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Uncontrolled Movements, Anger, and Insomnia
Editor's Note: The Case Challenge series includes difficult-to-diagnose conditions, some of which are not frequently encountered by most clinicians, but are nonetheless important to accurately recognize. Test your diagnostic and treatment skills using the following patient scenario and corresponding questions. If you have a case that you would like to suggest for a future Case Challenge, please email us at ccsuggestions@ with the subject line "Case Challenge Suggestion." We look forward to hearing from you. Background A 35-year-old man presents to the neurology clinic due to abnormal movements over the past 6 years. The involuntary movements began in the right upper limb, followed sequentially by the left upper limb, left lower limb, and finally the head and neck. The movements occur during wakefulness and are absent in sleep. They are described as jerky and nonpurposeful. His gait has assumed a dancelike character. He also has had behavioral changes that include frequent outbursts of anger, aggressive behavior, depressive mood, and insomnia. His abnormal movements are aggravated during outbursts of anger and disturbances in mood. He has no weakness in any limbs but is unable to perform regular household activities. Family members have also noted memory impairment. He has been unable to continue his work as a machine operator for the past 3 months. He has no history of psychoactive drug intake, including phenytoin, phenothiazines, haloperidol, L-dopa, lithium, isoniazid, amphetamines, tricyclic antidepressants, or any other relevant drugs. He reports no history of chest pain, breathlessness, or joint pain. His family history includes a paternal grandfather and father who had similar forms of abnormal movements and died at the age of 60 years and 55 years, respectively. The patient has five siblings (two brothers, three sisters). His elder brother died by suicide at age 25 years, and his elder sister died at age 33 years. Both had abnormal movements and abnormal behaviors. One of his younger sisters (age 22 years) also has similar abnormal movements and depressed attitude. His younger brother (age 17 years) and other younger sister (age 14 years) are healthy and symptom-free. The patient's children, an 8-year-old son and a 10-year-old daughter, are symptom-free. His past medical history is positive for hypertension, which is well controlled with lisinopril (20 mg daily). He has no surgical history. He does not smoke, drink, or use recreational drugs. Physical Examination and Workup A general examination reveals a pleasant man who is well built and in no acute distress. His blood pressure is 140/80 mm Hg, his heart rate is 78 beats/min, his respiratory rate is 12 breaths/min, his SpO 2 level is 98% on room air, and his body mass index (BMI) is 20. He is afebrile. A cardiovascular examination reveals normal peripheral pulses and normal heart findings. A chest examination reveals normal auscultation and expansion. His abdomen is soft. Head, eyes, ears, nose, and throat (HEENT) examination findings are unremarkable. He does not have a skin rash. A visual examination reveals normal acuity, field, and fundi. His affect is flat. A neurologic examination of the higher mental functions reveals that the patient is awake and alert, with normal orientation, attention, concentration, fund of knowledge, and language function. His memory is impaired, with recall one-third at 3 minutes. He has a normal past memory. His speech is normal. A cranial nerve examination reveals normal extraocular movements, increased blink rate, normal facial sensation, a symmetric face with abnormal fidgety movement, normal hearing, and normal palate movement. He has abnormal tongue movement and cannot protrude his tongue more than 20 seconds (darting tongue movement). He has normal shoulder shrug. No Kayser-Fleischer ring is noted during slit-lamp examination. An examination of the motor system reveals decreased muscle tone, normal bulk, and 5/5 strength in both upper and lower extremities. No atrophy or fasciculation is noted. Deep tendon reflexes are normal (2+ with flexor planters). Sensory examination findings are normal. Finger-nose test findings are normal. An examination of the extrapyramidal system reveals reduced tone and involuntary choreoathetoid movements that affect both upper and lower extremities as well as his face. He has a dancing gait. Diagnostic tests reveal normal complete blood cell count (CBC) and comprehensive metabolic panel findings. He has normal serum findings and urine copper levels. His erythrocyte sedimentation rate (ESR) is 22 mm/hr (reference range, 0-22 mm/hr). He has normal ECG findings, a normal thyroid-stimulating hormone (TSH) level, a normal transthoracic echo (with ejection fraction 65%), and normal chest radiography findings. Brain MRI can be used to evaluate for selective atrophy of deep gray structures, to document disease burden, and to provide a baseline for future comparison. Whole-body 18-FDG PET/CT may be used to screen for occult neoplasm and paraneoplastic chorea, but this is exceedingly rare and typically subacute. NMDA receptor antibody panel may be used to investigate for autoimmune encephalitic chorea, but the features of this (ie, seizures, psychosis, and autonomic instability) are absent in this case. RPR and FTA-ABS may be used to evaluate for neurosyphilitic chorea, but this is also very uncommon and unnecessary without risk factors or acute symptoms. In this patient, brain MRI reveals evidence of bilateral caudate atrophy, with increased intercaudate distance (Figure). Figure. Cerebrospinal fluid (CSF) examination findings are normal. Discussion This 35-year-old man has Huntington disease. He has insidious-onset, slowly progressive movement disorder, and movements are absent during sleep. His movements are described as choreoathetoid. He has family history that suggests autosomal dominant transmission. Apart from the movement disorder, he also has neuropsychiatric manifestations, with death at an early age in the family. A CT scan of the head revealed evidence of caudate nucleus atrophy. Brain MRI revealed evidence of caudate atrophy (Figure). Figure. In evaluating the differential diagnoses, the patient has no history of antipsychotic medication use to suggest tardive dyskinesia. He has no clinical or diagnostic evidence of infection or heart involvement, which makes Sydenham chorea unlikely. No acanthocytes were observed, helping to exclude neuroacanthocytosis. The strong family history of progressive abnormal movements and neuropsychiatric symptoms across generations supports a genetic etiology, specifically autosomal-dominant Huntington disease. Huntington disease is a rare neurodegenerative disorder of the central nervous system (CNS) characterized by choreiform movements, behavioral and psychiatric disturbances, and dementia.[1] Huntington disease is caused by an autosomal-dominantly inherited expansion of CAG trinucleotide repeats in the huntingtin ( HTT ) gene on chromosome 4; this leads to production of a mutant huntingtin (mHTT) protein, with an abnormally long polyglutamine repeat.[2] Individuals with more than 39 CAG repeats develop the disease, whereas reduced penetrance is seen in those with 36-39 CAG repeats. The disease can be anticipated when the gene is passed down the paternal line, as in this case; a father with a CAG repeat length in the intermediate range may have a child with an expanded pathogenic repeat length. This is because sperm from males shows greater repeat variability and larger repeat sizes than somatic tissues. Mutant huntingtin protein leads to death and neuronal dysfunction through various mechanisms. Postmortem studies reveal diffuse atrophy of the caudate and putamen. The progressive worsening of Huntington disease leads to a bedridden state with cognitive deterioration, and death typically occurs about 20 years after the onset of symptoms.[3] Prevalence in the white population is estimated at 1 in 10,000 to 1 in 20,000. The mean age at symptom onset is 30-50 years. In some cases, symptoms begin before age 20 years, with behavior disturbances and learning difficulties at school; this is termed juvenile Huntington disease (Westphal disease).