Doctors' Newsletter - Autumn 2008 - Douglass Hanly Moir Pathology

Doctors’ Newsletter
Autumn 2008
Pathology
Industry Update
Primary buys Symbion
Page 2
Pathology Industry Consolidation
Dr Colin Goldschmidt
Page 3
New Pathologists
The Pathologists of DOUGLASS HANLY MOIR and BARRATT & SMITH PATHOLOGY
Pages 4-5
Acquired Bleeding Disorders
Dr Vera Stoermer
Pages 6-8
Neutrophils: The Good,
The Bad and the Ugly
Dr Debbie Clark
Pages 9-10
Allergy to Stinging Insects
Dr Karl Baumgart
Page 11
Medicare Update
• Tryptase
• Diagnosis of Helicobacter pylori Infection
“We take it personally”
“We take it personally”

Pathology Industry Consolidation
Dr Colin Goldschmidt
Chief Executive Officer
You may be aware that, after a
protracted takeover battle, Primary
Healthcare has emerged as the new
owner of Symbion Health. Primary
Healthcare is the owner of SDS
Pathology in Sydney, but it is perhaps
better known for its medical centre
operations under its founder, Ed
Bateman. Symbion Health operates
Symbion Laverty Pathology in NSW
and other pathology companies
around Australia – all of these will
now come under the control of
Primary Healthcare. It is expected
that a physical merger of the SDS
laboratory and Symbion Laverty
Pathology will take place in the
coming months.
Corporatisation and consolidation
of Australian pathology gathered
momentum through the nineties and
was principally driven by the need
to achieve economies of scale and
improved efficiencies in the face of
declining fee levels.
In order to avoid the potentially
negative impacts of corporatisation
and consolidation, Sonic Healthcare
(the parent company of both
Douglass Hanly Moir and Barratt &
Smith Pathology) adopted a `Medical
Leadership’ model to guide our
progression in this new environment
and to preserve our professional
image and personalised service to
you. It was this fervent desire for
us to remain a Specialist Medical
Practice – notwithstanding increasing
size or corporate structure – which
led me to relinquish my role as
a histopathologist in favour of a
management position in 1993!
Our Medical Leadership model
is formally characterised by a set
of `Foundation Principles’, which
specifically guide our behaviour and
service to you, our referring doctors.
They are depicted below for your
interest.
Our Foundation Principles
These Foundation Principles reflect
the essential medical core of the
company and express features which
are specifically appropriate for a
healthcare company – and which we
believe are most important to you and
your patients. They are:
• Technical excellence in our medical
testing and reporting
• Delivering localised and
personalised services to you
• The showcasing and sharing of our
highly specialised medical
knowledge
• Providing our patients with the best
possible service.
The integral involvement of
pathologists and other experienced
medical professionals in this
leadership model is essential.
The CEO of Douglass Hanly Moir
Pathology, Barratt & Smith Pathology
and Sonic Healthcare is a pathologist!
And the CEOs of almost all our other
pathology practices are pathologists
too.
Our Medical Leadership model
has served to differentiate us from
competitors. I believe that we are
generally well-recognised for our
medically focussed culture and values
and, if there is a `DHM difference’ or
a `Barratt & Smith difference’, then
it surely resides most fundamentally
at this level. This difference is
essentially a commitment to involve
our pathologists at every level of our
operations, so that the best interests
of our referring clinicians are served.
In the setting of pathology sector
consolidation, we believe that a
healthy future for Australian pathology
will be ensured under such a
medical model.
So, despite the significant industry
changes inherent in the Primary/
Symbion consolidation, you can
expect no change to our operations,
style or vision at DHM or at Barratt
& Smith Pathology. In particular, our
Medical Leadership model, which
sits proudly at the very heart of our
organisation, remains steadfast.
