Martin Pistorius 3

https://www.youtube.com/watch?v=JtLw5KXm09U

https://www.youtube.com/watch?v=WD1IX1AFRZg

https://www.youtube.com/watch?v=GaAp7Q-fFiw

See: https://childnervoussystem.blogspot.com/2018/07/martin-pistorius-2.html

https://childnervoussystem.blogspot.com/2015/04/an-aromatherapist-saw-something-in-his.html

Recommendations for the assessment and management of idiopathic intracranial hypertension in children

Amin S, Monaghan M, Forrest K, Harijan P, Mehta V, Moran M, Mukhtyar B, Muthusamy B, Parker A, Prabhakar P, Whitehouse WP, Krishnakumar D. Consensus recommendations for the assessment and management of idiopathic intracranial hypertension in children and young people. Arch Dis Child. 2024 May 9:archdischild-2023-326545. doi: 10.1136/archdischild-2023-326545. Epub ahead of print. PMID: 38724065.

Abstract

Background: Idiopathic intracranial hypertension (IIH) is a potentially disabling condition. There is a lack of evidence and national guidance on how to diagnose and treat paediatric IIH, leading to variation in clinical practice. We conducted a national Delphi consensus via the Children's Headache Network to propose a best-practice diagnostic and therapeutic pathway.

Methods: The Delphi process was selected as the most appropriate methodology for examining current opinion among experts in the UK. 104 questions were considered by 66 healthcare professionals, addressing important aspects of IIH care: assessment, diagnosis, treatment, follow-up and surveillance. General paediatricians, paediatric neurologists, ophthalmologists, opticians, neuroradiologists and neurosurgeons with a clinical interest or experience in IIH, were invited to take part.

Results: The Delphi process consisted of three rounds comprising 104 questions (round 1, 67; round 2, 24; round 3 (ophthalmological), 13) and was completed between March 2019 and August 2021. There were 54 and 65 responders in the first and second rounds, respectively. The Delphi was endorsed by the Royal College of Ophthalmologists, which engaged 59 ophthalmologists for round 3.

Conclusions: This UK-based Delphi consensus process reached agreement for the management of paediatric IIH and has been endorsed by the Children's Headache Network and more broadly, the British Paediatric Neurology Association. It provides a basis for a pragmatic clinical approach. The recommendations will help to improve clinical care while minimising under and over diagnosis.

From the article:

Management: therapeutic LP

CSF pressure, if over 28 cm CSF (21 mm Hg) should be reduced down to 20–25 cm CSF (15–18 mm Hg).

The maximum number of (therapeutic) LPs a patient should have over the course of their illness is five, as other therapeutic options should be instigated before this point.

Management: weight management

A dietetic service should be available for weight management for patients with IIH.

Overweight or obese patients with IIH should be referred to a dietician for weight management or to a weight management team.

Management: first-line therapy in patients with IIH who do not have visual impairment

There was no consensus on medical management but the most selected answer by 46% of responders was that acetazolamide should be considered for all patients as first-line medical treatment, regardless of their BMI. This did not reach the threshold for consensus. The leading answer after ‘acetazolamide’ (46%) or ‘other’ (26%) was ‘information, general advice, safety netting but no drug treatment for now’ (18%). A minority of respondents supported topiramate (4%), no intervention (4%) or surgical approaches (2%).

Management: first-line therapy in patients with new visual impairment/loss of vision

If a patient is taking acetazolamide, blood urea, electrolytes and bicarbonate levels should be checked. Bicarbonate should be corrected when the value is equal to or lower than 18 mmol/L.

Management: second line

Repeated therapeutic LP should be offered when visual changes progress and there is a threat to vision on medical management and/or when symptoms are not responsive to medical management.

Management: neurosurgical

ICP bolt monitoring for 48 hours should be considered for patients with persistently raised LP opening pressure measurements (on two LPs) and papilloedema.

VSS should be considered if there is evidence of stenosis of the dominant venous sinus.

Recommendations for the assessment and management of Individuals With CDKL5 deficiency disorder

Amin S, Monaghan M, Aledo-Serrano A, Bahi-Buisson N, Chin RF, Clarke AJ, Cross JH, Demarest S, Devinsky O, Downs J, Pestana Knight EM, Olson H, Partridge CA, Stuart G, Trivisano M, Zuberi S, Benke TA. International Consensus Recommendations for the Assessment and Management of Individuals With CDKL5 Deficiency Disorder. Front Neurol. 2022 Jun 20;13:874695. doi: 10.3389/fneur.2022.874695. PMID: 35795799; PMCID: PMC9251467.

