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Medscape
24-06-2025
- Health
- Medscape
Episode 3: Cracking the Code: Insulin Resistance in HS
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. Ginette A. Okoye, MD: Hi. I am Dr Ginette Okoye. Welcome to Medscape's InDiscussion podcast series on hidradenitis suppurativa (HS). Today, we'll discuss insulin resistance in HS with our guest, Dr Lindsey Bordone. Dr Bordone is a board-certified dermatologist and assistant professor of dermatology at Columbia University Irving Medical Center. Dr Bordone specializes in complex medical dermatology, particularly in autoimmune skin diseases. Thank you for joining us today, and welcome to the Medscape InDiscussion podcast. Lindsey Bordone, MD: Thank you for having me. This is very exciting. Okoye: I have been looking forward to this conversation for a long time because today we're focusing on one of the major comorbidities of HS, which is metabolic syndrome — in particular, insulin resistance. Dr Bordone, you have quite a bit of experience evaluating and treating insulin resistance, and you work closely with an endocrinologist. This topic is fascinating. I think you might be the US expert on the intersection of insulin resistance and dermatology, and so we cannot wait to learn from you. Bordone: Thanks. I hope I live up to it. Okoye: Tell me a little bit about your experience with HS. Bordone: With HS patients, I had always thought something was missing. These patients would come in and they would have terrible inflammation, and nothing seemed to work. Even biologics that would suppress the inflammation always left them maybe slightly improved, but they still had pretty terrible disease that seemed to me, in some cases, not compatible with normal life. I started to notice in many of them that they had signs of insulin resistance on their skin, such as acanthosis nigricans, which is thickening of the skin that leaves a dark, velvety appearance on the back of the neck and in the armpits. And many patients were overweight, which can happen with autoimmune conditions in general, because it's very hard to exercise if you're not feeling comfortable. I also knew from work in immunology that inflammation causes insulin resistance. But then I started to ask questions about the family history of diabetes or personal history of gestational diabetes, and there seemed to be a strong trend, which made me start to evaluate their labs. The funny thing is that for the most part, they all had normal blood sugars. Their labs looked pretty good, but then if you looked a little bit deeper, some things didn't seem quite right. Their liver enzymes were inverted, meaning the liver enzyme that's typically higher, aspartate aminotransferase (AST), was lower than the alanine aminotransferase (ALT) level. For the layman, this means your liver isn't behaving like it should, and that's an indicator of insulin resistance. I just started to notice a trend. It seemed like an obvious fit. I reached out to an endocrinologist, and we started discussing it. We put our heads together and started to dig deeper. And then I spoke to you, and you solidified things for me when I met with you and the other person you were doing research with. You were talking about neutrophil webs, and there was an overlap between the inflammatory response of the liver in fatty liver and liver disease from metabolic illnesses and HS. It was years ago now that I spoke about it with you, and I was like, okay, this is it. This has to be it. Okoye: That was an important day in my career as well, because it felt like we both independently were concerned about the fact that people's blood sugars were normal, but they couldn't be. Something was off. For me, the real epiphany was when you taught me to check for insulin resistance using the appropriate labs. Can you tell us more about how to evaluate people for insulin resistance? It's not the A1c. Bordone: Definitely not. The other unifying trend among all these HS patients is that they have a very hard time losing weight. Even if they were dieting and exercising, they seemed to hold onto weight. Their sugar looked great. But what I started checking was their homeostatic model assessment for insulin resistance (HOMA-IR) score, where you check their fasting insulin and fasting sugar between 8 and 9 in the morning. That's usually the best time. Once you get further into the morning, around 10:00 AM, your circadian rhythm lowers your insulin. You want to see it first thing in the morning, after you've been fasting for 8 hours. I tell patients to stop eating at midnight and roll out of bed and have their blood drawn. In New York, it's a little bit of a challenge because people walk 20 blocks to a lab. I have to remind them that walking is still exercise; it'll bring your sugar down. If they had a meal at something like 8:00 PM and then at 8:00 AM their blood sugar is over 100 mg/dL and their fasting insulin is high, as if they had just eaten a meal, there's something very abnormal about that. Normal fasting insulin, you want it to be around 5 μIU/mL. I had patients coming in with fasting insulin counts of 40, 60. It's almost universal. In the HS patients, they have very high insulin production, and it seems to happen 24 hours a day, whether they're eating or not. Okoye: You mentioned the homeostatic