Doctors Newsletter - Douglass Hanly Moir Pathology

SUMMER 2000
Page 2
Editorial –
Partnership
and Core Values
Dr Colin Goldschmidt
Page 3
New Medical Director
Dr Annabelle Farnsworth
New Serology Tests
for Infectious Diseases
Page 4-6
No Spleen – So What?
Dr Debbie Clark
Page 7-9
Infections in Pregnancy
Dr Ian Chambers
Dr Miriam Paul
Page 10-11
TTG – A New Test
for Coeliac Disease
Dr Karl Baumgart
Page 12
Olympic wrap-up
Our Closing Ceremony
Doctors ’ Newsletter
www.dhm.com.au

Editorial
Dr Colin Goldschmidt
Managing Director
Partnership
and
Core Values
Service in Partnership
At Douglass Hanly Moir Pathology, we pride ourselves on
the quality of our testing and on the service we provide to
you and to your patients. In addition, as pathologists,
we see our interaction with you fundamentally as a
professional partnership.
Our principal pursuit is to maintain the very highest standard
of scientific accuracy and, to this end, our pathologists,
managers and scientific staff are fully involved in overseeing
all specimen testing and reporting on your patients.
However, we recognise that there are many other facets of
our operation that are important in your assessment of our
service. These include the relationships between our liaison
staff and your practice, our electronic download services,
our couriers and our collection centres and their staff.
Also, because we are committed to offering a personalised
service, we spend much time developing programs on our
mainframe computers that allow customised options to be
made available to satisfy the different needs of our doctors.
In essence, everything that we do is centred on the
concept of a partnership between your practice and
ourselves. In this partnership, we wish to help you,
wherever possible, in your day-to-day practice needs.
Practice Core Values
It is inevitable that the values a company follows impact
directly on the type of service it can provide. Therefore, you
may be interested to know what sort of behaviour we
encourage and adhere to within our organisation, and how
these principles have been developed.
We recently polled the majority of our staff members,
asking them to indicate what core values they believed
were important in an organisation such as ours.
Interestingly, there was significant agreement across our
company and this has allowed us to formalise our core
values in five “plain English” key statements.
These core values affirm that we:
• Commit to service excellence
• Treat each other with respect and honesty
• Demonstrate responsibility and accountability
• Strive for continuous improvement
• Maintain confidentiality
Our core value statements are relevant to each and every
one of us at Douglass Hanly Moir, no matter what our role
or the nature of our job. I believe that we can all be proud
to undertake a commitment to uphold these values and,
in so doing, strengthen and consolidate a culture that
benefits our partnership with you.
Recent Merger
We have recently initiated a merger with our sister practice,
Barratt & Smith Pathology, in order to eliminate unnecessary
overlap of our operations and to enhance the delivery of
our services, through the sharing of testing between our
central laboratory in North Ryde and the Barratt & Smith
laboratory in Penrith.
I would like to take this opportunity to warmly welcome
all Barratt & Smith doctors to Douglass Hanly Moir.
I thank you for your cooperation and understanding
through the past weeks of the merger and hope that you
find the new arrangements to your satisfaction. I trust
that this will mark the beginning of a professional
partnership between us.
To all our referring doctors, on behalf of our pathologists
and managers, may I wish you and your families a safe and
peaceful festive season. We thank you very much for your
ongoing support and look forward to further enhancing our
partnership with you into the future.
I warmly invite your comments at any time
and encourage you to contact me via
Phone 98 555 333 or Fax 9878 5066 or
Email colgold@msn.com.au
2

New Medical Director
We are pleased to inform you that, earlier this year,
Dr Annabelle Farnsworth accepted the position of Medical
Director of Douglass Hanly Moir Pathology. This senior
medical role was previously held by Dr Colin Goldschmidt,
concurrently with his role as Managing Director. Annabelle
will now fulfil the many functions relating to medical
management at Douglass Hanly Moir. Ours is a practice
that has always been managed by doctors for doctors,
and so the role of Medical Director is an extremely
important one.
