Pathology rent cap will cost patients, doctors

The AMA has warned that Federal Government proposals to cap pathology collection centre rents will likely drive up patient out-of-pocket costs and could force some medical practices out of business.

In a strongly worded letter, AMA President Dr Michael Gannon has appealed to the Small Business and Family Enterprise Ombudsman, Kate Carnell, to intervene and help try to convince the Government to drop its plan.

Dr Gannon said the proposal, announced during the Federal election, to change provisions in the Health Insurance Act would allow the two major pathology companies that dominate the market to unilaterally cut the rents they paid to medical practices for co-located collection centres (ACCs), delivering a big financial blow to small business already reeling under the effects of the Medicare rebate freeze.

“The proposed changes fundamentally alter the intent of the existing law…by imposing a blunt cap on the commercial rents that GPs and other specialists can receive for co-located ACCs,” the AMA President said. “It delivers two major listed companies with an unwarranted and unfair advantage…estimated to save [them] between $100 million and $150 million per annum.”

Under the deal, which was sprung on the medical profession without warning, the Government has promised to bring down rents in exchange for a promise from pathology companies that they will sustain bulk billing rates despite the loss of the bulk billing incentive.

Dr Gannon warned that the Government’s proposed changes would have “a big impact” on medical practices.

“Medical practices are [already] feeling the impact of the current MBS indexation freeze, and policy changes like this will simply have a further negative impact on their cash flow and on practice viability,” he said. “For those practices that have used this source of rental income to help keep them viable during the current extended freeze, it may it may mean higher costs to patients or simply selling their business.”

Many, the AMA President said, had made decisions about hiring staff and purchasing equipment based on anticipated revenue streams from ACC rents, and the policy would put their finances under strain.

Dr Gannon said it was unlikely the Government comprehended the full impact of the “poorly targeted” policy when announcing it, including the massive windfall it would deliver to the big pathology providers and the hefty financial blow it would deliver to many medical practices.

Adrian Rollins

Government targets quality in proposed PIP overhaul

The AMA has expressed concern that a proposed major shake-up of the Practice Incentives Program is not being supported by increased investment in general practice.

The Health Department has unveiled plans to “refresh” the 18-year-old PIP system by slashing the number of incentive payment categories on offer, reducing the administrative burden on practices and intensifying the focus on quality.

Under the proposal, outlined in a discussion paper released by the Department, seven existing payments covering asthma, cervical screening, diabetes, aged care access, prescribing, Indigenous health and procedural GP incentives would be axed; four existing payments, covering rural loading, after hours services, teaching and e-health – would be maintained; and a new Quality Improvement Incentive payment would be introduced.

The AMA has welcomed the increased focus on quality, and is in consultation with the Department over the proposal to collapse the PIP payment categories.

But it voiced concern that the changes were not being supported by an increase in financial support for GPs, particularly given that many practices are being pushed to the financial brink by the Medicare rebate freeze and the prospect of cuts to pathology collection centre rents.

The Department has indicated that there will be no extra money injected in the PIP scheme.

It said the quality incentive payment would be used to “give general practices increased flexibility to improve their detection and management of a range of chronic conditions, and to focus on issues specific to their practice population”.

The push to overhaul the PIP system comes at the same time the Government is launching the initial stage of its Health Care Home model of care and undertaking a comprehensive review of the 5700 services listed on the MBS.

The Department said the initiatives together would “take the health system towards services that are aligned with contemporary practice”.

The case for changes to the PIP has been mounting in recent years, with a number of organisations including the Australian National Audit Office, the Organisation for Economic Co-operation and Development and the Grattan Institute all raising concerns that the system imposed an unduly heavy administrative burden on practices and was failing to keep up with evolving health needs and priorities.

The Department said the evidence showed that many existing incentives might be no longer appropriate, and that the more could be achieved by intensifying the focus on quality, including by making better use of data.

“Redesigning the PIP would enable it to move away from process-focused funding towards a simpler system that encourages quality improvement and innovation, and allows practices to see improvements in measures that are important to them,” it said.

Precisely how this could be achieved was up for consultation and debate, the Department added.

It suggested two options. One would be to merge all five PIP items (including the new Quality Improvement Incentive) into a single payment administered by the Department of Humans Services – essentially building on and adapting existing arrangements. Eligible practices would receive sign-on and quarterly payments, to be used to make quality improvements of their choosing.

Under the second option, the Department would no longer directly fund practices. Instead, practices would use PIP funds to engage third-party providers to support their quality improvement work.

Whatever the option chosen, practices would be required to regularly share data to map quality improvements, individually, locally and nationally.

The Government is inviting submissions on the proposed PIP overhaul. The deadline is 30 November.

The Department’s consultation paper can be downloaded here.

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A review of maturity onset diabetes of the young (MODY) and challenges in the management of glucokinase-MODY

Case presentation

A 63-year-old lean female of Asian ethnicity was referred to our service in 2006 with a 12-year history of well controlled type 2 diabetes (T2D) in the absence of micro- or macrovascular complications. She had undetectable β-cell antibodies. Her fasting glucose levels were 6–7 mmol/L and her glycated haemoglobin (HbA_1c) level was 7.3% (56 mmol/mol). She was previously diagnosed with gestational diabetes mellitus (GDM) in three of five pregnancies, requiring insulin with the fourth pregnancy. All children were born without complication and of normal weight. Her father and five of six siblings were diagnosed with T2D. Over time, her management included diet and exercise, metformin 850 mg three times a day, modified release gliclazide 60 mg daily, and pioglitazone 45 mg daily. Ten years after referral, her HbA_1c level was 7.6% (60 mmol/mol). She trialled basal insulin (glargine), but it was ceased as it was apparently ineffective. Her weight remained stable and her HbA_1c levels showed little variation with escalating oral therapy. She developed postmenopausal osteoporosis and pioglitazone was ceased. Her daughter, who was also lean, was diagnosed with GDM during routine antenatal care. Given the autosomal dominant penetrance of diabetes in the family, she underwent genetic testing for maturity onset diabetes of the young (MODY) subtype 2 due to a glucokinase gene mutation (GCK-MODY), for which she tested positive. Our index patient also underwent genetic testing, and similarly tested positive for the same heterozygous mutation (aberrant splicing of intron 8c.1019+1G>A).

