG mutation were about two to three times as likely to develop eczema in the first year of their life than those without the mutation. However, after this age, there was no significant increase in the risk of developing eczema with the mutations.

Of the 503 children in the Manchester study, 187 (37%) were reported by their parents to have developed eczema; 50 (10%) had mutations in the FLG gene. It made similar findings with regards to the increased risk of eczema with the FLG mutations.

Children with the mutation who were exposed to cats were more likely to develop eczema in both studies. However, the extent of this risk differed, with risk increasing about 11-fold in the Copenhagen study, compared with about 4-fold in the Manchester study. Exposure to cats among children without the FLG mutation did not affect the risk of developing eczema. Although exposure to dogs reduced the risk of eczema in the Copenhagen study, this reduction did not quite reach significance after other factors were taken into account. There was no association between dog ownership and eczema in the Manchester study. Exposure to mite allergens did not significantly alter the risk of eczema, regardless of the presence or absence of the FLG mutation in either study.

What interpretations did the researchers draw from these results?

The researchers concluded that the two groups had shown an interaction between the FLG mutation and exposure to cats from birth in the risk of developing eczema in the first year of life. They suggest that individuals with the FLG mutation “may need to avoid cats but not dogs in early life.”

What does the NHS Knowledge Service make of this study?

This study has some limitations, which should be taken into account when interpreting its results:

  • As with all studies of this type, where people self-elect into groups rather than being randomly allocated, there may be differences between the groups other than the exposures of interest responsible for the results. This study did not assess or adjust for any confounding factors that might affect the risk of developing eczema.
  • Some of the analyses were based on very small numbers of children, which can make the results more susceptible to chance. For example, in the Copenhagen study, only five children with eczema had a cat in their home and carried an FLG mutation.
  • The Manchester and Copenhagen studies used slightly different methods, therefore their results may not be comparable.
  • It is not clear whether the assessments of eczema were carried out blinded to either genetic status or pet exposure status. This may have affected the results.
  • The FLG mutation is estimated to account for about 11% of cases of eczema. Therefore, these findings will not apply to the majority of people with eczema.

In light of these limitations, the results should be interpreted with caution. Although they indicate a potential interaction between genes and environment, the exact amount by which the co-existence of FLG mutations and cat ownership increases the risk of developing eczema in early life is unclear. Further studies will be required to confirm these findings and quantify this risk.

 

Sir Muir Gray adds...

The logic is good, but don’t kill the cat yet.

 

Analysis by Bazian

Edited by NHS Choices

Links to the headlines

Cats increase risk of eczema in some babies. The Daily Telegraph, June 24
2008

Own a cat and run the risk eczema, researchers warn. Daily Mail, June 24
2008

Cats 'spark eczema in vulnerable'. BBC News, June 24 2008

Study suggests cat and eczema link. Channel 4, June 24 2008

Links to the science

Bisgaard H, Simpson A, Palmer CNA, et al. Gene-Environment Interaction in the Onset of Eczema in Infancy: Filaggrin Loss-of-Function Mutations Enhanced by Neonatal Cat Exposure. PLoS Med 2008; 5(6): e131

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