assessment. That is the HOMA-IR test, How is that calculated? Can you tell us a bit more about that? Bordone: Truth be told, I just punch it into an online calculator. It just assesses whether or not your insulin is reducing your glucose enough, because for high insulin, your sugar should be low. But if your sugar is high and your insulin is also high, then that insulin is not having an effect. You check it between 8 and 9 in the morning, with no exercise ahead of time. I tell people, don't lift weights or exercise the night before. Because if they want to be a go-getter and exercise for an hour the night before, their blood sugars are good for about 24 hours after, so that can skew the results quite a bit. What the HOMA-IR score shows is your insulin sensitivity. All patients with a good HOMA-IR have a score of 1 or 2, sometimes even lower than that, meaning they're very sensitive to their insulin. Once they're above 2, they're insulin resistant. And then I have some patients with an HOMA-IR score that should be under 2 but instead is 14, and they're walking around with totally normal blood sugars because they just produce more and more insulin to reduce whatever blood sugar they have to a fine level. But that amount of insulin production is so abnormal that it leads to other health issues. Okoye: And because that high insulin is keeping their blood sugar normal, it's keeping their A1c relatively normal as well, which for me was the real epiphany. Testing glucose and A1c is not enough, right? You have to test the fasting glucose and fasting insulin. Plug those two numbers into that online calculator, and then really make decisions based on the HOMA-IR score, not A1c. Bordone: Yes, and it's heartbreaking because I think a lot of these patients know there's something wrong with them. They've flown under the radar because their A1c is fine. They don't feel well, but no one gives them an explanation because it hasn't been part of the general workup that a primary care doctor does, or dermatology has ever done. But I think that's changing, particularly if it's a young, healthy person who doesn't have high blood pressure or anything that they're aware of, but they see something's going on with their skin. They'll see a dermatologist. We're the ones who are going to have to identify it, test for it, and diagnose it. Okoye: I agree. You mentioned that when the insulin level is high, people don't feel well. Can you tell us a bit more about that? What are the effects of an elevated insulin level? Bordone: This is so interesting to me, and it is so diverse. First, insulin is a growth hormone, so it increases cell division. One of the things we see aside from acanthosis nigricans is thickened ear lobes. People develop what's called the Frank sign, where their ear lobe gets so puffy that it almost folds. That soft tissue in the ear lobe growth mirrors what happens with the soft palate at the back of the throat, where soft tissue also grows. As it grows in the throat, it starts to obstruct your breathing when you sleep at night. It relaxes when you're lying back, and your muscles in your throat have relaxed. People develop obstructive sleep apnea and always feel tired. The problem with having high insulin is that there are times when you haven't eaten for a while, and your insulin finally starts to go down, and then, for whatever reason, your body starts listening to it in that moment. Then you become hypoglycemic and your sugars get too low, and then you feel tired and woozy. So, people's sugars can go up, and they can go very low too. It makes it even more of a challenge to lose weight. They're often fatigued. They have these weird symptoms where they just don't feel right when their sugars get low, and they cannot lose weight, and they get depressed because they are counting micro- and macronutrients and keeping track of everything. Nothing works, and they're told, just try harder. That's the opposite of what they need to hear because then they think, well, what the hell else am I going to do? Most of the time, they don't even realize how bad they feel because it's such a slow creep into insulin resistance. But then, when you treat them for it, they feel so much better and their fatigue improves, their energy levels increase, and weight starts melting off. They can think more clearly. They don't have food noise anymore. There are just so many things that insulin influences. Okoye: You mentioned food noise. Insulin makes you hungry. Bordone: It's good to have a lot of insulin in a famine because you're always seeking out food, and then you're storing it as fat, very quickly, so you can get hungry again because your sugar can get low. It's great in the right setting, but we evolved for so many years, and now we don't need it. So when people are just producing it all the time and they have access to food, it takes on a life of its own and spirals. Okoye: Based on that, it sounds like we need to address insulin resistance in any of our patients who present with signs of insulin resistance. But certainly, in our patients with HS, weight loss can help decrease friction in their intertriginous areas. Weight loss can help them be more sensitive to our anti-inflammatory medications. Just milligram per kilogram wise, if only to help our patients in that weight loss journey, to help them feel