Abstract

CDKL5 Deficiency Disorder (CDD) is a rare, X-linked dominant condition that causes a developmental and epileptic encephalopathy (DEE). The incidence is between ~ 1:40,000 and 1:60,000 live births. Pathogenic variants in CDKL5 lead to seizures from infancy and severe neurodevelopmental delay. During infancy and childhood, individuals with CDD suffer impairments affecting cognitive, motor, visual, sleep, gastrointestinal and other functions. Here we present the recommendations of international healthcare professionals, experienced in CDD management, to address the multisystem and holistic needs of these individuals. Using a Delphi method, an anonymous survey was administered electronically to an international and multidisciplinary panel of expert clinicians and researchers. To provide summary recommendations, consensus was set, a priori, as >70% agreement for responses. In the absence of large, population-based studies to provide definitive evidence for treatment, we propose recommendations for clinical management, influenced by this proposed threshold for consensus. We believe these recommendations will help standardize, guide and improve the medical care received by individuals with CDD.

From the article:

There were many areas of consensus recommendations identified. The majority of these are for completion at baseline. There is an emphasis upon holistic care, such as the monitoring of systemic functions and educational needs, with certain areas recommended to be reviewed, not only at baseline, but also annually and if clinically indicated. These included the monitoring of growth, the need for a regular review of feeding and swallowing, and non-specialist screening for respiratory difficulties.

A comprehensive neurological assessment is encouraged at baseline. The consensus recommendations are for the individual with CDD to be reviewed by a pediatric neurologist with experience in managing epilepsy, clinician discussion to inform families about the risk of SUDEP, completion of a baseline MRI and EEG, consideration for epilepsy surgery, screening for the presence of a movement disorder, registration with the CDKL5 international registry and a review of the individual's sleep. Despite limited published evidence on the use of novel antiseizure drugs for CDD in the literature, Ganaxolone and Epidiolex are encouraged to be offered for epilepsy associated with CDD, if clinically indicated, dependent on FDA and EMA approvals and legal and regulatory requirements, respectively.

Discussion

CDD is a debilitating condition where there is an urgent need for further development of management options. To achieve these necessary advances will require large scale and international, collaborative efforts to evaluate potentially effective interventions in sufficiently powered clinical trials. Progress will rely heavily on cooperation between international medical and scientific professionals, affected families, industry and funding organizations. The extensive experience of the author group includes those with direct experience in CDD management including authors of a clinically relevant CDD severity assessment tool. We hope that this survey adds to the current knowledge base concerning clinical aspects of care and provides a useful proposed standard of care elucidated by the agreed areas of consensus. These recommendations can support clinicians with less experience of CDD and act as a catalyst for further research that would aim to increase capacity for evidence-based management in CDD.

Dell'Isola GB, Antonella F, Francesco P, Mario M, Cordelli DM, Piero P, Pasquale P, Alessandro F, Operto FF, Maurizio E, Marco C, Dario P, Sara M, Elisabetta S, Alberto S, Giovanna S, Savasta S, Paolo P, Di Cara G, Fruttini D, Vincenzo S, Pasquale S, Alberto V. CDKL5 deficiency-related neurodevelopmental disorders: a multi-center cohort study in Italy. J Neurol. 2024 Jun 14. doi: 10.1007/s00415-024-12421-1. Epub ahead of print. PMID: 38874638.

Abstract

CDKL5 deficiency disorder (CDD) is a complex clinical condition resulting from non-functional or absent CDKL5 protein, a serine-threonine kinase pivotal for neural maturation and synaptogenesis. The disorder manifests primarily as developmental epileptic encephalopathy, with associated neurological phenotypes, such as hypotonia, movement disorders, visual impairment, and gastrointestinal issues. Its prevalence is estimated at 1 in 40,000-60,000 live births, and it is more prevalent in females due to the lethality of germline mutations in males during fetal development. This Italian multi-center observational study focused on 34 patients with CDKL5-related epileptic encephalopathy, aiming to enhance the understanding of the clinical and molecular aspects of CDD. The study, conducted across 14 pediatric neurology tertiary care centers in Italy, covered various aspects, including phenotypic presentations, seizure types, EEG patterns, treatments, neuroimaging findings, severity of psychomotor delay, and variant-phenotype correlations. The results highlighted the heterogeneity of seizure patterns, with hypermotor-tonic-spasms sequence seizures (HTSS) noted in 17.6% of patients. The study revealed a lack of clear genotype-phenotype correlation within the cohort. The presence of HTSS or HTSS-like at onset resulted a negative prognostic factor for the presence of daily seizures at long-term follow-up in CDD patients. Despite extensive polypharmacotherapy, including medications such as valproic acid, clobazam, cannabidiol, and others, sustained seizure freedom proved elusive, affirming the inherent drug-resistant nature of CDD. The findings underscored the need for further research to explore response rates to different treatments and the potential role of non-pharmacological interventions in managing this challenging disorder.

