Experts comment on emerging treatments for anhedonia and highlight lifestyle modifications that support patients with Major Depressive Disorder.

Emerging Treatments of Anhedonia in Patients with Major Depressive Disorder

In addition to the dextromethorphan-bupropion combination, the clinicians review other evidence-based treatments for anhedonia. These include medications modulating dopamine, glutamate, kappa opioid receptors, and psychedelics. Lifestyle approaches like exercise, diet, sleep, social connection, and purpose are also critical, improving motivation and pleasure by enhancing BDNF, endorphins, and dopamine while decreasing inflammation.

They emphasize assessing and tracking residual symptoms like anhedonia even in patients considered asymptomatic or “in remission” on rating scales, as lingering lack of enjoyment, drive, or interest predicts later recurrence and dysfunction. Using practical measures of life engagement and specific hobbies, relationships, or tasks is recommended over formal rating scales to identify ongoing areas of impairment.

In closing, the clinicians express excitement about the expanding treatment options to address unmet needs like motivation and pleasure that have been resistant to standard interventions. They urge clinicians to utilize both new tools emerging from ongoing research as well as digital measures and benchmarking to ensure treatment gets patients to optimal functioning, not just minimal symptom reduction. Keeping skills updated and identifying patients struggling with residual symptoms is key to enabling fuller recovery.

This summary was AI-generated and edited for clarity. 

Dr Andrew Cutler and Dr Greg Mattingly comment about emerging treatments to treat anhedonia and highlight lifestyle modifications that support the wellbeing of patients with Major Depressive Disorder.

Gregory Mattingly, MD

A panel of ophthalmologists discuss strategies for improving patient outcomes in retinal vein occlusion with anti-VEGF and other therapies.

Optimizing Treatment Outcomes in Retinal Vein Occlusion

Optimizing Treatment Outcomes in Retinal Vein Occlusion (RVO)

Hong-Uyen Hua, MD

Ken reports on medical innovations and advances in practice and edits presentations for news and professional education publications. He previously taught and mentored pharmacy and medical students, and provided and managed pharmacy care and drug information services. He regularly contributes to Contagion Live, HCP Live, and Neurology Live.

Kenneth Bender, PharmD

Maddy Pontius is a Master’s Student in Forensic Psychology at the University of Denver with interests in rehabilitation psychology, health psychology, and neuropsychology. She is hoping to work within the overlap of offender rehabilitation and healthcare in the future.

Maddy Pontius, BA

Discussions about migraine treatment often revolve around a single topic: triggers. Patients with migraine are always eager to learn about factors that activate migraine in order to avoid them. Tracking and avoiding triggers is often one of the few means of control migraine patients feel they have over an otherwise unpredictable disease. However, this is an oversimplification. In practice, trigger avoidance is usually ineffective, and sometimes even detrimental to patients. That’s because:

Many supposed “triggers” are not triggers at all, but rather are premonitory symptoms signaling an attack is already underway.

Rarely does a single trigger produce a migraine attack.

Avoiding triggers can erode patients’ quality of life, since it can lead to avoidance of enjoyable activities

 as well as feelings of helplessness and self-blame.

Migraine Triggers Versus Prodromal Symptoms

Research has confirmed several triggers of migraine attacks:

 are perhaps the most common migraine trigger among women. The drop in estrogen levels just prior to menses is likely the cause.

, including for religious reasons such as Ramadan

 Links between chronic stress, pain, migraine, and catastrophic thinking have been demonstrated by many studies.

 However, removing a stressful situation alone is unlikely to improve migraine. In fact, the abrupt cessation of stress is often itself a migraine trigger.

Many environmental factors may affect migraine (such as altitude, lightning, and barometric pressure changes) but the effects are relatively mild and in some cases nonsignificant.

It’s important to emphasize that rarely does any single trigger invariably produce a migraine attack. Much depends upon the patient’s own migraine threshold, which fluctuates over time. For example, sudden changes in daily activity or environment increase migraine susceptibility,

 making triggers more potent than usual. This can be disorienting for patients, who may find that activities that were tolerable one day become triggering the next.

Further confusing for patients is the difficulty figuring out which of the events or symptoms that preceded a migraine attack was the trigger. This has led to a plethora of reported triggers, most of which have not been borne out by research. Rather, data supports the idea that many of these symptoms are actually premonitory, or prodromal symptoms,

 which occur 2 to 48 hours prior to the headache phase of a migraine attack.

