Patient name: J.S.

Date of Presentation: 6/20/16, 3:30pm

Setting: CHAM ED
Informant: Patient
Accuracy of Information: Reliable
CC: pain with breathing
HPI: J.S. is a 20 year old Hispanic male with PMH of asthma. He presents
with dyspnea/SOB, wheezing, and expiratory pleuritic chest pains that are
described as a dull achy localized lower chest and back pain. Pain is a 8/10.
His dyspnea/SOB began 2 weeks ago while he was swimming in a pool. This
was followed by a 2 week course of severe nonproductive coughing and
wheezing. Patient says that he felt like something was stuck in his chest.
During this time, physical exertion would exacerbate his symptoms while
resting would make them better. He has not had an asthma attack in 3 years
and, therefore, did not have any albuterol at home to take. Today he began
having expiratory pleuritic chest pains which caused him to come to the ED.
He has had no associated symptoms of fever, chills, night sweats, rhinorrea,
soar throat, ear pain, rashes, vomiting, diarrhea, constipation, or headaches.
He reports no recent travel or known sick contacts.
Initial ED course: upon admission patient was given albuterol 2.5 mg/3 mL
nebulizer solution (FULL) 5 mg (every 20 min PRN), but it was discontinued
because it made the patient feel jittery. Patient was then given a course of
the following:
prednisone tablet 60 mg (once)
ipratropium 0.02 % nebulizer solution 2.5 mL (every 20 min PRN)
levalbuterol 1.25 mg/3 mL nebulizer solution 3 mL (once)
ibuprofen tablet 600 mg (once), for pain.

After administration of medications, patients wheezing, coughing, and SOB

resolved and pain improved. A CXR was ordered.
PMH:
-Asthma, last attack 3 years ago
-Regular health care provider, Margaret S Rosenberg, MD
PSH:
-Left knee surgery for a torn MCL, age 17
Medications:
Albuterol HFA (PROVENTIL HFA;VENTOLIN HFA) 90 mcg/actuation inhaler
every 4 (four) hours PRN
Allergy:
Sulfa (sulfonamide antibiotics) - rash - 12/07/2015
Birth History:
J.S. was born full term via normal spontaneous vaginal delivery in a hospital
in Bronx.
Prenatal and perinatal courses were uneventful.
Growth and Development:
J.S. appears to have developed and grown well with no social, language, fine
or gross motor deficiencies. Tanner stage 5 in all categories.
School History:
J.S. has received high school diploma and is currently in college majoring in
business.

Immunizations:
Immunizations received:
Influenza

12/08/1998 11/30/2001 10/15/2008 11/10/2010

HepB

04/30/1996 05/30/1996 11/27/1996

DTP

07/03/1996 09/09/1996 11/27/1996

DTP/Hib

08/15/1997

DTap

04/27/2000

Td

07/20/2007

Tdap

11/10/2010 10/22/2012

Hib NOS

07/03/1996 09/09/1996 11/27/1996

Polio

07/03/1996 09/09/1996 11/27/1996 08/15/1997

MMR

05/01/1997 04/27/2000

Varicella

09/10/1998

Meningococcal 10/22/2012
HPV4-Gardasil

11/10/2010 10/22/2012

Immunizations for Hep A, second varicella, third HPV, and pneumococcal

vaccines (PCV13 and PPSV23, these should be given a year apart) should be
scheduled [1.] Otherwise J.S. is up to date.
Immunizations he should have received by age 20. [1]
HPV: should start age 11-12, 3 dose series - 0, 1-2, and 6 months
RV: at 2mo, 4mo, 6mo

PCV: at 2mo, 4mo, 6mo, 12-15mo

Varicella: 12-15mo, 4-6 years
HepA: begin 2-dose HepA vaccine series at 12-23 months, separating 2
doses by 6-18mo

Social History:
J.S. lives in an apartment in the Bronx with his mother and younger sister
(18) and brother (8). His mother works as case manager for helping
homeless people in shelters find homes and supports the family. No smoking
or pets at home. Dad is not in the picture.
HEADSSS:
H: J.S. has a positive relationship with his mom. She cares for him and
is very supportive and is helping him financially get through college.
E: J.S. has a positive attitude towards school, good relationship
teachers, getting good grades, and hopes to go into business.
A: enjoys playing basketball and drawing/art. Spends time with family
D: has taken marijuana in high school but does not anymore. No other
drugs. Does not smoke and drinks alcohol occasionally.
S: Not currently sexually active. In the past has had sex with only one
girl. Engages only in vaginal sex and uses condoms.
S: positive self-esteem. Denies depressed mood or thoughts of suicide
S: safe at home and school. Wears a seatbelt in car.
FH:
-Asthma: mom and maternal grandmother
-Diabetes: both grandmothers

