Single Payer Healthcare: Case study in running out of The People’s money

Currently there is significant and contentious debate about providing and paying for healthcare in America. In 2010, the Affordable Care Act (ACA) was passed by Congress and included a dozen different new taxes, a specific cadre of policy designs, and mandates for employer participation as well as mandates for individuals to carry insurance. Penalties went along with the mandates, of course. A full discussion of the ACA is beyond the scope of this blog, but suffice it to say that a major issue was how to pay for the expansion of healthcare services. Insurance companies signed up to provide healthcare policies to many individuals, Medicaid rolls were expanded in many states, and a unique provision was made to ‘bail out’ insurance companies if they sustained significant losses.

In short, with its continued funding of Medicare, and its role in partially funding Medicaid and [through bailouts] insurance companies, the extensive role of the federal government makes the United States almost a ‘pseudo’ single payer system with many of the provisions found in other single payer systems (SPSs).

While various factions continue to argue about the future of the ACA, and whether or not it was designed to devolve into a SPS, it would be prudent to look at well-established SPSs to see if there are lessons to be learned. The National Health Service (NHS) in the United Kingdom is a classic and longstanding example of a SPS. The NHS has separate bodies to handle the separate countries in the system. England, Wales, Ireland and Scotland each have separate, very complex organizational systems (1).

From the development of the NHS until now, the evolution of the system in England has devolved to decision-making bodies called Clinical Commissioning Groups, which are regional groups of general practitioners, nurses and consultants that plan and commission the best services for their local patients and population, and collectively have a fiduciary responsibility to the NHS in doing so. (1,2). Over the years, the National Institute for Health and Care Excellence (NICE) has evaluated new therapies and technologies to see if they are worthy to be reimbursed by the NHS. (3)

NICE is not known for readily adopting new medications and technologies. It withdrew NHS funding for newer and more expensive modalities that could potentially impact over 20,000 cancer patients, and more recently rationed treatments for Hepatitis C treatments (4,5,6,7)

No coverage for some products or rationing of others is just the tip of the iceberg in England. Surgery for cataracts is not permitted until the patient is nearly blind (x), knee and hip replacements are denied until “pain is so severe that it interferes with your quality of life and sleep….everyday tasks, such as shopping or getting out of the bath, are difficult or impossible.”(8, 9) And most recently, the “most severe [rationing] ever” by NHS, already adopted by several Clinical Commissioning Groups, is the ban of obese patients and smokers from ‘routine’ surgery. (10)

In addition to these specific issues, there is a movement within the NHS/NICE system to establish a new (lower) financial cap for costs per Quality Adjusted Life Year (QALY) as well as a potentially not approving any treatment that will cost the system more than 20 million pounds during the first three years. (10)

Rationing is the unseemly underbelly of Single Payer healthcare, and when discussed in abstract terms tends to lose its true meaning for the individual. If it is your mothers pain awaiting a new hip, your grandmothers inability to read her romance novels, or even your fathers heart attack while awaiting surgery because he is overweight or some other of the myriad possibilities these very real possibilities need to be discussed openly in light of what is going on with the NHS .

Despite these measures, the NHS is still several billions of dollars in the hole. Clearly these draconian measures are an attempt at slowing the rising healthcare debt, yet they haven’t cut any of the huge bureaucracy that adds to these costs. (12) Think the US government can do a better job? I have a bridge I’d like to sell you…

1. The organisation of the NHS in the UK: comparing structures in the four countries. Doheny S., National Assembly for Wales – Research Service. May 2015.