As Medical Director, Annabelle is responsible, in
association with our other pathologists and with our
department managers, for ensuring that the highest
clinical and ethical standards are maintained in all areas
of our practice.
In this position Annabelle also takes on the role of
medical representative of our company and, as such, she
welcomes enquiries from doctors, medical practice staff,
hospital staff and others regarding any aspect of our
practice.
Dr Annabelle Farnsworth
Medical Director
Director of Cytopathology
Annabelle continues in her role of Director of
Cytopathology, an area where her considerable expertise
is well recognised. She does, of course, invite doctors to
continue to contact her if they wish to discuss any matter
concerning cytopathology.
We encourage you to contact Annabelle if
she can assist you in any way on
98 555 150 or Toll Free 1800 222 365
New Serology Tests for Infectious Diseases
Herpes specific serology
Herpes simplex type specific serology is now available.
This test reliably identifies those patients who have been
infected with HSV-2 and is of use when lesions are
beyond the stage where culture will be successful,
or when the patient is between episodes.
The test is performed on serum in our Immunochemistry
Department.
Treponemal Antibody Enzyme Immunoassay
Recently DHM has begun to use a Treponemal Antibody
Enzyme Immunoassay in screening for syphilis.
This assay has very high sensitivity and specificity for
the diagnosis of syphilis and will be a useful adjunct to
the other tests currently in use.
Enquiries regarding either of these tests
can be directed to Dr Ian Chambers or
to Dr Miriam Paul on 98 555 311
3

No spleen – So what?
A past history of splenectomy, especially if performed many
years previously, is easily overlooked in a consultation by
both patients and doctors alike. A patient may not be aware
of the details of past surgery or may have forgotten which
organ was removed!
Splenectomy is a not uncommon operation, affecting
around 1 in 1000 members of the population. A practitioner
would therefore expect to have several such patients in his
or her practice.
Lack of a spleen carries a significant lifelong risk of
serious and potentially preventable infection.
Some patients with inflammatory bowel disorders, coeliac
disease, or dermatitis herpetiformis develop splenic atrophy
and so are also at risk.
What are the life-long risks of
splenectomy?
Dr Debbie Clark
Haematologist
All asplenic patients carry the life-long risk of a
fulminant, often rapidly fatal, septicaemia associated
with disseminated intravascular coagulation.
This is usually caused by Streptococcus pneumoniae
(pneumococcus). Such cases have been described more
than 20 years post-splenectomy. (1), (2)
The risk of dying, although unquantifiable, is clinically
significant and the risk lifelong. It is highly likely that most
of these deaths are preventable by means of patient
education, prophylactic antibiotics and vaccination. (3)
It is most important that a patient who has had a
splenectomy knows that it is vital to seek medical attention
immediately if he or she develops a flu-like illness.
Long-term risks of splenectomy
are commonly overlooked.
Recent surveys reveal that only a minority of patients
without a spleen are aware of the risk of sudden
fulminant sepsis.
One reason is that it used to be thought that there
were no long-term problems associated with splenectomy,
and many patients were specifically told at the time
of their operation that there would be no serious
consequences.
Nowadays, however, the increased susceptibility to sudden
and severe infection in splenectomised patients is well
recognised. (4)
It is therefore recommended that splenectomised
patients should be actively sought out and given
appropriate advice. (5)
Who is at greatest risk?
• Children
• Patients in the early post-splenectomy period
• Patients whose surgery was performed for malignancy
or haemoglobinopathy (as compared to those who lost
their spleens as a result of trauma)
How can I know if my patient has had a
splenectomy?
Sometimes, as previously mentioned, the patient may not
be aware of, or has forgotten, details of previous surgery.
• Clues from the blood film
An unexpected clue to the absence of the spleen may
come from a routine full blood count. Patients who have
no spleen commonly have a subtle constellation of
changes on the blood film.