-HTN: maternal grandparents

-Cancer: maternal great aunt
Siblings are healthy and no family history of congenital heart problems.
ROS:
Constitutional: mild weakness and fatigue due to lots of coughing and SOB.
No weight change, fever, chills, night sweats
Skin: no itching, rashes, sores, lumps, moles
Head: no head trauma, headache, visual changes
Neuro: no dizziness, tremors, LOC, unsteadiness
Psych: no thoughts of harm self/others
Eyes: No redness or exudates.
Ears: no ear pain, discharge, hearing loss
Nose: no rhinorrhea, stuffiness, sneezing, itching, allergy
Mouth / throat / neck: no hoarseness, sore throat, trouble swallowing or
swollen neck
Cardiac: dyspnea on exertion but no HTN, murmurs, palpitations, edema
Respiratory: complains of asthma, SOB, wheeze, cough. No sputum,
hemoptysis.
GI: No change in appetite. No nausea, vomiting, diarrhea, constipation,
dysphagia, bleeding, abdominal pain, or jaundice. Normal bowel movement
frequency/change, stool color.
Musculoskeletal: complains of pain in both knee joints. No joint swelling or
muscle weakness. Has mid back pain due to all the coughing
Urinary: normal frequency. No dysuria, hematuria, incontinence, stones, or
infection
Sex: Has sex with women only and vaginally. Always uses condoms.
Currently not sexually active

PE:
Vitals: BP 118/70 mmHg | HR 66 | Temp 98.1 F (Oral) | Resp 21 | SpO2 98%
room air
General: Alert and Oriented. Well groomed. In moderate respiratory distress
and was able to speak in full sentences with difficulty. In bed throughout
interview and physical exam while taking medications for asthma.
Ht 1.86 m (6' 1.23") | Wt 110.8 kg (244 lb 4.3 oz) | BMI 32.03 kg/m2 (96.9%)
Skin: normal color, texture, and moisture. No rashes or petechiae. Scar on R
knee due to surgery.
Head: NCAT
Eyes: Normal sclera and conjunctivae without evidence of anemia,
conjunctival icterus, or injection. PERRLA, EOMI.
Ears: No hearing deficits and tympanic membrane intact bilaterally. No
discharge
Nose: moist mucous membranes. Patent airways. No discharge or polyps
Mouth/Throat: Moist mucus membranes. No lesions, erythema or exudates,
dentition excellent. No tongue deviations. Normal papilla. Throat is clear
Neck: Supple, carotid pulse WNL, midline trachea. No JVD, thyromegaly,
lymphadenopathy, or stiff neck
Spine: no kyphosis
Chest: Expiratory wheezing bilaterally. Subcostal and intercostal retractions.
Nasal flaring. No hyperresonant percussion, dullness to percussion or
decreased breath sounds.
Heart: RRR normal S1, S2. No murmurs, rubs, or gallops
Abdomen: soft NT ND +BS no hepatosplenomegaly or ascites

GU: Tanner stage 5 male, bilateral descended testicles

Extremities: radial and carotid pulse 2+ B/L. Warm and well perfused. No
leg edema or clubbing. Capillary refill < 2 seconds.
Musculoskeletal: FROM in neck, shoulders, elbows, wrists, hands, spine,
hips, knees, ankles, and toes. No joint deformities, swelling, erythema, or
warmth.
Neuro: no cranial nerve deficits. No sensory or motor deficits. Strength 5+
throughout. Biceps, brachioradialis, achilles, and patellar reflexes 2+ B/L
Normal FTN test

Labs: no labs were ordered

Imaging: CXR ordered in the ED: results pending
Summary Statement:
J.S. is a 20 year old Hispanic male with a PMH of asthma, who presents with
acute sudden onset of moderate progressive respiratory distress and severe
constant nonproductive cough for the past 2 weeks, as well as severe
expiratory pleuritic chest pains that began today. He is afebrile, hydrated
and cardiac exam is normal. Results for CXR are pending.
Problem list:
1) Wheezing, cough, SOB (asthma attack) with pleuritic chest pains
2) Pain in both knee joints
3) Immunization update
Differential diagnosis:

Asthma
Pneumonia
Pulmonary embolism

Pneumothorax

Asthma:
Asthma is a reversible hyperresponsive bronchoconstriction of smooth
muscle cells, most often due to allergic stimuli (atopic asthma), where the
airways in the lungs become inflamed, narrow and swell, and can produce
extra mucus, which makes it difficult to breathe [2,3]. In addition,
abnormalities in airway smooth muscle function and airway remodeling in
response to injury appear to add to the effects of airway inflammation [4].
Signs and symptoms of asthma include intermittent dyspnea, cough, chest
tightness and wheezing. These may occur a few times a day or a few times
per week. Also they may become worse at night or with exercise [2]. The
strongest identifiable risk factor for the asthma is atopy or the genetic
predisposition to develop specific IgE antibodies directed against common
environmental allergens [5], while non allergic/atopic causes may include
virus infection, occupational exposure, exercise, and aspirin. Diagnosis of
asthma is usually determined by the history of symptoms, response to
asthma therapy over time, and pulmonary function testing via spirometry.
Spirometry measurements of FEV1 and FVC provide information that is
essential to the diagnosis of asthma [6]. Tests such as CBC allergy tests, and
imaging are not helpful for diagnosis. Imaging will appear normal. CBC and
allergy test, however may show elevated eosinophil count and positive
allergy test due to allergic triggers. There is no cure for asthma; rather
medication is used to relieve symptoms. Treatment is divided into two
categories: short-relief medications used to treat acute symptoms and longterm control medications used to prevent further exacerbation. For acute
symptoms short-acting beta2-adrenoceptor agonists (SABA), such
as salbutamol (albuterol) are the first line treatment for symptoms.
Anticholinergics, such as ipratropium bromide, offer additional benefit when
used in combination with SABA in people with moderate or severe symptoms
[3]. For long-term control corticosteroids are the most effective treatment
available. Inhaled forms (beclomethasone) are used except in the case of
severe persistent disease, in which oral corticosteroids are used instead.
Other medications include Long-acting beta-adrenoceptor agonists (LABA)
(such as salmeterol and formoterol) and Leukotriene receptor
antagonists (such as montelukast and zafirlukast) which may be used in
conjunction with inhaled corticosteroids [3,7].

J.S.s 2 week course of wheezing, dyspnea, tachypnea, and non-productive

cough support a diagnosis for acute asthma attack, especially considering
his PMH for asthma. His pleuritic chest pain can be attributed to a strain in
his chest muscles due to his constant forceful coughing. Furthermore, his
relief of symptoms upon administration of asthmatic medications may
support this diagnosis. His lack of signs of infection, and low clinical
probability for PE, as discussed below make these diagnoses less likely. A
normal CXR can confirm this by helping ruling out pneumothorax and
pneumonia.
Pneumonia:
Pneumonia is an inflammatory condition of the lung parenchyma. It is usually
caused by an infection due to a virus or bacteria. Risk factors for infection
are impaired cough reflex, mucus plugging/cystic fibrosis, asthma, smoking,
immunocompromised etc Signs and symptoms include dullness to
percussion, decreased breath sounds, productive cough with yellow-green or
rusty (blood) sputum or dry cough (atypical pneumonia), pleuritic chest
pain, fever, chills, dyspnea, tachypnea, and elevated WBC count. Diagnosis is
made by symptoms and physical exam and confirmed by CXR, blood culture,
and sputum culture [8]. There are three patterns that are seen on CXR: lobar
pneumonia, bronchopneumonia, and interstitial/atypical pneumonia. A lobar
pneumonia is a consolidation of an entire lobe of the lung and is most
commonly caused by S. pneumoniae which has traditionally been the most
common cause of community-acquired-pneumonia (CAP)
[9]. Bronchopneumonia are scattered patchy consolidations centered around
bronchioles and can be caused by S. aureus and other bacteria. Finally,
interstitial/atypical pneumonia is characterized by diffuse interstitial
infiltrates with minimal or no sputum and low fever. These can be caused by
bacteria (M. pneumoniae is the most common cause of atypical pneumonia
and infection rates are highest in school-aged children, military recruits, and
college students. Transmission is via close contacts and respiratory droplets.)
or viruses (RSV in infants and influenza in the elderly, immunocompromised,
and preexisting lung disease). Treatment/antibiotics will depend upon the
identity of the infecting pathogen.
J.S. lacks signs for infection such as fever, night sweats, chills, vomiting,
diarrhea, sore throat, lymphadenopathy, dysuria, hematuria, rashes, ear
pain, rhinorrhea and more specifically for pneumonia, lacks decreased
breath sounds, dullness to percussion, and hemoptysis which would make a
diagnosis for pneumonia less likely, despite his positive signs of pleuritic