[4] The first description, by Waters, dates to 1842. However, after a description in 1872 by George Huntington, it became known as Huntington chorea. In 1983, a linkage on chromosome 4 was established, and in 1993 the gene for Huntington disease was found.[1] Diagnosis of Huntington disease is confirmed by demonstration of autosomal dominant transmission or gene testing in the presence of clinical features.[5] The clinical features of Huntington disease consist of motor, cognitive, and neuropsychiatric manifestations. Huntington disease has a biphasic course of hyperkinetic phase with chorea in the early stages of disease that then plateaus into a hypokinetic phase, consisting of bradykinesia dystonia, balance issues, and gait disturbance. The younger-onset variant is associated with predominant bradykinesia.[6] Cognitive disturbance can be seen many years before other symptom onset and is characterized by impaired emotion recognition, processing speed, and executive function abnormality. Neuropsychiatric symptoms widely vary, including apathy, anxiety, irritability, depression, obsessive-compulsive behavior, and psychosis. A lack of awareness of early and progressing behavioral, cognitive, and motor symptoms is a hallmark of Huntington disease. This unawareness is caused by the disease itself (specifically, impaired insight or anosognosia) and is not the result of intentional denial, avoidance, or suppression of symptoms.[7] Therefore, a comprehensive history, including information from a knowledgeable family member/caregiver, is advisable.[7] Numerous conditions can mimic Huntington disease, including a spinal cerebellar ataxia 17, spinocerebellar ataxia 1-3, and Friedreich ataxia, which involve neuropathy. If seizures are also present, dentatorubropallidoluysian atrophy should be considered. Acanthocytes are seen in patients with neuroacanthocytosis.[8-10] Isolated chorea can be seen in acquired conditions, including chorea gravidarum, systemic lupus erythematosus, antiphospholipid syndrome, thyrotoxicosis, postinfectious syndromes, polycythemia vera, and some drug use. Genetic testing for the mHTT mutation can be either diagnostic or predictive.[6] A diagnostic test may be performed when a patient presents with typical motor features of Huntington disease. Prior to testing, the patient should be informed about Huntington disease and its hereditary nature, as a positive test result has implications for the patient and family. Predictive testing is performed in asymptomatic patients, mostly for reproductive reasons. Treatment of Huntington Disease The optimal management of Huntington disease involves a multidisciplinary approach that includes neurology, nurses, physical therapy, speech-language pathology, and dietitians and other healthcare professionals. The goal is to optimize the quality of life based on the changing need of the patient. These consist of combined pharmacologic and lifestyle changes, including behavioral therapy. Symptoms may be worsened by stress, fatigue, and intercurrent disorders (eg, anxiety, digestive disorders, infectious or painful conditions), so these aspects must be assessed and treated alongside the primary symptoms of Huntington disease.[3] In clinical practice, information about symptoms should be obtained from both the patient and caregivers, since patients may have impaired awareness of their condition.[11] Identifying coexisting psychiatric symptoms, comorbid medical conditions, and environmental factors is crucial.[11] Educating caregivers about the nature and presentation of symptoms and methods to modify triggers is also vital.[11] Medication choices should be guided by coexisting symptoms and disease stage, and regular reassessment of drug need and potential for dose reduction is important because of adverse effects that can mimic disease progression.[11] Nonpharmacologic interventions, including behavioral therapies and environmental modifications, should be prioritized for neuropsychiatric symptoms in Huntington disease. Pharmacologic agents may be considered if these measures are insufficient, and consultation with a psychiatrist knowledgeable in Huntington disease is recommended for individuals whose symptoms are resistant to standard pharmacologic therapy.[11] Tetrabenazine and its modified version, deutetrabenazine, are commonly used to treat choreiform movements. Side effects of tetrabenazine can include depression, anxiety, sedation, sleep problems, restlessness, and parkinsonism.[7] Citalopram is a selective serotonin reuptake inhibitor used to manage depression. Modafinil and atomoxetine are used to manage apathy. Tiapride, although unavailable in the United States, is considered a first-line treatment option for chorea outside the United States.[7] Other antipsychotics such as olanzapine, risperidone, and quetiapine are also used to manage chorea. Risperidone may also help with psychomotor restlessness, and olanzapine and quetiapine can have additional benefits like weight gain (which can be desirable in Huntington disease) and mood stabilization. Haloperidol has also shown effectiveness.[7] Medications used to suppress chorea (eg, tetrabenazine and deutetrabenazine and certain antipsychotics) should be used sparingly and mainly for subjectively disabling hyperkinesias, starting at low doses and titrating gradually. They make take 4-6 weeks to show results.[7] The choice of medication depends on the individual patient's symptoms, tolerability, and co-existing conditions.[7] Evidence regarding the treatment of psychiatric symptoms in Huntington disease is limited, with recommendations often based on expert opinion owing to a lack of robust controlled studies.[7,11] Nonpharmacologic interventions such as cognitive-behavioral therapy and psychodynamic therapy are recommended, especially for depression, anxiety, obsessive-compulsive behaviors, and irritability. Behavioral strategies (eg, structured routines and distraction) are important for managing irritability and agitation.[3,11] Depression: Selective serotonin reuptake inhibitors (SSRIs) such as citalopram, fluoxetine, paroxetine, sertraline, and venlafaxine are recommended as pharmacologic options. [3,7] Mianserin (unavailable in the United States) or mirtazapine are alternatives, particularly in patients with sleep disruption. [3,7,11] Electroconvulsive therapy (ECT) may be considered for severe or resistant cases, although it can significantly impair short-term memory. [3,7] Mianserin (unavailable in the United States) or mirtazapine are alternatives, particularly in patients with sleep disruption. Electroconvulsive therapy (ECT) may be considered for severe or resistant cases, although it can significantly impair short-term memory. Anxiety: SSRIs or serotonin-noradrenaline reuptake inhibitors (SNRIs) are first-line treatments, especially when anxiety coexists with depression. [3,11] Mirtazapine is an option in patients with sleep disorders. [11] Long-term use of benzodiazepines is generally discouraged for ambulatory individuals because of the risk of falls and dependence but can be used short-term or as needed. [3,11] Mirtazapine is an option in patients with sleep disorders. Long-term use of benzodiazepines is generally discouraged for ambulatory individuals because of the risk of falls and dependence but can be used short-term or as needed. Obsessive-compulsive behaviors/perseverations: For true obsessive-compulsive phenomena, SSRIs are considered first-line treatment. [3] Olanzapine and risperidone may also be valuable for ideational perseverations, particularly if associated with irritability. [3] Clomipramine is an option, especially if needed for coexisting obsessive perseverative behaviors. [11] Olanzapine and risperidone may also be valuable for ideational perseverations, particularly if associated with irritability. Clomipramine is an option, especially if needed for coexisting obsessive perseverative behaviors. Irritability and aggression: SSRIs are a first-line treatment. [3] For aggressive behavior, neuroleptics are recommended. [3,7] Mood stabilizers (eg, valproate, lamotrigine, lithium, carbamazepine) can be added if irritability is resistant to other treatments or for mood lability. Risperidone and olanzapine may help reduce irritability. [3,7] For aggressive behavior, neuroleptics are recommended. Mood stabilizers (eg, valproate, lamotrigine, lithium, carbamazepine) can be added if irritability is resistant to other treatments or for mood lability. Risperidone and olanzapine may help reduce irritability. Psychosis (hallucinations/delusions): Second-generation neuroleptics (antipsychotics) are the first-line pharmacologic treatment. [3,7,11] Options include olanzapine, risperidone, quetiapine, aripiprazole, and haloperidol. [7] Clozapine may be considered for severe or resistant cases, particularly in akinetic forms of Huntington disease but requires regular monitoring. [3,7,11] Underlying causes, such as the use of psychotropic agents or somatic triggers, should be investigated and addressed. [3,11] Options include olanzapine, risperidone, quetiapine, aripiprazole, and haloperidol. Clozapine may be considered for severe or resistant cases, particularly in akinetic forms of Huntington disease but requires regular monitoring. Underlying causes, such as the use of psychotropic agents or somatic triggers, should be investigated and addressed. Apathy: Personalized cognitive stimulation and structured routines and activities are recommended.