Characteristic changes include the presence of Howell
Jolly bodies, often in combination with target cells, burr
cells, a mild thrombocytosis and occasionally a mild
lymphocytosis. When these changes are seen our
haematologists will comment on possible asplenia.
This may act as a reminder that your patient may
require advice and vaccination.
• If there is any doubt as to the status of a patient
then an ultrasound can be performed.
4
This patient did not know what the scar in the left
upper abdomen signified.

No spleen – So what?
Ideally these are given 14 days prior to splenectomy
– they may be given simultaneously but in separate
syringes and at separate sites.
Booster doses of pneumococcal vaccine and
meningococcal vaccine are recommended every 5 years.
• Prophylactic antibiotics
Consider continuous prophylactic antibiotics for all
patients, but especially for children and for all patients
during the first two years post-splenectomy.
Suggested regimens are: (6)
Blood film from showing post-splenectomy changes
Target cell
Howell Jolly body
Which organisms pose a risk?
• Streptococcus pneumoniae (more than half of cases)
• Neisseria meningitidis
• Haemophilus influenzae type b
• Capnocytophaga canimorsus (animal bites)
• Malaria
• Babesiosis
How can post-splenectomy sepsis be
prevented?
• Increased awareness by clinicians
The risks of splenectomy may not have been
generally appreciated throughout the medical
profession. However, this condition poses an important
public health issue, in that healthy, and often young,
individuals may suffer a serious and potentially
preventable illness. The implication for litigation must
also be recognised, should a doctor fail to inform a
patient of possible risks.
• Patient education
At Douglass Hanly Moir Pathology we have
recognised the need for patient education and so, to
assist referring doctors and their patients, we have
published a pamphlet for patients dealing with the
implications of splenectomy. Titled “Have you had
your spleen removed? Facts you need to know”,
this pamphlet is available for you to use in your
practice. The information in the pamphlet is also
available on our website.
• Recommended immunisations for splenectomy (6)
The available vaccines to protect against infections
post splenectomy are:
• 23 valent pneumococcal vaccine
• quadrivalent meningococcal vaccine
• Haemophilus influenzae type b (Hib) vaccine for those
with close contact with children under 5 years of age
• Children under 2 years:
amoxycillin 20mg/kg orally daily
or
phenoxymethylpenicillin 125mg orally 12-hourly
• Adults and older children:
amoxycillin 250mg orally daily
or
phenoxymethylpenicillin 250mg orally 12-hourly
• Patients hypersensitive to penicillin:
roxithromycin 150mg
or
erythromycin 250mg orally daily
• Patient initiated treatment
In view of the fulminant nature of some of the infections
in question, it may be advantageous for the patient
to have a supply of antibiotics to take in case of the
onset of a flu-like illness. Suggested regimens are:
Augmentin 2 tablets stat. (or Bactrim if penicillin
sensitive).
• General practitioner initiated treatment
If the patient consults the doctor with a significant
flu-like illness then Ceftriaxone 1G imi/ivi stat. may be
given prior to transfer to hospital.
• Written information
It may be advisable to provide your patient with written
information to the effect that a splenectomy has been
performed and what is the status of immunisations and
prophylactic treatment. It is also advisable for a patient
to wear a Medic-Alert bracelet indicating their asplenic
condition.
• Travel overseas
Malaria is a much more serious disease in a
splenectomised person. A patient without a spleen
should avoid malarious areas if at all possible. If travel
to these areas cannot be avoided then the importance
of rigidly following prophylactic regimens must be
emphasised.
• Miscellaneous
Animal bites may transmit Capnocytophaga
canimorsus, one of the organisms mentioned above.
Patients should be advised to notify their doctor of any
animal bite.
5

No spleen – So what?
Checklist for doctors
Do you have any patients with a past history of
splenectomy?
If so…
✓ Are they aware of the lifelong risk of overwhelming
post-splenectomy infection?
✓ Have they been given clear instructions about the need
to seek immediate medical attention for flu-like
illnesses?