Benke TA, Demarest S, Angione K, Downs J, Leonard H, Saldaris J, Marsh ED, Olson H, Haviland I. CDKL5 Deficiency Disorder. 2024 Apr 11. In: Adam MP, Feldman J, Mirzaa GM, Pagon RA, Wallace SE, Bean LJH, Gripp KW, Amemiya A, editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993–2024. PMID: 38603524.

Excerpt

Clinical characteristics: CDKL5 deficiency disorder (CDD) is a developmental and epileptic encephalopathy (DEE) characterized by severe early-onset intractable epilepsy and motor, cognitive, visual, and autonomic disturbances. Movement disorders include chorea, dystonia, and stereotypical hand and leg movements.

Although females are more commonly affected than males (female-to-male ratio is approximately 4:1), the severity of manifestations in heterozygous females and hemizygous males can be equivalent. However, the severity of the phenotype can vary depending on the type and position of the CDKL5 pathogenic variant, pattern of X-chromosome inactivation in females, and presence of postzygotic mosaicism in males or females, who can have mild manifestations.

Diagnosis/testing: The diagnosis of CDD is established in a female proband with suggestive clinical findings and a heterozygous CDKL5 pathogenic variant identified by molecular genetic testing.

The diagnosis of CDD is established in a male proband with suggestive clinical findings and a hemizygous CDKL5 pathogenic variant identified by molecular genetic testing.

Management: Treatment of manifestations: International consensus recommendations for the assessment and management of individuals with CDD have been published. The management of individuals with CDD is complex and requires multiple specialty evaluations; referral to a CDKL5 Center of Excellence may allow families to coordinate care more easily for affected individuals.

Targeted therapy: Ztalmy® (ganaxolone) is a targeted therapy for the treatment of epilepsy associated with CDD in individuals aged two years and older. This is the first approved treatment for seizures associated with CDD and the first treatment specifically for CDD.

Supportive care: Multidisciplinary care by specialists in the fields of pediatric neurology including pediatric epilepsy, feeding and nutrition, sleep disorders, behavioral disorders, orthopedics, physical therapy, occupational therapy, speech-language disorders, and genetic counseling.

Surveillance: Annual assessments by a medical home / primary care physician and specialists.

Genetic counseling: CDD is inherited in an X-linked manner. Approximately 99% of affected individuals represent simplex cases (i.e., a single occurrence in the family). The majority of individuals who represent simplex cases have the disorder as the result of a de novo germline or (rarely) postzygotic CDKL5 pathogenic variant. Rarely, an individual with CDD has the disorder as the result of a CDKL5 pathogenic variant inherited from a heterozygous or mosaic mother. If the mother of the proband has a CDKL5 pathogenic variant, the chance of transmitting it in each pregnancy is 50%. Females who inherit the pathogenic variant will be heterozygous and are at high risk of being affected, although skewed X-chromosome inactivation and the possibility of other attenuating factors may result in a variable phenotype. Males who inherit the pathogenic variant will be hemizygous and will most likely be severely affected. Once the CDKL5 pathogenic variant has been identified in an affected family member, prenatal and preimplantation genetic testing are possible.

See: https://childnervoussystem.blogspot.com/2019/10/cdkl5-genetic-disorder.html

Electrographic seizures and EEG background features in pediatric neuro-oncology patients admitted to the pediatric intensive care unit

Pickup EES, Keenan JS, Packer RJ, Wells EM, Conley C, Staso K, Harrar DB, Sansevere AJ. Electrographic seizures and EEG background features in pediatric neuro-oncology patients admitted to the pediatric intensive care unit. Neuro Oncol. 2024 Jun 18;26(Suppl 4):0. doi: 10.1093/neuonc/noae064.682. PMCID: PMC11183668.

Abstract

BACKGROUND

Electrographic seizures (ES) are common in critically ill children with the incidence of ES ranging from 10-50%. Continuous EEG (cEEG) is frequently obtained in children with brain tumors due to encephalopathy or concern for seizures. Despite this, little is known about the incidence of ES, EEG background features, or the impact of EEG on clinical management in this population.

