Government of Western Australia
Department of Health
Public Health
Dear Colleague
BonSoy soy milk: information for Medical Practitioners
5 Key points for Medical Practitioners
BonSoy soy milk has been withdrawn from the marketplace following detection of
1.
high levels of iodine in this product. This product should not be consumed.
Several adult cases in NSW have been diagnosed with thyroid conditions
2.
believed to be associated with consumption of BonSoy soy milk.
In addition, a newborn has been diagnosed with hypothyroidism secondary to
3.
iodine excess following maternal consumption of BonSoy during the pregnancy.
Doctors should be alert to seek information about BonSoy soy milk consumption
4.
by any persons presenting or who have presented in the past months with
thyroid conditions.
Medical practitioners should report all suspected cases of thyroid disease where
5.
BonSoy soy milk is involved to the Communicable Diseases Control Directorate
during business hours on tel. 9388 4999 or fax 9388 4848.
BonSoy is a soy milk product distributed nationally in Australia. Tests have shown it to
contain extremely high levels of iodine and consumption has been linked to clinical
thyrotoxicosis and, less commonly, hypothyroidism. Iodine crosses the placenta and may
cause foetal and neonatal hypothyroidism which can cause developmental problems in the
newborn.
Exceeding the safe upper limit for iodine intake may occur when 30ml is consumed per day
by an adult, or 5ml for a child.
Recommended levels of Iodine
The recommended daily intake for iodine depends on age and life stage:
• Younger children (1 to 8 years) – 90µg
• Older children (9 to 13 years, boys and girls) – 120µg
• Adolescents (14 to 18 years) – 150µg
• Men – 150µg
• Women – 150µg
• Pregnancy and breastfeeding – 220µg and 270µg respectively.
The recommended safe upper limit for iodine is:
• Young children (1 to 3 years) – 200µg
• Older children and Adolescents (14 years) – 900µg
• Adults – 1,100µg
Signs and Symptoms excessive iodine intake
Excessive iodine can lead to hyperthyroidism or, less commonly in adults, hypothyroidism.
Infants appear more susceptible to hypothyroidism following excessive iodine exposure.
The commonest symptoms of hyperthyroidism are palpitations, fatigue and weight loss.
Hypothyroidism is often insidious and, in mild cases, may only be detected on routine
screening but it can cause fatigue, weight gain and mental clouding.
Medical Management
• Patients should be advised not to consume the product and to dispose of it either
down the drain or in the garbage bin.
• Iodine has a half life of approximately 30 days.
• When a patient presents with a history of prolonged BonSoy soy milk consumption
together with symptoms or signs listed above, Medical Practitioners should consider
measurement of TSH. If the TSH is abnormal, proceed to measurement of the
urinary iodine level (normal range in children 100-500 ug/L) and thyroid antibodies
and consider referral to an endocrinologist or at least try to obtain phone
consultation with an endocrinologist. There is no need to measure the urinary iodine
level if the TSH is normal (Normal range 0.3-4.0 mU/L, can vary between
laboratories) as stopping the ingestion of the milk will return the body’s iodine levels
to normal within a few weeks.
• Advice to patients who report they have drunk the milk and are pregnant: see your
GP or obstetrician for a TSH measurement. The baby may also need additional TSH
and free T4 measurement after birth (but this is usually routinely done with the
Guthrie heelprick test); If the TSH is abnormal, then thyroid ultrasound and thyroid
scan are indicated. The effect of the high iodine levels will be to block synthesis of
thyroid hormones causing hypothyroidism which in the neonatal period could cause
a permanent loss of cognitive function.
• Suspected cases should be reported during business hours to the Communicable
Disease Control Directorate on 9388 4999, fax number 9388 4848.
Advice for the general public about the recall of BonSoy soy milk product and a fact
sheet about iodine is available on the Food Standards Australia and New Zealand
website: http://www.foodstandards.gov.au/
Thank you for your support in this matter.
Yours sincerely
Dr Tarun Weeramanthri
Chief Health Officer
Department of Health