After being treated for more than 20 years, the patient was advised to cease treatment. She did so reluctantly, mainly due to the years of advice stressing the importance of treatment adherence. Her HbA_1c level remained at 7.8% (62 mmol/mol) 3 months after treatment cessation. A 1-week continuous glucose monitoring study revealed fasting glucose levels of 7.5–8.4 mmol/L with the largest postprandial glucose excursion of about 3.0 mmol/L.

Literature search and sources

The sources used in this narrative review were obtained from original publications or reviews from groups renowned for their work in the definitions and genetics of MODY subtypes. Other publications were obtained from the MEDLINE and EMBASE databases and limited to English language; they were preferably recent publications (within < 10 years) and published in high impact journals. Information on specific genetic mutations and clinical phenotypes for the MODY subtypes were also obtained from the Online Mendelian Inheritance in Man online catalogue (www.omim.org).

What is MODY?

MODY is a heterogeneous group of monogenic diabetes disorders due to pancreatic β-cell dysfunction.1,2 Patients with MODY have early onset of diabetes and typically lack features of insulin resistance or autoimmunity. The MODY subtypes, of which there are currently 14, were first identified in the 1970s.3–5 They have an estimated population prevalence of 1.1:1000, or about 1–2% of diabetes cases (Box 1) in white Europeans, but are present in every race and ethnicity.6

The three most common MODY subtypes are mutations of hepatocyte nuclear factor 1A (HNF1A, MODY3), HNF4A (MODY1) and GCK genes. The GCK mutation, known as MODY subtype 2 (MODY2), or more recently as GCK-MODY, constitutes 10–60% of all MODY cases (Box 2).2,9–11 Rarer mutations resulting in β-cell dysfunction are also considered as separate MODY subtypes, and include alterations to insulin promoter factor 1 (MODY4), HNF1B (MODY5), and neurogenic differentiation factor 1 (MODY6) (Appendix). Patients with MODY5 constitute 5% of all MODY subtypes; MODY5 has been named the “renal cysts and diabetes syndrome,” as it often encompasses other urogenital malformations, pancreatic atrophy and deranged liver function tests.

The reference list includes succinct and lengthier reviews for further reading on MODY subtypes7,10,12,13 and on GCK-MODY.2,7,14

MODY subtypes 1 (HNF4A) and 3 (HNF1A)

Although driven by different mutations, the clinical phenotypes due to alterations of the HNF4A (MODY1) and HNF1A (MODY3) are best regarded as similar entities, because the features and management are similar.7,10,15 It is believed that mutations in HNF4A and HNF1A, which function as transcription factors, specifically result in dysfunction of the α, β and pancreatic polypeptide cells within pancreatic islets, resulting in reduced or delayed insulin secretion in response to glucose.15,16 In general, both MODY1 and MODY3 may present with mild diabetes, although usually postprandial blood glucose excursions are greater than those seen in GCK-MODY (ie, ≥ 5 mmol/L).17 Clinical features of MODY3, in addition to those listed in Box 2, include young onset diabetes usually before the age of 25 years in at least one family member, not normally requiring insulin initially, with generally good glycaemic control with less insulin than anticipated, detectable C-peptide in the presence of a blood glucose level (BGL) of over 8 mmol/L, family history spanning at least two generations, postprandial glucose excursions over 5 mmol/L with or without normal fasting glycaemia, absence of pancreatic autoantibodies and glycosuria when BGLs are under 10 mmol/L (given the low renal threshold for glucose wasting).18 These patients usually have a profound response to low doses of sulfonylurea therapy,16,19 with one randomised cross-over trial demonstrating about a 5-fold greater response with gliclazide compared with metformin. Patients also typically lack features of metabolic syndrome or insulin resistance (eg, obesity, acanthosis nigricans, elevated or normal high density lipoprotein cholesterol, and normal triglycerides).10,12

In contrast, MODY1 (HNF4A) is much less common, although the clinical features are similar to MODY3 (HNF1A), aside from a later age at diagnosis and the lack of pronounced glycosuria. Patients with MODY1 also share sensitivity to sulfonylureas. Offspring of women with MODY1 are often born with macrosomia (> 4.4 kg in 56% of carriers) and there may be transient neonatal hyperglycaemia.8 Clinical suspicion should be raised when there is a strong family history of pronounced macrosomia, or less commonly, if there is diazoxide (a medication used to treat hypoglycaemia) responsive neonatal hyperinsulinism in the context of familial diabetes.

