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DAVAO DOCTORS COLLEGE Gen. Malvar St., Davao City BACHELOR OF SCIENCE IN NURSING Case Presentation of ALLERGIC RHINITIS Presented to the Nursing Clinical Instructor of Davao Doctors College In partial Fulfillment of the Requirements in Nursing Care Management 103 Christine Joy Catacata, Harlene Climaco, Dinalyn Dalayap, Angelika Dublas, Katreena Anne Dumapias, Art Benedict Esteves
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Page 1: ALLERGICRHINITIS.FINNEW

DAVAO DOCTORS COLLEGE

Gen. Malvar St., Davao City

BACHELOR OF SCIENCE IN NURSING

Case Presentation of

ALLERGIC RHINITIS

Presented to the Nursing Clinical Instructor of

Davao Doctors College

In partial Fulfillment of the Requirements in

Nursing Care Management 103

Christine Joy Catacata, Harlene Climaco, Dinalyn Dalayap,

Angelika Dublas, Katreena Anne Dumapias,

Art Benedict Esteves

August 2015

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TABLE OF CONTENTS

A. Objectives

I. General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . i

II. Specific . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . i

B. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ii

C. Definition of Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iv

E. Patient’s Profile

I. Biographic Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

I. Past Health History . . . . . . . . . . . . . . . . . . . . . . . .. . . .1

II. Present Health History . . . . . . . . . . . . . . . . . . . . . .. . . .2

III. Family History (with Genogram) . . . . . . . . . . . . . . .. . . 3

F. Review of Anatomy and Physiology.. . . . . . . . . . . . . . . . . .. . ..4

G. Comprehensive Health Assessment . . . . . . . . . . . . . . . . . . . . . 7

H. Pathophysiology

I. Etiology (Tabular) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .15

II. Symptomatology (Tabular) . . . . . . . . . . . . . . . . . . . . . . . 18

III. Schematic Diagram . . . . . . . . . . . . . . . . . . . . . . . . . . . . .20

IV. Narrative . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

I. Course in the ward/ Treatment/ Interventions

I. Medical Management

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1.) Doctors Progress Notes . . . . . . . . . . . . . . . . . . .. 24

2.) Laboratory/ Diagnostic Examinations. . . . . . . . . . .27

3.) Pharmacologic (Drug Study) . . . . . . . . . . . . . . . . .37

II. Surgical Management (Tabular) . . . . . . . . . . . . . . . . . . . . 57

III. Nursing Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58

J. Discharge Plan

I. METHODS Format . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .74

K. Bibliography

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E. PATIENT’S PROFILE

Name: Jumamil, Nenita Dimalaluan Hospital Number: 00261058

Address: B7, L25, P2, Aguila St., Patient Number: IP15-008715

Awang Subd, Bacaca, DVO

Age: 61Y3M3D Attending Physician: Dr. Batalla

Sex: Female

Nationality: Filipino

Civil Status: Married

Religion: Christian

Occupation: Govt. Employee

Chief Complain: Cough and Fever

Admission Diagnosis: Urticaria, SVI, allergic rhinitis; ess hpn

Past Health History:

Patient was known having thyroid disorder, essential hypertension that started 11

years ago. She is taking Losartan 50mg, once per day as her maintenance. She

had undergone TAHBSO in the early 1990’s as well as Laparoscopic

Cholecystectomy last 2013. She had bronchial asthma that started last year and

taking Avamyst as her emergency drug but effect has poor compliance. She has

allergy in Levofloxacin.

3 days prior to admission, patient had onset of fever with a temperature of 38.

4*C associated with productive cough with yellow phlegm seen. Patient self

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medicated Paracetamol 500 mg/tab and Sinecod(Ambroxol) which only provided

temporary relief. Patient also noticed muscle pain on the same day, medicated

with Norgesic Forte, still temporary relief was provided. On the night prior to

admission, patient still have persisted condition, hence the admission.