With my warm regards,
Technical
and
Operational
Excellence
Medical Practice
Medical Leadership
Personalised
Service for
Doctors
Professional
and
Academic
Expertise
Satisfying
Patient
Needs
Dr Colin Goldschmidt
MB BCh, FRCPA
CEO Douglass Hanly Moir Pathology/
Barratt & Smith Pathology
CEO Sonic Healthcare
2

New Pathologists
Dr Nick Taylor B.Med.Sc, MB, BS, MAACB, FRCPA
Chemical Pathologist, Director of Chemical Pathology, Automated Laboratory
Dr Nick Taylor is a graduate of the University of New South Wales. He trained
in chemical pathology at Westmead and Royal Prince Alfred Hospitals. In 1991
he was appointed as staff specialist in chemical pathology at Concord Hospital,
before moving into private pathology practice in 1994. Most recently, Dr Taylor was
employed by Laverty Pathology as Clinical Head of Chemical Pathology from 2002
until December 2007.
Dr Taylor’s areas of clinical speciality include general biochemistry, endocrinology
and toxicology. His main laboratory interests involve the development of useful
reference intervals and improved interpretive comments on pathology reports.
Dr Taylor has served on the NSW Branch Committee of the Australian Association
of Clinical Biochemists in different roles, from 1988 to 1992, and from 2002 to
2004. He has also been a NATA medical laboratory assessor since 1992.
Dr Taylor is available for consultation in all areas of biochemistry and endocrinology,
while his main role in the laboratory will be in the area of automated testing.
Dr Lye Lin Ho MB, BS (Hons), FRACP, FRCPA
Haematologist
Dr Lye Lin Ho is a graduate of the University of Sydney. She trained in both
clinical and laboratory haematology at Royal Prince Alfred and St George
hospitals. At present she is completing her thesis for a PhD in the field of
cancer drug resistance, investigating the relationship between oncogenes and
multidrug transporters. Dr Ho has joined Douglass Hanly Moir Pathology as a
laboratory haematologist. Her particular interest is in malignant haematology and
haemoglobinopathies.
Dr Peter Kyle BScAgr, MB, BS, FRCPA, FRCPath
Haematologist
Dr Peter Kyle is a graduate of the University of Sydney. His residency at Prince of
Wales Hospital included two haematology terms. This experience stimulated his
interest in haematology, which he pursued by completing specialist haematology
training at Charing Cross Hospital in London. Following his return to Australia in
1986, he spent periods at Newcastle Mater, Royal Newcastle, Prince of Wales and
St George hospitals. From 1990 to 2006, he was Staff Specialist in Haematology at
St George Hospital. Dr Kyle’s particular interests are in blood banking, coagulation
and haemoglobinopathies.
3

Acquired Bleeding Disorders
Dr Vera Stoermer
Haematologist
Acute and chronic acquired
bleeding disorders in outpatients
are common and often difficult
to evaluate. They are initially
dependent on subjective evaluation
of an increased tendency to
bleed, firstly by the patient and
secondly by the clinician. What is
considered significant bleeding by
one patient may be disregarded by
another. If a significant bleeding
tendency is being considered,
subsequent laboratory testing is
guided by the clinical history and
physical examination of the patient.
A correct diagnosis is essential
if appropriate therapy is to be
instigated, particularly for those
patients undergoing a diagnostic or
invasive procedure.
Picture 1:
Ginko biloba
leaf
Initial assessment
In the initial consultation, questions
need to be asked to ascertain
whether the patient has excessive,
prolonged, recurrent, or delayed
bleeding, or abnormal bruising. A
family history of significant bleeding
should be excluded, even if the
onset of abnormal bleeding is
recent. Any history of excessive
bleeding after physical trauma, skin
lacerations, dental extractions, or
surgery, is likely to be significant.
The presence of epistaxis, gum
bleeding and menorrhagia should
also be ascertained. Ecchymoses
after trauma are normal; however,
the sudden development of new or
multiple ecchymoses may be due to
an underlying medical condition.
Questions should concern general
health and possible underlying
disease which may be associated
with a bleeding tendency.
Examples include chronic liver and
renal disease, and myelodysplastic or
myeloproliferative disorders.