PLEASE note scheduling changes for the following OTC Cough and Cold medicines for children aged 2-12 years old:

1. Anthistamines: Brompheniramine, Chlorpheniramine (PIRITON), Dexchlorpheniramine, Diphendyramine (BENADRYL), Doxylamine, Pheniramine, Promethazine (Phenergan), and Triprolidine.
2. Antitussives: Codeine, Dextromethorphan, Dihydrocodeine, Pentoxyverine and Pholdodine.
3. Expectorants/mucolytics: Ammonium chloride, Bromhexine, Guaifenesin, Ipecacuanha, Senega and Ammonia.
4. Decongestants: Oxymetazoline, Phenylephrine, Pseudoephedrine and Xylometazoline.

Regulatory authorities for 5 countries: Australia, USA, UK, Canada and New Zealand have conduct safety and efficacy reviews of these medicines for children under 2 years old and concluded they should not be given to children in that age group.

The TGA (Australia) proposes that:

* OTC cough and cold should NOT be used ofr children <6 years old and only for children between 6-12 years old on the advice of doctors and pharmacists.

It is definitely good to be back in KL,albeit for a very short visit.

For friends who were interested in doing the MRCGP as an alternative to the Fellowship exams;please take note.

For the MRCGP Int, i was just informed last week that the RACGP Assessment Unit in Melbourne have no idea how to "assess" it. Apparently between June 23rd (when i sat for my AKT exam of the FRACGP as part of the specialist pathway) and now, they have changed theri minds yet again and do not think it is "equivalent"

I wrote to the RCGP UK and UK PMETB and apparently with the MRCGP Int you can actually apply under the CESR pathway to obtain a certificate equal to the CCT. Please see the quote below regarding the process you need to go through:

In the first instance, you will need to pass the General Medical Council’s PLAB test before you can apply for a license to practice in the UK. In order to practice in the UK as a substantive Consultant, you must also be registered on the GMC’s Specialist register.



Please see link below for more information regarding the PLAB test:

http://www.gmc-uk.org/doctors/plab.asp



Furthermore, in order to be registered on the GMC’s specialist register you will need to get the Certificate of Eligibility for Specialist Registration (CESR) award from PMETB.

This will ascertain whether your training abroad matches the UK standard. After being awarded a CESR, you will be eligible for specialist registration.



Below is a link with more information and Frequently Asked Questions (FAQs) about the equivalence routes to the specialist register and GP registers.



http://www.pmetb.org.uk/index.php?id=961


It is a bit fairer as the pathwya is clear and they do not change it every minute like the RACGP in Australia.


For instance take a look at this letter they sent in March 2009:

Further to our correspondence, we acknowledge your desire to undertake the RACGP assessment in March 2009. As you are aware, in July 2008 the RACGP Specialist Pathway (SP) was introduced as a tailored program for international medical graduates (IMGs) wanting to work in Australian general practice. This pathway is intended for IMGs who do not have Australian medical registration.

According to your application, you have already been granted medical registration in Australia, hence you were notified that enrolment in the RACGP assessment could not take place unless you met the enrolment eligibility criteria for the practice eligible route. We identified that this may have created an obstacle with the medical board, as your registration was conditional pending the undertaking of the RACGP Applied Knowledge test (AKT). Hence we offered you the opportunity to enter into the Specialist Pathway which will enable you to sit the AKT without meeting your GP experience time requirements. Please see 'The Assessment Handbook for Candidates- eligibility for Assessment' http://www.racgp.org.au/assessmenthandbook.

The policy still remains the same; that you either continue down the practice eligible route and fulfil the GP experience time requirements or enter into the SP. Due to the difficulty this presents to you, the RACGP are reconsidering this policy and a review is underway. As you can appreciate, this review may take some months before an outcome is published. We are aware of the time constraints you are under hence we propose a short term solution to your current situation.

We have made arrangements for a special sitting of the AKT on 23 June 09 in Sydney. We anticipate that by the time your results are released, we will be better positioned to advise you of what is required to proceed with the final exam segments and eventually achieving the Fellowship of the RACGP.