[3,7,11] If depression is suspected as a contributor, an SSRI should be tried.[3,11] In patients without depression, activating antidepressants or stimulant drugs (eg, methylphenidate, atomoxetine, modafinil) may be considered.[11] Sedative medications may increase apathy, so their dosage should be monitored or reduced.[3,11] Currently, no pharmacological treatment is specifically recommended for cognitive symptoms in Huntington disease.[3,7] Rehabilitation strategies, including speech therapy, occupational therapy, cognitive and psychomotor therapy, may help transiently improve or stabilize cognitive functions.[3,7] Coping strategies can be useful as an alternative to medication. Certain medications, such as sedative drugs, neuroleptics, and tetrabenazine, can negatively affect memory, executive functions, and attention.[3] Apart from symptomatic treatment, pharmacologic agents have failed to show benefit in clinical trials as disease-modifying agents. The most promising approaches in regard to disease modification are emerging therapies aimed at lowering levels of mHTT by targeting either the DNA or RNA of the mHTT gene.[12] RNA-targeting using antisense oligonucleotides (ASOs) have shown disappointing results in clinical trials. This has shifted significant research focus and toward orally available small molecules that modify HTT mRNA splicing, thereby reducing mHTT protein production. DNA-targeting approaches using gene editing tools like CRISPR/Cas9, while demonstrating success in preclinical models, remain in the early stages of development.[13,14] The patient in this case was diagnosed with Huntington disease with CAG repeat 78. He was started on tetrabenazine for abnormal movements and citalopram for depression. He opted to apply for federal disability. His children are asymptomatic, and the family decided not to investigate until symptoms develop or they are age 18 years.
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Jul 18 2025 This Week in Cardiology
Please note that the text below is not a full transcript and has not been copyedited. For more insight and commentary on these stories, subscribe to the This Week in Cardiology podcast , download the Medscape app or subscribe on Apple Podcasts, Spotify, or your preferred podcast provider. This podcast is intended for healthcare professionals only. In This Week's Podcast For the week ending July 18, 2025, John Mandrola, MD, comments on the following topics: Finerenone, what not to consider when choosing treatment of AS, brain health after atrial fibrillation ablation, early rhythm control for AF, and Watchman reimbursement cuts. I received an email from an academic EP who is involved with regulation, regarding my coverage of pulmonary embolism (PE) devices two shows back. He clarified my thoughts on the 510(k) approval pathway where devices get approved by being similar to an already approved device. I called it extremely problematic and called for FDA to reform it. My colleague writes that it's not up to FDA to reform the program. The 510(k) pathway and the rules around substantial equivalence are in federal law and Congress would need to change these rules. Speaking of 510(k) pathway, he agrees it can be problematic. It works well for devices like blood pressure (BP) cuffs and diagnostic EP catheters, in which the underlying technology is well established. It's harder in things like artificial intelligence or machine learning-based devices or anything that is sort of—but not completely—new. He said we spend a lot of time on these, often focused on whether the intended use is the same, whether we have enough bench and clinical data, etc. And, he writes, 'substantial equivalence' means we need to be assured that the device performs as well as the predicate and that often requires clinical data. I have come to really appreciate listener feedback because it is so instructional. I did not know that Congress has to change the 510(k) pathway. Keep coming with the listener feedback. Finerenone FDA Widens Indication of Finerenone for Heart Failure Patients Medscape news has a good summary of the FDA approval of finerenone. It's actually an expansion of the indication of the nonsteroidal mineralocorticoid receptor antagonist (MRA). The FDA initially approved finerenone in 2021 to reduce the risk for cardiovascular death heart failure hospitalization (HHF), myocardial infarction (MI), and kidney complications in adults with chronic kidney disease (CKD) associated with type 2 diabetes—a rather specific indication. The new expansion will be for patients with heart failure (HF) and left ventricular ejection fraction (LVEF) of at least 40%. This is based on the FINEARTS-HF trial published in New England Journal of Medicine in 2024. This was a big 6000+ patient trial comparing finerenone to placebo in patients with heart failure with preserved ejection fraction (HFpEF). Mean age 72, LVEF 53%, most with NYHA Class 2 and 3 HF. The primary endpoint was a composite of total worsening HF events (HHF or urgent visit) and CV death. Follow-up was 2.5 years. There was a 16% reduction in the primary endpoint. The hazard ratio was 0.84 and confidence intervals were significant. The absolute risk reduction (ARR) was 2.8%, or a number needed to treat (NNT) of 35. The primary composite was driven almost completely by HF events as there was no statistical difference in CV death or all-cause death. This came at a cost of more increases in creatinine and potassium. High potassium more than 6 was 3.0% vs 1.4%. FINEARTS-HF is fine. It was a positive trial. My criticism of the trial and finerenone use in HFpEF centers on three main issues. First issue: Wrong comparator. Finerenone should have had to beat spironolactone. I say that because the Americas part (US, Canada, Brazil, Argentina) of the TOPCAT trial clearly show that spironolactone improved outcomes in HFpEF. Of course it does. MRA drugs as a class help in HFrEF and likely do in HFpEF. The question facing clinicians is which MRA to start—one that costs pennies, spironolactone, or one that will surely cost bunches, finerenone. The lack of head-to-head comparison is what we get when we let industry control regulatory trials. If I were at FDA, I would have pushed for a spironolactone arm. The second issue was that the benefit from finerenone was modest. Despite enrolling 6,000 patients, there were only 200 fewer events in the finerenone arm, and no difference was seen in cardiovascular death. The 16% reduction in the primary endpoint was driven solely by heart failure events, not mortality. Finerenone is a diuretic after all. HFrEF patients have 4 classes of 'disease-modifying' drugs. Finerenone cannot be called disease-modifying. The third issue I have with FINEARTS is that the authors surely have — but don't share — the effect on total hospitalizations. As I have shown in other HFpEF trials, most hospitalizations in these patients is not HF. So, if a drug or device reduces one type of hospitalizations (here for HF), but this type is only a small fraction of the total burden of hospitalizations, the