In addition, medication or
nutritional supplements which affect
platelet function will enhance bruising
or bleeding due to an underlying
bleeding tendency. A detailed history
of all drugs and medications is
essential, especially with regard to
any 'over-the-counter' medication or
herbal remedies which the patient
may not consider relevant.
The commonest cause of an
acquired bleeding disorder is drugrelated,
due to the increasing use of
anticoagulant therapy, which includes
antiplatelet therapy and warfarin.
Antiplatelet agents, such as aspirin,
clopidogrel and non-steroidal antiinflammatory
drugs are in widespread
use throughout the community.
Individual response to these
drugs is extremely variable
and will produce a significant
bleeding tendency in some
patients. Herbal remedies
and other over-the-counter
medications may have antiplatelet
or other haemostatic
effects, and produce a bleeding
tendency. This may especially be
seen when these medications are
taken in combination with other
anticoagulants; for example, Gingko
biloba in addition to warfarin.
Another common cause of an
acquired bleeding or bruising
tendency is thrombocytopenia
which may result from a wide
variety of causes. Primary or
secondary immune-mediated
destruction, including drug-induced,
viral infections, or autoimmune
diseases, should be considered.
Decreased production, sequestration,
or increased consumption of platelets
are all possible causes.
A less common cause of a bleeding
tendency includes inhibitors or
antibodies directed against specific
factors e.g. factor VIII or IX, which
may arise spontaneously in elderly
patients, in pregnancy or in patients
with autoimmune disorders. These
inhibitors, although rare, may result
in catastrophic bleeding, especially
in patients undergoing surgery.
Paraproteins also act as inhibitors by
interfering with platelet or coagulation
factor function. Common medical
conditions have a range of effects on
the haemostatic system.
4

Acquired Bleeding Disorders
Chronic liver disease produces
thrombocytopenia and reduced
synthesis of almost all coagulation
factors as well as abnormal
fibrinogen synthesis. In severe liver
disease, chronic disseminated
intravascular coagulation (DIC) is
often present. Vitamin K deficiency
occurs especially with cholestatic
jaundice and results in impaired
synthesis of vitamin K-dependent
coagulation factors. Other systemic
disorders with increased bleeding
include severe renal impairment
resulting in platelet dysfunction and
hypothyroidism with an acquired von
Willebrand disorder.
Conditions such as myeloproliferative
disease and myelodysplasia
are often associated with a
bleeding tendency. Patients with
myeloproliferative disorders may
develop a range of defects, including
acquired von Willebrand disorder.
The bleeding tendency in these
disorders is compounded by the
use of aspirin to reduce the risk of
thrombosis which also occurs in
these conditions. In myelodysplasia,
not only thrombocytopenia but
also dysfunctional platelets are a
common occurrence, and may cause
significant bleeding if the patient
undergoes surgery.
A less common cause of a
bleeding tendency is disseminated
intravascular coagulation
(DIC), which may arise with
some malignancies, such as
adenocarcinoma, or suddenly in
acute promyelocytic leukaemia
(APML), and may have catastrophic
effects. Disseminated intravascular
coagulation in association with
cancer does not generally result
in bleeding, unless the patient
undergoes surgery.
and blood film, platelet function
analysis (PFA-100) if available,
activated partial thromboplastin
time (APTT), prothrombin time
(PT), thrombin time (TT) and
fibrinogen level are indicated.
These tests, if abnormal, warrant
further investigation, such as factor
assays, von Willebrand and platelet
aggregation studies, depending on
the abnormality. If the haemostatic
screening tests are normal, as may
be the case for mild defects in
haemostasis, further investigation
may still be required if the clinical
history is highly suspicious or the
patient is to undergo a higher risk
procedure, such as cardiovascular
surgery.