 Seen in this light, such symptoms are not triggers that can be avoided; rather, they signal to the patient that an attack is already underway.

Common premonitory symptoms often confused for triggers include:

Chocolate is probably the best example of a food craving misunderstood as a trigger. Although patients rank chocolate number one of all food-based triggers, placebo-controlled studies have failed to show that chocolate triggers migraine.

 The same can be said of caffeine, an oft-cited food “trigger” that 

Prodromal symptoms are individual to each patient. Identifying their prodromal symptoms can help a patient with migraine recognize that the headache phase is imminent, lessening the element of surprise and allowing them to take mitigation steps such as leaving work early, seeking out a dark room, notifying caregivers, or obtaining childcare for during the attack.

Reframing Triggers for Effective Migraine Treatment

Asking patients to avoid triggers does not appear to be effective, based on studies comparing the practice to a control group that didn’t change their behaviors. Trigger avoidance was also found less effective than cognitive therapy or an approach of learning to cope with triggers.

 Avoiding stress, for example, has been found less effective for chronic pain than coping or adaptive strategies and may lead to anxiety, increased disability, and catastrophic thinking.

Focusing extensively on migraine triggers during an office visit is not only an ineffective use of provider-patient time, but it may also have a host of negative consequences on the person with migraine’s quality of life:

Patients can feel blamed or self-blame for a migraine attack (e.g., “This is my fault because I drank wine”).

A patient may find it impossible to identify their triggers, especially in those with very frequent attacks (where everything can appear to be a trigger) or infrequent attacks (where it’s difficult to find consistent patterns).

The triggers identified may not be avoidable, such as stress or weather.

Focusing on triggers can increase anxiety or lead to anticipation of attacks. It may even pave the way to more migraine attacks. Nocebo is a major problem in headache, both in clinical trials and practice.

 Studies of other pain disorders have shown that increased pain expectations cause an increase in symptoms

; the suggestion that a specific trigger will cause a migraine attack may create similar expectancy mechanisms.

It does not address the underlying cause of the disorder.

With all this in mind, here are a few strategies when advising patients on triggers.

 Maintaining a regular diary or calendar eliminates recall bias and focuses on overall migraine control. It may also allow the discovery of unrecognized triggers amenable to treatment, such as caffeine withdrawal on weekends or menstrual migraine. In addition to tracking attacks, ask patients to write down strategies that worked, both preventively and abortively (medical and non-medical), to reduce their migraine symptoms.

Focus on healthy lifestyle choices that raise migraine threshold. 

Rather than trigger avoidance, focus on engaging in proactive behaviors that, done consistently, raise patients’ threshold for migraine triggers. Those include good sleep, regular nutrition patterns, regular exercise, and stress management techniques.

For further practical details on healthy lifestyle changes that improve migraine, see my colleagues’ Stephen Silberstein, MD and William Young, MD’s article “Lifestyle Changes for Migraine: Practical Tips for the Neurologist & PCP.”

To help patients understand the concept of threshold and their ability to raise their own migraine resistance level, try this patient-centric article from Ctrl M Health.

Recognize and treat “cephalgiaphobia.” 

Ask patients if they worry about migraine when they are headache-free or restrict activities due to fear of migraine. Fear of migraine between attacks is an important predictor of chronification and medication overuse.

 Finding effective acute medication may reduce the risk of chronification.

 Cognitive behavioral therapy can be particularly effective.

 Patients with very frequent migraine—for whom triggers appear to be everywhere—may benefit from effective preventive medication.

Expect that patients will be new to the idea of replacing trigger-avoidance strategies with proactive behaviors. They will need encouragement and guidance to follow through. Until recently, evidence-based, expert-reviewed programs to help patients with lifestyle change for migraine were rare. That is a guiding reason why we at the Jefferson Headache Center and Thomas Jefferson University Hospital have partnered with Ctrl M Health, whose app-delivered program makes this information widely accessible.

Providers have the ability to help patients redirect their efforts into the factors within their control that are shown to actually make a difference. I find patients also benefit from the empowerment this behavioral approach brings, making them more confident in their ability to manage migraine. Those gains, in turn, allow them to continue making progress in reducing migraine frequency and severity, improving their quality of life.

The Jefferson Headache Center and Thomas Jefferson University have partnered with Ctrl M Health to create comprehensive, evidence-based programming and support for people with migraine. For free provider resources, best practice tips, and patient handouts, visit their For Providers page.