patient does not win. HHF are a reasonable surrogate in HFrEF, because in those patients a weak LV is the primary issue. But in HFpEF, these patients are older and burdened with much higher co-morbidity, so HHF becomes a weak surrogate measure. I don't have a problem with FDA approving the drug for this indication. But they should have been stronger in the regulatory input regarding the seminal trial. Drug companies will jump over the bar we set for them. We help them when we set the bar low. For clinicians, we shall see what the cost of this drug is. I still believe we start with spironolactone and keep finerenone in the bullpen for relief when the first line fails. One of the most common decisions in the field of valvular HD is whether to do transcatheter aortic valve implantation (TAVI) or surgical aortic valve replacement (SAVR) in patients with severe aortic stenosis (AS). There are obvious cases when patients are clearly poor surgical candidates. TAVI is the choice. There are also obvious surgical choices when the patient is very young or has the need for concomitant surgical procedures, such as left atrial (LA) ablation, mitral disease, or coronary artery disease (CAD) requiring revascularization. Then SAVR. For the large number in the middle, patients and doctors have to translate the nuances of the PARTNER, EVOLUT, Notion 1 and 2, DEDICATE, and UK-TAVI trials. You could have day-long conferences on sorting through the details of these trials. Ultimately, there is a tension between the much lower burden of TAVI vs its long-term durability relative to SAVR. Editors of the European Heart Journal and authors, mostly from Columbia University, tempt us to consider another factor in the decision: the carbon footprint of the two procedures. I kid you not. EHJ has the top impact factor of all cardiology journals, and it has now published a comparison of the carbon footprint of 10 patients who had SAVRs and 20 patients who had TAVIs (10 in the OR and 10 in the cath lab). They used a model that measured the kilograms of CO 2 equivalents based on the primary data, such as the materials, procedures, energies, in the preoperative, operative, and postoperative setting. TAVI used less CO 2 equivalents than SAVR (about half less). The numbers were 300 kg of CO 2 equivalents in TAVI vs 600 kg of CO 2 equivalents in SAVR. Postoperative intensive care unit and floor care accounted for the largest portion of the carbon footprint. The intraoperative footprint of SAVR was driven by biological waste, postoperative length of stay, and inhaled anesthetic gases. The authors concluded: The carbon footprint of SAVR is about twice as high as those from OR–TAVI or CATH–TAVI. These findings should potentially be considered when making population level decisions and guidelines moving into the future. I don't know what is happening to us as a field. The authors write this in the discussion: While carbon emissions should not be the deciding factor in the treatment strategy for individual patients, relative emissions should play a role in the future when deciding between different treatment options. I did a simple Google search on carbon emissions. Even if we accept their calculations, the difference was about 300 kg of CO 2 equivalents. To fly across the US is 1000 kg of CO 2 equivalents per passenger. So if you take your family of 4 that's like 13x more than the difference in these two procedures. Walk through Atlanta, Dulles, Newark, or LAX airports and just eyeball the number of people flying. I am all for climate stewardship. I ride a bike to work. I live close to everything in town. I don't litter. I like European hotels that minimize wasteful energy use. But my friends, the role of carbon footprint should have exactly zero influence on medical decisions such as TAVI vs SAVR. Number 1, it is miniscule relative to other human activities, and number 2, we take care of patients not the environment. Public health should have no bearing on individual decisions. Finally, I used to think coffee, blueberry, and quinoa studies were the most wasteful of time and effort. Now I think studying the carbon footprint of two medical procedures may have earned top honors in the most useless and wasteful studies. Come on you all. Post-Ablation Visual Auras a Sign of Transient Brain Injury? The group of Dr Greg Marcus at UCSF continue to do interesting work in EP. Their latest, led by fellow Adi Elias, investigated the possible association of a transseptal puncture during catheter ablation for ventricular arrhythmias with post-procedural visual auras. As well as to assess the relationship between occipital and parietal lobes acute brain emboli and migraine-related visual auras. The questions are important because it goes to the health of the brain during left-sided ablation, which is undergoing a massive increase due to the use of pulsed-field ablation (PFA) in the left atrium (LA). This work is actually an observational substudy of a recent randomized controlled trial called TRAVERSE. I will discuss both because both papers are making the rounds in the EP. Note also that this isn't just an EP topic because visual auras and micro-emboli to the brain also occur with coronary angiography, percutaneous coronary intervention (PCI) and valvular procedures. Let's talk first about the TRAVERSE trial, published in Circulation , in February 2025, first author Greg Marcus. TRAVERSE randomized only 146 patients who were to have a left sided ventricular tachycardia (VT) ablation to either retrograde aortic (RA) approach vs transseptal approach. The primary endpoint was an acute brain lesion on MRI. The main result: in the retrograde aortic approach, 28 of 62 (45%) exhibited an acute brain lesion compared with 19 of the 69 (28%) of those randomized to a transseptal puncture ( P = .036). No differences in clinically manifest complications or procedural efficacy were observed. No patient had a clinical stroke. Notable in the study was 10% of patients did not get an MRI—which means that they did not have a primary endpoint measured. The authors conclude from this data that: A transseptal approach may be the more favored strategy over a retrograde aortic approach for catheter ablation of endocardial left ventricular arrhythmias to reduce brain injury. The heightened risk of new brain lesions detected using MRI without overt clinical manifestations in the retrograde aortic arm may suggest a higher risk of other organ damage that is not immediately clinically occult. It is possible other procedures conventionally performed through a retrograde aortic approach might incur similar harms, and that novel transseptal approaches may yet prove beneficial. The first thing to say is that they have convinced many in the EP world that transseptal is the preferred approach to the LV. I sent a message to private EP group about access for a VT case and the overwhelming answer was transseptal and [quote] 'I am impressed by the UCSF data.' Well, my friends, I like many of the authors of this multicenter trial, but the trial is a mess, and it does not tell us the best approach. The first thing to say is that there were only 47 primary outcome events, and the primary outcome events were white spots on an MRI that disappear and have no know permanent sequalae. So even if there were a statistically robust difference, would it be clinically significant? I am not sure, and likely neither are you. I put the numbers into a Fragility Index calculator, which tells us how many non-events or events in each group would have been required to make the results nonsignificant or greater than P value of .05. The Fragility Index is 1. If one more patient in the transseptal group had a white spot, then the trial is negative. That is not a statistically robust finding. Not at all. What's even worse is that 10% of patients did not have an MRI. So the missing data is 10x the Fragility Index. The authors acknowledge this limitation but soft roll it. The academic editorialists don't mention the fragility of the data, nor the massive missingness. I think it is an existential problem with this study. We simply do not know. Imagine a drug or device outcome trial where 10% of the patients did not have a primary outcome measured. My final take of this study is that EP doctors might