Like T2D, both MODY1 and MODY3 are progressive forms of diabetes, and insulin secretion reduces over time.13 It is expected that micro- and macrovascular complications should be screened for, especially retinopathy and nephropathy. Treatment with insulin may be needed in 30–40% of affected individuals.12 Mutations in HNF4A favourably affect lipid biosynthesis and are associated with a 50% reduction in serum triglyceride levels and a 25% reduction in certain serum apolipoproteins.10

MODY2 (GCK-MODY) is often misdiagnosed

Based on the frequency of diagnoses, referral rates and prevalence in the United Kingdom, it is likely that GCK-MODY is underdiagnosed (or misdiagnosed as T2D) as more than 80% of patients with GCK-MODY do not undergo genetic testing.20 The condition is driven by an inactivating, heterozygous mutation of GCK, the glycolytic enzyme that catalyses the conversion of glucose to glucose 6-phosphate, the initial step in the chain of glucose metabolism in the β cell, consequently required for the release of insulin.21 In GCK-MODY, GCK is abnormal and functions at a higher glucose sensing threshold, earning its reputation as the “glucose sensor” of the β cell and the hepatocyte.22

The clinical phenotype is asymptomatic, mild hyperglycaemia present from childhood, usually ranging from 5.4 to 8.3 mmol/L. Most patients have an HbA_1c level of 5.6–7.3% (41–56 mmol/mol) if they are less than 40 years old, or 5.9–7.6% (41–60 mmol/mol) if they are more than 40 years old.23

Special groups

All children with fasting hyperglycaemia need exclusion of GCK-MODY

Chronic childhood hyperglycaemia is exceptionally abnormal and, therefore, GCK-MODY along with type 1 diabetes (T1D) are the major differential diagnoses to consider, as GCK-MODY is present in 10–60% of all children with fasting hyperglycaemia.2 One cohort study of 82 children with fasting hyperglycaemia (BGL, ≥ 5.5 mmol/L) and negative β-cell antibodies found a GCK mutation in 48% of the cases.24 The major discriminating features favouring T1D are the presence of one or more islet cell antibodies, more pronounced hyperglycaemia, requirement for insulin within 5 years of diagnosis, and a stimulated C-peptide level lower than 200 pmol/L, as these are usually lacking in GCK-MODY.1,25

Pregnant women with GCK-MODY may need treatment

Epidemiological studies suggest that GCK-MODY is present in 1–2% of mothers diagnosed with GDM, and it usually presents as asymptomatic, mild fasting hyperglycaemia.6 A lower body mass index (BMI, < 25 kg/m²) and a fasting glucose level greater than or equal to 5.5 mmol/L have sensitivity and specificity of 68% and 96%, respectively. It is estimated that among lean women with mild fasting hyperglycaemia, the number of women needed to test is 2.7 to detect a single case of GCK-MODY.6 With new diagnostic thresholds adopted in Australia defining the diagnosis of GDM (ie, fasting BGL, 5.1–6.9 mmol/L),11 it is likely that more cases will be detected incidentally. Treatment in mothers with a known GCK-MODY mutation is indicated only if the fetus has a confirmed normal genotype (via chorionic villus sampling or amniocentesis) or if there is sonographic evidence of accelerated fetal growth on ultrasound, since this likely reflects fetal hyperinsulinaemia as the fetus attempts to overcome maternal hyperglycaemia. Treatment is with insulin, which is normally ceased postpartum.2,26,27

Diagnosis

Mild, fasting hyperglycaemia in younger, slimmer patients

There are no distinct clinical features of GCK-MODY. Suspicion is based on the findings of persistently elevated fasting hyperglycaemia (5.4–8.3 mmol/L), HbA_1c levels of 5.8–7.6% (40–60 mmol/mol), young age (< 30 years old), non-obese phenotype, post-prandial glucose excursions lower than 3 mmol/L, and autosomal dominant pattern of inheritance of diabetes.2,7 With respect to the latter, a strong clinical clue is that many relatives of patients with known GCK-MODY will have been diagnosed with prediabetes, T1D or T2D, yet they rarely require insulin despite being diagnosed for many decades, and seemingly few, if any, develop complications. Despite this, about 20% of family members with GCK-MODY receive treatment with oral hypoglycaemic therapy and a minority with insulin.4,28,29

Genetic testing is the gold standard

Confirmation of GCK-MODY is performed by molecular genetic testing using Sanger sequencing and requires 5–10 mL of ethylenediaminetetraacetic acid (EDTA)-treated blood. There are over 620 gene mutations identified throughout the ten pancreatic β-cell exons of the GCK gene in more than 1400 families.30 Samples can be sent to a number of laboratories.31,32 For example, one laboratory’s cost and processing time (4–8 weeks) will depend on whether the mutation is known to be due to a GCK mutation (cost ∼ $600) or either of HNF4A or HNF1A (∼ $800).2 A 16-gene MODY panel may also be requested for about $1145. Local laboratories can also perform the analysis for GCK mutations for $745 with a turn-around time of 4 weeks.32 Other mutations (ie, HNF4A, HNF1A) may be analysed by requesting a MODY 10-gene panel (next generation sequencing), inclusive of GCK gene mutation testing. A 4 mL EDTA blood sample is required (or 2 μg genomic DNA) and the cost is about $1100 with a 4-week turn-around time. As whole genome sequencing becomes more widely available, testing for heritable diabetes syndromes will become easier to access and new syndromes will be discovered (this information is current at the time of printing).

Testing patients greatly influences management

Because a diagnosis of GCK-MODY will significantly alter management, the clinician should be alert for suspected cases and refer suitable patients for genetic testing. However, as our case illustrates, in patients treated with diabetes medications for many years, the physician should discuss testing in an unbiased manner, without assuming that the patient will embrace a positive result that will allow them to cease therapy. If patients are amenable to ceasing treatment, as in our patient, this may cause significant stress and anxiety due to a feeling of guilt and perceived future morbidity. This is due to multiple previous clinical discussions with the patient stressing the importance of treatment adherence and tight glycaemic control. This is similarly important in patients with MODY3, in whom a positive diagnosis allows cessation of insulin and a switch to a sulfonylurea, which is likely to have been administered in a basal-bolus regimen or via an insulin pump for many years. Patients should be alerted that confirming a diagnosis of GCK-MODY not only significantly influences the number of investigations and reduces the treatment burden to them, but it also carries implications for relatives who may be undiagnosed, with offspring having a 50% chance of inheriting the gene.