2. The NHS in England

3. NHS Commissioning

4. National Institute for Health and Care Excellence

5. Betrayal of 20,000 cancer patients: Rationing body rejects ten drugs (allowed in Europe) that could have extended lives

6. 25 cancer drugs to be denied on NHS

7. NHS ‘abandoning’ thousands by rationing hepatitis C drugs

8. Thousands of elderly are losing their sight as NHS rations cataract surgery

9. Pain-level rationing of hip and knee surgery due to cash crisis, admits NHS

10. Obese patients and smokers banned from routine surgery in ‘most severe ever’ rationing in the NHS

11. Daniel Zeichner MP: Proposed changes to NICE & NHS England must not be implemented without a real debate

12. Perspectives on the European Health Care Systems: Some Lessons for America


The Rodney Dangerfield of Cardiovascular Risk Factors in Diabetes

Some of you may remember the great comedian Rodney Dangerfield who passed away in 2004. While some may remember his roles in Caddy Shack or Back to School (my favorite), he was best known for his catchphrase “I don’t get no respect” which was the basis for many comedy monologues.

When we speak of cardiovascular risk in diabetes, we invoke cholesterol, chronic hyperglycemia, reactive oxygen species (ROS), AGE’s, the presence of kidney disease and perhaps others. But almost no one talks about, measures, or attempts to treat one risk factor that is well recognized and treatable (or at least the effects of it seem to be). Have you guessed it yet?

Haptoglobin (Hp) was first described in 1938. It is an α2-sialoglycoprotein coming mainly from hepatocytes in response to the secretion of cytokines such as IL-6, IL-1 and TNF. Haptoglobin is a tetrameric protein that structurally resembles immunoglobulins because it has two light chains (α) and two heavy chains (β) covalently bound to each other by disulfide bridges (S-S). Its main function is to rapidly bind free hemoglobin from intravascular hemolysis to keep it from oxidatively damaging the vascular endothelium. Although present in all vertebrates, in humans Hp is characterized by molecular heterogeneity caused by genetic polymorphism. In the 1940s and 1950s structural heterogeneity was establish when alleles of different structures and lengths were identified, categorized as Hp 1-1, Hp 2-1, and Hp2-2. While these variants can be found in patients without diabetes, much of the work on their role as risk factors has been done in the context of diabetes (both type 1 and type 2). Biologic functions of Hp include prevention of renal damage from intravascular hemolysis, protection against ‘toxic radicals’, and sparing of nitric oxide when unbound to hemoglobin. It has also been found to have a variety of different effects comprising an immune-modulating action. All of these effects seem to differ with the haptoglobin phenotype, and in general a protective role is seen in patients with the Hp 1-1 variant, and a lack of protective effect or more pathological role is seen with the Hp 2-2 variant. Approximately 40% of patients with diabetes carry the Haptoglobin 2-2 gene variant (1)

Increased oxidative stress in diabetic patients results from oxidation of glucose and the modification of low-density lipoproteins (LDL). These changes may stimulate the production of inflammatory cytokines that have been implicated in the morphological and pathological changes found in macrovascular and microvascular complications, and different degrees of susceptibility to the development of vascular problems have been observed in studies of the antioxidant properties of Hp. In diabetic patients, those with Hp 1-1 show better protection against complications than Hp 2-1 and Hp 2-2 individuals. The Hp 2-2 phenotype has been found more frequently in people developing type 2 diabetes (2). Hp 2-2 has been shown to be a major risk factor in diabetic vascular disease (3), an increased risk of Coronary Heart Disease (4) an increased cardiovascular mortality in type 1 diabetes (5), an increased risk of renal function decline (6), an increased risk of death following stroke (7), retinopathy (8) and many other risks of complications in people with diabetes.

Also, as many of you know, both type 1 and type 2 diabetes are associated with the so called ‘leaky gut’. In type 1 diabetes various antigens are presented to the maturing gut which can stimulate the development of activated T-cells which, over time, destroy pancreatic beta cells. In type 2 diabetes, the ‘leaky gut’ allows lipopolysaccharides into the circulation, releasing cytokines and adipokines causing inflammation, insulin resistance and eventually diabetes with loss of beta cell mass due to glucose and lipid toxicity. A major factor associated with ‘leaky gut’ is zonulin, discovered in 2000 by Fasano. Zonulin is pre-haptoglobin-2. (9) It is fascinating that the haptoglobin 2 allele (especially in those individuals who are homozygous [hp 2-2] would confer risk of diabetes, and risk within diabetes likely due to its role in gut permeability and ongoing inflammation…