spend less time destroying LA during AF ablation and more time learning to look at evidence. TRAVERSE was a good effort, but its internal validity issues, small differences in a surrogate outcome and no difference in stroke tells us near zero about what approach to use when ablating LV sources of arrhythmia. To me, the doctor should choose the approach most likely to achieve success. Retrograde aortic access is clearly superior to transseptal for some areas of the V. TRAVERSE should not discourage them from using it. In the meantime, the question of best approach is an answerable question: it simply requires a larger study with more primary outcome events and less loss to follow-up. The second paper, first author fellow Adi Elias, was published in Heart Rhythm last week. This observational study asked two questions: (a) did the access site (RA vs transseptal) affect visual auras and (b) was there an association between occipital and parietal white spots and migraine-related visual auras. In total, 121 patients of the 146 had assessment of visual auras. A total of 18 reported a visual aura in the first month after the procedure and 103 did not. Pause there. Because the authors will soon be making conclusions about 18 reported visual auras. This paper also suffers from serious missingness, as 15% of those in the transseptal arm and 21% of those in the RA arm did not complete the 1-month questionnaire about having a visual aura, which was the primary endpoint. The first main result was that there was no difference between post-ablation visual auras observed between transseptal (16% of 63) and retrograde aortic approaches (14% of 57; P = .78). The second main result was that more participants with acute brain emboli in the occipital or parietal lobes experienced migraine-related visual auras (38% vs. 11%; P = .014). The actual numbers are 7 of 18 of those with occipital/parietal lesions vs 12 of 103 patients without parietal/occipital lesions. I calculated the Fragility Index on this difference, and it was 2. If 2 of the 103 without a white spot in the occipital/parietal area had a visual aura, then the association is non-significant. And again, recall that loss to follow-up was more than 15% in both groups. The authors make positive conclusions from this fragile data. Transseptal puncture was not associated with visual auras, however acute brain emboli involving the visual cortex was associated with such symptoms. These data suggest that transseptal punctures are not causal in migraine-related visual auras and that post-procedure acute brain emboli are apparently not always clinically silent. They then double down in their interviews on Medscape. Marcus says, 'These findings demonstrate that, contrary to a long-held belief that these post-ablation MRI-detected small brain lesions are asymptomatic — in fact, they are often referred to as 'asymptomatic cerebral emboli' or 'ACEs' — these small acute brain lesions actually can, and perhaps often do, manifest in clinical symptoms.' Dr Elias, too, is too strong. He says, 'The data show that these post-ablation brain lesions are not clinically silent. It may be the case that we haven't known what to look for and assessed for symptoms immediately without enough time for the subsequent visual auras that would occur.' Again, maybe they are correct, but the data is not statistically robust. They're making big conclusions based on 18 MRI scans and nearly 1 in 10 patients did not have an MRI and 1 in 5 patients did not have an assessment for visual auras. Only 2 events would change the conclusions. The data, therefore, do not support their conclusions. I would conclude only that there may be a signal, but we need more data to understand the relationship of postprocedure brain emboli and visual auras. Finally, my criticism of these studies is not meant to downplay the issue of brain emboli after procedures. These are potentially quite serious because even if the effect size on cognition is small, the large numbers of procedures being done means there could be a huge public health crisis in the future. As it is in all of medicine: everything turns on patient selection. When we do TAVI in an older person who has less than 6 months to live due to severe AS, and he or she gets asymptomatic brain emboli, we worry a little. In contrast, when we blast a 50-year-old with persistent AF with PFA, ablating the pulmonary veins, posterior wall and God knows what else, creating oodles of microbubbles that then cause multiple brain lesions, we should worry a lot. The best way to avoid brain emboli is to avoid procedures. That's not happening now. The reverse is. Early AF ablation is a money maker for doctors and hospitals. PFA lowers the threshold for doing AF ablation because it's faster and less likely to cause catastrophic complications. But our profession should be wise enough to be concerned about these observations. We should demand better data on brain MRIs as well as cognitive testing, especially with the advent of PFA. A small harm could turn into a huge problem. European Heart Journal has published a rapid communication from EAST-AFNET authors, regarding the short-term benefit of early rhythm control (ERC) vs rate control. To briefly review, NEJM published EAST-AFNET 5 years ago in 2020. About 2800 patients with newish AF were randomized to two strategies: early rhythm control (mostly with antiarrhythmic drugs) vs rate control. The primary endpoint was a composite of CVD, stroke, heart failure hospitalization, or acute coronary syndrome. The 5-year trial found a 21% statistically significant reduction in the primary endpoint. The primary safety endpoint did not differ. However, the authors combined death and stroke as both primary efficacy and safety endpoints. If you don't double count stroke and death, there were nearly 3x more safety events (68 vs 19) in the early rhythm control group (ERC) vs rate control. A couple notables: EAST-AFNET was not an ablation trial. Less than 1 in 5 patients in the ERC had ablation. So you have to posit that antiarrhythmic drugs (AAD) reduced hard outcomes—a first for sure. Another notable, there was only a 20% difference in the presence of sinus rhythm (80% vs 60%) at 2 years. So you also have to posit that a difference in sinus rhythm of only 20% drove hard outcomes. I am pretty sure — no, highly sure — that the better outcomes in EAST-AFNET were just performance bias, in that the ERC transmitted ECGs with symptoms had many, many more interactions with their clinicians. I am not against ERC, and do it often, but I oppose the use of EAST-AFNET to foster lucrative early AF ablations. I believe strongly that patients with AF who do not have HF or decompensation should be treated slowly and given a chance to let nature (or natural history) or risk factor modification help with their AF. One more thing about EAST-AFNET: the Kaplan-Meier curves for the primary endpoint do not separate for about 1.5 to 2 years , which is what you expect with patients with new AF. If there is a benefit of SR or enhanced medical interactions, it should take time to reduce cardiac outcomes. Now to the rapid communication of a post-hoc study. Here the EAST-AFNET authors look specifically at outcomes in the first 30 days both in the overall population and in the subset with HF. First result: A primary outcome event occurred in 9 of the 1400 patients randomized to early rhythm control and in 21 of the 1400 patients in the usual care group hazard ratio (HR) 0.43, 95% CI, 0.20–0.93). Second result: Deaths in first 30 days were observed in 1 of 1400 patient randomized to early rhythm control and in 4 of the 1400 patients randomized to usual care (HR 0.25, 95% CI, 0.03–2.24). The third result involved HF patients in EAST-AFNET 4. Slightly less than one third of all patients had prevalent heart failure, of which 400 patients were randomized to early rhythm control therapy and 400 to usual care. Within 30 days after randomization, a primary outcome occurred in 3 vs 14 patients with prevalent heart failure randomized to early rhythm control vs rate control, respectively (HR 0.22, 95% CI, 0.06–0.77; Figure 1). The authors concluded that: This exploratory analysis suggests immediate beneficial effects of early rhythm control therapy within 30 days after