To treat or not to treat

Arguments against treatment

With the exception of pregnancy, GCK-MODY has been regarded as a lifelong subtle abnormality in glucose homeostasis that is not progressive and shows little deterioration over time.16,33 This is in contrast to MODY3 (20–50% of cases), MODY1 (∼ 5% of cases)7 as well as T1D and T2D. GCK-MODY should therefore be considered a distinct clinical entity.2 As the fasting hyperglycaemia is often mild, varies little with time, and rarely results in the development of micro- or macrovascular complications, treatment is thought unlikely to change clinical outcomes.2,33 In a recent, large cross-sectional study involving GCK-MODY patients with a mean duration of 49 years, patients developed only mild background retinopathy when compared with healthy controls. Moreover, macrovascular complications developed in 4% of GCK-MODY patients versus 30% in patients with T2D, possibly reflecting the more favourable lipid profile in this condition.33

It is also known that the mild fasting hyperglycaemia in patients with GCK-MODY is resistant to oral diabetes therapy as well as dietary changes, due to the altered set point at which glucose homeostasis is maintained by the loss-of-function mutation of GCK.28 Therefore, treatment may not alter a patient’s glycaemic control or their trajectory towards developing complications as a result of mild fasting hyperglycaemia.

Arguments for treatment

As with the rest of the population, which is affected by genetic susceptibility, advancing age and rising rates of obesity, patients with GCK-MODY may also concurrently develop the metabolic derangements typical of T2D, such as progression of insulin resistance and β-cell failure.34 For example, one retrospective study of 33 patients with GCK-MODY over an 11-year period illustrated a small but significant deterioration in fasting (6.8–7.1 mmol/L) and 2-hour glucose levels (8.2–9.0 mmol/L), as well as decreases in insulin sensitivity when baseline and repeat oral glucose tolerance tests were compared.34 This was also associated with a mean increase in BMI from 19.2 to 22.3 kg/m². More recently, it has been suggested that patients with GCK-MODY should be considered for treatment when the HbA_1c level clearly and repeatedly exceeds 7.6 (60 mmol/mol).2,23 However, the question of whether to treat or not, based on a specific HbA_1c level in patients with GCK-MODY, remains controversial; notwithstanding, HbA_1c itself has limitations in predicting the development of microvascular complications.35

The verdict is divided

The decision to treat the patient should take into consideration the patient’s age, the current mild to moderate hyperglycaemia, the observation of postprandial glucose intolerance, the patient’s preference and the suboptimal HbA_1c level, which may increase the risk of both micro- and macrovascular complications. This is in the context of an anticipated trajectory of deteriorating glycaemic metabolism that often accompanies advancing age and weight gain. This would naturally be weighed against the risks, cost and inconvenience of multiple investigations and the need for medical appointments, frequent self-monitoring of glucose levels, cost of glucose test strips, as well as patient anxiety.36 Furthermore, many patients may suffer from side effects from pharmacologic therapy; notwithstanding, weight gain, hypoglycaemia (especially if on sulfonylurea or insulin), gastrointestinal upset and vitamin B12 deficiency with metformin, as well as the adverse metabolic consequences to bone metabolism, bladder cancer risk and heart failure with thiazolidinediones, as in our index patient, should be considered. To date, there are no data on the efficacy of dipeptidyl peptidase 4 inhibitors, glucagon-like peptide-1 receptor agonists, or sodium glucose cotransporter 2 inhibitors, in these patients. Therefore, a careful examination, by an attentive clinician, of the patient’s goals, quality of life, comorbidities and an estimation of benefit, should form the basis when considering the decision to treat.

Genetic testing is underutilised but may be cost-effective

The burden and cost, both personally and to the community, are difficult to estimate when considering the implementation of a screening strategy at a national level. A recent cost-analysis simulation of a one-time genetic screening test (with a cost of US$2580) for the three most common MODY subtypes (GCK, HNF1A, HNF4A) — which account for more than 90% of all MODY cases — within the first year of diagnosis, was undertaken in a hypothetical cohort of young individuals (aged 25–40 years old) with a diagnosis of diabetes.36 The study assumed that the prevalence of GCK-MODY was 6% (similar to other countries), and when diagnosed, patients with GCK-MODY received no treatment. The screening test yielded an average small gain of 0.012 quality-adjusted life years and an incremental cost-effectiveness ratio of US$50 000.36 The cost-effectiveness extends to children, and arguably more so, with savings of about €1500 per year from time of diagnosis, as intensive treatment for presumed T1D in children is reduced to conservative management in the case of a positive diagnosis of GCK-MODY.37

It is not just MODY; diabetes genes are common in the general population

It is worth noting that not all genetic causes of diabetes can be ascribed simply to monogenic (single gene) mutations such as in MODY, or that there are a small number of rare genes inherited within generational lines that specifically affect an individual’s risk of developing diabetes. This approach, although clinically useful, is simplistic and may inadvertently overlook the fact that, on the whole, the population carries multiple, common genetic alterations in a single gene (ie, variants) that may collectively increase the risk of developing diabetes.38 A recent large analysis of exomes (protein-coding regions which comprise a fraction, 1–2%, of the whole human genome), from 6500 subjects with T2D matched to an equal number of healthy controls from five ethnic groups, has cast doubt on the evidence that rare or low frequency disease-associated variants affect the risk of developing diabetes. The authors note that most of the diabetes-associated genetic variants are quite common in the population.39