A recent onset of a bleeding
tendency may be due to a previously
undiagnosed mild inherited bleeding
disorder. This may not become
evident until the patient has
undergone a haemostatic challenge,
such as surgery, or complains of
menorrhagia. In these cases, the
haemostatic screening tests, which
are insensitive to mild reductions in
factor levels, may be within reference
limits, so that further investigation
is warranted.
In the investigation of all bleeding
disorders, the importance of a careful
history cannot be overemphasised,
as it is the key to directing both the
initial tests and judging the extent to
which further investigation will
be required.
If you have any questions regarding
the investigation of a bleeding
diathesis, Dr Vera Stoermer, Director
of Coagulation at Douglass Hanly
Moir Pathology, or any of our
Haematologists, will be pleased
to advise.
Suggested Initial Haematological
Tests for an Acquired Bleeding
Disorder
FBC/platelet count and blood
film examination
PT, APTT, TT and fibrinogen
PFA-100 (if available)
Picture 2: Petechial rash due to DIC in patient with APML
Investigations
For those patients with a clinical
history or physical examination
suspicious of a bleeding tendency,
haemostatic screening tests which
include a FBC/platelet count
If you have any enquiries, please contact Dr Vera Stoermer on (02) 98 555 312
5

Neutrophils: The Good, The Bad and the Ugly
Dr Debbie Clark
Haematologist
Neutrophilia
In the normal adult full blood count,
neutrophils form the majority
cell percentage of the white cell
differential count. Their main function
is to fight bacterial infection and the
majority of cases with neutrophilia will
be due to infection, an association
that doctors are universally familiar
with.
The absolute neutrophil count is
of greater significance than the
percentage. Reference range in a
normal adult is: 2.0 – 7.5 x 10^9 /L.
Commonly, a left shift is also
reported at the time of a neutrophilia.
This simply means that less mature
cells of the same series, such as
band forms or even myelocytes,
are also present in the film.
See diagram 1.
Although most neutrophilias
will be secondary to obvious
infection, sometimes there is no
clinical indication of this and then
the question arises: what is this
neutrophilia due to and should I be
worried about it At the back of
everyone’s mind is the possibility of
an early myeloid leukaemia. There
are, however, a substantial number of
other causes of a neutrophilia which
are more common than primary
marrow disorders. Table 1 lists them.
Physiological causes of a
neutrophilia are a result of circadian
rhythms and reaction to physiological
processes. The neutrophil count
rises after a meal and after physical
exertion.
Pregnancy is frequently associated
with a neutrophilia and our quoted
reference ranges on the full blood
count report reflect these changes, if
we have sufficient clinical information
to that effect. However, the ranges
are not so readily fixed as in the
non-pregnant state and should be
interpreted with a degree of flexibility.
Myelocytes are a common finding.
Many factors influence the neutrophil
count in pregnancy: the stage of
pregnancy and the presence of a
multiple pregnancy, for example.
Some drugs are often associated
with a neutrophilia: steroids are
a frequently observed cause of a
neutrophilia and myelocytes are often
seen in the film. Of course, patients
on steroids may have an increased
risk of infection, which complicates
the interpretation of this finding.
Other drugs include: lithium, and
GCSF.
Inflammation of tissue without
bacterial infection may also give rise
to a neutrophilia. Examples include
myocardial infarction, tissue necrosis,
trauma and vasculitis.
Acute haemorrhage or
haemolysis, neoplasia, as well as
some acute metabolic disorders
may all sometimes be associated
with a neutrophilia. Lastly, a
neutrophilia may be an early sign of
a myeloproliferative disorder. In
chronic myeloid leukaemia, it is
the predominant feature of the blood
count, with a white count often in the
200-300 x 10^9 /L range. In its very
early stages, there may be a milder
neutrophilia, but there is often quite
a marked left shift. The presence
of a basophilia or eosinophilia, plus
changes in other parameters, such
as the platelets, may give a clue to
the underlying disorder.
Other myeloproliferative disorders,
such as polycythaemia rubra
vera and myelofibrosis, may
also include a neutrophilia
among their features. Chronic
myelomonocytic leukaemia,
a disorder of the elderly which
includes both myeloproliferative and
myelodysplastic features, usually
shows a marked monocytosis with
an accompanying neutrophilia and
left shift.