randomization, including a lower incidence of the primary outcome, fewer deaths, and a reduced composite of death or heart failure hospitalization—in both the overall population and in those who have HF at baseline. This supports its early implementation in patients at risk of heart failure or with acute and advanced heart failure. Again, I offer no malice to the authors, but this is a really problematic study. The numbers are tiny. I don't care what the P value or confidence interval say. EAST-AFNET was powered to tell differences over many years , not 30 days. So small are the differences in the first year, the Kaplan-Meier curves do not separate at all in the main paper. I am not sure why the authors set out to look at a comparison with so few events, or why the EHJ published something so unhelpful. But it depresses me to see stuff like this. Not only does it not help us , the small numbers of events (9 vs 21, for instance, in a study of 3000 patients) is more likely to deceive us . EAST-AFNET was a great effort. Strategy trials are hard; they are noisy. Performance bias was likely. But looking at 30 days with its few events only adds more noise to a noisy piece of evidence. I will close on a positive note. Our government, and likely yours too, makes a lot of mistakes. We should celebrate when government does something smart. This week, the Centers for Medicare & Medicaid Services announced that reimbursement will be cut by 27% for percutaneous LAAO. Since I strongly believe there is little to no benefit for these procedures—perhaps even a net harm—I consider this a positive. Better would have been zero reimbursement unless the patient is in a trial. Then we would have an idea of whether this procedure works. Keep in mind, my friends, that the PROTECT AF trial of warfarin vs Watchman did not pass FDA scrutiny due to internal validity issues. PREVAIL missed its first primary endpoint of stroke, systemic embolism, or CV death. Watchman did not meet noninferiority vs warfarin. Most patients having left atrial appendage occlusion (LAAO) would not have been included in the regulatory trials. And no clear data exist comparing LAAO to direct oral anticoagulants or no anticoagulation. Also, a note to my enthusiastic EP colleagues. Go ahead. Keep posting on Twitter that you can do LAAO or AF ablation in 6.5 minutes. We get that you are fast. Do you think that payers don't follow you on social media? Finally, I am still trying to understand the new National Coverage Determinations (NCD) criteria for tricuspid transcatheter edge-to-edge repair (T-TEER). The matter in question is the coverage with evidence criteria wherein patients having T-TEER have to be enrolled in a proper study. I don't know of one of those but will continue searching.
Medscape
5 days ago
- Business
- Medscape
Infographic: Doctors' Experiences With the Tax Man
The average tax bill for a US physician and their family rose by about 4.6% in 2024. Eighty-two percent of doctors told Medscape that tax bill was too high, and 68% said they understand how the tax system works. Still, of the 1 in 7 physicians who have been audited, most of those said they were treated fairly. This infographic presents key insights from a new report asking US doctors about their experiences with taxation and auditors. To learn more, check out the Medscape Physicians and Taxes Report 2025. Medscape Physicians and Taxes Report 2025
Medscape
6 days ago
- Health
- Medscape
S3 Episode 3: Young-Onset Adult Cancer Survivorship
This transcript has been edited for clarity. For more episodes, download the Medscape app or subscribe to the podcast on Apple Podcasts, Spotify, or your preferred podcast provider. Kathryn J. Ruddy, MD, MPH: Hello, I'm Dr Kathryn Ruddy. Welcome to season three of the Medscape InDiscussion Cancer Survivorship podcast series. Today, we'll discuss young-onset cancer survivorship. First, let me introduce my esteemed guest, Dr Narjust Florez. Dr Florez is the associate director of the Cancer Care Equity Program, co-director of the Young Lung Cancer Program, and a thoracic medical oncologist at Dana-Farber Brigham Cancer Center. Dr Florez's clinical interests include targeted therapy for lung cancer and the care of women and young individuals with lung cancer, including their cancer survivorship. Dr Florez, welcome to the Medscape InDiscussion Cancer Survivorship Podcast. Narjust Florez, MD: Thank you, I'm very happy to be here. Dr Ruddy was one of my mentors when I was at Mayo Clinic, and there were around 6 months during my training that I was considering specializing in breast cancer. So, this feels full circle, coming back and having this discussion with one of the individuals I learned how to conduct survivorship research with. Thank you. Ruddy: Thank you, Dr Florez. Some of you may remember that Dr Florez was part of this podcast series in previous years, so we're thrilled to have her back again in season three. Dr Florez, could we start by having you talk about the incidence of young-onset cancer and how young-onset cancers can present? Florez: Thank you for that very important question. Since 2010, and even before that, we have seen an increased number of cases of young-onset cancer. What is young-onset cancer? These are patients who are usually diagnosed before the age of 50 or 45. These patients are diagnosed with cancer during a very disruptive time of their lives and often don't have any other person in their circle who has been diagnosed with cancer. The number of cases is increasing. Colorectal cancer is one where we have seen the highest rise in the number of cases, and that's why a large campaign is pursuing colorectal cancer screening to start at age 45 instead of 50. So 45 is the new 50. Dr Kimmie Ng spearheaded a lot of these efforts. When I was at Mayo with you, Dr Ruddy, we saw increased incidences of lung cancer in younger women. Young-onset lung cancer is higher in younger women compared to colorectal cancer, which can be seen in either sex. Young breast cancer is rising in certain groups and declining in others. This is the reality. Younger patients are getting cancer. Cancer should no longer be seen as a disease of older adults. We have to open our eyes to this diagnosis, because often, these patients don't get a timely diagnosis because of the lack of association with these solid tumor cancers in younger individuals. We often see testicular cancer and lymphoma in this subgroup. Now, a new group of cancers is affecting this population. Ruddy: In addition to those potential diagnostic delays, what are the unique challenges that your patients face during and after treatment when they are diagnosed at a young age? Florez: When we talk about young-onset cancers, we must consider their challenges across the entire spectrum. Let's start with the first one, which is diagnostic delays. This is very unique to this population and to patients with colorectal and lung cancer, in which the symptoms cannot be as specific. We know from our own study that young women with lung cancer are often told that they may have a mental health issue instead of lung cancer. The number one misdiagnosis in this group was anxiety. This data will soon be presented. We interviewed over 114 young women with lung cancer and identified that chest pressure was often attributed to anxiety when in fact it was the tumor growing. For diagnosis in young individuals with colorectal cancer, mental health is often included, and these patients with [gastrointestinal] symptoms are diagnosed with irritable bowel syndrome based on symptoms without specific imaging: leading to delays in diagnosis. And a lot of these patients are, unfortunately, diagnosed via stage IV when there are limited treatment options. That brings up a very important aspect that affects the entire spectrum of survivorship, which is stress and the healthcare system. Many young patients have had to seek care multiple times due to the diagnosis. Many of them believe that they could have been diagnosed at an earlier stage. Issues of trust affect survivorship because, up until the diagnosis, the patient was not heard. After diagnosis, we know isolation is a big challenge in their survivorship. They don't have peers who have gone through this. They often have a parent or a grandparent who