Conclusion

Despite the availability of genetic testing, there are a significant number of patient- and physician-related factors that may be prohibitive to uptake, including the perceived lack of possibilities for treatment (if coexistent MODY and T2D develop over time, many would argue that it may not change management if hyperglycaemia is mild; however, we believe that it makes a difference to management and monitoring) and prevention, cost implications of a positive diagnosis to patients, and lack of awareness of MODY as a diagnosis.40 These factors should all be discussed with the patient when considering genetic or genomic testing. The patient should be counselled regarding the treatment implications of a positive diagnosis, including the possibility that they may have not required the treatment they were prescribed many years prior. The points raised by this review will be increasingly relevant to the medical practitioner given the rapid development of genetic and genomic testing.

Box 1 –
Subtypes of diabetes according to relative prevalence

CF = cystic fibrosis. DIDMOAD = diabetes insipidus diabetes mellitus optic atrophy deafness. GDM = gestational diabetes. HCV = hepatitis C virus. LADA = latent autoimmune diabetes of the adult. MELAS = mitochondrial myopathy, encephalopathy lactic acidosis and stroke-like episodes. MIDD = maternally inherited diabetes. MODY = maturity onset diabetes of the young. PCOS = polycystic ovarian syndrome. WFS1 = wolframin gene.

Box 2 –
Prevalence, genetic and key clinical features of the common forms of diabetes and subtypes of maturity onset diabetes of the young (MODY)

Type 2 diabetes

Type 1 diabetes

Gestational diabetes

MODY1

MODY2

MODY3

Prevalence

1 in 13 people (∼ 870 000 in Australia)

10% of all diabetes (∼ 170 000 in Australia)

5–10% of all pregnancies

∼ 5%*

10–60%*

20–50%*

Causative mutation

Multiple polymorphisms (eg, class II HLA genes)

Multiple polymorphisms

HNF4A7,8

GCK2

HNF1A10

Clinical features

Older (usually > 45 years), overweight or obese, often family history, insulin resistance

Slim, family history of autoimmune disorders, usually childhood or early adolescence or adulthood (includes LADA)

Older (> 40 years); pre-pregnancy obesity (BMI, > 30 kg/m²); family history (30%) and ethnicity; previous GDM; PCOS; macrosomic babies, diagnosed 24–28 weeks’ gestation

Young age (< 25 years), strong family history of diabetes, absent antibodies, detectable C-peptide

Diagnostic glucose and HbA_1c

75 g OGTT: fasting BGL, ≥ 7 mmol/L; random or 2-h postprandial BGL, ≥ 11.1 mmol/L; HbA_1c, ≥ 6.5% (48 mmol/mol)

Similar to type 2 diabetes

75 g OGTT: fasting BGL, 5.1–6.9 mmol/L;1-h, ≥ 10 mmol/L; 2-h, 8.5–11 mmol/L11

As with type 2 diabetes; postprandial glucose excursions, ≥ 5 mmol/L

Fasting BGL, 5.4–8.3 mmol/L; postprandial glucose excursions, ≤ 3 mmol/L, HbA_1c, 5.8–7.6% (40–60 mmol/mol)

As for MODY1

Treatment

Diet, exercise, OHG, injectable GLP1 RA, insulin

Insulin

Diet, exercise, metformin, insulin

Respond to sulfonylureas, 30–40% apparent insulin-requiring

None required (controversial)

As for MODY1

Special features

Progressive β-cell dysfunction with development of micro- and macrovascular complications

Negative C-peptide and DKA without insulin (outside of honeymoon period), positive antibodies in majority to GAD, IA-2, ICA, IAA and ZnT8

Hyperglycaemia remits postpartum

Glycosuria common; develop micro- and macrovascular complications as in type 1 and 2 diabetes

Favourable lipid profile; lean; minimal or no micro- or macrovascular complications; minimal effect of treatment on glycaemic control

As for MODY1; strong family history of macrosomic babies

* Denotes approximate percentage prevalence of all MODY subtypes. DKA = diabetic ketoacidosis. GAD = glutamic decarboxylase autoantibody. GCK = glucokinase gene. GDM = gestational diabetes mellitus. GLP1 RA = glucagon-like peptide 1 receptor agonists. HLA = human leukocyte antigen. HNF1A = hepatocyte nuclear factor 1α gene. HNF4A = hepatocyte nuclear factor 4α gene. IA-2 = insulinoma-associated-2 autoantibody. IAA = insulin autoantibody. ICA = islet cell cytoplasmic autoantibody. LADA = latent autoimmune diabetes of the adult. OGTT = oral glucose tolerance test. OHGs = oral hypoglycaemic therapy. PCOS = polycystic ovarian syndrome. ZnT8 = zinc transporter 8 autoantibody.

Big pathology to get massive windfall at expense of patients, doctors

The AMA has warned that Federal Government proposals to cap pathology collection centre rents will likely drive up patient out-of-pocket costs and could force some medical practices out of business.

In a strongly worded letter, AMA President Dr Michael Gannon has appealed to the Small Business and Family Enterpirse Ombudsman, Kate Carnell, to intervene and help try to convince the Government to drop its plan.

Dr Gannon said the rapid increase in ACC rents since they were deregulated in 2010 had been driven by competition for market share between the two big pathology companies, and the Government itself had attested to the fact that there was no evidence of a link between the pathology referrals made by doctors and ACC rents.