Present Medical History: During rounds, Patient was received lying on bed in

moderate high back rest. With ongoing #1 PNSS @ 80cc/hr at her left

metacarpal vein. Patient was alert, conscious and coherent during interaction

and can clearly verbalize her thoughts and concerns. Non productive cough was

observed. Patient still complained about chest pain during coughing.

Family History: On the paternal side,

Current Lifestyle:

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F. ANATOMY AND PHYSIOLOGY

Anatomy of the nasal cavity

The nasal cavity extends from the external opening, the nostrils, to

the pharynx (the upper section of the throat), where it joins the remainder of the

respiratory system. It is separated down the middle by the nasal septum, a piece

of cartilage which shapes and separates the nostrils. Each nostril can be further

divided into roof, floor, and walls. The nasal cavity can be divided into the

vestibule, respiratory and olfactory sections.

Nasal vestibule

The nasal vestibule is the dilated area at the nostril opening.

Respiratory section

The respiratory section of the nasal cavity refers to the passages through which

air travels into the respiratory system. The respiratory section of each nostril

contains four conchae (protrusions or bumps) which are also referred to as

turbinate bones or lobes and are covered by the nasal mucosa. Underlying these

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conchae are meatuses (passages to interior body structures). The meatuses of

the nasal cavity connect to the paranasal sinuses.

Olfactory region

The olfactory receptors (receptors for smell sensations) are found in this section

of the nasal cavity. Bowman’s glands are also found in this section of the nasal

cavity.

Surrounding structures

Para-nasal sinuses

The nasal cavity is surrounded by a ring of paranasal sinuses and meatuses in

the nasal cavity connect to these structures. The sinuses develop as outgrowths

of, and drain into, the nasal cavity. The mucosa of the sinuses connects to the

nasal mucosa.

Nasolacrimal ducts

Nasolacrimal ducts are the ducts which connect the lacrimal (tear) ducts in the

eye to the nasal cavity.

Oral cavity

The nasal cavity is separated from the oral cavity (interior of the mouth) by the

hard palate.

 

Anatomy of the nasal mucosa

The nasal mucosa, also called respiratory mucosa, lines the entire nasal cavity,

from the nostrils (the external openings of the respiratory system) to the pharynx

(the uppermost section of the throat). The external skin of the nose connects to

the nasal mucosa in the nasal vestibule. A dynamic layer of mucus overlies the

nasal epithelium (the outermost layer of cells of the nasal mucosa).

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The initial one-third of the nasal cavity is lined by stratified squamous

epithelium (smooth epithelium consisting of flat surfaced cells), several cell layers

thick. The outmost layer of squamous cells overlies a layer of proliferative cells

(cell which divide and replicate to form new cells) which is attached to a

basement membrane, a network of tough fibres which supports the epithelium.

The posterior two-thirds of the cavity is lined with pseudo-stratified columnar

ciliated epithelium (a type of epithelium in which cells arrange themselves in

columns and project tiny hairs called cilia) containing goblet cells (mucus

producing cells), and which overlies a basement membrane.

The nasal sub-mucosa underlies the basement membrane. This layer is made up

of glands which secrete watery substances and mucus, nerves, an extensive

network of blood vessels and cellular elements like blood plasma. The entire

mucosa is highly concentrated with blood vessels and contains large venous-like

spaces; bodies which have a vein-like appearance and swell and congest in

response to allergy or infection.

Mucosa of the olfactory system

Unlike other nasal mucosa, the epithelium of the olfactory system does not

project cilia. This mucosa contains nerves which connect to the olfactory nerve.

Physiology of the nasal cavity

The nasal cavity functions to allow air to enter the respiratory system upon

respiration. Structures within the cavity regulate the flow of air and particles it

contains. The olfactory region of the nasal cavity regulates the sense of smell.

Conchae (turbinate bones)

The conchae (turbinate bones) of the nasal mucosa expand the total surface

area of the mucosa and create turbulence in air entering the respiratory passage.

This causes air to swirl as it moves through the nasal cavity and increases

contact between infiltrating air and the nasal mucosa, allowing particles in the air

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to be trapped before entering other parts of the respiratory system (e.g. the

lungs).