However this has changed AGAIN and now they switched me to a Practice Based Assessment!.

Latent Autoimmune Diabetes in Adults (LADA) is a slow progressive form of Type 1 Diabetes.

* autoimmune destruction of pancreatic B-islet cells leading to an absolute insuloin deficiency within 2-6 years.
* Distinguished from Type 2 DM by presence of Islet autoantibodies especially to Glutamic Acid Decraboxylase (GAD)

TYPE 2 DM:

* progressive deterioration in glucose tolerance caused by insullin sensitivity and insulin secretion defects.
* Risk factors are: Obesity, hypertension, dyslipidemia and insulin resistance; a strong family history is also a risk factor.

TYPE 1 DM:

* absolute deficiency in Insulin secretion, and usually arises in children aged 15 years or younger.
* 13% of all diabetes in Australia
* Specific autoimmune destruction of insulin producing B-cell in pancreas leading to a dependency in insulin replacement.
* Serological markers for this autoimmune process include: Islet cell cytoplasmic autoantibodies (ICA), autoantibodies to to GAD and insulin or to the tyrosine phosphate IA2.

Patients with LADA:

* more likely to be symptomatic
* poor glycemic control
* existence of other autoantibodies (GAD)
* present clinically as osmeone with Type 2 DM, do not require insulin immediately after diagnosis and may be overweight.
* UKPDS 1997: one in 10 adults aged 25-65 years with Presumed Type 2 DM actually had GAD antibodies.

SUMMARIZED FROM AUSTRALIAN DOCTOR DIABETES SUPPLEMENT NOV 2009
8 different classes of medications are now available for treatment of diabetes:

1. GLP-1 and DPP-IV
2. insulin 1921
3. Sulfonylureas:stimulate insulin release 1946
4. Metformin:reduced hepatic glucose production and insulin resistance 1957
5. Acarbose: reduces carbohydrate digestion 1995
6. Thiazolidinediones "glitazones": reduce insulin resistance 1997
7. Repaglinide: short term insulin stimulation 1997
8. Exenatide GLP-1 Analogue 2005
9. Sitagliptin DPP-IV inhibitor enhances GLP-1 action 2006

GLP-1 resembles the structure of glucagon but has an OPPOSITE physiological effect:

1. PROMOTES insulin secretion
2. INHIBITS glucagon release
3. REDUCES circulating glucagon levels

GLP-1 is released from the gut wall in response to food. it is degraded very rapidly by enzyme dipeptidyl peptidase-IV (DPP-IV)

New GLP-1 based therapies are: Exenatide an INJECTABLE GLP-1 analogue or mimetic, DPP-IV INHIBITORS such as sitagliptin which slow degradation of GLP-1 and boosts its effects.

LOW RISK HYPOGLYCEMIA FROM TREATMENT AS EFFECT of GLP-1 DECLINES as blood glucose levels fall.

EXENATIDE
developed from exendin-4 compound of Gila monster salivary gland.
In clinical trials: S/c EXENATIDE BID decreased HBA1C by 0.8-0.9% and associated with INCREASED SATIETY, REDUCED APPETITE, WEIGHT LOSS and low rate of hypoglycemia.

side effects"nausea, sweating, vomiting, dizziness,
weight loss 2.5kg at 12 momths using exenatide compared to 2.9kf weight gain with insulin.

PROF DRUCKER from Banting and Best Diabetes Centre in Toronto recommends: EARLY combination therapy with METFORMIN and Sitagliptin.
METFORMIN ALSO STIMULATES GLP-1 SECRETION!
GLP-1 is also CARDIOPROTECTIVE.
Sitagliptin is indicated in Australia for combination therapy woth metformin, sulfonylureas and thiazolinedinediones.

Consensus recommendations from American Diabetes Association and European Association the Study of Diabetes (Diabetes Care 2009;32:193-203):

* Tier 1 medications with well-established safety records and efficacy are diet, eexrcise, metformin, insulin and sulfonylureas.
* Tier-2 less 'well validated" are pioglitazone and GLP-1 agonist exenatide. Useful if recurrent hypoglycemia or for promotion of weight loss.
* Other therapy includes: acarbose, repaglinide, DPP-IV inhibitors such as sitagliptin.