✓ Have they discussed with you the pros and cons of
penicillin prophylaxis or keeping a supply of antibiotics
at home in case of emergency?
✓ Have they had pneumococcal and other recommended
vaccinations?
✓ Are they aware of the special need for caution when
travelling overseas?
Websites
1. For doctors:
www.rph.wa.gov.au/labs/micro/spleen.html
2. For patients:
www.leukaemia.demon.co.uk/spleen.htm
(Note that this is part of the Leukaemia Research Fund
website but the information is good quality and
applicable to all splenectomised patients. Patients
would of course need advising, where applicable, that
their own condition had no connection with leukaemia.)
3. This article and our patient information leaflet are
available on the Douglass Hanly Moir Pathology
website: www.dhm.com.au
References
(1) Cullingford G.L. et al. Severe late post splenectomy
infection. Br. J. Surg. 1991 78:716-721.
(2) Lambert H.P. Guidelines for the prevention of infection
in the patient with an absent or dysfunctional spleen.
British Medical Journal. 1996 312; 430-434.
(3) Management of risk of overwhelming sepsis in adult
patients post splenectomy Dr Roger Wilson,
Department of Microbiology and Infectious disease,
Royal Perth Hospital, Perth. 1996.
www.rph.wa.gov.au/labs/micro/spleen.html
(4) Whittaker A. N. Infection and the spleen: association
between hyposplenism, pneumococcal sepsis and
disseminated intravascular coagulation. Med. J. Aust.
1969 1:1213-19.
(5) Spelman D.W. Editorial: Postsplenectomy overwhelming
sepsis: reducing the risks. Med. J. Aust. 1996 164: 648.
(6) Therapeutic Guidelines: Antibiotic
11th Edition 2000/2001
➜
Patient pamphlet
“Have you had your spleen removed?
Facts you need to know”
This pamphlet can be obtained from your Area
Manager or our Stores Department (98 555 210).
For further advice on the issues raised in
this article please do not hesitate to contact our
haematologists or microbiologists
on 98 555 311 or Toll Free 1800 222 365
6

Infections in Pregnancy
Although many women may attend an obstetrician for
ante-natal care, general practitioners are often consulted
for medical problems during pregnancy. One such area is
that of infectious diseases. This article deals with some of
the more serious infections which can occur during
pregnancy and which can be difficult to diagnose.
Many infectious agents can cause problems for either the
mother or fetus in pregnancy. Among these are:
Bacteria
• Syphilis
• Gonorrhoea
• Chlamydia trachomatis
• Group B Streptococcus
• Listeria
• Mycoplasmas
• UTI
Viruses
Others
• Rubella
• Parvovirus B19
• Cytomegalovirus (CMV)
• Varicella-Zoster virus (VZV)
• HIV
• Hepatitis B and C (HBV/HBC)
• Toxoplasma gondii
• Malaria
Dr Ian Chambers
Director of Microbiology
What are the potential problems of
maternal infection?
• Transplacental transmission of some agents to the
fetus during pregnancy can cause congenital
malformations.
e.g. CMV, Rubella, VZV, Syphilis
• Stillbirth and premature labour are possible
complications of some infections.
e.g. Listeria, Bacterial Vaginosis.
• Other organisms may be transmitted in the
peri-natal period.
e.g. Gonorrhoea, Hepatitis B and HIV.
Ante-natal screening in Australia currently
involves testing for:
Rubella (IgG)
Syphilis
Hepatitis B (surface antigen to detect carriers)
Group B Streptococcus
Urine microscopy and culture
The above protocol has been adopted because these
infections can cause significant morbidity. There are
sensitive and specific screening tests for them and safe
and effective intervention is available if infection (or
susceptibility to infection) is detected.
The protocol detects:
• Maternal infection which can be treated
e.g. Syphilis, UTI
• Maternal infection which may require intervention
e.g. Rubella
• Maternal susceptability to infection
e.g. Rubella
• Carriage of infectious agents which require prophylactic
treatment at the time of delivery
e.g. HBV, Group B Strep.