He warned that the Government’s proposed changes would have “a big impact” on medical practices.

Many, the AMA President said, had made decisions about hiring staff and purchasing equipment based on anticipated revenue streams from ACC rents, and the policy would put their finances under strain.

Adrian Rollins

Health costs rise as rebate freeze bites

Patients face higher out-of-pocket costs as the medical profession struggles under pressure from the Federal Government’s Medicare rebate freeze.

As a result of the Government’s freeze, the gap between the Medicare rebate and the fee the AMA recommends GPs charge for a standard consultation will increase to $40.95 from 1 November, up from $38.95, continuing the steady devaluation of Medicare’s contribution to the cost of care.

The increase comes on top of the effects of the Medicare rebate freeze, which is forcing an increasing number of medical practices to abandon or reduce bulk billing and begin charging patients in order to remain financially viable.

Adding to the financial squeeze, the Government is considering changes that would cut the rents practices receive for co-located pathology collection centres that the AMA estimates would rip up to $150 million from general practice every year.

Under the changes recommended by the AMA, the fee for a standard Level B GP consultation will increase by $2 to $78, while the Medicare rebate remains fixed at just $37.05.

AMA Vice President Dr Tony Bartone said doctors had kept medical fee increases to a minimum, but Medicare indexation lagged well behind the cost of providing medical care.

“The MBS simply has not kept pace with the complexity or cost of providing high quality medical services,” Dr Bartone said.

The rise is roughly in line with Reserve Bank of Australia forecasts for underlying inflation, currently at 1.5 per cent, to rise anywhere up to 2.5 per cent by the middle of next year, and reflects steady increases in medical practice costs.

Staff wages, rent and utility charges have all increased, as have professional indemnity insurance premiums, continuing professional education costs and accreditation fees.

While practice running costs are rising, the Government’s contribution to the cost of care through Medicare has been frozen for more than two years, and in many cases far longer.

The Medicare rebate for GP services has not been indexed since mid-2014, while the last rebate increase for most other services was in November 2012. In the case of pathology and diagnostic imaging the rebate freeze is even longer, going back more than 15 years.

Dr Bartone said the rebate freeze was pushing up patient out-of-pocket costs.

“Many patients will pay more to see their doctor because of the Medicare freeze,” he said. “The freeze is an enormous burden on hardworking GPs. Practices cannot continue absorbing the increasing costs of providing quality care year after year. It is inevitable that many GPs will need to review their decision to bulk bill some of their patients.”

The AMA is pressing the Government to reverse the rebate freeze, and AMA President Dr Michael Gannon has declared he would be “gobsmacked” if it was still in place by the time of the next Federal election, due in 2019.

But Health Minister Sussan Ley has played down hopes that indexation will soon be reinstated, warning that there will not be a change of policy “any earlier than our financial circumstances permit”.

The Government is trying to curb the Budget deficit and rein in ballooning debt.

As part of its strategy, it is increasingly pushing the cost of health care directly onto patients.

Australian Institute of Health and Welfare figures show the Commonwealth’s share of the nation’s health bill slipped down to 41 per cent in 2014-15, while patients’ share has increased to almost 18 per cent, and Australians now pay some of the highest out-of-pocket costs for health care among Organisation for Economic Co-operation and Development countries.

The cost of health

How AMA recommended fees compare with the frozen Medicare rebates

Medical Service	AMA Fee (2015)	AMA Fee (2016)	MBS Schedule Fee (2016)
Level B GP consult (MBS item 23)	$76.00	$78.00	$37.05
Level B OMP consult (MBS item 53)	$76.00	$78.00	$21.00
Blood test for diabetes (MBS item 66542)	$48.00	$49.00	$18.95
CT scan of the spine (MBS item 56219)	$990.00	$1,055.00	$326.20
Specialist – initial attendance (MBS item 104)	$166.00	$170.00	$85.55
Consultant Physician – initial attendance (MBS item 110)	$315.00	$325.00	$150.90
Psychiatrist attendance (MBS item 306)	$350.00	$355.00	$183.65

Adrian Rollins

Government pathology changes could cost practices up to $150m

Federal Government plans to change the rules regarding rents for pathology collection centres could be a disaster for medical practices, ripping up to $150 million a year from their income, the AMA has warned.

AMA President Dr Michael Gannon has told Health Minister Sussan Ley that a significant number of general practices will become “collateral damage” if the Government persists with plans to change the definition of ‘market value’ that applies to rents for pathology collection centres, with serious consequences for the provision of health care.

Dr Gannon said the Minister needed to re-think the proposed changes and adopt a more nuanced approach “consistent with the original intent of the…laws”.

“If you do not get this right, a significant proportion of general practices will become collateral damage, which would be a disastrous policy outcome and contrary to your stated support for the specialty,” he told Ms Ley.

Last month it was revealed that the Government had put off plans to axe bulk billing incentives for pathology services and abandoned its threat to impose a moratorium on the development of new collection centres.

In a climb-down, the Government pulled back from its threat to scrap the incentives on 1 October and advised it would not be proceeding with the moratorium, which was announced during the Federal election in order to head off a protest campaign by the pathology industry against the axing of a bulk billing incentive.

Instead of a ban, the Government has directed that collection centre leases be put up for renewal every six months, down from the usual 12 months, until a new regulatory framework is put in place. Existing leases will be grandfathered for up to 12 months, after which the new rules will come into effect.

The bulk billing incentive cut, meanwhile, which was originally due to come into effect from 1 July and save $332 million, will now not be implemented until 1 January 2017.

“Bulk billing incentives for the pathology sector will continue until new regulatory arrangements are put in place and the Government will continue to consult with affected stakeholders,” a spokesman for Ms Ley told the Herald Sun.