CHANGING CONCEPTS TYPE 1 & 2 DIABETES.
Summarized from Australian Doctor Supplement November 2009

Prof Len Harrison at IMR Melbourne reviewed links between "diabetogenic" environment and causes and classification of diabetes (Nature Reviews Endocrinology 2009;5:483-89).

* increasing numbers children,adolescents and adults have BOTH autoimmunity against beta cells (typical of Type I DM) AND Insulin resistance (classical of Type 2 DM)
* =DOUBLE DIABETES=Latent autoimmune diabetes in youth, latent autoimmune diabetes in adults and type 1.5 diabetes
* likely environment that fosters expressions of genes once posed only a low risk.

ENVIRONMENTAL CHANGES PROMOTING DIABETES:

1. Increased total intake of food:high fat, trans fatty acids, fructose, low fibre
2. Changes in exposure to pathogens (hygiene hypothesis)
3. Low levels Vitamin D as hormone as well as Vitamin assoc with increased risk Type 1&2 DM.
4. Heating and cooling of buildings has reduced need to expend energy to thermoregulate.
5. Shorter periods of sleep tend to increase weight gain.

POSSIBLE INTERVENTIONS:

1. healthy diet and exercise
2. normalizing sleep
3. re-acquaint with temperatures outside thermoneutral zone
4. vitamin D therapy serum levels >70ng/ml target
5. EARLY use METFORMIN and THIAZOLINEDIONES which might preserve beta cell function in type 2 and even type 1 DM.
6. PREVENTION IS ONLY SUSTAINABLE APPROACH

Protecting beta cells:

* 80% of beta cells have been destroyed by the time a patient presents with Type 1 DM, 60% when presenting with Type 2 DM.
* METFORMIN, STIGAGLIPTIN, THIAZONELINEDIONES might slow rate decline of beta cells.

CLASSIFICATION DIABETES (American diabetes association)

* >50 types!!Type 1 DM 10%
* Type 2 DM
* Gestational DM (5% all Aussie women), 13% women aged 45-49 and higher in Aboriginals, torres straits islanders and south Asian women.

TREATMENT TARGETS FOR DIABETES
UKPDS Study 1998

* looked at patients with newly diagnosed DM assigned intensive control with METFORMIN, Sulfonylurea or insulin or conventional treatment with diet alone.
* Median HbA1C of 7.0-7.9% only achieved.
* only half achieved target 7.0% even after intensive treatment.
* better control lead to 12% reduction in all diabetes endpoints ESP. microvascular events.
* MI and all-cause mortality reduced in obese patients treated with MTF as firstline.

ACCORD STUDY 2008

* 10,000 patients, average age 62 years with longstanding disease and had established CVD or increased risk
* randomised to intensive therapy to reach HBA1C 6.0% or conventional therapy 7.0-7.9%

Trial stopped: all-cause MORTALITY INCREASED with INTENSIVE glucose lowering ( 5.0% vs 4.0%)
-->reasons for death unknown

AUSTRALIAN TREATMENT TARGETS

* general target: <7.0%
* Diabetes if short duration (10 years in younger patients/<20 years in older patients and no cardiovascular disease)
* + require lifestyle modification=<6.0%
* +require antidiabetics other than MTF and insulin=<6.5%
* requiring insulin =<7.0%
* Pregnancy or planning pregnancy=<6.0%
* Diabetes of longer duration or clinical cardiovascular disease=<7.0%
* Recurrent severe hypoglycemia or hypoglycemia unawareness <8.0%

HBA1C vs estimated average glucose (mmol/L)

* 5% = 5.4mmol/L
* 6% =7.0mmol/L
* 7%=8.6 mmol/L
* 8%=10.2 mmol/L
* 9%=11.8 mmol/L
* 10%= 13.4 mmol/L
* 11%=14.9 mmol/L
* 12%=16.5 mmol/L

DATA FROM DIABETES CARE;2008; 1473-1478.