In general, screening for other agents is not recommended
unless there is a specific clinical illness being investigated,
or in situations of specific risk (e.g. HIV).
In particular, the use of IgM assays in asymptomatic
women is inappropriate, as misleading, positive results
can occur.
For example:
Dr Miriam Paul
Clinical Microbiologist
Infectious Diseases Physician
• Persistent positive rubella IgM may occur in pregnancy
• Toxoplasma IgM may persist for many months after
infection
• CMV IgM is commonly seen during reactivation, which
is of little risk to a pregnancy
7

Infections in Pregnancy
Cytomegalovirus (CMV)
Primary infection with CMV in pregnancy is the
commonest cause of congenital abnormality in
Australia. Reactivation is rarely a problem.
Around 50% of the Australian population are immune
to cytomegalovirus (IgG positive). Reactivation during
pregnancy occurs in 10-30% of seropositive women
but rarely causes fetal problems, despite virus being
transmitted to the fetus in 10%.
women who have not received ZIG, once blistering
lesions appear.
The highest risk of fetal damage (2%) from maternal
infection occurs at 13-20 weeks gestation. Skin scarring
in a dermatomal distribution (which occurs due to the
occurrence of shingles in utero), with occasional
associated limb hypoplasia is the commonest malformation.
Neurological abnormalities are much less common.
Primary CMV infection in pregnancy is significant.
• This occurs in 1-2% of seronegative pregnant women,
causing a glandular-fever type of illness.
• Transmission across the placenta causes fetal infection
in 20-50% of cases, leading to fetal damage apparent
at birth in 10% of those infected (i.e. an incidence <
1/1000 pregnancies).
• Severe fetal damage may manifest as a purpuric rash,
hepatosplenomegaly and jaundice, and neurological
damage.
• A further 15% of congenitally infected infants appear
normal at birth but develop late sequelae, particularly
deafness.
Diagnosis of maternal infection is made by serology in a
symptomatic woman, with IgG seroconversion occurring in
association with the presence of IgM. Confirmation of
fetal infection is then made by culture and PCR testing of
amniotic fluid, which is most sensitive after 20 weeks
gestation. CMV viral load in amniotic fluid may be predictive
of the degree of fetal impairment. Serial ultrasound testing
is insensitive.
Varicella-zoster virus (VZV)
This is the causative agent of chickenpox and shingles.
Approximately 90% of Australian adults are immune, even
if they do not recall a past illness.
Primary VZV infection in pregnancy may cause:
• severe, possibly fatal, maternal chickenpox
• congenital malformations in the fetus
• severe neonatal chickenpox (if infection occurs
around term)
Chickenpox in pregnant women only comprises 2%
of all adult chickenpox cases but 25% of all chickenpox
deaths occur in this group. Infection may be more severe,
with pneumonitis, encephalitis and myocarditis occurring.
Prevention of maternal chickenpox is achieved by
administration of Zoster Immune Globulin (ZIG) to
seronegative pregnant women within 72 hours of
significant exposure to a case of chickenpox. Of note, this
may not prevent fetal infection. Aciclovir can be given to
Scarring which occurred as a result of in utero infection with VZV
Neonatal chickenpox can be life-threatening when maternal
chickenpox occurs within the 7 days prior to delivery and
up to 7 days after birth. The high infant mortality rate of
30% is due to transplacental transmission of a large amount
of virus, with no protective maternal antibody yet present.
Management of perinatal maternal chickenpox involves
administration of ZIG to the neonate within 72 hours of
delivery. Maternal shingles is not an indication for ZIG as the
baby receives the mother’s protective antibody transplacentally.
Toxoplasma gondii
This is an ubiquitous protozoan parasite. The cat family is
the definitive host but humans and other animals can also
become infected. In humans infection most commonly
occurs due to eating tissue-cysts in undercooked meat
(e.g. rare steak). Transmission can also occur through
contact with soil and working with animals.