But the Minister is persisting with plans to change the regulations governing rents for approved collection centres, particularly regarding the definition of market value as applied under the prohibited practices provisions of the Health Insurance Act.

Dr Gannon said that in talks earlier this year, the AMA had agreed with moves to strengthen compliance with existing regulations and “weed out examples of rents that are clearly inappropriate”.

But he said the Government at that stage had given no hint it was considering changes to the regulations, and its election announcement had taken all stakeholders, except Pathology Australia and Sonic Healthcare, by surprise.

Dr Gannon said the Government’s clear intent was to control collection centre rents, and the AMA opposed the proposed changes.

There are more than 5000 collection centres across the country, many co-located with medical practices.

“These practices are small businesses and have negotiated leases in good faith,” Dr Gannon said, and had made business decisions based on projected rental revenue streams, including staffing and investment.

He warned that ripping this source of revenue away could be disastrous for many.

“For many practices feeling the impact of the current MBS indexation freeze, this source of rental income has helped keep them viable,” he said, adding that AMA estimates were that the Government’s changes would cost practices between $100 million and $150 million a year in lost rent revenue.

“The magnitude of this cut goes well beyond an attempt to tackle inappropriate rental arrangements. It is causing significant distress, particularly for general practice,” Dr Gannon said. “I doubt the Government truly contemplated the extent of the impact of its election commitment when it was announced.”

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Cancer registry privacy fears

The AMA has raised concerns sensitive patient information will be in the hands of a for-profit operator following the Federal Government’s decision to award a $220 million contract to Telstra to build and operate a national cancer screening register.

The AMA has told a Senate Committee inquiring into the decision that although it did not have any in-principle objection to outsourcing clinical registries, it was worried by Telstra Health’s lack of experience in the field, and the implications of giving a profit-making enterprise access to commercially valuable and highly sensitive personal information.

“Telstra Health does not have direct previous experience in operating registries of this kind,” the AMA said in a submission to the Senate Standing Committee on Community Affairs.

Under the Government’s plan, data from nine separate cancer screening registers will be consolidated into a single National Cancer Screening Register containing the bowel and cervical cancer screening records of all participating Australians. Information on the register will be used to support the expansion of bowel cancer screening to cover almost 10 million people, and cervical screening for 1.4 million women.

The AMA said it would be “more comfortable” if the registry, which will contain sensitive information about a person’s cancer risk, medical procedures and health status, was in commercially disinterested hands.

“Given the potential commercial value of the data contained in the register, the AMA would be more comfortable with it being operated by Government, a tertiary institution, or not-for-profit entity that has little interest in how the data in the register might otherwise be used,” it said. “This would go a long way to allaying concerns about the secondary use of data for commercial reasons.”

The AMA’s concerns were echoed by health policy expert Professor Lesley Russell, of the Menzies Centre for Health Policy.

“Telstra Health will have the ability to access data from the Australian Immunisation Register, from the Australian Institute of Health and Welfare, and from Medicare claims, and the registers will be integrated with GPs, specialists and pathology laboratories,” Professor Russell said in a submission t the Senate Committee.

“Will the Australian population be comfortable with the fact that a for-profit business knows whether they have had a full or partial hysterectomy, if they are at risk of bowel cancer…and when they last had a colonoscopy?

“Will GPs, specialists and diagnostic labs be happy that Telstra Health can, at least potentially, scrutinise their diagnoses and treatment?”

Privacy Commission Timothy Pilgrim said the centralisation of such sensitive information in a database that can be accessed from many points posed “a number of security and privacy risks”, and suggested the operation of the register be subject to additional requirements under the Privacy Act.

But Telstra Health said it was “uniquely placed” to provide the register, with the size, scale and expertise to ensure its secure and successful operation.

It said Telstra already manages “extremely sensitive” data for hospitals, financial institutions and Government, and all information contained in the register would be hosted in Australia and controlled by the Government.

“Telstra will build and operate the Register in accordance with strict data security requirements determined by the Australian Government. These are the same requirements that would apply to any Australian Government or not-for-profit agency.”

Concerns have also been raised about how Telstra Health was awarded the job, and what might happen to the register and the data it contains when the five-year contract expires.

Telstra said it won the contract following an open tender, but the AMA is among those complaining the process has been opaque.

“There has been a lack of transparency around the process for awarding this contract,” it said. “The awarding of such a contract to an entity that has hitherto had no direct role in establishing or operating a register of this kind sets a challenging and potentially troublesome precedent.”

Professor Russell said the basis on which Telstra won the contract over other applicants had not been disclosed, and the Government had not explained why other entities such as the Department of Human Services, the AIHW and Cancer Australia had not been considered for the work.

“What happens when the Telstra Health contract expires in five years’ time – will it automatically be renewed, will it be up for competitive bids? How will this contestability affect the continuity, ongoing resources and work needed for the registers?” she asked.

Shadow Health Minister Catherine King said “clearly there are questions that need to be answered about handing these records to a for-profit company with no experience in this area”.

“This is sensitive, personal information about people’s health – we need to get it right,” she said.

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Many living a long but not-so-healthy life

Australia’s latest check-up shows that although we are living longer than ever before poor diets, excessive drinking and inadequate exercise are undermining our health and almost half have a chronic illness.

In a comprehensive snapshot of the nation’s health, the Australian Institute of Health and Welfare reported that a baby boy born between 2012 and 2014 will, on average, live for 80.3 years and a baby girl born at the same time will live even longer, to an average 84.4 years.