Table 1: Causes of a neutrophilia
Bacterial infection
Tissue inflammation / necrosis
Drugs (e.g. steroids)
Pregnancy
Acute haemorrhage or haemolysis
Neoplasia
Severe metabolic disorders
Myeloproliferative disease
6

Neutrophils: The Good, The Bad and the Ugly
Diagram 1: Maturation of neutrophils
Neutropenia
Another common abnormality in
the full blood count is the finding
of a neutropenia. The lower limit
of the reference range for adults
in our laboratory is 2.0 x 10^9 /L.
However, it is generally accepted
that in patients of Middle Eastern
and African descent, the absolute
neutrophil count may normally be as
low as 1.5 x 10^9 /L. The underlying
cause of a neutropenia is often
more difficult to establish than for a
neutrophilia.
An increased tendency to infection
may become significant in patients
with an absolute neutrophil count
below 1 x 10^9 /L, and a risk of
severe or spontaneous infection is
frequently seen below 0.5 x 10^9 /L.
The underlying cause will influence
the likelihood of this, infection being
much commoner in patients with
bone marrow failure disorders. Some
causes of a neutropenia are listed in
Table 2.
Overall, and especially in children, a
viral illness is by far the commonest
cause and is, of course, usually selflimiting.
Drug therapy is probably
the second commonest cause of
neutropenias seen in our laboratory
and a very wide range of drugs are
potentially implicated. A neutropenia
is often seen in autoimmune disease
and, interestingly, may precede its
onset by months or even years.
Sometimes, particularly in the
elderly, a persisting neutropenia may
be the only sign of an underlying
bone marrow disease, such as
myelodysplasia.
Table 2: Causes of a neutropenia
Infection (especially viral)
Drug induced
Autoimmune disease
Hypersplenism
Bone marrow disease
Cyclical neutropenia
Congenital neutropenia
Idiopathic
Morphological Changes
When a blood film is examined, we may comment on morphological abnormalities. Although these are less common than an
increase or decrease in neutrophil numbers, their presence may give important clues to underlying disease.
Leukoerythroblastic film
This term is used to indicate the presence of both immature white cells
(usually myelocytes) and nucleated red blood cells. If persistent, it
suggests an underlying bone marrow abnormality, particularly metastatic
carcinoma in the marrow or a primary marrow disease. Occasionally, this
change is seen in patients with severe sepsis, haemorrhage or haemolysis,
and represents simply a reactive process in the marrow.
Picture 5: Leukoerythroblastic film (A nucleated red cell and myelocyte are shown) >
7

Neutrophils: The Good, The Bad and the Ugly
Hypersegmented neutrophils or a ‘right shift’
When the normal lobulation of the neutrophil nucleus becomes more
pronounced, cells with five lobes or more may be readily seen in the film.
Because the appearance is the opposite of the unsegmented band cells
or myelocytes seen in a left shift, the term ‘right shift’ is sometimes used.
Hypersegmented neutrophils are classically an early sign of B12 or folate
deficiency, however they may also be seen in patients on some drugs
(e.g. hydroxyurea) and occasionally in uraemia.
Picture 2: Hypersegmented neutrophil >
Hyposegmented neutrophils, hypogranulation and the pseudo-
Pelger-Huet anomaly
In myelodysplastic syndromes, neutrophils may become abnormally
segmented, often with only two lobes connected by a thin strand of
nuclear material; there may also be a loss of granulation. Typical cells
are illustrated. The abnormality is known as the pseudo-Pelger-Huet
abnormality and strongly suggests an underlying myelodysplasia. The term
pseudo-Pelger-Huet derives from a benign and uncommon congenital
abnormality of nuclear segmentation known as Pelger-Huet.