The risk associated with the presence of the Hp 2-2 genotype can be mitigated with vitamin E treatment to a striking degree. While vitamin E has not been shown to affect surrogates of risk in individuals with Hp 1-1, its effect is clear for those with Hp 2-2. The summary abstract below speaks for itself:

Clinical trial data from the HOPE, ICARE, and WHS studies is presented showing a pharmacogenomic interaction between the Hp genotype and vitamin E on the development of CVD. Specifically, in individuals with diabetes and the Hp2-2 genotype, vitamin E has been shown to be associated with an approximately 35% reduction in CVD. Cardioprotection by vitamin E in individuals with the Hp2-2 genotype appears to be mediated in part by an improvement in HDL functionality as demonstrated in three independent trials in both type 1 diabetes and type 2 diabetes. (10)

Despite this positive review, and others like it, over 300 articles in PubMed regarding haptoglobin in diabetes, and several presentations at ADA Annual meetings, the current ADA Standards of Medical Care don’t even mention haptoglobin.(11) It truly is the ‘Rodney Dangerfield of risk factors in diabetes’!

So my question to all of you is: With the clear role of haptoglobin genotype 2-2 in the risk of micro and macrovascular complications AND with the clear indication that treatment with Vitamin E can substantially reduce that risk…when was the last time you suggested obtaining a haptoglobin genotype for your patient with diabetes?

1) Changing the Face of Diabetic Care with Haptoglobin Genotype Selection and Vitamin E Nina S. Levy, Ph.D. and Andrew P. Levy, M.D., Ph.D. Rambam Maimonides Med J. 2011 Apr; 2(2): e0047

2) Shi X, et al. Haptoglobin 2-2 Genotype Is Associated with Increased Risk of Type 2 Diabetes Mellitus in Northern Chinese. Genetic Testing and Molecular Biomarkers 2012;16:563-568

3) Asleh R. and Levy AP. In vivo and in vitro studies establishing haptoglobin as a major susceptibility gene for diabetic vascular disease. Vascular Health and Risk Management 2005;1:19–28

4) Cahill LE, et al. The Risk of Coronary Heart Disease Associated With Glycosylated Hemoglobin of 6.5% or Greater Is Pronounced in the Haptoglobin 2-2 Genotype. Journal of the American College of Cardiology 2015;66:1791-9

5) Costacou T. and Orchard TJ. The Haptoglobin genotype predicts cardio-renal mortality in type 1 diabetes. J. Diabetes Complications. 2016;30:221-6

6) Costacou, T, et al. Haptoglobin Genotype and Renal Function Decline in Type 1 Diabetes. Diabetes 58:2904–2909, 2009

7) Ijas P, et al. Haptoglobin Hp2 Variant Promotes Premature Cardiovascular Death in Stroke Survivors. Stroke. 2017;48:1463-1469

8) Mukund R, et al. Haptoglobin2-2 phenotype is an additional risk factor of retinopathy in type 2 diabetes mellitus. Indian Journal of Human Genetic. 2013 Apr-Jun; 19(2): 154–8.

9) Fasano A., Physiological, Pathological, and Therapeutic Implications of Zonulin-Mediated Intestinal Barrier Modulation. The American Journal of Pathology 2008;173:1243-1252

10) Hochberg I, et al. Interaction Between the Haptoglobin Genotype and Vitamin E on Cardiovascular Disease in Diabetes. Current Diabetes Reports 2017_online Jun 17

11) American Diabetes Association. Standards of Medical Care in Diabetes. Diabetes Care 2017; 40: Supplement 1

Metformin: Stepchild of Diabetes Care

The Merriam Webster definition of Stepchild is: “one that fails to receive proper care or attention”. We all know that metformin is pretty much a ‘given’ when we initiate care for diabetes based on nearly all type 2 diabetes treatment guidelines. We also know that metformin has been used effectively in diabetes prevention in patients with prediabetes with long-term effectiveness (1) and that this effect was dose and adherence related (2). Yet despite this, one survey suggested that only 36% of primary care providers prescribe metformin for patients with prediabetes at all (3). Combine this with the fact that we that there is a relationship of dose to the intensity of the hypoglycemic effect in diabetes in clinical trials (4) and that there is an association of glucose control in early treatment with ‘regression’ of pre-diabetes (5).