Interestingly, a recent study found no significant
association between infection and the presence of
cats (adult or kitten) in the household. Although cysts
are passed in cat faeces they must mature in soil for
several days prior to becoming infective. The prevalence
of infection is high in some countries (e.g. in France and
Central America it is 80-90%), whereas in Australia only
30-40% of the population are seropositive (i.e. immune).
Congenital infection follows PRIMARY maternal
infection and transmission to the fetus depends on the
stage of pregnancy, being lowest in the 1st trimester (25%)
and rising in later pregnancy (2nd trimester 54%, 3rd
trimester 65%). Conversely, the magnitude of fetal damage
is greatest early in gestation. The majority (85%) of infected
fetuses have mild or sub-clinical infection. Symptomatic
infection at birth consists of neurological abnormalities,
chorioretinitis, jaundice and rash.
8

Infections in Pregnancy
There is no significant association
between infection with
toxoplasmosis and
the presence
of cats or
kittens
in the
home.
Diagnosis
Diagnosis of
infection during
pregnancy can be
difficult, as maternal infection
may be asymptomatic. In symptomatic
women, maternal serology is performed to demonstrate
IgG seroconversion in association with the presence of
IgM. It is important to note that IgM can persist for many
months and even years after infection. IgA detection may
be useful in establishing the timing of infection, as it does
not persist as long. Amniocentesis is then performed at 18
weeks gestation to confirm fetal infection. PCR performed
on this fluid is extremely accurate. Fetal blood sampling in
utero is occasionally performed to measure IgG, IgM, and
IgA, and serial ultrasound may reveal neurological
abnormalities in utero.
Rubella
?
At least 95% of women of childbearing age in Australia
are rubella immune, but congenital rubella still occurs,
especially when primary infection occurs in the first
trimester.
Primary infection in the first trimester results in up
to 90% of fetuses developing major congenital
malformations. Approximately four congenitally infected
children are born annually in Australia, and 25% of the
mothers have no history of exposure or clinical illness.
• When rubella exposure occurs during pregnancy the
index case should be confirmed by serology (detectable
IgM) and the pregnant woman should have IgG and
IgM measured.
• Repeat serology 4 weeks after exposure is
recommended, looking for seroconversion or a
significant IgG rise.
When a positive IgM result is found in pregnancy it has
been established that only 42% are due to acute rubella
infection (this is particularly important in asymptomatic
patients). Sucrose gradient fractionation testing can be
performed at a reference laboratory to confirm whether
this IgM is of recent origin, and thus likely to be associated
with fetal infection.
Reinfection with rubella in pregnancy may occur,
particularly in women with low-level immunity following
vaccination, but the infection is not usually viraemic and
therefore fetal problems are much less common
(around 5%) than in primary rubella infection.
Parvovirus
Fifth disease (also known as slapped cheek disease and
erythema infectiosum) has an incubation period of 1-3
weeks and occurs mainly in primary school age children.
Infection in pregnancy does not result in congenital
malformations but can cause stillbirth in 5-10%, due
to fetal hydrops.
Hydrops develops within 8 weeks of maternal infection
(average 5 weeks) and is most likely when infection occurs
in the second trimester. The condition is due to the
development of anaemia in the fetus, which is more likely to
occur in the second trimester when major RBC
production is occurring.
When exposure occurs in pregnancy
• Maternal immunity (IgG) should be checked, as 50-60%
of the population is immune.
• Symptomatic non-immune women should have infection
confirmed (IgM detected with IgG seroconversion).
• If maternal infection is confirmed, weekly fetal
ultra-sound is performed for 6-8 weeks, looking for
hydrops.
• If hydrops occurs in the fetus, cordocentesis is
performed for fetal diagnosis (by Parvovirus PCR or
IgM) and intrauterine transfusion may be undertaken,
with an 85% success rate.
The overall survival rate of hydropic fetuses is 63%; with
34% of these spontaneously resolving, 33% stillborn and
33% requiring intrauterine transfusion.