Olfactory system

The olfactory system functions to process sensory information related to smell.

Bowman’s glands

Bowman’s glands secrete the majority of the mucus which overlies the nerves of

the olfactory system. They also secrete the pigment which gives this mucus its

yellow colour. Mucus secreted by these glands dissolves odours as they enter

the nose, enabling them to interact with the olfactory receptors.

Surrounding structures

Paranasal sinuses

The paranasal sinuses function to resonate speech and produce mucus which

enters the nasal passage. Other functions of the sinuses are not well understood.

Nasolacrimal ducts

The nasolacrimal ducts drain tears from the lacrimal (tear) ducts of the eyes, to

the nasal mucosa.

Physiology of the nasal mucosa

The nasal mucosa plays an important role in mediating immune responses to

allergens and infectious particles which enter the nose. It helps

prevent allergens and infections from invading the nasal cavity and spreading to

other body structures, for example the lungs. The mucus secreted by and

which lines the mucosa provides a physical barrier against invasion by

pathogens (harmful microorganisms). It is sticky and traps pathogens when they

enter the nasal cavity.

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Trapping pathogens enables components of the mucus to attack and destroy the

microbes. For example, an antibody called IgA prevents pathogenic microbes

from attaching to cells of the mucosa and in doing so prevents them from

invading the cells. Lysozyme (enzymes which breakdown bacteria) is another

component of the nasal mucus. It works to degrade pathogenic microbes. The

epithelial or outer cells of the nasal mucosa are constantly being worn away and

replaced by new cells from the underlying proliferative (regenerative) layer. This

provides additional protection as it ensures that pathogens which do manage to

invade the outer cell layer are removed as the epithelial cells are sloughed off.

However, in some individuals abnormal responses of the nasal mucosa occur

and immune responses are mounted against allergens which the body does not

usually recognise as pathogenic and thus does not usually mount an immune

response to. In these individuals the mucosa, which usually functions to protect

the body from invading microorganisms, is also thought to play a role in the

pathological allergic response referred to as a type 1 hypersensitivity reaction.

This type of allergic response is mediated by B cells (antibody producing cells of

the immune system), which begin producing immunoglobulin type E (IgE).

Epithelial cells

Epithelial cells form the epithelium or surface layer of the nasal mucosa.

Historically nasal mucosa epithelial cells were thought to simply:

1. Provide a physical barrier to the invasion of infectious microorganisms and

allergic particles;

2. Work in conjunction with mucus glands and cilia to secrete and remove

mucus and foreign particles from the nasal cavity.

However, recent evidence suggests the functions of epithelial cells are much

broader and that they also regulate immune responses which occur if the

physical barrier fails and pathogens infiltrate cells of the nasal mucosa. The

epithelium contains antigen-binding proteins (protein chain sections of an

antibody that recognise and join to antigens). These proteins are involved in the

processes through which allergens are presented to antigen presenting cells.

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These cells are responsible for introducing pathogens to the T-lymphocyte cells

(T cells) which in turn function to mount an immune response to destroy

allergens presented to them. Antigen presenting cells capture antigens as they

enter the body and present them to naïve T cells. That is; T cells that have not

previously encountered, and therefore do not yet recognise as pathogenic, the

specific antigen being presented. Thus, antigen-binding proteins in the epithelium

catalyse the series of processes through which T cells begin to recognise and

respond to allergens.

Epithelial cells also release factors which enhance inflammatory responses. The

most important of these factors are cytokines (proteins which regulate the

duration and intensity of immune responses). Allergens can directly activate the

epithelial cells to produce an inflammatory response, or the epithelial cells may

mount such a response in response to T cell recognition of the antigen. Epithelial

cells also appear be involved in the IgE-producing processes which perpetuate

allergic responses.

Endothelial cells

Endothelial cells are cells which line the walls of the arteries that feed the nasal

mucosa. They are also involved in allergic responses. They primarily function to

attract leukocytes (white blood cells) circulating in the blood to the site of

inflammation.