Guidelines are clear on the need to aggressively intensify therapy in patients with newly diagnosed type 2 diabetes to get to the A1C goal, but patients and physicians may feel less urgency early in the course of the disease, and ‘clinical inertia’ or lack of appreciation of the benefits of early control mean that many patients will be at increased risk of later cardiovascular complications from inadequate intensity of metformin dosing even in the few years subsequent to diagnosis (6). With more recent publications suggesting more flexibility in dosing metformin in patients with impaired renal function, we have even more reason to be comfortable with dosing this important medication (7). When was the last time you recommended metformin for a patient with prediabetes? When was the last time your reviewed your type 2 diabetes patients’ doses of metformin and pushed the envelope on dosing? Sounds like there’s a need to me!

1. Diabetes Prevention Program Research Group. 10-year follow-up of diabetes incidence and weight loss in the Diabetes Prevention Program Outcomes Study Lancet. 2009 November 14; 374(9702): 1677

2. The Diabetes Prevention Program Research Group. Long-Term Safety, Tolerability, and Weight Loss Associated With Metformin in the Diabetes Prevention Program Outcomes Study. Diabetes Care 2012;35:731

3. Mainous AG, et al. Prediabetes Screening and Treatment in Diabetes
Prevention: The Impact of Physician Attitudes. J Am Board Fam Med 2016;29:663

4. Hirst JA, et al. Quantifying the Effect of Metformin Treatment and Dose on Glycemic Control. Diabetes Care 2012;35:446

5. Perreault L, et al. Effect of regression from prediabetes to normal glucose regulation on long-term reduction in diabetes risk: results from the Diabetes Prevention Program Outcomes Study. Lancet 2012;379:2243

6. Svensson E, et al. Early Glycemic Control and Magnitude of HbA1c Reduction
Predict Cardiovascular Events and Mortality: Population-Based Cohort Study of 24,752 Metformin Initiators. Diabetes Care 2017;40_online April 17

7. Inzucchi, SE, et al. Metformin in Patients With Type 2 Diabetes and Kidney Disease: A Systematic Review. JAMA. 2014;312:2668

Laugh and the World Laughs With You… …Snore and You Sleep Alone!


Of course, all snoring isn’t necessarily bad (unless you are a sleep partner), but most of us have heard about Obstructive Sleep Apnea (OSA) and have pre-conceived notions about risk factors, prevalence and outcomes. It is safe to say, however, that obstructive sleep apnea is the  ‘elephant in the room’ of cardiovascular risk.  It is true that most individuals who have OSA are overweight or obese, as that is the most common risk factor.  We know that the upper airway collapses in some people who have more tissue in the upper airway (tonsils, adenoids, tongue, palate and uvula).  When the OSA sleeper lays in his/her back, gravity is not in their favor as muscles relax during sleep.  When the sleeper attempts to breath in, the tissue obstructs resulting in snoring or gasping sounds and either a decrease in flow (hypopnea) or a cessation of airflow into the lungs (apnea).  The more often this happens the more likely the sleeper is to develop the consequences of chronic intermittent hypoxia.  OSA affects men about 2-3 times more commonly than women. An older study suggested that roughly 26% of a primary care population was potentially at risk of OSA, yet screen was very rare (1,2). If we look at one specific population, among an estimated 14 million US commercial drivers, 17–28% or 2.4 to 3.9 million are expected to have OSA (3).  In this population the effects of sleep deprivation secondary to OSA can be disastrous.