better. I feel like we need to think about how we, as dermatologists, treat insulin resistance. I know that you do this all the time, so can you give us some tips? Bordone: I love the GLP-1s. That's probably my go-to medication. I first ask patients about their dietary habits. I think some people start craving sugar because that's what insulin does to the satiety circuits in your brain; it makes you crave sugar. I often discussed with them what they're eating and if they're having any drinkable calories or things that dissolve very quickly. For example, I'll tell patients, if you take a bucket of water and throw cereal in, it turns into mush in 2 seconds; anything like that disintegrates and becomes sugar almost instantly is not your friend. We go through some dietary counseling. Exercise is something we discuss. A lot of times, they're in such a sad mental state because they've tried so hard and they failed for so long, I go right to using medication. It's almost cruel to ask them to just keep trying without giving them a boost. Some patients say, I don't want to be on medication, but I say, look, let's just get the ball rolling. We can always take you off it. You are never handcuffed to anything. But I'd rather see you in a healthy place and have you struggle for another 5 years like you've already been doing. Okoye: How do you use the GLP-1? Do you do any screening tests? What doses are you using? Bordone: I start with checking, obviously, a HOMA-IR score. Especially in my HS patients, there's a very high burden of fatty liver. I check liver enzymes, and I'll check lipids to see if they have high triglycerides. They often have high triglycerides, low high-density lipoprotein cholesterol, and high low-density lipoprotein cholesterol. And because vitamin D is fat-soluble, their vitamin D levels are always low. So, I'll check all of those and just confirm and show them yes, in fact, you do have insulin resistance, and you have abnormal cholesterol readings and liver abnormalities. If their liver abnormalities are significant, I also do what's called a Fibrosis-4 (FIB-4) score, and I'll screen them for fatty liver and fibrosis. If it's high enough, I'll get a liver scan and send them for a gastrointestinal (GI) medicine consult. I almost always, if someone has liver issues, will start them off with tirzepatide since the data on tirzepatide for fatty liver are that this is so far the superior drug. I start them on 2.5 mg of tirzepatide. I like semaglutide, but the nausea seems to be a limiting factor. The weight loss with tirzepatide is double, so if insurance will cover it, I almost always start with tirzepatide, 2.5 mg. Okoye: You mentioned the FIB-4 score, so that's a score for liver fibrosis. In order to calculate FIB-4 score, just in an online calculator, you put in AST, ALT, platelets…. Bordone: And age. Okoye: And you're finding patients with HS with elevated FIB-4 scores? Bordone: Yes. The younger ones tend to be okay. But when you have someone who has high liver enzymes and lower platelets, it's an issue. I've been surprised by how many people have abnormal FIB-4 scores. That has been eye-opening, and they're not getting screened. I wouldn't say it happens all that frequently, but it's much more frequent than I expected. I thought that maybe once in a blue moon I would see it, and it's more than that. It's to the point where I have to warn them about taking certain medications that are metabolized through the liver, and I get them to see GI as soon as possible, and it solidifies the need for tirzepatide, because of the data showing it helps so much with fatty liver. Okoye: And when you have these data — the FIB-4 score, the AST-ALT inversion, the HOMA-IR score — does that help with insurance coverage of the GLP-1 agonist? Bordone: No, and that's been frustrating. I will say that this year, more insurance companies are starting to cover it, I think because they're seeing the cost savings. Patients are hospitalized less. They wind up having fewer doctor visits. I don't have patients with HS coming in with flares every other minute. Their HS gets better, but normally you have to make a good case for either sleep apnea or sometimes I'll have them wear a continuous glucose monitor and show that yes, their A1c is not high but their blood sugars do get high, and I will diagnose them with type 2 diabetes under different criteria or enlist the help of an endocrinologist. I write appeal letters, but insurance can be very difficult. I think that's the major barrier at this point for these drugs that work so well. Okoye: Do you use metformin? Bordone: I use metformin quite a bit. Metformin is great. It has been around for a very long time, and overall, it's very inexpensive, accessible. The stomach upset can be a problem. I rarely now use the immediate release. I use the extended-release versions. It can help, quite a bit, but I don't see it doing as much as the GLP-1. If I can get someone on a GLP-1, that's my preference. Okoye: Would you ever have someone on both metformin and the GLP-1? Bordone: Yes, I do that. Sometimes, if the patient has nausea on a GLP-1, like let's say I can only get semaglutide, and I have a patient with significant nausea, I'll have them take that and then metformin. I don't combine any other diabetes meds with those two because it's too far out of my