Picture 3: Neutrophil in myelodysplasia (Pseudo-Pelger-Huet abnormality) >
Döhle bodies and toxic granulation
Neutrophil granules become enlarged, dark and prominent in severe
infections. In these cases, we will comment on the FBC to this effect. In
the most severe cases, a pale blue structure is seen within the cytoplasm,
known as a Dohle body and, when seen in the context of possible
infection, is often a marker of severe bacterial infection.
Picture 4: Neutrophil with toxic gramilation and a Dohle body near lower edge >
Blast cells
Blast cells are very immature cells and may be of either the granulocyte
series or lymphoid cells. Their presence raises the possibility of an
underlying leukaemia, therefore a new finding would normally prompt
further investigation. When these, or other less common abnormalities
of the granulocyte series, are noted on the FBC report, the blood
film will have been reviewed by a haematologist or one of our senior
scientists. If you have any questions arising from one of our reports, our
haematologists will always be happy to review the blood film further at
your request and discuss the abnormalities present.
Picture 5: Blast cells >
Dr Debbie Clark recently retired from haematology practice, after a long and distinguished career at
Douglass Hanly Moir Pathology. This article was written prior to her retirement.
Discussion and enquiries may be directed to any of our other Haematologists on 98 555 312.
8

Allergy to Stinging Insects
Dr Karl Baumgart
Director of Immunology
How common is stinging
insect allergy and what
do these stings do
Around 1% of adults have
experienced an allergic reaction
to a stinging insect. These allergic
reactions have their onset within four
hours of a sting. They encompass
local but limited reactions, large local
reactions and systemic reactions.
Delayed reactions can also occur.
These have their onset four hours
after the sting, and can include
serum sickness, Guillain-Barre
syndrome, glomerulonephritis,
myocarditis and sometimes a flu-like
syndrome. Occasional patients with
longstanding chronic inflammatory
disorders have been reported to
develop clinical remission after stings!
We know little about mortality from
insect sting allergy, as there are no
specific autopsy findings.
What stinging insects do
we have in Australia
Important stinging insects belong to
the orders of:
• Hymenoptera - apids (bees)
• Vespids (wasps)
• Formicids (ants)
Allergy to “jumper ants” is very
common in Tasmania and in
Southern Australia. We have nonsocial,
stingless native bees, as well
as social native bees and European
honeybees that can sting. We also
have a wide range of wasps that can
sting.
What should I know
about bees
Apids (honeybees) have been
domesticated by humans for
thousands of years and most live
in constructed hives, although
feral colonies in trees do occur.
Honeybee venom is bacteriostatic,
so secondary infections are rare.
The venom is a complex mixture
of phospholipase, hyaluronidase,
melittin, acid phosphatase, apamin
and other peptides. There are some
common components with vespid
(wasp) venoms.
Do we have “killer”
or africanised bees in
Australia
NO. African bees are highly
aggressive and in Brazil were
crossbred with European bees,
resulting in “africanised” or “killer”
bees. They have gradually spread
northward from South America and
now occur in Southern states of
the USA. These bees can attack
individuals without clear provocation,
which has resulted in a number
of deaths each year in the United
States. There are a large number of
Websites dedicated to this issue.
What should I know
about wasps
Yellow jackets (Vespula spp)
scavenge for food in waste bins
and rotting vegetation. Their stings
commonly result in cellulitis. They are
very aggressive and can sting with
little provocation when food supplies
are reduced.
Yellow hornets (Dolichovespula
arenaria) and white-faced hornets
(D. maculata) build nests in trees,
bushes and near roofs. They can
become aggressive when exposed to
vibrating tools or other disturbances
of the plant where their nest is
situated. Paper wasps (Polistes spp)
are less aggressive. They make nests
that have a paper like appearance
under leaves and in other sheltered
areas around buildings.
Vespid venoms include
phospholipase (with minimal
cross-reactivity to that of bees),
hyaluronidase, acid phosphatase,
kinin and other peptides common
to ant-venoms. Unlike honeybees,
vespid venoms are not bacteriostatic.