chest pains, dyspnea, cough, tachypnea, and PMH of asthma. A normal CXR
can confirm this diagnosis by helping ruling out pneumonia. Also a CBC can
be done to check for elevated WBC, which is another sign of infection.
Pulmonary embolism:
A pulmonary embolism (PE) is a blockage of an artery in the lungs by an
intravascular mass that has traveled from elsewhere in the body. The most
common source of pulmonary embolism is a DVT of the lower extremity
usually involving femoral, iliac, or popliteal veins. It is often clinically silent
due to the dual blood supply of the lungs and the emboli are usually are
small/self-resolve. Therefore, only about 10% of PEs cause infarction. Sudden
death can occur when a large saddle embolus blocks both the left and right
pulmonary arteries. Risk factors for PE include prolonged bed
rest/inactivity, smoking, stroke, pregnancy, obesity, surgery, and cancer [10].
Signs and symptoms include dyspnea, tachypnea, cough, pleuritic chest
pain, and sometimes hemoptysis. Diagnosis is initiated using the Wells
score; which is a scoring system that is used to assign point values to risk
factors such as, immobility, prior history of DVT or PE, suspected DVT, etc
to assess the clinical probability of PE (low, intermediate, high). Following
assessment if clinical probability is low then a D-dimer test, which has a high
sensitivity but low specificity (around 50%), should be done to rule out PE. IF
D-dimer is elevated then diagnostic imaging should be considered. In
addition, if clinical probability is high, then a CT pulmonary angiogram should
be performed followed by Doppler ultrasound in the lower extremity and V/Q
lung scan if necessary [11,12]. Treatment for PE consists mainly of
anticoagulants (low molecular weight heparin for 7-10 days followed by/with
warfarin for 3-6 months) and if necessary thrombolytics/tPA where there is
extensive and hemodynamically compromising PE [13].
Although J.S presents with signs/symptoms/risk factors of a PE such as
dyspnea, tachypnea, cough, pleuritic chest pain, and obesity, his clinical
probability of PE based on the Wells score is low. For example he has no
prior history of DVT or PE, no hemoptysis, no recent surgeries within the past
month, he has not been immobile, and there is no diagnosis that is less likely
than PE (asthma is more likely). Thus, PE is less likely his diagnosis.
However, D- dimer test can be done to help rule out PE.
Pneumothroax:
Pneumothorax is an abnormal accumulation of air in the pleural space. This
causes an uncoupling of the lung from the chest wall and may interfere with

normal breathing. It can be described as either traumatic or spontaneous.

Spontaneous pneumothorax often occur at rest and can be caused by a
rupture of an emphysematous bleb (the trachea will shift to the side of
collapse) which can be seen in young adults. Traumatic pneumothorax is
caused by a blunt trauma, penetrating chest wall injury or as a consequence
of mechanical ventilation. In some cases this can lead to a tension
pneumothorax, where air enters the pleural space but cannot exit (the
trachea will be pushed to the opposite side of the injury). This will result in a
medical emergency that can cause a steadily worsening oxygen
shortage, hypotension, and ultimately death if not treated. Risk factors for
pneumothorax include patients with a tall/thin body habitus, smoking, and
patients with an underlying lung problem such as asthma, cystic fibrosis,
necrotizing pneumonia, and interstitial lung disease. Signs and symptoms of
pneumothorax include dyspnea, pleuritic chest pain, non-productive cough,
diminished breath sounds, hyperresonant percussion, and tachypnea.
Diagnosis is made with CXR and if possible should be taken in the upright
position [14]. Treatment for pneumothorax depends on its severity and can
include options such as observation, supplemental oxygen, needle
aspiration, and chest tube insertion. Traumatic/tension pneumothorax are
medical emergencies and therefore require the insertion of a chest tube.
Although J.S presents with signs/symptoms/risk factors of pneumothorax
such as dyspnea, pleuritic chest pain, non-productive cough, tachypnea, and
PMH of asthma he lacks diminished breath sounds, hyperresonant
percussion, and has no history of smoking. J.S. has not sustained any trauma
so a traumatic pneumothorax can be ruled out. A spontaneous
pneumothorax, however, cannot be entirely ruled out. J.Ss 2 week history of
wheezing, cough, and dyspnea are most likely due to an asthma attack but
his 1 day history of pleuritic chest pain could have resulted from a
spontaneous pneumothorax due to his asthma and constant coughing. The
relief of his symptoms by asthma medications makes pneumothorax less
likely but a CXR should be done to confirm this.
Molecular Science: Airway inflammation in asthma
Airway inflammation in asthma generally involves the same cells that are
involved in the allergic response in the skin and nasal airways. Therefore,
mast cell activation, mediated by a variety of cytokines, cells and other
mediators, is important in this process.