Mucus glands

Glands in the nasal mucosa produce a sticky mucus which moistens air and

traps bacteria as they enter the respiratory passage.

Cilia

Cilia or small hairs which project from the epithelium and line the nasal mucosa

create motions which drain mucus from the nasal passage to the throat from

where it is swallowed and digested by stomach juices. The activity level of cilia is

dependent on temperature and in cold temperatures cilia become less active.

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Mucus may accumulate in and drip from the nostrils (runny nose) in these

conditions. Infectious particles and allergens also impair cilia activity and can

lead to symptoms such as a congested or runny nose.

Underlying blood vessels

The thin walled veins on which the nasal mucosa rests function to warm air

entering the respiratory passage. Due to the high concentration of blood vessels

in the nasal cavity, changes in these blood vessels contribute to nasal

congestion. For example, constriction of these blood vessels decreases airway

resistance, making it easier for air to enter the respiratory system. The nasal

nerves also regulate the congestion response.

Nerves

Innervation of the nasal mucosa is regulated by the trigeminal and maxillary

nerves which also provide sensations to other areas of the face. The trigeminal

nerve regulates sensations including touch, pressure and temperature in the

nose, while sympathetic and parasympathetic innervation (innervation which

controls involuntary movements like constriction and dilation of the blood

vessels) occurs via the maxillary nerve. The different types of nerves found in the

nasal cavity and mucosa have various functions. For example, constriction of

blood vessels which feed the nasal cavity is regulated in part by the sympathetic

nervous system, while the parasympathetic nervous system plays a role in

regulating secretions of mucus from nasal glands. Other nerves in the nasal

cavity influence the dilation of blood vessels, nasal secretions, inflammation and

interactions between nerves and the mast cells which mediate allergic

responses.

Venous-like spaces

Venous-like spaces found throughout the nasal mucosa swell and become

congested in response to allergens and infection.

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H. PATHOPHYSIOLOGY

I. ETIOLOGY

PREDISPOSING FX (✔) JUSTIFICATION

Pneumonia ✔ Pneumonia is found among people with Allergic

rhinitis, especially people who are female, 50-59

old, also have Allergic rhinitis, and take

medication Singulair. We study 86 people who

have Pneumonia and Allergic rhinitis from FDA

and social media. (http://www.ehealthme.com/cs

/allergic+rhinitis/pneumonia)

Bronchial Asthma ✔ Rhinitis and asthma have been evaluated and

treated as separate disorders, but recent

advances in the understanding and knowledge of

the underlying processes have moved current

opinion towards the concept of unifying the

management of these disorders. The “united

airway disease hypothesis” proposes that upper

and lower airway diseases are both

manifestations of a single inflammatory process.1

The upper and lower airways interface more than

the air and the blood but regulate most of the

human body interactions within its environment.

Living an entire life with a clean and silent two-

step air filter which is not replaceable suggests

abilities of plasticity, regulation, teaching, renewal

and local to systemic control functions. Togias A.

Rhinitis and asthma: evidence for respiratory

system integration. J Allergy Clin Immunol

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2003;111:1171–84.

Age ✔ Structural changes in the nose associated with

aging, predisposes the elderly to rhinitis. It would

be safe to say that the many changes that occur

in the connective tissue and vasculature of the

nose predisposes aging individuals to chronic

rhinitis making the percentage of the elderly with

nasal symptoms significantly higher than the

general population. (Curr Allergy Asthma Rep.

2006 Mar; 6(2):125-31.)

Genetic ✔ Allergic rhinitis is an atopic (genetic) condition

which often runs in a family. Those with a family

history of the disorder have a greater likelihood of

experiencing the condition themselves. Some

evidence suggests that irregular IgE responses

and sensitisation to specific environmental

allergens is genetically determined, although the

genetic components of the allergic rhinitis are not

well understood. Specific genes which might

pass on the irregular IgE response trait have not

been identified. . Maternal factors (e.g. exposures

of the mother during pregnancy) are also known

to influence the likelihood of allergy in the

offspring. (Kneepkens CM, Brand PL: Clinical

practice: Breastfeeding and the prevention of

allergy. Eur J Pediatr 2010, 169:911-917.)