1. Martin PR. Managing headache triggers: think ‘coping’ not ‘avoidance.’ Cephalalgia. 2010;30(5):634–7. DOI: 10.1111/j.1468-2982.2009.01989.x

2. Loder EW. Menstrual migraine: pathophysiology, diagnosis, and impact. Headache. 2006;46(Suppl 2):S55–60. DOI: 10.1111/j.1526-4610.2006.00555.x

3. Abu-Salameh I, Plakht Y, Ifergane G. Migraine exacerbation during Ramadan fasting. JHeadache Pain. 2010;11(6):513–7. DOI: 10.1007/s10194-010-0242-z

4. Drescher MJ, Elstein Y. Prophylactic COX 2 inhibitor: an end to the Yom Kippur headache. Headache. 2006;46(10):1487–91. DOI: 10.1111/j.1526-4610.2006.00609.x

5. Meng ID, Cao L. From migraine to chronic daily headache: the biological basis of headache transformation. Headache. 2007;47(8):1251–8. DOI: 10.1111/j.1526-4610.2007.00907.x

6. Kunz M, Chatelle C, Lautenbacher S, Rainville P. The relation between catastrophizing and facial responsiveness to pain. Pain. 2008;140(1):127–34. DOI: 10.1016/j.pain.2008.07.019

7. Lipton RB, Buse DC, Hall CB, Tennen H, Defreitas TA, Borkowski TM, et al. Reduction in perceived stress as a migraine trigger: Testing the “let-down headache” hypothesis. Neurology. 2014;82(16):1395–401. DOI: 10.1212/WNL.0000000000000332

8. Marmura MJ, Hernandez PB. High-altitude headache. Curr Pain Headache Rep. 2015;19(5):483. DOI: 10.1007/s11916-015-0483-2

9. Prince PB, Rapoport AM, Sheftell FD, Tepper SJ, Bigal ME. The effect of weather on headache. Headache. 2004;44(6):596–602. DOI: 10.1111/j.1526-4610.2004.446008.x

10. Martin VT, Behbehani MM. Toward a rational understanding of migraine trigger factors. The Medical clinics of North America. 2001;85(4):911–41. DOI: 10.1016/S0025-7125(05)70351-5

11. Schulte LH, Jurgens TP, May A. Photo-, osmo- and phonophobia in the premonitory phase of migraine: mistaking symptoms for triggers? J Headache Pain. 2015;16:14. DOI: 10.1186/s10194-015-0495-7

12. Becker WJ. The premonitory phase of migraine and migraine management. Cephalalgia. 2013;33(13):1117–21. DOI: 10.1177/0333102412437390

13. Maniyar FH, Sprenger T, Schankin C, Goadsby PJ. Photic hypersensitivity in the premonitory phase of migraine—a positron emission tomography study. Eur J Neurol. 2014;21(9):1178–83. DOI: 10.1111/ene.12451

14. Pavlovic JM, Buse DC, Sollars CM, Haut S, Lipton RB. Trigger factors and premonitory features of migraine attacks: summary of studies. Headache. 2014;54(10):1670–9. DOI: 10.1111/head.12468

15. Marcus DA, Scharff L, Turk D, Gourley LM. A double-blind provocative study of chocolate as a trigger of headache. Cephalalgia. 1997;17(8):855–62. DOI: 10.1046/j.1468-2982.1997.1708855.x

16. Martin PR, Reece J, Callan M, MacLeod C, Kaur A, Gregg K, et al. Behavioral management of the triggers of recurrent headache: a randomized controlled trial. Behav Res Ther. 2014;61:1–11. DOI: 10.1016/j.brat.2014.07.002

17. Ramirez-Maestre C, Esteve R, Lopez-Martinez A. Fear-avoidance, pain acceptance and adjustment to chronic pain: a crosssectional study on a sample of 686 patients with chronic spinal pain. Ann Behav Med. 2014;48(3):402–10. DOI: 10.1007/s12160-014-9619-6

18. Volders S, Boddez Y, De Peuter S, Meulders A, Vlaeyen JW. Avoidance behavior in chronic pain research: a cold case revisited. Behav Res Ther. 2015;64:31–7. DOI: 10.1016/j.brat.2014.11.003

19. Peris F, Donoghue S, Torres F, Mian A, Wober C. Towards improved migraine management: determining potential trigger factors in individual patients. Cephalalgia. 2017;37(5):452–63. DOI: 10.1177/0333102416649761