may have had cancer treatment. There is a lack of having that community. Luckily, social media has helped with some of that isolation, but my patients often report that they're the only young person in the entire waiting room. They don't have anybody to lock eyes with. They don't even have anyone in the hallway to say, 'Man, this is difficult.' So we have created a lounge at Dana-Farber, specifically for young adults with cancer, so they can have this little space in which they can connect, even if it's not the same type of cancer, they have the same challenges with diagnosis. One thing that we often forget to talk about with young-onset cancer is the effect on families. Young-onset patients are often the backbone of caring for others and the family nucleus. So, younger women, younger men, and non-binary individuals are often taking care of younger children, ages 4-18 or more. They also care for older adults, such as their parents or grandparents. In society, this group of patients is the caregivers. The issue is, who cares for the caregiver when the caregiver gets sick? Finally, these patients tend to have more aggressive treatments because they're able to tolerate them. The consequences of that are a large number of long-term side effects that affect all aspects of their survivorship. Ruddy: Can you discuss fertility concerns and fertility preservation? This is a topic near and dear to my heart because of my own interest in fertility preservation during cancer therapy, which was inspired by a close friend's cancer diagnosis during medical school. It was actually what led me to become an oncologist and sparked my passion for cancer survivorship research. I would love to hear you tell our audience a bit about how this plays a role. Florez: We both have a mentor who also studies fertility. We're all passionate about this. Through my own personal experience with fertility, I have firsthand experience with this challenge. One main issue is that oncologists get very limited training about fertility and fertility preservation. You may get a lecture or two, and if you are fortunate, like me, my mentors specialize in this, so you receive extra training; but you have to go out of your way to learn about it. Most patients are not provided the opportunity for fertility preservation, regardless of the subtype of cancer. Breast cancer has been at the forefront, and they have done more research and have more options. Lung cancer is on the back burner. It's behind like it is 1995. The lack of training is a big issue. There is also a rush to treat many of these young patients who are often very sick. We often discuss delays in diagnosis, so these patients need to begin treatment immediately. But it is not our role as providers to decide fertility preservation for our patients. It is our duty to give them options. There are many options for fertility preservation. It can be easier for biological men. For them, we have sperm collection. For women, it tends to be a little more complicated. It can range from injections all the way to full stimulation and preservation. However, the main thing is that we keep the options open for patients to make their own decisions, rather than making the decision for them, because we don't know what their cancer journey will bring. With new advancements in therapies, I have patients with metastatic lung cancer living for 12 years. It is not my role to decide if and when they want to be parents or if they want to have additional children. It's not only about those who haven't had children, but also about those who may want more children. Having the discussion is the first step, and it is not expected of medical oncologists or community oncologists to know what to do, but to know who to refer the patient to. We have nurses, nurse practitioners, and specialists. Dr Elizabeth Ginsburg is a remarkable individual who has conducted extensive research in this area. The main thing is to ask our patients about fertility preservation. I have a template in Epic because we're often so busy that we forget about so many things. However, if you have it in your template, before closing the note, you need to click 'Discuss' or 'You will discuss' so that you can close the note. That's a little tip that has helped me remember. Ruddy: That's a great tip. The Epic templates are so helpful for so many aspects of our care, so thank you for that. Can you talk about your pregnancy and lung cancer registry? Florez: When I talked about pregnancy and lung cancer registry on the podcast the last time, we were not even live. It was an idea and a journey. It all started with a phone call from one of my friends, an OB attending physician, who said, 'NJ, I need your help.' I said, 'Do you need help moving?' Do you want me to pet sit your cat? What is happening?' They said, I have a pregnant patient with lung cancer. I still remember the feeling. My belly just fell. They said, 'Well, you take care of young patients.' I was like, yeah, but not pregnant patients. This led to an examination of the literature, revealing that there are no established guidelines. Most of the data precedes targeted therapy. There is no data available on immunotherapy, and all of these agents are what we are using most frequently in these young patients. As a result of that experience and having to give chemotherapy to a pregnant woman, for the first time in my career, I remember texting my mentor, saying I can't sleep. My patient starts chemotherapy tomorrow. My mentor said, 'Yeah, I've done it a hundred times.' We created the registry. The registry is housed at Dana-Farber, but is an international registry, so anybody across the globe can enter cases. The cases are anonymous, and we ask for a follow-up 6 months and 12 months after the case has been entered. To meet the goal of processing as many cases as possible, patients can enter their cases. This process is fully IRB-approved. And it's because sometimes I don't remember the Apgar score of the offspring that may have been treated, but the mothers have the capacity to get such detailed information. Providers from around the world can submit cases to the registry, including nurses, nurse practitioners, and physicians. Families and patients can also enter the cases. We have 72 cases so far. So we have the largest cohort of pregnancy and lung cancer. We learned that there's a significant lack of uniformity in treatments. We have cases from many countries around the globe, and we have seen a lack of uniformity. And it's risky, because a lot of these targeted therapies have not been approved, and they have not been studied for this population whatsoever. Immunotherapy, for example, was studied in non-sexually mature baboons. That's the data we have. As a consequence of the registry, we have launched the Pregnancy and Lung Cancer Consortium with Dr Imbimbo in Switzerland and Dr Marina Garassino, in which people can bring pregnant cases to us. We're happy to guide them because the literature is so diverse. Ruddy: That's a phenomenal resource and design. I'm very excited to hear more about your future results. Another topic you talked about last year on the podcast was the importance of sexual health. Have there been any new data or interventions over the last year that you'd like to update the listeners on? Florez: As we're talking about young-onset cancer, sexual health has to be at the forefront. It's unfair to expect a 32-year-old woman diagnosed with colorectal or lung cancer or breast or lymphoma to remain celibate until the end of her days. Sexual health has many benefits, including health, self-esteem, and well-being. It can decrease even the amount of opiates that you may need. Sexual health is cancer care. That's the first thing I want to talk about. As a result of her studies and the Sexual Health Assessment in Women with Lung Cancer study (SHAWL study), which is our study, Dr Sharon Bober has launched the SHARE study, which is sexual health after cancer treatment, focused on younger patients. This is for women aged 19-49 and is based at Dana-Farber Cancer Institute. No medications are involved in the intervention. The interventions focus on cognitive behavioral therapy, physical therapy, and provide educational online sessions about body changes that these patients