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J ALLERGY CLIN IMMUNOL
VOLUME 129, NUMBER 2
Abstracts AB125
SUNDAY
474 Maternal IgE Levels Are Associated With IgE Levels At Ages10 And 18 In Girls But Not In Boys, Isle Of Wight Birth Cohort
A. Sadeghnejad1, W. Karmaus2, S. H. Arshad3; 1Department of Medi-
cine, Capital Health System, Trenton, NJ, 2University of South Carolina,
Columbia, SC, 3The Asthma and Allergy Centre, Isle of Wight and
University of Southampton, UNITED KINGDOM.
RATIONALE: We have previously shown that parental history of asthma
exerts a higher risk on asthma in the same gender offspring, ‘‘parent of
origin effect’’. To investigate this concept, IgE was utilized as an objective
measure of atopy. We conducted gender-specific analyses for the relation-
ships between maternal IgE and IgE levels at ages 10 and 18.
METHODS: Of 1456 subjects in this birth cohort, maternal IgE was
available for 1057 (73%). IgE levels were available for 954 (66%) at 10
years and for 560 (38%) at 18 years. To evaluate the associations between
maternal and adolescence IgE we used linear and logistic regressions. IgE
levels were either logransformed (linear regression) or dichotomized
(logistic regression). We adjusted the effect of maternal IgE for pet
exposure, smoking and birth weight. Raised IgE levels were defined as
levels above median.
RESULTS: In linear regressions, maternal IgE was associated with IgE
levels at ages 10 (p50.0005) and 18 (p50.02) in girls but not in boys. In
logistic regressions, the odds ratios (OR) for the association of raised
maternal IgE levels on raised IgE levels at ages 10 and 18 were larger in
girls (OR52.07, p50.001 and OR51.72, p50.07) compared to boys (OR
1.93, p50.004 and OR51.04, p50.90).
CONCLUSIONS: This is the first study investigating the association of
maternal IgE and adolescence IgE. Maternal serum IgE seems to have
stronger relationship with IgE levels at ages 10 and 18 years in girls
compared to boys. These findings suggest that there is a gender-specific
imprinting of the maternal atopy status.
475 An Unusual Case of Mast Cell Activation SyndromeR. Patel1, J. Celestin2, M. Frieri1; 1Nassau University Medical
Center, East Meadow, NY, 2Albany Medical College, Albany, NY.
RATIONALE: Mast Cell Activation Syndrome (MCAS) can be difficult
to diagnose. This is due in part to commonmultiple organ involvement and
overlap with other disorders. Most recently, criteria to diagnose this entity
have been published. It can be primary, secondary due to chronic
autoimmune urticaria (CAU), or idiopathic.
CASE PRESENTATION:Wedescribe a 74 year old Caucasianmalewho
is being treated for Neuroendocrine Antral Carcinoid since 2008, with
Sandostatin. Since 2003, he has been having intermittent episodes of
urticaria, sometimes associated with flushing and diarrhea. His current
medications are H1 and H2 blockers, ketotifen, and opioids for spinal
stenosis. Physical examination shows dermatographia, without urticaria or
Darier’s sign.
METHODS: CBC and differential, 24 hr urine 5-HIAA, and serum
gastrin, serotonin, and chromogranin A were normal. He had elevated
levels of alkaline phosphatase (157 U/ml), serum tryptase (17 ng/mL),
plasma histamine (8.44 ng/ml), and anti-IgE receptor antibody (10.7%).
Skin biopsy revealed lichenoid keratosis, patchy mononuclear cells, and
papillary dermal fibrosis, but no visible mast cells. Gastric biopsy showed
small neuroendocrine tumor cells (positive for chromogranin A) and
synaptophysin without mitosis.
CONCLUSION: This patient’s MCAS is secondary and probably due to
his neuroendocrine antral tumor or hyperactive mast cells that may have
degranulated. However, his CAU may have been triggered by neurohor-
mones, histamine release, or intermittent opioid analgesics for spinal
stenosis. Incubation in vitro of his mast cells along with his tumor cells
would confirm that hypothesis.