20. Becker WJ. The premonitory phase of migraine and migraine management. Cephalalgia. 2013;33(13):1117–21. DOI: 10.1177/0333102412437390

21. Peres MF, Mercante JP, Guendler VZ, Corchs F, Bernik MA, Zukerman E, et al. Cephalalgiaphobia: a possible specific phobia of illness. JHeadache Pain. 2007;8(1):56–9. DOI: 10.1007/s10194-007-0361-3

22. Giannini G, Zanigni S, Grimaldi D, Melotti R, Pierangeli G, Cortelli P, et al. Cephalalgiaphobia as a feature of high frequency migraine: a pilot study. J Headache Pain. 2013;14:49. DOI: 10.1186/1129-2377-14-49

23. Lipton RB, Fanning KM, Serrano D, Reed ML, Cady R, Buse DC. Ineffective acute treatment of episodic migraine is associated with new-onset chronic migraine. Neurology. 2015;84(7):688–95. DOI: 10.1212/WNL.0000000000001256

24. Grazzi L, Andrasik F. Non-pharmacological approaches in migraine prophylaxis: behavioral medicine. Neurol Sci. 2010;31(Suppl 1):S133–S5. DOI: 10.1007/s10072-010-0306-5

Forget what you think you know about red wine or chocolate ‘activating’ migraine. Many commonly accepted “triggers” aren’t triggers at all.

Helping Your Patients Avoid the Migraine Trigger Trap

Michael Marmura, MD

Ralph DeFronzo, MD is a Professor of Medicine and Chief, Diabetes Division at UT Health San Antonio.

Ralph A. DeFronzo, MD: Noxious Nine and Mifepristone for Hypercortisolism in T2D

22nd Annual World Congress Insulin Resistance Diabetes & Cardiovascular Disease (WCIRDC)

, Ralph DeFronzo, MD, a professor of medicine and chief of the diabetes division at UT Health San Antonio, discussed the evolution of his influential concept, the Ominous Octet, which outlines the multiple defects contributing to 

Initially introduced in 1987 as the "triumvirate," focusing on insulin resistance in the liver and muscle and beta-cell dysfunction, the model expanded in 2008 to include five additional key players: obesity, the gastrointestinal tract, excess glucagon secretion, the kidney, and the brain, all of which exacerbate insulin resistance and beta-cell failure.

DeFronzo then shifted focus to a novel discovery about hypercortisolism in patients with difficult-to-control T2D, a condition in which the adrenal glands secrete excess cortisol, aggravating many of the defects in the ominous octet. The CATALYST study revealed that approximately 24% of these patients have elevated cortisol levels, which significantly contribute to their poor glycemic control. Treatment with mifepristone (Korlym), a glucocorticoid receptor blocker, led to a surprising 1.5% reduction in HbA1c, compared with 0.15% for placebo (placebo-adjusted reduction, 1.32%; P <.0001). In addition, mifepristone achieved a notable decrease in medication requirements, showcasing a promising new therapeutic avenue for this previously under-recognized cause of diabetes.

DeFronzo emphasized the importance of educating clinicians about hypercortisolism as a contributing factor in hard-to-treat diabetes, intending to integrate the Noxious Nine into clinical practice to improve patient outcomes. These findings represented a significant breakthrough in the understanding and management of complex T2D cases, with an FDA-approved treatment available for affected patients.

Relevant disclosures for DeFronzo include Corcept Therapeutics, AstraZeneca, Novo Nordisk, Alynylam Pharmaceuticals, and others.

DeFronzo R. Noxious Nine. Presented at the 22nd Annual World Congress Insulin Resistance Diabetes & Cardiovascular Disease (WCIRDC). Los Angeles, California. December 12-14, 2024.

Iapoce C. Mifepristone Notably Reduces HbA1c in Treatment Phase of Catalyst Trial. HCP Live. December 12, 2024. Accessed December 13, 2024. https://www.hcplive.com/view/mifepristone-notably-reduces-hba1c-in-treatment-phase-of-catalyst-trial.

Ralph DeFronzo, MD, discussed the evolution of his Ominous Octet concept to the Noxious Nine, highlighting the role of hypercortisolism in difficult-to-control type 2 diabetes (T2D). Initially focusing on insulin resistance and beta-cell dysfunction, the model expanded to include additional factors like obesity and excess glucagon secretion. The CATALYST study found that 24% of patients with challenging T2D have elevated cortisol levels, significantly impacting glycemic control. Mifepristone treatment showed a 1.5% reduction in HbA1c, suggesting a new therapeutic approach for these patients.