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PRECIPITATING FX (✔) JUSTIFICATION

Air pollution ✔ In addition to previously described allergens,

exposure to high levels of pollutants including

oxides of nitrogen, ozone, sulfur dioxide, black

smoke– large particulate matter, small

particulates, carbon monoxide, and volatile

organic compounds have been considered as

important contributing factors in both

exacerbation and etiology of allergic airway

diseases (Utell and Samet 1993; Devalia et al

1994; Krishna et al 1995)

Lack of proper Hygienic

Measures

✔ According to the hygiene hypothesis, infections

with viruses and perhaps other intracellular

organisms also influence the developing immune

system: the T-cell responses to these infections

generate Th1-like cytokines such as IL-12 and

IFN-γ that down-regulate Th2 responses. Thus,

the core of the hygiene hypothesis is based on

the observations that Th1 responses induced by

microbial stimulation can counterbalance

allergen-induced Th2 responses. (Matricardi et al

1997, 2000)

Nutrient Intake ✔ There has not been much data published on the

effects of diet on symptoms of seasonal allergies

yet, however I have observed in my medical

practice that the change to a high-nutrient diet is

accompanied by a wide variety of benefits,

including an improvement in allergy symptoms. I

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have seen many allergic patients slowly reduce

the severity of their allergies and over time many

became entirely non-allergic. When you follow a

high-nutrient diet, you are creating an

environment in your body that promotes proper

immune function and regulation of the

inflammatory response, which may help to blunt

allergy symptoms. (Nagel G, Nieters A, Becker N,

et al: The influence of the dietary intake of fatty

acids and antioxidants on hay fever in adults.

Allergy 2003, 58:1277-1284.)

Ownership of pets ✔ Pet ownership was found to markedly increase

the risk of sensitization to pets (Al-Mousawi et al

2004). The prevalence of asthma, rhinitis, and

skin allergy was significantly more common in

families with animals than in those without (Bener

et al 2004). The secretary proteins from a large

number of animals carry or contain powerful

allergens capable of causing severe

hypersensitivity reactions. (Nolte H, Backer V,

Porsbjerg C: Environmental factors as a cause

for the increase in allergic disease. Ann Allergy

Asthma Immunol 2001, 87:7-11.)

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II. SYMPTOMATOLOGY

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III. SCHEMATIC DIAGRAM

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IV. NARRATIVE

In allergic rhinitis, your body overreacts to some stimulus in the

environment that stimulus is called an allergen. The most common culprit is

pollen. Pollen can come from trees or grass. Pollen also tends to be seasonal. In

other words, some types of pollen are out in the type of environment with

different temperature and that gives rise to yet another term that’s synonymous

with allergic rhinitis or seasonal allergies. Basically anything that can get into the

air that you can inhale can act as an allergen to somebody who suffers from

allergic rhinitis. When allergen goes into the nose and that allergen is going to

come into contact with this mast cell over here. Being a mast cell or basophil, on

its surface it has a particular protein that’s shaped like a Y and that protein is

called an Immune Globulin which is shorten to “Ig” and this particular type of

immune globulin is called IgE. This pollen is going to get bound by this IgE

molecule, and that IgE molecule, just a protein sitting on the surface of this

basophil is going to alert that cell to its presence. In a person with allergic rhinitis

this cell over reacts and it overreacts big time. And when it sees that pollen grain

it starts letting out little molecules into its environment that tell all the celld around

it to get excited as well. So this whole group of nasal mucosa gets overreacted.

The most common type of molecule that gets excited is called histamine.