specialty, so I will enlist the help of endocrinology. But I'm very comfortable with metformin and the GLP-1s, and also using them together. Okoye: What dose do you aim for with metformin? Bordone: I find that once I get above 1500 mg/d, people complain about stomach upset, and even at 1500 mg/d, they're pretty unhappy. At the beginning, I'll tell them to take 500 mg extended-release every day, and if you don't have any stomach upset, double it within 2 weeks. And then we go from there. Okoye: You mentioned that in your experience, in patients with HS on the GLP-1 agonists, you're seeing improvements in their HS? Bordone: Undoubtedly. I have one patient I saw 2 days ago; I've maybe been seeing her for about 8 years. I cannot believe the difference in this woman. She used to have flares. Every day, she was wearing maxipads in her armpits because she was constantly draining. She never dated, never exercised, and was so limited in life. She has lost 70 pounds on tirzepatide. And now she never calls my office. I never do injections. She has no problems. She has a lot of scarring, which will probably need to be surgically corrected at some point, and maybe once or twice a year, she'll say that she has soreness in one of her armpits. She's my classic example of someone who just needed to get their insulin down, and it runs in her family. I have other patients who are like her, too. Okoye: Interesting. Those patients, are they on a GLP-1 agonist and a typical HS therapy, such as a biologic? Bordone: I still have some patients on combinations of adalimumab and tirzepatide. Most of them have gotten off the biologic, though, and are just on tirzepatide as monotherapy, and they've done great. Okoye: That has been my experience as well. But I have to say some, some of my colleagues in the HS world, that has not been their experience, and the data that are coming out seems to be mixed. The latest study I saw showed modest benefit, if any. But the doses were quite low. The doses of semaglutide were quite low in that study. I think more needs to be done, and I think better studies need to be done, but certainly anecdotally, I think this provides benefit to the right patient. Bordone: I agree. I think low doses don't do much, and I haven't been as impressed with the first GLP-1s. I think tirzepatide is better for HS, and it does take longer and higher doses. Okoye: What would you say is the average time for you to see efficacy? Bordone: For most of my HS patients, I need to get them to the highest possible dose and then get their weight down to a BMI of less than 27, usually, before I start seeing the impressive response. If I have a thin patient with HS, I think that's a different situation. Then I do genetic testing on them. I do immunodeficiency panels, and I've had several with the JAK1 mutation, and those patients are a different category. But my obese patients with HS do beautifully on the GLP-1s — well, GLP-1 plus glucose-dependent insulinotropic polypeptide (GIP), the tirzepatide. Okoye: Something important that I'll take away from your last statement is that you're not seeing improvement until their BMI is below 27. That could take months. I wonder if people are giving up too quickly or if people aren't staying on them long enough because of the cost. I know that's been a barrier for some of my patients. Bordone: It's a huge barrier, and I have a few patients where the problem is if you have someone with a BMI of 60, for instance, once your weight gets very high, it's interesting: Your body becomes more efficient. Your metabolism goes down a bit. And even if you fix their BMI to a point with GLP-1s or with a gastric bypass, you never quite get them all the way there. There are cases where I've sent them for endocrinology assessment, and they've needed a combination of gastric bypass plus a GLP-1 to keep their insulin down, because even if you bring the weight down, if the insulin's still high, you're still going to have a problem. For those patients who are very overweight, I still get them into an obesity clinic and have someone assess them to see what will get them to their best health situation. Okoye: Sounds great. Well, this has been illuminating, and I hope that our audience has gotten as much from it as I have. Do you have any parting words? Bordone: I think for HS patients, it's really important to see someone who specializes, like you, or someone at an academic center. I see a lot of patients who go to dermatologists who see it once in a while, and they're just on antibiotics endlessly, and I think there are more exciting things happening and better help on the way. Okoye: There's a lot of hope, and the HS experts are trying to do a better job of teaching all our colleagues how to manage HS so that people everywhere can have access. But thank you. Today we've talked to Dr Bordone about insulin resistance in HS, and some key takeaways from my perspective include the importance of testing our patients with HS for insulin resistance by checking a fasting glucose and fasting insulin to calculate their HOMA-IR score. Check their AST, ALT, lipid panels, and a platelet score to calculate their FIB-4 score, to make sure they don't have liver fibrosis. I think that is a practice-changing takeaway from today's session. Thank you all for joining us. Please take a moment to download the Medscape app to listen and subscribe to this podcast series on HS. This is Dr Ginette Okoye for the Medscape InDiscussion podcast. Assessing Insulin Sensitivity and Resistance in Humans HOMA-IR Online Calculator Aural Sign of Coronary-Artery Disease Exploring the Therapeutic Potential of GLP-1 Agonists in Hidradenitis Suppurativa Risk of Liver Dysfunction and Non-Alcoholic Fatty Liver Diseases in People With Hidradenitis Suppurativa: A Systematic Review and Meta-Analysis of Real-World Evidences Tirzepatide for Metabolic Dysfunction-Associated Steatohepatitis With Liver Fibrosis FIB-4 Score The Therapeutic Potential of GLP-1 Receptor Agonists in the Management of Hidradenitis Suppurativa: A Systematic Review of Anti-Inflammatory and Metabolic Effects