Ralph A. DeFronzo, MD discusses the Noxious Nine and the impact of hypercortisolism on difficult-to-control type 2 diabetes.








Ralph DeFronzo, MD 

Ryan Oakley, MD, takes a closer look at the recent history of ketamine in depression. He also explores the differences between ketamine and esketamine.

Ketamine for the Treatment of MDD

 I'm going to be talking about the interventional options that move a little bit away from direct electrical stimulation, using a more advanced neurochemical intervention. I would be surprised if most of you haven't at least heard of ketamine at this point as being used for mental illness in some way. It's all over the news, it's being marketed for a lot of different things. We're going to discuss a little bit about what it has actual evidence for and clear some of that up, including talking about what the FDA just released to combat some of that marketing. We're also going to talk about the evolution and the creation of the FDA-approved insurance-covered form of ketamine, which is esketamine, and how we use that in our clinics as an intervention.

So, what's special about ketamine, why is this being developed as an interventional treatment? First, to understand where ketamine is right now what it's been used for, its primary use is the procedural anesthetic and medicine. It started being explored for depression specifically based on some animal studies that showed that, when intervening on the glutamate system, the animals depressed behaviors improved, also based on some human clinical studies with medications that act on the glutamate system, like lamotrigine or alprazolam, also found to have some antidepressant activity. So then, a group decided to see if we could intervene directly on the glutamate system with an NMDA antagonist, like ketamine, to see what kind of effect would that have on depression. This group did a study, a randomized controlled trial, double-blind crossover study, and showed that it did, in fact, have a pretty dramatic, rapid, and sustained antidepressant activity. It was then explored a lot more as a treatment for depression.

We talked about ketamine a little bit. Esketamine was developed later. Essentially, ketamine is a combination of two different mirror images of a molecule. Esketamine is one of those mirror images of the molecule that they've designed and created to be delivered intranasally in an office setting, which sort of improves its scalability (ie, how easily we can deliver this treatment). So that's where esketamine is. “Es” is actually the name of the mirror image of ketamine, [and] this how it gets its name.

So, breaking down the difference between ketamine and esketamine, the biggest one is which one's actually insurance-based, which one has approval. Ketamine is not approved by the FDA for any kind of mental health treatment at this point. It's also not covered by insurance. Esketamine is approved by the FDA for treatment-resistant depression or major depression with suicidal ideation. The FDA recently put out a warning on compounded ketamine, because ketamine is getting marketed almost like a snake oil treatment for all the different types of mental illness where there's not a lot of evidence to support it (except for in depression, IV formulation, and a specific way of delivery). Whereas esketamine has evidence, we have a well-defined means of how to deliver it.

[What are] other differences between them? Ketamine, the drug itself or the medication is actually quite inexpensive. Esketamine, the drug, is actually quite expensive. However, insurance covering esketamine actually makes it more affordable for patients, whereas ketamine treatments, you're not just paying for the medication, you're paying for staff, you're paying for monitoring, paying for IV, all these things. It actually becomes less affordable for the patient, whereas esketamine is a very affordable option for people with treatment and depression. Other things to note is that there's no federally mandated program that tells us how to use ketamine. There are no guidelines for it. Esketamine does have guidelines. Ketamine doesn't have a risk evaluation mitigation system. So, we don't have a place where we can find out more about the side effects of how safe ketamine actually is, whereas esketamine does have that. We're continually monitoring how safe it is, and also able to update information for patients to make sure we deliver it the most safe way possible.

Transcript was AI-generated and edited for clarity. 

Ryan Oakley, MD

metabolic dysfunction-associated steatotic liver disease (MASLD)

 and bariatric surgery are becoming increasingly common in light of the rising obesity epidemic. Bariatric surgery offers well-established benefits on MASLD outcomes, including reduced adverse liver and cardiovascular events, improvement in steatohepatitis, and potential histologic regression of fibrosis.

Despite this, patients may still develop cirrhosis following bariatric surgery, either through progressive steatosis or other mechanisms. While many have sought to validate the efficacy and safety of performing bariatric surgery on patients with compensated cirrhosis, there is a paucity of literature describing the effect of bariatric surgery on outcomes of cirrhosis decompensation events.

We performed a retrospective, population-based analysis using the National Inpatient Sample database from October 2015 - December 2020 to identify all adults with obesity hospitalized with decompensated cirrhosis, including ascites, variceal hemorrhage, hepatic encephalopathy, or portal hypertension. These patients were then stratified into those with (n = 14,500) or without (n = 1,010,955) a history of bariatric surgery (Roux-en-Y gastric bypass or sleeve gastrectomy).