However, more than 11 million Australians had at least one of eight chronic conditions, including about 1.2 million identified with diabetes – 85 per cent of whom had the largely preventable type 2 version of the condition.

In addition, 13 in every 100 smoke daily, 18 drink alcohol at risky levels and 95 do not eat the recommended servings of fruit and vegetables. Despite 55 out of 100 completing daily recommended physical activity levels, 63 per cent of Australians are overweight or obese.

The long-term decline in smoking rates has continued. The proportion of people aged 14 years and older who report never smoking rose from 58 per cent in 2010 to 60 per cent in 2013.

What kills us is changing. Cancer has overtaken heart disease for the first time as Australia’s biggest overall killer. It is predicted that 46,900 Australians will succumb to cancer this year – slightly more than 128 people a day. Nonetheless, survival rates for cancer are increasing.

More than 45 per cent of Australians aged 16 to 85 will experience a common mental disorder such as depression or anxiety, and one in seven will have suicidal thoughts in their lifetime.

Indigenous Australians continue to have a lower life expectancy and higher rates of many diseases, including diabetes, end-stage kidney disease and coronary heart disease.

AMA Vice President Dr Tony Bartone told ABC Radio National’s PM program that it was good news that Australians were living longer and that cancer survival rates were increasing, but lamented that around half of Australians had a chronic disease that was mainly caused by lifestyle choices.

“We still need to ensure the lifestyle prescription is the cornerstone of good preventative health care,” Dr Bartone said.

“Good preventative care is worth exceedingly more than the cost of the consultation, in terms of improved outcomes.

“Thirty-one per cent of the burden could have been prevented by reducing risk factors such as smoking or excess weight, and that’s a significant amount of suffering, morbidity, and of course health care.”

In 2013-14, $2.2 billion or 1.4 per cent of total health expenditure went to public health activities, which included prevention and health promotion. This proportion has fallen from 2.2 per cent in 2007-08.

AMA President Dr Michael Gannon recently urged the Government to invest in preventive health measures to improve the health and wellbeing of all Australians.

“The lack of investment, coupled with the freeze on Medicare patient rebates and cuts to bulk billing incentives for pathology tests and x-rays, is affecting GPs’ ability to provide primary health care,” Dr Gannon said

“Preventive health is not only an investment in the health of our nation, it is an investment in Australia’s economic productivity.

“When risk factors for chronic diseases and conditions are detected early and addressed, it reduces the need for more expensive hospital admissions.

“Australia spends significantly less on prevention and public health than comparable countries including New Zealand, Finland, and Canada.

“With the exception of tobacco control, there has been little or no progress against the national targets for preventing and controlling risk factors for chronic disease.”

The AMA calls on the Government to commit to:

fund prevention and early intervention as a sound and fiscally responsible investment in Australia’s health system;
increase investment to properly resource evidence-based approaches to preventive health; and
deliver sustainable funding for non-government organisations (NGOs) that advocate, educate and provide services to those affected by chronic diseases and health problems, including alcohol and substance abuse, domestic violence, blood-borne viruses, aged care, mental health and public health awareness.

The AIHW report is available at http://www.aihw.gov.au/publication-detail/?id=60129555544

Kirsty Waterford

Billions start flowing for medical research

Almost $1.3 billion of funds stripped from the Health portfolio have been funnelled to the Medical Research Future Fund as the Federal Government makes good on its controversial plan to divert billions of dollars from other areas of health to support research.

Late last month the Government, with little fanfare, transferred $1.277 billion to the MRFF’s Special Account, the first instalment of what is expected to be $20 billion injected into the Fund in coming years.

Prime Minister Malcolm Turnbull is persisting with the Medicare rebate freeze, reduced public hospital funding and cuts to bulk billing incentives in pathology and diagnostic imaging, with a share of the savings being directed to the MRFF.

The plan, unveiled in the 2014 Budget, was heavily criticised at the time by the AMA, which argued that although increased investment in medical research was welcome, it should not come at the expense of medical services and other areas of health.

But the $1.2 billion transfer is the clearest demonstration yet that the Government has no intention to abandon or scale back its plan, which has the backing of parts of the medical research community.

The Research Australia alliance, which claims to have 160 members and supporters, welcomed the initial investment as a “significant step to secure Australia’s health and medical research future”.

Research Australia Chief Executive Officer Nadia Levin said the transfer of the money to the MRFF Special Account was “words in action”.

“This is Prime Minister Turnbull and Health Minister Ley doing exactly what they said they would do – build our health system and build an innovation nation,” Ms Levin said. “This is not just words. It’s action and it’s money, and it is going to make an enormous difference to the health of Australians and the health of the economy.”

Following months of consultation, the MRFF is developing a document setting out the strategy and principles which will guide its investment in research projects.

Initially, the Fund intends to direct $61 million toward health and medical research project this financial year.

Under the Government’s plan, the Fund will expand rapidly in the next few years to reach $20 billion in the early 2020s, enabling it to invest around $1 billion a year in research.

Adrian Rollins

[Review] The frontotemporal dementia-motor neuron disease continuum

Early reports of cognitive and behavioural deficits in motor neuron disease might have been overlooked initially, but the concept of a frontotemporal dementia-motor neuron disease continuum has emerged during the past decade. Frontotemporal dementia-motor neuron disease is now recognised as an important dementia syndrome, which presents substantial challenges for diagnosis and management. Frontotemporal dementia, motor neuron disease, and frontotemporal dementia-motor neuron disease are characterised by overlapping patterns of TAR DNA binding protein (TDP-43) pathology, while the chromosome 9 open reading frame 72 (C9orf72) repeat expansion is common across the disease spectrum.