The Independent
14-06-2025
- Health
- The Independent
How a handful of almonds could improve your health
A new study in the journal Nutrition Research suggests that eating a handful of almonds daily can significantly reduce metabolic syndrome, a condition linked to heart disease, diabetes, and dementia. The 12-week clinical trial involved adults aged 35 to 60 with metabolic syndrome, with one group consuming 320 calories of almonds daily and the other eating the same number of calories from crackers. Participants who ate almonds experienced significant health improvements, including reductions in total cholesterol, LDL (bad) cholesterol, and waist circumference. Blood tests of the almond group also showed increased levels of vitamin E and lower levels of gut inflammation, indicating a positive shift in gut health. Researchers highlight that almonds contain beneficial nutrients like vitamin E, polyunsaturated and monounsaturated fats, fibre, and other minerals that contribute to the observed health improvements.
Medscape
02-06-2025
- General
- Medscape
Fibrosis-4 Index Finds New Role in Rheumatoid Arthritis
Up to 20% of patients with rheumatoid arthritis (RA) had abnormal fibrosis-4 (FIB-4) index values, reflecting an indeterminate to high risk for liver fibrosis; a significant correlation was seen with insulin resistance but not with disease activity. METHODOLOGY: Researchers conducted a cross-sectional study to calculate FIB-4 index values in patients with RA and assess their relationship with disease characteristics and cardiovascular comorbidities. They recruited 465 adults with RA (mean age, 55 years; 81% women) between 2019 and 2021, all of whom had a disease duration of at least 1 year and were taking ≤ 10 mg/day of prednisone or an equivalent dose. The FIB-4 index was calculated using an equation considering age, platelet count, and alanine aminotransferase and aspartate aminotransferase levels, with the risk for fibrosis classified as low, indeterminate, or high on the basis of defined cutoff values. Participants underwent evaluations for disease activity, complete lipid profiles, the presence of metabolic syndrome, anthropometric parameters, and insulin resistance using the Homeostatic Model Assessment, as well as carotid ultrasound to detect subclinical carotid atherosclerosis. Cardiovascular risk was estimated using t he Systematic Coronary Risk Evaluation-2 (SCORE2) tool. TAKEAWAY: SCORE2 classified 66% of patients with RA as having low cardiovascular risk, 28% as having moderate cardiovascular risk, and 6% as having high cardiovascular risk; the prevalence of cardiovascular risk factors was generally high. FIB-4 values indicated an indeterminate risk for fibrosis in 18% of patients with RA and a high risk in 1%, whereas 81% had a low risk. Several factors, including age ( P < .001), cardiovascular risk measured by SCORE2 ( P < .001), and metabolic syndrome ( P = .008), showed positive correlations with FIB-4 values; however, in multivariable analysis, the presence of hypertension, insulin resistance indices, and statin use maintained significant positive associations. < .001), cardiovascular risk measured by SCORE2 ( < .001), and metabolic syndrome ( = .008), showed positive correlations with FIB-4 values; however, in multivariable analysis, the presence of hypertension, insulin resistance indices, and statin use maintained significant positive associations. Disease activity (measured by multiple scores), acute phase reactants, and the presence of rheumatoid factor or anti–citrullinated protein antibodies showed no significant association with FIB-4 values, whereas the presence of erosions at recruitment was associated with FIB-4 ( P = .044). IN PRACTICE: "This index may serve as a surrogate marker for CV [cardiovascular] risk and insulin resistance in patients with RA," the authors concluded. SOURCE: This study was led by Iván Ferraz-Amaro, Hospital Doctor Negrín, Las Palmas de Gran Canaria, Spain. It was published online on May 21, 2025, in Rheumatology . LIMITATIONS: The cross-sectional design of this study prevented the establishment of causal relationships between variables. Data on hepatic ultrasound or liver biopsy were lacking. Information on cumulative methotrexate use was not collected. DISCLOSURES: This study was supported by a grant from Instituto de Salud Carlos III and additional funds from the European Union. Two authors reported receiving grants or research support and consultation fees from speaker bureaus associated with several pharmaceutical and healthcare companies, including AbbVie, Roche, and GSK.