A much more insidious and common occurrence of OSA is in people with diabetes.  If we look at the type 2 diabetes patient population, the proportion at risk is significantly higher, due to the higher prevalence of older patients, and those with obesity. A recent review suggested the overall prevalence of diagnosed OSA in diabetic patients is approximately 71% based on the average data from five studies including a total number of nearly 1200 patients with type 2 diabetes (4). In 2008, the IDF Taskforce on Epidemiology and Prevention released a consensus statement that recommended a targeted approach to “screen individuals with type 2 diabetes and obesity for sleep disordered breathing (SDB)”. Briefly, the IDF recommended that healthcare professionals should consider the possibility of OSA in patients with type 2 diabetes and work in tandem with the local ‘sleep service’ to provide a clinically appropriate process of assessment, referral and intervention (5).

Several screening tests are available and include the Berlin Questionnaire, the STOP-BANG Questionnaire, and the Epworth Sleepiness Scale.  This last screener may be less effective than the others primarily due to the fact that daytime sleepiness, while common, is not universal, and appears less often in women and in individuals with heart failure. I prefer the “Canadian modifications” of the STOP-BANG screening tool (6).  Further diagnostic tests include the ‘gold standard’ sleep study (polysomnography), and within the last several years more and more products have been introduced that can be used as home diagnostic tests (7).

Studies have shown that cardiac remodeling occurs In OSA patients and that the changes are similar to predisposing changes for heart failure.  There is a significant increase in cardiovascular risk from the downstream consequences of chronic intermittent hypoxia from repeated episodes of apnea or hypopnea during sleep: atherosclerosis, cardiovascular disease including conditions such as myocardial infarction, congestive heart failure, cerebrovascular accident, resistant hypertension, and cardiac arrhythmia, as well as cognitive dysfunction, depression, poor glucose control in diabetes and motor vehicle accidents to name just some of them.

So, the prevalence in people with diabetes is high, and the outcomes of cardiovascular morbidity and mortality are well described.  Yet, the screening rate is abysmally low (in one study around 5%).  Routine screening of diabetes patients should lead many more people to a diagnostic procedure and to CPAP as the most effective treatment.  An old saying about how to eat an elephant is “one bite at a time”.  In the case of OSA, I would submit that some of these bites are up to you.  Pharmacists, involved in screening for OSA you ask (?) Of course! In this era of patient-centered care, how could a credible “diabetes practitioner” [yes, that’s you…] NOT screen patients for Obstructive Sleep Apnea!

  1. Hiestand DM, Britz P, Goldman M, Phillips B. Prevalence of symptoms and risk of sleep apnea in the US population: results from the National Sleep Foundation sleep in America 2005 poll. Chest 2006; 130:780 – 6.
  2. Grover M, et al.  Identifying Patients at Risk for Obstructive Sleep Apnea in a Primary Care Practice. J Am Board Fam Med 2011;24:152–160
  3. Kales S, and Straubel,M. Obstructive Sleep Apnea in North American Commercial Drivers. Industrial Health 2014, 52, 13–24
  4. Pamidi S and Tasali E . Obstructive Sleep Apnea And Diabetes-IsThereALink_Pamidi FrontNeurol_2012_v3_Article128
  5. Seetho I, et al. Obstructive sleep apnoea in diabetes – assessment and awareness. British Journal of Diabetes  2014(3):105-108