may experience during their cancer treatment and after the cancer treatment and how to cope with that and see your new body, your new sexual health, activity, and intimacy. This study is very interesting. Patients will be randomized to either group sessions or individual sessions. It's called the SHARE study, which is sexual health and rehabilitation. While we have documented the sexual dysfunction, this study is the next step, which is an intervention to improve sexual health in young patients with cancer, and the SHARE study is regardless of the type of cancer. If people are interested, they can Google SHARE study, with Dr Bober, who's here at Dana-Farber. I think the time for sexual health interventions is now. Ruddy: That sounds like an extremely important study, so congratulations on taking that forward with Dr Bober. Do you want to say anything about the potential for integrative approaches to be helpful for young patients, specifically, with regard to other areas of survivorship? Florez: Yes. I think early onset cancer care is multidisciplinary care, because we have to look at these patients very long term, right? One, two, three decades after they have been diagnosed with cancer. The plan is not to fix issues after we have caused them. The plan is to address them before that. So, a very important aspect is cardio-oncology and survivorship. I currently have two football players who underwent treatment. Now they're resuming their strenuous activity. I have to work with cardio-oncology to ensure their heart is in shape to run on a football field. Another important aspect of multidisciplinary care is psycho-oncology for these patients. These patients struggle with significant mental health issues. As a millennial myself, we were born with a little touch of anxiety to start with. My patients say I'm only 42 years old, and I'm tired of being part of historical events. So, I had the pleasure of working with Dr Cristina Pozo-Kaderman, a psycho-oncologist. She helps these patients cope with the diagnosis and new ways of treating some of these mental health issues outside of medications. Medications are very helpful, but therapy plays a very important role in their survivorship. In breast cancer, colorectal, and lung cancer, mental health issues have a higher prevalence in younger patients. There's a higher prevalence of depression, adjustment disorder, and anxiety. Working with psycho-oncology is key for the survivorship of these patients because it goes by in phases. At the beginning, everybody's all hands on deck, right? And eventually, the layers of support peel off as the patient moves in their cancer journey. Another multidisciplinary care that we often forget for young-onset patients is financial advisors and social work. These patients don't have lifetime savings. These patients often need to remain in their jobs to keep their insurance, which affects their survivorship, including whether they can make it to appointments, and worrying about switching to COBRA insurance when they can't work. So financial advisors and social workers are essential for treating young patients because it allows them to apply to foundations, adjust things as needed, and know about resources that, often, even doctors don't know about. I'm in Massachusetts. I'm very fortunate to be in a state with Medicaid expansion. There are a lot of things I'm not familiar with, so these are only three of the things that are very important when we're looking at survivorship for young-onset cancer patients. The fourth thing is family members and caregivers. They are part of the cancer care team as much as the surgeons, as much as radiation oncologists, because sometimes grandma needs to help with childcare. Sometimes grandma needs to help drive somebody. So they need to be included in conversations as well. Young-onset cancer care is no longer just the medical oncologist's job; it is everybody's responsibility, including society as a whole. Ruddy: I completely agree, and I hope we can come up with new and better ways to support caregivers in future years, because this is, as you say, a very critical part of our care team. Is there anything else you want to tell our audience today before we close, Dr Florez? Florez: I would like to ask our audience to look at patients with their eyes open. And remember that what we learned in medical school has changed; the patient we learned about in our USMLE step 1, 2, and 3 is no longer the full reality. Lung cancer is not limited to older men with a previous tobacco history anymore. Colorectal cancer is not limited to older men. Come with open eyes. See the patient's needs because, unfortunately, this phenomenon will continue to grow, and more and more younger patients will be diagnosed with cancer. Remove some of the gender bias, remove some oncologist bias, and see these patients with higher needs instead of assuming they can do it on their own. They actually need additional support. Ruddy: Thank you so much, Dr Florez. Today, we spoke with Dr Narjust Florez about cancer survivorship issues in young adults. Thank you for tuning in. Please take a moment to download the Medscape app to listen and subscribe to this podcast series on cancer survivorship. This is Dr Kathryn Ruddy for the Medscape InDiscussion Cancer Survivorship podcast. Listen to additional seasons of this podcast. Cultural Competency and Cancer Survivorship: Humility, Lifelong Learning, and Effectively Communicating With Patients Trends in Cancer Incidence and Mortality Rates in Early-Onset and Older-Onset Age Groups in the United States, 2010-2019 US Preventive Services Task Force Recommendations for Colorectal Cancer Screening: Forty-Five Is the New Fifty Lung Cancer in Women: The Past, Present, and Future Cancer Statistics, 2025 "Too Young to Have This Kind of Diagnosis": A Qualitative Exploration of Younger Adults' Experiences of Colorectal Cancer Diagnosis Dana Farber Young Adult Program (YAP) From Approximation to Precision: Fertility and Pregnancy Questions in Young Patients With Lung Cancer Oncofertility in Children and Adolescents When the Unimaginable Happens: Lung Cancer Diagnosis During Pregnancy Sexual Health Assessment in Women With Lung Cancer Study: Sexual Health Assessment in Women With Lung Cancer Sexual Health and Rehabilitation Online (SHAREonline)
Medscape
7 days ago
- Health
- Medscape
FDA Warns Companies Hawking ‘Legal Morphine' Products
The FDA has sent warning letters to seven companies for illegally marketing products containing added or concentrated 7-hydroxymitragynine (7-OH), a potent metabolite of kratom. 'This action reflects the agency's growing concern around novel potent opioid products being marketed to US consumers and sold online and in smoke shops, gas stations, and corner stores,' the FDA said in a statement. Since late 2023, there has been a surge in 'kratom' products marketed as '7-OH,' '7-Hydro,' or 'legal morphine,' as reported by Medscape Medical News. 7-OH occurs naturally in trace amounts in kratom. By contrast, concentrated 7-OH preparations are 30-40 times more potent at opioid receptors and produce rapid-onset analgesia, euphoria, respiratory depression, and classic opioid-type withdrawal. As previously reported by Medscape Medical News, research has shown that 7-OH has high abuse potential and may also increase the intake of other opiates. The FDA warning letters focus on companies illegally selling tablets, gummies, drink mixes, shots, and other products that contain 7-OH as an added ingredient or at concentrated levels. According to the agency, some products are adulterated conventional foods or dietary supplements because 7-OH does not meet the relevant safety standard. Others are unapproved new drugs with unproven claims such as relieving pain and managing anxiety, the FDA said. '7-OH is not lawful in dietary supplements and cannot be lawfully added to conventional foods. Additionally, there are no FDA-approved drugs containing 7-OH, and it is illegal to market any drugs containing 7-OH,' the FDA warned. The warning letters were sent to the following companies: Images of the products being illegally marketed by the seven companies that received warning letters can be viewed online. The FDA has requested a response from each company within 15 business days.
