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By Louis Kuritzky, MD
Hepatitis C Treatment: Just How Much is it Worth to Cure a Dreadful Disease?
Source: Brennan T, Shrank W. JAMA 2014;312: 593-594.
The trouble with the expense of treating hepatitis C virus (HCV) infections is that very few patients are acutely "choking" on it, since the largest pool of HCV patients are asymptomatic. Progression to end-stage liver disease, liver transplantation, and hepatocellular carcinoma — the three most dreaded HCV consequences — may seem distant to the asymptomatic or even modestly symptomatic patient. The current costs of some HCV regimens appear, at least at first glance, extraordinary. For instance, once-daily oral sofosbuvir, one of the most highly effective HCV treatments, is a startling $84,000 for a standard 12-week course ($1000 per pill)!
Although neither the public nor clinicians are readily aware of the per-tablet costs of actually creating a new therapeutic entity, it is perhaps noteworthy that the initial purchase of the company that first developed sofosbuvir was $11 billion. This number does not include any of the costs for subsequent manufacture and marketing, and of course it will take many, many courses of sofosbuvir to recoup even these initial expenses. On the other hand, if every HCV patient in the United States were to enjoy a curative treatment course of sofosbuvir at the standard price, that could generate as much as $250 billion.
Certainly the costs of treatment for liver transplantation, end-stage liver disease, and hepatocellular carcinoma would readily eclipse even this apparently extravagant tariff for sofosbuvir and some other agents like it, such that in the long-term perspective, it becomes "pay me a lot now or pay a lot more later." In any case, many voices are calling for the industry to be economically and socially responsible stewards of the treatments they offer.
DPP-4 Inhibitors: Should We Worry About Risk
Source: Raz I, et al. Diabetes Care 2014;37: 2435-2441.
Although not well recognized
until the advent of DDP-4 inhibitors (e.g., alogliptin, linagliptin, saxagliptin, sitagliptin) and GLP-1 agonists (e.g., albiglutide, dulaglutide, exenatide, liraglutide), diabetes is associated with pancreatitis. The mechanisms by which diabetes might lead to pancreatitis are not well understood, although comorbid hypertriglyceridemia and hypertension (which is often treated with thiazides, leading to triglyceride elevation) might be contributing factors.
In the last 2-3 years, case reports of pancreatitis in patients taking GLP-1 agonists and DPP-4 inhibitors have prompted closer scrutiny of the potential relationship between these two classes of agents. Indeed, FDA labeling for some agents from both classes includes warning/caution comments on pancreatitis. Do DPP-4 inhibitors or GLP-1 agonists increase risk for pancreatitis? Recent trial data on saxagliptin provides reassuring commentary that likely merits consideration in reference to other members of the DPP-4 group as well.
Raz et al report data from the Saxagliptin Assessment of Vascular Outcomes Recorded in Patients with Diabetes Mellitus-Thrombolysis in Myocardial Infarction (SAVOR-TIMI) 53 trial. Among the 16,492 patients randomized to DPP-4 treatment (saxagliptin) or placebo, the risk for pancreatitis was both small (< 0.5%) and not different between saxagliptin and placebo.
Current recommendations suggest that incident pancreatitis in patients taking DPP-4 inhibitors or GLP-1 agonists merits at least temporary discontinuation of such treatment. The SAVOR-TIMI 53 data provide reassurance that DPP4 inhibitors, specifically saxagliptin, do not increase risk for pancreatitis.
Obesity and Cancer
Source: Bhaskaran K, et al. Lancet 2014;384: 755-765.
The link between obesity and adverse cardiovascular outcomes can be fairly directly attributed to readily visible obesity comorbidities such as increases in blood pressure, dyslipidemia, and sedentary lifestyle. But what about cancer?
According to a recent analysis in the Lancet based on records from primary care records in the United Kingdom (n = 5.24 million), there is a meaningful relationship between increasing body mass index (BMI) and cancer.
For instance, for every 5 kg/m2 increase in BMI, statistically significant hazard ratios increased for cancers of the uterus (HR = 1.62), gallbladder (HR = 1.31), kidney (HR = 1.25), cervix (HR = 1.10), and thyroid (HR = 1.09). Not all cancer risks were magnified by increasing BMI. For instance, prostate cancer and premenopausal breast cancer were inversely associated with BMI.
According to this analysis, as many as 41% of uterine cancers and 10% of gallbladder, kidney, liver, and colon cancers are related to being overweight in the United Kingdom. The mechanism(s) by which increasing weight is associated with cancer in general is by no means clear. On the other hand, it has been demonstrated that overweight women more often feel like they get a negative reception from their health care provider and hence do not attend cervical cancer screening opportunities as assiduously as age-matched, more slender women.
In addition to well-recognized cardiovascular consequences of obesity, risk for some cancers is also meaningfully increased.