Low hanging fruit

Hopefully everyone had a good holiday break, and maybe even the chance to curl up with a good book…or better, with the Federal Register!  Yes, you heard that right, the Federal appleRegister from 2016 has a number of positive developments in areas that are or will soon be ‘ripe’ for pharmacist intervention.  Notices and rulemaking for Medicare are published by CMS in the Federal Register. These notices are often accompanied by CMS’ responses to comments received on proposed rulemaking as well as some interesting background data.  So let’s look at what CMS considers important (i.e. what they are willing to pay for).  First, they recognize that medication misadventures often result in costly adverse effects including ED visits and hospitalizations.  They recognized MTM as needed (Ref 1), and when it was clear that it wasn’t being used as often as they wanted, they expanded the criteria to qualify more patients for MTM.  Realizing that medication misadventures were more likely during care transitions, CMS decided to reimburse for Transitional Care Management (CPT 99495, 99496) that included Medication Reconciliation. (Ref 2) With CMS’ announced aggressive plan to move to a system of more value-based reimbursement, new payment models were recently release as MACRA-MIPS (Ref 3), and medication reconciliation was a key component for the Merit-based Incentive Payment System (Ref 3, see pgs 77225 and 77230).

Switching gears to a key condition recognized by CMS, diabetes, it is clear that they value Diabetes Self Management Education (CPT G0108, G0109), and that they have increased the reimbursement for provision of that service. (4) Recently, CMS has announced that it will reimburse diabetes prevention in the proposed Medicare Diabetes Prevention Program (Ref 5, see section III.J)  The preliminary structure proposal is in Ref 5, and establishes how you can be prepared for the final rulemaking in 2017, and implementation in 2018.  In this document you can find links to the proposed standards and to the proposed curriculum developed by CDC. This is a must read if you want to be prepared to offer this service!

Finally, CMS has not only established reimbursement for Chronic Care Management (CPT 99490), but updated their rules with new codes for more complex patients who are involved in CCM (CPT 99487-99489) so that the reimbursement could better reflect the amount of work involved with CCM in highly complex patients (Ref 5, see section E.4 and Table 11).  As most of you already know, CCM can be provided to patients with 2 or more chronic diseases, and thus nearly all your patients with diabetes would qualify.

It is clear that medications, diabetes and chronic care are not only on the CMS’ radar screen, but they are addressing concerns related to expansion of these services as well as augmenting reimbursement.  Members of the ACCP Endocrine & Metabolism PRN are particularly well positioned to take advantage of many of these services!

At the 2016 ACCP Annual Meeting in October, a session discussing TCM and CCM was poorly attended, yet just down the hall a session on PCSK-9 inhibitors was packed.  While being the local guru on pharmacodynamics of PCSK-9 inhibitors may bring personal satisfaction, providing services such as TCM, CCM, DSMT, and soon MDPP brings revenue.  We are fighting for recognition as ‘providers’, and in any fight, you are lucky when the other guy telegraphs his moves.  CMS is not telegraphing, they are shouting it from the rooftops, yet only a few ACCP members are doing any of these services.  My bias is obvious, if you want to be recognized as ‘providers’, then start providing what your customer wants!

  1. The Medicare Prescription Drug, Improvement, and Modernization Act of 2003. Public Law 108-173. December 8, 2003. Available at: [accessed 12/27/2016]
  2. [accessed 12/27/2016]
  3. Medicare Program; Merit-Based Incentive Payment System (MIPS) and Alternative Payment Model (APM) Incentive Under the Physician Fee Schedule, and Criteria for Physician- Focused Payment Models. Federal Register / Vol. 81, No. 214 / Friday, November 4, 2016 / Rules and Regulations. [accessed 12/27/2016]
  4. Medicare Benefit Policy Manual Chapter 15 – Covered Medical and Other Health Services [accessed 12/27/2016]
  5. Medicare Program; Revisions to Payment Policies Under the Physician Fee Schedule and Other Revisions to Part B for CY 2017; Medicare Advantage Bid Pricing Data Release; Medicare Advantage and Part D Medical Loss Ratio Data Release; Medicare Advantage Provider Network Requirements; Expansion of Medicare Diabetes Prevention Program Model; Medicare Shared Savings Program Requirements. [accessed 12/27/2016]