On outcomes analysis, inpatient mortality rates were lower in the bariatric surgery cohort (2.9% vs 4.1%; 

= .002), as were rates of acute kidney injury (24% vs 27%; 

<.001), respiratory failure requiring mechanical ventilation (0.7% vs 1.5%; 

<.001), and upper GI bleed (6.7% vs 9.6%; 

<.001). On univariate logistic regression analysis, bariatric surgery was protective against inpatient mortality (odds ratio [OR], 0.72; 95% confidence interval [CI], 0.58-0.89; 

= .002). However, after adjusting for age, race, Baveno stage, and Charlson Comorbidity Index, protective significance was lost (OR, 0.82; 95% CI, 0.66-1.03; 

Weight loss is the primary treatment for MASLD, and despite a growing armamentarium of non-surgical weight loss strategies, bariatric surgery remains the most effective and enduring treatment for obesity. A recent systematic review reported an overall lower risk of adverse liver outcomes among patients with obesity who underwent bariatric surgery compared to those who did not (Hazard ratio, 0.33; 95% CI, 0.31-0.34), including significantly reduced risk of developing cirrhosis.

 However, despite surgery, fibrosis may still progress and patients remain susceptible to other causes of cirrhosis, such as viral hepatitis or alcohol-associated liver disease. In fact, bariatric surgery is known to increase the risk of alcohol use disorder post-operatively, facilitating more rapid and higher peak alcohol delivery to the systemic circulation.

Regardless of etiology, our study illustrates improved outcomes among patients with obesity and a history of bariatric surgery hospitalized with decompensated cirrhosis compared to nonsurgical patients. This likely relates to overall improved metabolic and comorbid health conferred by bariatric surgery. Though an important finding, future analyses are needed to further understand this relationship, including identifying temporal relationships between surgery and the onset of cirrhosis and decompensation, as well as subanalysis based on cirrhosis etiology and ongoing risk factors.

Aminian A, Al-Kurd A, Wilson R, et al. Association of Bariatric Surgery With Major Adverse Liver and Cardiovascular Outcomes in Patients With Biopsy-Proven Nonalcoholic Steatohepatitis. 

. Nov 23 2021;326(20):2031-2042. doi:10.1001/jama.2021.19569

Lassailly G, Caiazzo R, Ntandja-Wandji LC, et al. Bariatric Surgery Provides Long-term Resolution of Nonalcoholic Steatohepatitis and Regression of Fibrosis. 

. Oct 2020;159(4):1290-1301.e5. doi:10.1053/j.gastro.2020.06.006

Verrastro O, Panunzi S, Castagneto-Gissey L, et al. Bariatric-metabolic surgery versus lifestyle intervention plus best medical care in non-alcoholic steatohepatitis (BRAVES): a multicentre, open-label, randomised trial. 

. May 27 2023;401(10390):1786-1797. doi:10.1016/S0140-6736(23)00634-7

Are VS, Knapp SM, Banerjee A, et al. Improving Outcomes of Bariatric Surgery in Patients With Cirrhosis in the United States: A Nationwide Assessment. 

. Nov 2020;115(11):1849-1856. doi:10.14309/ajg.0000000000000911

Bai J, Jia Z, Chen Y, Li Y, Zheng S, Duan Z. Bariatric Surgery is Effective and Safe for Obese Patients with Compensated Cirrhosis: A Systematic Review and Meta-Analysis. 

. May 2022;46(5):1122-1133. doi:10.1007/s00268-021-06382-z

Wang G, Huang Y, Yang H, Lin H, Zhou S, Qian J. Impacts of bariatric surgery on adverse liver outcomes: a systematic review and meta-analysis. 

. Jul 2023;19(7):717-726. doi:10.1016/j.soard.2022.12.025

Pepino MY, Okunade AL, Eagon JC, Bartholow BD, Bucholz K, Klein S. Effect of Roux-en-Y Gastric Bypass Surgery: Converting 2 Alcoholic Drinks to 4. 

. Nov 2015;150(11):1096-8. doi:10.1001/jamasurg.2015.1884

King WC, Chen JY, Mitchell JE, et al. Prevalence of alcohol use disorders before and after bariatric surgery. 