HIV
Maternal HIV infection is uncommon in Australia, but only
60% of infected women are diagnosed ante-natally in
Australia. Counselling prior to testing is important as
indeterminate results may occur in uninfected people.
Intervention is possible if infection is diagnosed
ante-natally, and reduces transmission of HIV to the baby
by more than 70% (to about a 5% transmission rate).
Treatment consists of combination antiretroviral drugs for
mother and baby, caesarean section and the avoidance of
breast feeding, which can transmit the virus.
9

TTG – A New Test for Coeliac Disease
Dr Karl Baumgart
Director of Immunology
Autoantibody tests are important tools for the
initial investigation of coeliac disease, which is
then best confirmed by small bowel biopsy.
The recent identification of tissue transglutaminase
(TTG) as the main autoantigen provides a strong
biological basis for a new important laboratory test
for coeliac disease. Detection of TTG antibodies is
now our preferred specific laboratory marker for
coeliac disease, although we will continue to offer a
range of laboratory tests for coeliac disease.
Strategies for best use of these tests, their clinical
significance and common pitfalls in interpretation
of results are described below.
What laboratory tests do we have available
and can you tell me a bit more about them?
IgA and IgG Gliadin Antibodies
IgA and IgG antibodies can be detected by ELISA tests.
The results are reported in “units” and the values of these
results exhibit a good dynamic (broad) range of values.
Usually IgA gliadin antibodies are negative after 6-9
months of a gluten-free diet and IgG gliadin antibodies
become negative after 12-18 months of a gluten-free diet.
This assay is very sensitive, but less specific for
identification of patients with coeliac disease. The results
are almost invariably strongly positive in patients with
coeliac disease not on a gluten-free diet, but low-level
positives do not necessarily have clinical significance.
Thus, although human TTG has been identified as “the
autoantigen” in coeliac disease, the slight differences in
the TTG used in these assays may account for the
observation that this assay does not achieve 100%
sensitivity and specificity. The results exhibit a
reasonable dynamic range, and the results are reported
in units over a “cut-off” value. Although not perfect,
this assay has very high sensitivity and specificity.
IgA antibodies to TTG become negative 9-24 months after
commencement of a gluten-free diet.
This assay is now our preferred specific laboratory
marker for coeliac disease testing.
What are the pitfalls in interpreting these
test results?
• IgA-dependent serology is useless in patients with IgA
deficiency, which occurs in 1:300 of the population,
so measuring total IgA is a necessary part of the
laboratory investigation.
• Gluten restriction will result in lowering and
subsequently disappearance of all of the lab markers.
• Do not forget clinical syndromes from wheat
exposure may result from other mechanisms including
IgE-mediated wheat allergy, non-immunological
intolerance of wheat or preservatives used in wheat
products (propionates).
If I have to persuade the patient to eat
wheat again for the sake of some tests,
how long do they have to do this for?
?
These tests mainly have utility for monitoring patient
compliance with a gluten-free diet.
IgA Endomysial Antibody
This antibody is detected by indirect immunofluorescence
on a glass slide of primate oesophagus. Of the assays
available, this assay has the greatest specificity, but on
occasion it can be less sensitive. In most patients with
coeliac disease, this assay becomes negative after 12-18
months of a gluten-free diet.
10
IgA Tissue Transglutaminase Antibody (New test)
This antibody is detected by ELISA assays. There are
subtle differences between the different commercial
assays for this autoantibody since some use recombinant
antigens and others use TTG purified from guinea pig.
A minimum of two weeks of regular wheat intake would be
a reasonable “rechallenge” period.

TTG – A New Test for Coeliac Disease
What tests should I request when I am
considering the diagnostic possibility of
coeliac disease?
Coeliac screens should always include a total IgA,
one sensitive marker and one specific marker.
Our recommendations may alter along with further
changes in tests but at present we would recommend:
PREFERRED OPTION
Total lgA
Gliadin IgA, IgG antibodies
Tissue transglutaminase IgA antibody
Are the lab tests going to be helpful if I
am sending my patient for an endoscopy
anyway?