Co-Pays and Policy

An recent editorial in New England Journal of Medicine (N Engl J Med 2016; 375:2013-2015) from Dr. Leemore Dafny and others spoke of the U.S. DHHS announced goal of linking at least 50% of Medicare spending to value-based payment models. They noted that “health care providers are now scrambling to reorganize in a way that delivers value while preserving or enhancing ‘commercial success’ […of their health care businesses]…For years, insurers and pharmacy benefits managers have steered consumers toward generic and other ‘high-value’ drugs by categorizing drugs into ‘tiers’ and requiring lower copayments for ‘preferred’ drugs.” High value and preferred decisions are being made by the insurer/PBM based perhaps on criteria other than what a clinical pharmacist might consider high value… The authors note that “under tiering, insurers offer manufacturers favorable tier placement in exchange for better discounts” a clear benefit to the insurer or PBM. “Placement on a preferred-brand tier, with a [low] co-pay, will [arguably] yield higher sales than placement on a non-preferred-brand tier with a typical copayment of more than $50. Insurers can also negotiate lower prices for drugs that have therapeutic substitutes or questionable benefits by threatening to exclude them from their formularies entirely.”  The philosophy espoused by the authors of the article is that this is all good!  However, they note that the pharmaceutical industry “counterattacked” (…interesting choice of emotional vocabulary) “by offering ‘copayment coupons’. These coupons or discount cards — distributed by physicians’ offices, through the mail, and online — enable the manufacturer to pay some or all of a consumer’s copayment for a prescription. By severing the link between cost sharing and the ‘value’ generated by a drug, copayment coupons can undo the perceived beneficial effects of tiering.”  They estimate that “coupons increase the percentage of prescriptions filled with brand-name formulations by more than 60%” (!)

OK, I get it! The tiering process is one way to control costs, and healthcare policymakers like that!  I wanted to present a flip side view from the patient care perspective. It is well known that medication adherence is related in part to the size of co-pay assessments in an attempt at ‘cost sharing’ (1-2) both generally and for those entering the Medicare ‘donut hole’.(3)  The use of ‘high value’ [my definition is not necessarily based on medication cost…] drugs such as those that are still branded, may offer improved outcomes, but they are often made second or third tier by insurers to limit their own costs.   Adherence with a number of new medications, especially those with minimal co-pays suggests that there are adherence benefits to be gleaned from the discount cards or coupons.  Add to that the evidence that some of the older diabetes medications, available with little or no co-pays may have a higher rate of adverse effects. (4-7)

So ask yourself, if your mother or father were diagnosed with type 2 diabetes, would you want early aggressive therapy with agents that may have significantly more benefits (8-9), not to mention the benefit of early glucose control, or would you want them to start older agents (some with potential CV risk) and then stay with them for years in the clinical inertia that plagues diabetes care. I know what the policy makers prefer, and I know what my preference is for making new and better drugs more available regardless of ability to handle the co-pay…How about you?

  1. Effect of prescription copayments on adherence and treatment failure with oral antidiabetic medications. Barron J, Wahl P, Fisher M, Plauschinat C. P.T. 2008 Sep;33(9):532-53
  2. How patient cost-sharing trends affect adherence and outcomes: a literature review.Eaddy MT, Cook CL, O’Day K, Burch SP, Cantrell CR. P T. 2012 Jan;37(1):45-55
  3. Part D coverage gap and adherence to diabetes medications. Gu Q1, Zeng F, Patel BV, Tripoli LC. Am J Manag Care. 2010;16(12):911-8
  4. Sulphonylureas and risk of cardiovascular disease: systematic review and meta-analysis. Phung OJ1, Schwartzman E, Allen RW, Engel SS, Rajpathak SN. Diabet Med. 2013 Oct;30(10):1160-71
  5. Hyperinsulinemia and sulfonylurea use are independently associated with left ventricular diastolic dysfunction in patients with type 2 diabetes mellitus with suboptimal blood glucose control. Inoue T, Maeda Y, Sonoda N, Sasaki S, Kabemura T, Kobayashi K, Inoguchi T. BMJ Open Diabetes Res Care. 2016 Aug 18;4(1):e000223
  6. Cardiovascular risk associated with the use of glitazones, metformin and sufonylureas: meta-analysis of published observational studies.Pladevall M, Riera-Guardia N, Margulis AV, Varas-Lorenzo C, Calingaert B, Perez-Gutthann S. BMC Cardiovasc Disord. 2016 Jan 15;16:14
  7. Mortality risk among sulfonylureas: a systematic review and network meta-analysis.Simpson SH, Lee J, Choi S, Vandermeer B, Abdelmoneim AS, Featherstone TR. Lancet Diabetes Endocrinol. 2015 Jan;3(1):43-51
  8. Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes. Zinman B, Wanner C, Lachin JM, Fitchett D, Bluhmki E, Hantel S, Mattheus M, Devins T, Johansen OE, Woerle HJ, Broedl UC, Inzucchi SE; EMPA-REG OUTCOME Investigators. N Engl J Med. 2015 Nov 26;373(22):2117-28
  9. Empagliflozin and Progression of Kidney Disease in Type 2 Diabetes. Wanner C, Inzucchi SE, Lachin JM, Fitchett D, von Eynatten M1, Mattheus M, Johansen OE, Woerle HJ, Broedl UC, Zinman B; EMPA-REG OUTCOME Investigators. N Engl J Med. 2016 Jul 28;375(4):323-34