. Jun 20 2012;307(23):2516-25. doi:10.1001/jama.2012.6147

The retrospective analysis highlights improved outcomes among patients with obesity and a history of bariatric surgery hospitalized with decompensated cirrhosis.

Bariatric Surgery in Patients Hospitalized with Decompensated Cirrhosis: A Nationwide Analysis

Stephen Firkins, MD

Chief Pharmacist, Express Scripts® Pharmacy

Caregivers continue to face increased responsibilities and stress due to the 

 pandemic and knowing where to turn for help is not easy. A recent study shows that pharmacists will have an expanded role in patient care, and caregivers will want to take note of how they can tap into pharmacists’ expertise, which is often an underutilized resource.

Together, our organizations, Express Scripts® Pharmacy and Columbia University Mailman School of Public Health, partnered on new research to more deeply understand the expanding role of pharmacists in transforming patient care in the decade ahead. Between November and December 2021, we surveyed more than 3,000 patients, 1,000 pharmacists, and 500 providers (including physicians and nurse practitioners). The resulting Prescription of Trust report is the largest and most comprehensive research study ever conducted on this topic.

Our survey found that pharmacists currently spend about 50% of their time dispensing and filling medications, but that percentage is expected to decrease over the next decade. More than 80% of pharmacists agree they will see increased patient counseling responsibilities, take on an increased role in preventive care measures, and be more integrated in care management teams. We recognize this expansion of duties cannot happen fast enough, as the COVID-19 pandemic has accelerated the shortage of physicians and nurses available to serve patients.

The best part about the findings from our research is that patients and health care providers truly trust pharmacists to play a greater role in providing care. In fact, our research found that 72% of doctors and nurse practitioners already consider pharmacists to be part of the patient care team.In addition, nearly 80% of patients said they see pharmacists as an integral part of their health care team.

So, what should caregivers know about pharmacists, and how should they engage with them to make the most of their expertise?Caregivers should keep in mind that pharmacists do much more than dispense medications. Our research found pharmacists in ambulatory clinics, health systems (hospitals), and home delivery pharmacies often serve as specialists, advising patients with specific diseases or interacting with a larger health team to help manage complex patient care.

Pharmacists can help ease a caregiver’s stress by addressing medication issues including polypharmacy and adherence, as well as condition issues. Additional Express Scripts Pharmacy 

 shows there’s a link to better health outcomes when pharmacists get involved with patient counseling and chronic disease management

For example, patients with diabetes often need continuing care to help manage their condition. Caregivers can reach out to their pharmacist for medication consults but also for information about disease management and preventive care.

Similarly, pharmacists can assist with many other conditions, including high blood pressure and high cholesterol. As part of their expanding role, pharmacists can perform blood pressure and cholesterol screenings that allow them to make recommendations for potential future treatment. The more caregivers can partner with pharmacists to prevent emergency room trips, hospitalizations, or the advancement of a chronic disease by supporting adherence, the better we can affect a patient’s health outcomes.

Caregivers may also want to consider the benefits of telepharmacy services (via phone or video.) With the COVID-19 pandemic, the use of telehealth skyrocketed, but the use of telepharmacy has not been as quickly adopted. However, our study showed that nearly half (49.7%) of patients would find it extremely or very helpful to have routine testing and medical visits done from home. Telepharmacy is an underutilized resource for people to connect with a pharmacist anytime, anywhere. At many home delivery pharmacies, such as Express Scripts Pharmacy, their members can access pharmacists by phone 24/7.

Lastly, caregivers should keep in mind that most pharmacists chose their profession because of their desire to take care of patients, and the Prescription of Trust shows they are embracing their growing responsibilities with 70.1% saying they are excited about the evolving role of the pharmacist.

To learn more about The Prescription of Trust report, as well as how caregivers can make the most of patient care provided by pharmacists, please follow this link: 

Susan Peppers, RPh, Chief Pharmacist, Express Scripts® Pharmacy, is dedicated to quality and patient safety with responsibility for Pharmacy Practice, Patient Consultation, and Clinical Programs.

John McHugh, MBA, PhD is an Assistant Professor in the Department of Health Policy and Management at Columbia University’s Mailman School of Public Health. His research focuses on health care organizations and how they operate and respond to changing incentives.

The views expressed in this piece are those of the author, not necessarily those of the publication.

Clinicians and health care experts interested in contributing to HCPLive can 

Caregivers Can Lean on Pharmacists Who Are Taking on Expanding Role in Patient Care

Susan Peppers, RPh

In approximately 1 in 1000 women worldwide over the age of 40 and in the US, as many as 65 out of every 100,000 women are diagnosed with a rare, autoimmune disease that can cause significant liver damage and potentially lead to liver failure if left untreated.