In the allergic response an initial allergen exposure is followed by an increase

of specific IgE antibodies, which are produced and secreted by plasma cells.
Production and regulation of specific IgE appears to be related to an
overexpression of Th2 type T cell responses involving secretion of IL-4
(mediates class switching to IgE) and IL-5 (attracts eosinophils) relative to
the Th1 type. The IgE then bind to high-affinity Fc receptors on mast cells,
which are elevated in asthmatic airways and can be in close association with
airway smooth muscle cells. When an allergen is subsequently inhaled and
comes into contact with these mast cells, it crosslinks the allergen-specific
IgE on the cell surface and rapidly degranulates and releases
bronchoconstricting mediators such as histamine and leukotrienes/LTC4, D4,
and E4. Mast cells also store and release TNF-alpha, which recruits and
activates inflammatory cells and alters function and growth of airway smooth
muscle [14-17]. The above events are termed early phase reaction and can
happen within minutes upon allergen bronchoprovocation. Late phase
reaction on the other hand involves recurrence of bronchoconstriction
several hours later. This response coincides with an influx of inflammatory
and immune cells, such as monocytes, neutrophils, T- lymphocytes,
eosinophils, and basophils. These cells release mediators that cause airway
smooth muscle contraction that is mostly reversible by beta-2-agonists [18].

Studying/testing the efficacy or inefficacy of medications as treatment

enhances our understanding of airway inflammation and mast cell mediators
in the pathophysiology of asthma. For example targeting asthma
inflammation with medications such as glucocorticoids or anti-IgE block the
late phase response and improve control of asthma, while antihistamines and
leukotriene modifying agents block both early and late phase responses
[19,20].

Plan:
1) Wheezing, cough, SOB (asthma attack) with pleuritic chest pains:

Administration of the following medications given in the ED have

improved the patients wheezing, coughing, SOB, and pleuritic chest
pains:
o prednisone tablet 60 mg (once)
o ipratropium 0.02 % nebulizer solution 2.5 mL (every 20 min PRN)
o levalbuterol 1.25 mg/3 mL nebulizer solution 3 mL (once)
o ibuprofen tablet 600 mg (once), for pain.

These medications should be continued as needed as long as the

patient is in the ED.

A CXR was also ordered but the results are pending. If CXR is normal,
patient can be discharged with the following medications:
o albuterol HFA (PROVENTIL HFA;VENTOLIN HFA) 90 mcg/actuation
inhaler every 4 hours PRN. For asthma relief
o Ibuprofen 400mg PO every 4-6 hours PRN; Max 2400mg/day. For
chest pain
o Prednisone 50 mg tablet every 12 hours x3-10days; Max
60mg/day. For asthma control.
However, a D-dimer test should be ordered to rule out PE.

If CXR shows signs of pneumonia, then a blood or sputum culture can

be done to determine identity of pathogen. In the interim a macrolide
antibiotic such as azithromycin or clarithromycin can be given to cover
both M. pneumoniae and S. pneumoniae, which are the most likely
causing bacterial pathogen. If the pneumonia is viral then follow with
supportive care.
If CXR reveals pneumothorax the treatment will depend on its severity
and can include options such as observation, supplemental oxygen,
needle aspiration, and chest tube insertion. Pulmonology consult
should be called to best determine the severity and exact treatment
plan of the patient.

2) Pain in both knee joints:

Patient should be referred to orthopedics to evaluate joint pain in
knees.
Patient should not overuse/stress his knees
Ice packs can be used if patient experiences any swelling
3) Immunization update:
Immunizations for Hep A, second varicella, third HPV, and
pneumococcal vaccines (PCV13 and PPSV23, these should be given
a year apart) should be scheduled with his PCP Margaret S
Rosenberg, MD.
4) Patient should schedule a follow up in 2 days with his PCP Margaret S
Rosenberg, MD

Final ED course:
Imaging: CXR ordered in the ED revealed: cardiac silhouette is not
enlarged. The lungs are clear. There is no evidence of pneumothorax or
pleural effusion.
The patient was then discharged with the following medications:

albuterol HFA (PROVENTIL HFA;VENTOLIN HFA) 90 mcg/actuation

inhaler every 4 hours PRN
Prednisone (DELTASONE) 20 mg tablet daily

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