You know what CCM is, why aren’t you doing it?

In January of 2015, CMS initiated a new code for managing Chronic Care patients. (,
The code could be used when following patients with two or more chronic diseases from a rather extensive list of conditions we all know lead to higher medical care costs, and many which have significant morbidity and mortality associated with them. As you may know, identifying these patients and then providing follow up contact at a minimum of 20 minutes per month can result in reimbursement for the provider of roughly $40…which Medicare pays 80% of and the practice collects 20% from the patient. Of course the individual providing that 20 minutes needs to be part of the practice (employee or contractor), and the patient needs to agree to enroll in this service which is based on his/her plan of care. There are other requirements that are spelled out in the documents listed at the beginning of this Blog. It has been over a year, and yet only a few medical practices are offering this service, and only a very few members of ACCP are actually providing CCM. In a number of cases the service has been ‘assigned’ to the office nurse (read: Medical Assistant, or RN ‘chronic care coordinator,’ social worker, dietitian) or some other practitioner rather than the pharmacist. Indeed there are even commercial services that have sprung up to outsource this service.

ACCP rallies around the possibility of reimbursement for “Comprehensive Medication Management,” yet we have not been fighting tooth and nail for “Chronic Care Management” to be our responsibility. Indeed CCM is the low hanging fruit that could potentially lead to CMM. Nowhere will pharmacists be more valuable than the chronic care patient with multiple medications. It is a gateway to MTM (at least one of them) which has been recognized as valuable by CMS and worthy of extension to more and more patients as the provision of MTM was way less than CMS had planned yet was every bit a valuable as they knew it would be. Yes, a nurse can call patients and talk to them for 20 minutes. But having access to de facto risk stratified patients who are on multiple medications, often with conditions that have documented value via telemedicine follow-up is a gift that has been sitting under our Christmas Tree for over a year. Few ACCP members have taken up the gauntlet to ‘manage’ these patients. You can download blood glucose meters remotely, you can have patients monitor their blood pressure at home (a better way to do it anyway), you can monitor and reinforce medication adherence, or even find out patients who should be on certain medications (‘statins, ACE Inhibitors) yet somehow are not. There is even recognition that CCM services need to be expanded to increase reimbursement for more complicated patients, which means that reimbursement for those patients will be even higher in the future. Reimbursement for Diabetes Education was increased due to recognition of its value, MTM was expanded due to recognition of its value, Chronic Care Management was initiated and will likely soon be expanded due to recognition of its value ( [See:policy under consideration, pg 11].

The segue between CCM and the ‘holy grail’ of Comprehensive Medication Management seems obvious, and just needs to be fleshed out. Having clinical pharmacists involved in the first will more likely lead to the latter if we decide to make it so. So let’s get crackin’