If the laboratory tests for coeliac disease are negative,
you will not have to refer a patient for an endoscopy to
eliminate coeliac disease, but endoscopy may still be
appropriate if clinical entities other than coeliac disease
are to be considered.
Followup endoscopy may not be needed If patients
have a good clinical response to gluten-restriction and
demonstrate normalisation of laboratory markers of coeliac
disease (gliadin, endomysial or tissue-transglutaminase
antibodies) and its consequences (iron deficiency, changes
in blood count at presentation). However, for most patients,
a progress endoscopy after introduction of gluten restriction
is not unreasonable.
If discordant, then do Endomysial IgA
➜
➜
ALTERNATIVE OPTION
Total lgA
Gliadin IgA, IgG antibodies
Endomysial IgA antibodies
If discordant, then do TTG IgA
Normal duodenal mucosa. Note the long, “finger-like” villi on the surrface.
The alternate specific marker should be requested
if there are discordant results. The same antibody
markers should then be used for monitoring the
effect of gluten restriction.
How do serum markers relate to the need
for endoscopy and biopsy?
Patients with adequate gluten intake (at least two weeks
of regular wheat) should be referred for serology before
biopsy as negative serologic markers may raise the index
of suspicion for other clinical problems!
Patients with unequivocally positive coeliac markers or IgA
deficiency should be referred for endoscopy and biopsy to
document the extent of mucosal abnormality and confirm a
histological diagnosis.
Duodenal mucosa in coeliac disease. Note that the surface is almost flat
(“sub-total villous atrpophy”). These mucosal changes can revert to
normal or near normal on a gluten-free diet.
11

Olympic wrap-up
Our Closing Ceremony
We have now completed our involvement with the Sydney
2000 Olympic and Paralympic Games. Like other support
services associated with the staging of the Sydney 2000
Games, we are pleased to be able to say that all went
according to plan.
Sonic Healthcare was the Official Provider of Pathology
Services for athletes and Olympic Team members. Sonic
laboratories around Australia were involved in testing of
athletes prior to the Games, however, Douglass Hanly Moir
Pathology was responsible for setting up the laboratory in
the Polyclinic at the Athletes’ Village and for conducting
testing during the actual Games period. The laboratory was
completely fitted out and was functioning at a NATA approved
standard within a few weeks – something of a record!
Dr Grahame Caldwell was the Medical Director of the
laboratory and Sally Johnston, who is our Laboratory
Manager at Mater Hospital, Crows Nest, also took on the
role of Laboratory Manager at Homebush Bay. Geoff
Gibson, our Administration Manager, was Director of
Pathology at the Olympic laboratory and had overall
responsibility for our operation.
During the Games period our laboratory was open
15 hours a day and we also provided an out of hours
service for emergencies.
Although our on-site laboratory staff members were in the
centre of the “action” – the laboratory overlooked the main
stadium – because of the special involvement of our practice
at the Games, our entire staff felt part of the experience.
We were kept up to date with the happenings at Homebush
Bay through staff bulletins; our courier cars all flew the
Australian flag and, like many others around the country, we
followed the events on “the big screen” at every opportunity.
The Polyclinic had its own closing ceremony (a party!).
Then the lab was dismantled – again in record time. We
understand that the area where our laboratory was situated
will become part of a new primary school.
We are proud of the part our practice played during the
Sydney 2000 Olympic and Paralympic Games.
12
DOUGLASS HANLY MOIR PATHOLOGY PTY LIMITED • ABN 80 003 332 858 95 EPPING ROAD • NORTH RYDE • NSW 2113 • AUSTRALIA
A subsidiary of SONIC HEALTHCARE LIMITED
TEL 98 555 222 • FAX 98 555 111
MAIL ADDRESS • LOCKED BAG 145 • NORTH RYDE • NSW 1670 • AUSTRALIA