476 Effects of Omalizumab on Two Patients with Short Stature andAtopic Disease
N. B. Richards, S. McGeady, C. Chang, D. Doyle; Thomas Jefferson Hos-
pital, Philadelphia, PA.
RATIONALE: Up to 6% of children/adolescents with atopic diseases
have heights that are below the third percentile. While this high prevalence
of growth delay has been attributed to the impact of atopy on normal
development, the mechanism of this interaction is unknown. Decreased
prostaglandin E2 (PGE2) production may result in delayed skeletal
maturation and growth retardation. PGE2 synthesis in osteoblasts is
decreased by platelet activating factor (PAF). We describe 2 male
adolescents with longstanding linear growth retardation who experienced
growth spurts immediately following omalizumab therapy.
METHODS: Patient A is a 14 year old with severe asthma, allergic
rhinitis, and atopic dermatitis. Patient B is a 15 year old with severe atopic
dermatitis, asthma, and allergic rhinitis. Both required frequent oral
corticosteroids and had heights less than the third percentile.
RESULTS: Despite markedly elevated IgE levels, both were treated with
omalizumab and within 4 months following initiation of treatment had
rapid increases in linear growth. Patient A is now at the fifth percentile for
age and patient B is at the fifteenth percentile for height.
CONCLUSION: Omalizumab is thought to decrease the release of mast
cell mediators, which may reduce the amount of PAF released, enhancing
PGE2 production and allow accelerated linear skeletal growth to occur, as
was observed. While decreased therapeutic need for oral glucocorticoids
and/or serendipitous growth spurts in these patients cannot be ruled out, the
rapid growth observed pursuant to omalizumab therapy suggests that
clinical trials of omalizumab in severely atopic children with short stature
are indicated
477 Impact of Asthma Counseling by Pharmacist on AsthmaControl and Medication Adherence in Asia
T. Lim1, S. Kowalski2, K. Tan3; 1Department of Pharmacy, Singapore
General Hospital, Singapore, SINGAPORE, 2School of Pharmacy, Uni-
versity of South Australia, Adelaide, AUSTRALIA, 3Department of Res-
piratory and Critical Care Medicine, Singapore General Hospital,
Singapore, SINGAPORE.
RATIONALE: Published overseas studies demonstrated that asthma
counselling by pharmacists improved medication adherence and clinical
outcomes. We conducted a retrospective study to assess the impact of
asthma counseling by pharmacist on asthma control and medication
adherence in patients attended the pharmacist managed asthma counseling
clinic in Asia.
METHODS: Patients who attended the asthma counseling clinic and
received asthma counseling between September 2008 and March 2009
were recruited. The patients’ asthma control was assessed by comparing
the mean number of emergency department visits, hospitalizations and
Asthma Control Test (ACT) scores prior to counselling with the results 6
and 12 months after asthma counseling. Medication adherence was
assessed by medication refills during 6-months and 12 months after the
first clinic visit. Paired t-test and chi-squared test were used for comparing
mean values and categorical variables, respectively. The level of signifi-
cance was set at <0.05.
RESULTS: Total of 120 patients were recruited. The mean no of
hospitalization or emergency department visits due to asthma was reduced
from 0.61 60.71 and 0.74 60.77, 6 and 12 months before counseling, to
0.09 60.36 and 0.20 60.69, 6 and 12 months after counseling (p<0.01).
Mean ACT improved from 20 to 22.2(p<0.05). The proportion of patientswith medication adherence rates of more than 70%were 76.7% and 71.7%
respectively during 6 and 12 months after the first clinic visit.
CONCLUSIONS: Asthma counseling by pharmacists significantly re-
duces the hospitalization or emergency department visit; improves the
asthma control and maintains good medication adherence in Asia asthma
patients.