Histamine is going to cause all sorts of problems with inflammation and it can be

really severe that the mucosa can thicken up big time and get really engorged

and edematous, swollen that happens all through out the nose because these

basophils or mast cells arent just sitting in one particular area but they are

scattered everywhere. In adittion on being swollen, this mucosa is going to start

to produce mucus, the mucus is going to drip down along the turbinates that is

going to drip down the sides of the nose. Its going to pull on the base of your

nasal cavity, as this mucus pulls down in your nasal cavity it’s going to head

down towards your throat so you can cough up as well. Also as the mucosa

swells up, it can swell the nasolacrimal duct and shut, leading to watery eyes.

Also when the eustachian tube gets swollen bad enough, it can block the tube

and cause fluid to back up and that’s going to lead to symptoms that are stiffness

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and decreased ability to hear. Ofcourse theres also nerves in your nose that

ultimately end in your brain and as they get inflamed with all the process that’s

happening in your nose, they become irritated and send signals to your body

particularly the signal to sneeze and then swelling continues to get bigger and

more pronounce and more pronounced and it can actually completely block off

this entire nose. When that happens air cant get by and when that happens

breathing will become a problem.

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COURSE IN THE WARD

LABORATORY TESTS

URINALYSIS

EXAMINATION RESULT RANGE REMARKS/ JUSTIFICATION

RBC 229^/uL 0-11 High. Some crenated

RBC

Conventional

41^HPF 0-2 High

CBC,PLT

EXAMINATION RESULT RANGE REMARKS/ JUSTIFICATION

Heemoglobin 142^g/L 120-140 High

Neutrophils 0.50 0.55-

0.65

Low.

Lymphocyte 0.32 0.35-

0.45

Low.

Monocyte 0.14 0.6-0.12 High.

Absolute

Monocyte

0.9 0.0-0.8 High.

CHEST XRAY

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INTERPRETATION:

A comparison with the radiograph dated Feb 19,2015 discloses the same pleural

thickening in the left lateral hemithorax. Both lungs are clear lungs. The lateral

costrophenic sinuses are sharp. Heartsize is within normal limits. The

configuration is unremarkable. Pulmonary vascularity is normal. Hili are not

enlarged. Degenerative joint changes are again appreciated.

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MEDICATIONS

DATE MEDICATION TIME

July 27, 15 Losartan 50mg, 1tab, OD 8AM

Xanor 250mcg, OD 9PM

Montelukast+Levocitirizine10/5mg

1tab,OD, HS

9PM

Levopront 10mL, TID, PO 8AM, 2PM,8PM

PRN MEDICATIONS

DATE MEDICATION TIME

July 27, 15 Paracetamol 1tab (for fever) PRN

Norgesic Forte 1tab (for body pain) PRN

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K. BIBLIOGRAPHY

BOOKS:

1 Al-Mousawi MS, Lovel H, Behbehani N, et al. Asthma and sensitization in a community with low indoor allergen levels and low pet-keeping frequency. J Allergy Clin Immunol. 2004;114:1389–94.

2 Apter AJ, Gent JF, Frank ME. Fluctuating olfactory sensitivity and distorted odor perception in allergic rhinitis. Arch Otolaryngol Head Neck Surg. 1999;125:1005–10.

3 Ashmore M. Human exposure to air pollutants. Clin Exp Allergy. 1995;25(Suppl 3):12–22.

4 Baldini M, Lohman IC, Halonen M, et al. A polymorphism in the 5′ flanking region of the CD14 gene is associated with circulating soluble CD14 levels and with total serum immunoglobulin E. Am J Respir Cell Mol Biol. 1999;20:976–83.

5 Barnes KC, Neely JD, Duffy DL, et al. Linkage of asthma and total serum IgE concentration to markers on chromosome 12q: evidence from Afro-Caribbean and Caucasian populations. Genomics. 1996;37:41–50.

6 Bener A, Mobayed H, Sattar HA, et al. Pets ownership: its effect on allergy and respiratory symptoms. Allerg Immunol (Paris) 2004;36:306–10

7 Bodner C, Godden D, Seaton A. Family size, childhood infections and atopic diseases. Thorax. 1998;53:28–32.