What should I remember
when a patient has had a
sting
Remove the sting, if present
If there has been a bee-sting,
it can be removed by flicking it
with a fingernail, credit card or
pocketknife. Wasps do not leave
stingers.
Local reactions
These may require no treatment,
or may be treated (like large
local reactions) with rest and ice
compresses.
Large local reactions
These are commonly and, not
unreasonably, treated with rest, ice
compresses, antihistamines and
glucocorticoids.
9

Allergy to Stinging Insects
Systemic or generalised reactions
• Should be treated, like other
forms of anaphylaxis, with
adrenaline and iv fluids. Rapidacting
antihistamines, steroids
and H2-antihistamines are often
used.
• iv glucagon may be needed for
refractory patients or those on
beta blockers.
• Local measures should include
sting removal and ice
compresses. Some authors
recommend use of a tourniquet.
• Appropriate observation in a
supervised environment (e.g.
emergency department) for
several hours is usual. Further
antihistamines and oral steroids
may be needed over the next
24-48 hours.
• Antibiotics may be needed after
wasp stings.
What management
is appropriate after a
significant sting
Follow up testing, first aid measures
and consideration of desensitisation
should be reviewed after significant
stings. Mastocytosis should
always be excluded by testing
for Tryptase. Patients should be
given advice on handling “a nexttime
situation”. This may include
access to injectable adrenaline such
as Epi-Pen or Epi-Pen Jnr plus other
medications suitable for use in such
a setting.
Patients must not be
prescribed beta blockers.
Anaphylaxis action plans and
current contact details of Allergy
Specialists are available online at
www.allergy.org.au.
How can I confirm my
patient has stinging
insect allergy
Specific IgE antibodies to bee
venom, wasp venom and other
stinging insects may be detected by
in-vitro assays (RAST or ELISA tests)
on serum.
Specimens for these tests should
not be collected within one week
of a sting that caused a significant
reaction, as the levels may be
depressed following consumption of
the allergen-specific IgE antibodies
after the sting. Note that the actual
level of specific IgE antibodies to bee
venom may not correlate very closely
with the severity of the reactions
experienced by the patient.
A very small number of patients may
have negative in-vitro tests for insect
venom allergy but positive skin tests.
If your patient has a very definite
history of venom allergy but negative
in-vitro tests, further discussion with
your immunologist is recommended.
Some of these patients may have
IgG4 antibodies directed to bee
venom. Skin tests with insect venom
are another diagnostic option but
carry some risk of generalised
reactions. Tests for a range of ant
venoms are available. Jumper
ant venom tests are not routinely
available but have been performed in
a research laboratory environment.
Sometimes it is not clear that the
patient did, in fact, have a bite or a
sting and in-vitro tests can provide
strong circumstantial evidence that
this was the case!
Apart from first aid or
next-time strategy, what
else should I advise my
patients
Insect avoidance measures should
be stressed, including:
• Care with outdoor activities
• Use of covered footwear
• Avoidance of clothing with bright
colours or floral patterns
• Avoidance of scents. (This is
particularly appropriate for
bee-venom sensitive patients.)
• When patients eat outdoors, some
caution should be exercised with
food or beverages that have fruity
scents. Having a means to wash
hands and face is also important.
• When gardening, gloves and long
trousers may provide additional
protection.
Products with activity against flies
and mosquitoes have little value in
discouraging bees, wasps or ants.
Sprays that have activity against
wasps and bees are not suitable for
personal application.
When is venom
immunotherapy
indicated
Immunotherapy is indicated for
patients with a systemic reaction,
although there are certain issues
to consider. These include safety,
efficacy, relative risk of re-sting
vs risk of immunotherapy, cost,
convenience, as well as patient and
doctor preferences.
The risk of a second systemic
reaction in adults has been estimated
at 60-70%. In children this may be
10-20% if their initial reaction was
milder.
Immunotherapy is not indicated for
large local reactions, although most
have demonstrable venom-specific
IgE on RAST or skin prick tests.
