SUMMARY AND CONCLUSIONS
1, The present study comprised fifty Egyptian patients
suffering from bronchial asthma • and ·twenty normal
controls, The patients were devided into.four groups
namely : group "A" including those with atopic astrna ,
group "B" including those with non-atopic ·asthma ,
group "e" including both group "A" and "B" together,
and group "D" including asthmatic cases complicated
by emphysema.
2, The atopic group comprised IE· males and 7 females
their ages ranged from 15 to 42 years and the durations
of their disease ranged from 2 to 22 years ,
while the non-atopic group comprised 12 males , and
5 females, their ages ranged from 16 to 39 years,
and the durations of their disease ranged from 2 to
20 years.Df the cases complicated by emphysema 7
were males and 3 were females, their ages ranged
from 33 to 50 years, and the durations of their
disease ranged from 14 to 29 years,
3, All the asthmatic patients were subjected to the
following investigations :
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* Detailed clinical assessment.
* Urine and stool analysis.
X-ray chest.
Electrocardiogram (E.C.G.).
Skin tests by prick method using 7 antigens.
Pulmonary function tests including FVC, FEVl '
and PEFR.
*
*
*
*
* Arterial blood gas analysis including ,
*
PC02, pH and HC03•
Detection of total serum IgE levels using pharmacia
enzyme paper radio-immunosorbent test
*
(Phadezym IgE PRIST).
Platelet studies including
a) Platelet morphology: by examination of smears
prepared from capillary blood without -the
addition of anticoagulant "native blood".
b) Platelet count, by the direct method using
Formol-Citrated Red Cell diluent.
c) Platelet aggregation using ADP as aggregation
agent.
d) Platelet factor-3 availability (PF-3a).
e) Partial thrompoblastin time with Kaolin (PTT-K).
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4. Our results demonstrated the following:
* No considerable change in platelet morphology was
noticed apart from one case with many giant platelets
in his native blood smear.
Compared to normal controls, there was reduction
in the platelet count in all asthmatic groups with
statistically highly significant differences in
groups A, B, and C (P < 0.001) and only significant
for the cases complicated by emphysema (P < 0.01).
Four asthmatic cases had their counts that the relation
between the oxygen level, and the platelet
count is inversely proportional. The reduction of
platelet counts in our studied asthmatic cases was
attributed to diminished platelet synthesis, increased
platelet sequestration in the lungs, shortened
platelet survival time due to enhanced activity and
lastly due to increased platelet consumption,
As regarding the platelet aggregation, it has been found
to be impaired in all studied asthmatic groups. Comparing
the aggregation activity between each of studied asthmatic
groups and that of the control cases the difference
*
*
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was found highly significant for atopic and non
atopic cases (F ( 0.001) and was only signifi·
cant for cases complicated by emphysema (p( 0.01).
Impaired aggregation activity in our studied
cases was explained to be due to chronic stimulation
of platelets with subsequent defective
release of ADP. This stimulation could be due
to preformed immune-complexes in atopic cases or
by chronic hypoxia in non-atopic cases. The relation
between arterial blood oxygen level , and
platelet aggregation was stud~ed and showed that
hypoxaemia was associated with impaired aggregation
pattern. This was attributed to the possibility
that hypoxaemia inhibit platelet release
of ADP. The relation between pH of arterial blood
and platelet aggregation was also studied , and
it was observed that lowering pH of the arterial
blood was associated with inhibition of platelet
aggregation.
* Platelet factor-3 availability was assessed in our
studied cases and it has been found that 39.13 %
of non-atopic cases, and 30% of cases complicated
by emphysema had reduced platelet factor-3 availability.
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* As a test of coagulation in our studied asthmatic
cases, the partial thromboplastin time with Kaolin
(PTT-K) was used. The PTT was found to be normal
in all studied asthmatic groups and so the possibility
that bronchial asthma could be associated
with impaired coagulation system was excluded.
5. The number of cases is not enough to draw final conclusions,
yet the results of this work have stressed
the importance of stuyding the blood platelets in
bronchial asthma.
6. In this study we demonstrated how the platelet functions
are impaired in asthmatic patients , and we
think that there could be a pathogenic link between
megakaryocytes, platelet production and asthma.
7. We recommend for more detailed studies about the
relation between megakaryocytes, platelets , and
bronchial asthma using recent techniques of investigations
as isotopic studies for both lungs and
platelets, recent histopathologic studies and fibrooptic
lung studies. Other forms of parynchematous,
and vascular pulmonary diseases should also be
considered.
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8. Disodium cromoglycate (DSCG) a drug known for long
time to act through stabilizing mast cells has been
recently found to inhibit response to platelet activating
factor (PAF-Acether) in man, as an alternative
mode of its action in asthma. We think that
further studies are needed to clarify the possible
effect of the different drugs used 'in the treatment
of bronchial asthma on the megakaryocytes , and
platelets.
9. Drugs and substances which can affect megakaryocyte
fragmentation e.g. prostacyclin, 'or platelet activations
e.g. dipyridamole, should be considered in
further studies as a new hope for asthmatic patients.
10. It was concluded that the present study is an impetus
for further research in the role of pulmonary megakaryocytes
and blood platelets in the genesis of
asthma and may open new realms in the management of
this common and distressing disease.
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