Medscape
13-05-2025
- Health
- Medscape
Unusual Case of Psychosis Linked to Adrenal Tumour
In older patients, elevated blood pressure is often observed during visits to general practitioners. However, if it is not measurable, this should raise particular concerns. If a psychotic episode also occurs, prompt action is needed. Bastien Picut and his colleagues at Valais Hospital in Sion, Switzerland, reported an unusual case of a 60-year-old woman with decompensated metabolic syndrome and psychosis caused by a typical adrenal cortical carcinoma (ACC; adrenocortical oncocytic neoplasm, ACON). The Patient and Her History The woman presented to the hospital with symptoms of refractory arterial hypertension, accompanied by dizziness, headaches, and asthenia, and a weight gain of 20 kg within a span of 6 months. Despite maximal antihypertensive therapy, her systolic blood pressure remained at approximately 160 mmHg. Findings and Diagnosis Examination revealed the onset of type 2 diabetes, requiring immediate insulin, and mixed hyperlipidaemia associated with hypokalaemia and hypernatremia. While hospitalised under geriatric care, the patient experienced a psychotic breakdown characterised by persecutory delirium, noncritical visual hallucinations, and mistrust of contacts associated with anxiety. A comprehensive laboratory analysis was performed. Liver function tests were abnormal, with significantly elevated levels of gamma-glutamyl transpeptidase, total bilirubin, alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase. Additionally, hypernatremia (149 mmol/L) was noted (normal range, 135-145 mmol/L). The calcium and ammonia levels were normal at 2.31 mmol/L and 36 μmol/L, respectively. Urine analysis revealed proteinuria, ketonuria, urobilinogen, and haematuria. The levels of dehydroepiandrosterone sulphate and urinary catecholamines, including metanephrine, normetanephrine, and methoxytyramine, were marginally elevated. Following the initial evaluation, an ultrasound was performed, revealing a large, bilobed retro-pancreatic mass near the left kidney and para-aortic region. Subsequent abdominal CT confirmed a bilobed left adrenal mass measuring 8 × 5 cm and 1.8 × 2.2 cm, which was vascularised without calcifications. The CT scan ruled out the presence of any locoregional or distant spread of the disease. The differential diagnosis of pheochromocytoma was considered. Radiological findings and elevated urinary metanephrines, suggesting the secretion of catecholamine precursors. No other causes for the elevated urinary catecholamines were identified. Prior to the intervention, the patient was medically managed with haloperidol (1 mg orally three times daily) and clomethiazole (192 mg orally twice daily as needed) for psychiatric decompensation. For diabetes management, metformin 500 mg orally three times daily, linagliptin 5 mg orally, and insulin glargine 30U subcutaneously were administered. Hypertension was managed with metoprolol (50 mg), spironolactone (25 mg), lisinopril (20 mg), and doxazosin (4 mg) orally. Subsequently, laparoscopic left adrenalectomy was performed without intraoperative complications. The patient required adrenergic support until the fourth postoperative day. Additionally, all antihypertensive medications were discontinued, except for beta blockers. Discussion This is the first ACON case described in the literature with such an atypical clinical presentation, according to the authors. Psychotic manifestations of ACC have been previously described; however, they are associated with cortisol-secreting ACC as part of Cushing syndrome. Furthermore, the doctors could not conclusively determine whether the tumour was a pure non-secreting ACON. The clinical presentation resembled Cushing syndrome, and hypokalaemia could be attributed to vasospasm from secondary hyperaldosteronism. Aldosterone secretion from the tumour could not be clearly assessed due to the ongoing use of antihypertensive medications (beta blockers, spironolactone, calcium channel blockers, and angiotensin-converting enzyme inhibitors). This may have affected the aldosterone-renin ratio, leading to a potentially false-negative assessment. The variable clinical presentation and the lack of sensitivity and specificity of preoperative diagnostic procedures, such as imaging in aggressive malignant diseases, make adrenocortical oncocytic neoplasms a significant challenge for clinicians.