Varying practices exist for venom
immunotherapy in regards to the
reagents, the regime, duration and
monitoring of therapy.
Initial Evaluation Tests
IgE
Specific
IgE
(RAST)
TRYPTASE
Bee Venom I1
Paper Wasp Venom I4
Yellow Jacket Venom I3
If you have any enquiries, please contact Dr Karl Baumgart on (02) 98 555 286
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Medicare Update
Tryptase
Measurement of tryptase is now
reimbursed by Medicare for the
following indications:
• Exclusion of mastocytosis
• Monitoring of known mastocytosis
• Assessment of risk (by excluding
mastocytosis) in persons with
stinging insect anaphylaxis
• Confirmation of anaphylaxis
in persons with unexplained
acute hypotension or suspected
anaphylactic events.
Specimen
Serum (clotted or gel tube)
Testing Frequency
Tryptase estimations are performed
weekly (occasionally more urgently
following discussion with
Dr Baumgart on 02 98 555 286).
Reference Range
Normal value: less than 13.5 ug/l
Interpretation
Anaphylaxis not due to parenteral
agents (venom or drugs) will not
raise Tryptase levels. Occasional
persons with mastocytosis may have
levels just within the normal range.
Persons with elevated levels after
‘reactions’ should be retested 1-2
weeks later to document a return to
normal and exclude mastocytosis.
Direct mast cell degranulating agents
should not be given to persons with
mastocytosis. Allergic persons with
mastocytosis are at much greater
risk of anaphylaxis and should have
access to self-injectable adrenaline.
Diagnosis of Helicobacter pylori Infection
The non-histological methods
for the investigation of possible
Helicobacter pylori infection
include the Urea Breath Test (UBT),
detection of H. pylori faecal antigen
(HpAg) and H. pylori serology
(HpIgG).
Urea Breath Test
Until recently, the Medicare rebate
for UBT was restricted to patients
known to have peptic ulcer
disease. It can now be claimed
when the test is done for the
diagnosis of H. pylori infection
in ANY patient and also in the
assessment of response to
treatment. The UBT is the test of
choice, therefore, when the patient
is old enough and cooperative
enough to allow successful
specimen collection.
Because the amount of
radioactivity present in the
dose of 14C-labelled urea is
a small fraction of our daily
exposure to environmental
radioactivity, the test is not
contra-indicated in women
who are pregnant or who are
breastfeeding.
H.pylori Faecal Antigen
When age or disability make
successful specimen collection
for the UBT unlikely or impossible,
the faecal HpAg test is a
useful alternative. Its reliability
approaches that of the UBT and
specimen collection (a random
stool sample) is straightforward.
There is a Medicare rebate for this
test.
H.pylori Serology
There are very few clinical
situations where H. pylori
serology is useful. Detectable
HpIgG is not diagnostic of active
infection, nor is post-treatment
serology a useful assessment of
the success or failure of therapy.
One of the direct diagnostic
methods (UBT or HpAg) is always
preferable.
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DOUGLASS HANLY MOIR PATHOLOGY • ABN 80 003 332 858
A subsidiary of SONIC HEALTHCARE LIMITED
14 GIFFNOCK AVENUE • MACQUARIE PARK • NSW 2113 • AUSTRALIA
TEL (02) 98 555 222 • FAX (02) 9878 5077
MAIL ADDRESS • LOCKED BAG 145 • NORTH RYDE • NSW 1670 • AUSTRALIA
BARRATT & SMITH PATHOLOGY
A trading name of DOUGLASS HANLY MOIR PATHOLOGY PTY LTD • ABN 80 003 332 858
A subsidiary of SONIC HEALTHCARE LIMITED
31 LAWSON STREET • PENRITH • NSW 2750 • AUSTRALIA
TEL (02) 4734 6500 • FAX (02) 4732 2503
MAIL ADDRESS • PO BOX 443 • PENRITH • NSW 2751 • AUSTRALIA
www.dhm.com.au
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