 This disease is known as primary biliary cholangitis (PBC).

 Although PBC is more common in women, we now know that more men than previously thought also have this disease.

Many people may not experience symptoms in the early stages of the disease.

 If this chronic liver disease is left untreated, it can progress to cirrhosis.

The journey to a PBC diagnosis can be long and challenging, especially when there may not be any signs of the disease that others can see.

 For many patients, the path to a PBC diagnosis can involve numerous testing and procedures.

First-line and second-line treatment options are available to patients. After 1 year on first-line therapy, one’s health care provider will assess treatment goals by looking at biochemical response.

 Some patients don’t meet treatment goals—this is known as an inadequate response to therapy. In such cases, several second-line treatments are available for appropriate patients who qualify.

Routine liver blood tests can reveal abnormalities.

 If PBC is suspected by one’s doctor, an antimitochondrial antibody (AMA) test is generally used to confirm a PBC diagnosis.

 For people living with PBC, some treatment goals include normalizing or improving a protein called alkaline phosphatase (ALP) and managing symptoms of the disease, such as pruritus.

 A treatment plan that helps sustain ALP levels and more effectively manages symptoms may help improve disease outcomes.

Symptoms can range from mild to severe and can develop slowly over 5 to 20 years.

 As the disease progresses, there is an increased risk of inflammation of the bile duct and scarring of the liver that may cause serious complications.

More than half of people diagnosed with PBC are asymptomatic and not all symptoms of PBC are visible.

 The symptoms that commonly appear—such as pruritus (chronic itch) and fatigue—are often invisible to others and may negatively affect daily life.

 The debilitating itchy skin that may be associated with PBC can have a profoundly negative impact on a person’s daily life and those around them and may also be associated with sleep disturbance, fatigue, and depression.

For patients living with PBC, it is important to connect with others who have similar experiences who can provide crucial support, in addition to support from loved ones.

 It is also important to have a supportive care team that listens attentively, thoroughly explains the treatment process, and presents all available options.

As research and awareness of PBC continue to grow, there is hope for those living with the disease.

 Advancements in medical science aim to improve both the understanding and management of PBC, offering patients new avenues for care and support.

After receiving a PBC diagnosis, it’s essential for patients to maintain close communication with their care team. Regular check-ins with healthcare providers ensure that any changes in symptoms are promptly addressed and that the treatment plan is continually optimized.

 Beyond medical management, discussing ways to improve the patient’s daily life is key. Consider lifestyle adjustments for the patient, such as adopting a healthy diet and engaging in regular physical activity, along with treatment, which can help mitigate the progression of PBC.

By having the patient be proactive and informed, they can work alongside their care team to manage PBC effectively.

This content is sponsored by Gilead Sciences.

European Association for the Study of the Liver. EASL clinical practice guidelines: the diagnosis and management of patients with primary biliary cholangitis. 

 2017;67(1):145-172. doi:10.1016/j.jhep.2017.03.022

American Liver Foundation. Primary biliary cholangitis. Accessed September 30, 2024. Available at: https://liverfoundation.org/liver-diseases/autoimmune-liver-diseases/primary-biliary-cholangitis-pbc/

Levy C, Bowlus CL, Carey E, et al. A real-world observational cohort of patients with primary biliary cholangitis: TARGET-primary biliary cholangitis study design and rationale. 

. 2018;2(5):484-491. doi:10.1002/hep4.1173

Shaker M, Mansour N, John BV. Primary biliary cholangitis in males: pathogenesis, clinical presentation, and prognosis. 

 2022;26(4):643-655. doi: 10.1016/j.cld.2022.06.008

Bernal RB, Ferrigno B, Morales EM, et al. Management of primary biliary cholangitis: current treatment and future perspectives. 

 2023;34(2):89-100. doi:10.5152/tjg.2023.22239

Laschtowitz A, de Veer RC, Van der Meer AJ, Schramm C. Diagnosis and treatment of primary biliary cholangitis. 

. 2020;8(6):667-674. doi:10.1177/2050640620919585

Mayo Clinic. Primary biliary cholangitis diagnosis. Accessed September 17, 2024. Available at: https://www.mayoclinic.org/diseases-conditions/primary-biliary-cholangitis/diagnosis-treatment/drc-20376880

Authors