METHODS

This is a prospective single center study of critically ill children with brain tumors admitted to the pediatric intensive care unit (PICU) from July 2021 to July 2023. Patients with new or known primary brain tumors and cEEG completed during their admission were included. We excluded patients with planned admissions for EEG. Clinical variables included age, sex, oncologic diagnosis, tumor grade and location, indication for EEG, EEG features, and changes in management.

RESULTS

Thirty-six patients were identified who met the inclusion criteria. 21 patients were female. The median age was 11.0 years (IQR 6.6– 15.4 years). The most common indication for EEG was encephalopathy in 42% followed by clinical seizure in 31%. ES were captured in 19% (7/36) with the majority being subclinical; in patients with acute encephalopathy, ES were captured in 20% (3/15). The EEG background was abnormal in 97% of cases. The most common EEG background was slow disorganized with background asymmetry seen in in 74%. EEG background features met criteria for the ictal-interictal continuum in 14%. A higher rate of ES was seen in patients with disseminated tumors (p=0.03) and severe encephalopathy on EEG (p=0.006). EEG led to a change in management in 31% of patients.

CONCLUSIONS

ES are common in critically ill children with brain tumors and would go undetected without cEEG. EEG findings often led to a change in clinical management and is a vital tool for the evaluation of this population.

Acute disseminated encephalomyelitis

Background

Acute disseminated encephalomyelitis (ADEM) is an immune-mediated inflammatory demyelinating condition that predominately affects the white matter of the brain and spinal cord. The disorder manifests as an acute-onset encephalopathy associated with polyfocal neurologic deficits and is typically self-limiting. ADEM bears a striking clinical and pathological resemblance to other acute demyelinating syndromes (ADS) of childhood, including multiple sclerosis (MS). ADEM in children is readily distinguishable from alternative diagnoses on the basis of clinical features and findings on neuroimaging and laboratory investigations. However, given that ADEM lacks a specific identified biological marker rendering a reliable laboratory diagnosis, long-term follow-up is important as there are instances where an illness initially diagnosed as ADEM is ultimately replaced with a diagnosis of MS.

The onset of ADEM usually occurs in the wake of a clearly identifiable febrile prodromal illness or immunization and in association with prominent constitutional signs and encephalopathy of varied degrees. ADEM is typically a monophasic disease of pre-pubertal children; whereas, MS is typically a chronic relapsing and remitting disease of young adults. Abnormalities of findings on cerebrospinal fluid (CSF) immunoglobulin studies are less common in ADEM. However, the division between these processes is indistinct, suggesting a clinical continuum. Moreover, other conditions along the suggested continuum include optic neuritis, transverse myelitis, and neuromyelitis optica - clinical entities that may occur as manifestations of either MS or ADEM. Other boundaries of ADEM merge indistinctly with a wide variety of inflammatory encephalitic and vasculitic illnesses as well as monosymptomatic, postinfectious illnesses that should remain distinctfromADEM, such as acute cerebellar ataxia (ACA). A further indistinct boundary is shared by ADEM and Guillain-Barré syndrome as manifested in cases of Miller-Fisher syndrome and encephalomyeloradiculoneuropathy (EMRN).

Susceptibility to either ADEM or MS is likely the product of multiple factors, including a complex interrelationship of genetics and exposure to infectious agents and other environmental factors. Of particular interest are the indications that susceptibility to either condition is in part age-related. Most cases of ADEM possibly occur as the result of an inflammatory response provoked by pre-pubertal infection with a virus, vaccine, or other infectious agent. Typically, the manifestations of ADEM occur quickly after this pre-pubertal febrile systemic illness and are monophasic. In a minority of cases, patients with ADEM experience one or two pre-pubertal recurrences followed by remission. MS, on the other hand, typically manifests as a relapsing-remitting illness in ensuing adolescence or young adulthood, a significant and unexplained latency of effect with apparent permanency of immune dysregulation. Bouts of MS occur without a febrile prodrome. Uncommonly, MS develops in pre-pubertal individuals and ADEM develops in post-pubertal individuals. In very rare instances, individuals manifest pre-pubertal ADEM and, after long latency, MS in adolescence.

See more at: https://emedicine.medscape.com/article/1147044-overview

DEA training mandate: 8 hours of my life I'd like back

It's time to renew two of my three narcotic prescribing licenses. For the first time in my career, I've waffled on whether the financial outlay to the US Drug Enforcement Agency (DEA) is worth it. 

At $888 each, I've considered letting two licenses lapse because I only work part-time in Montana. But several friends advised me to keep a "spare" in case I transfer to a new location. 

I thought about just paying the fees until I could do a little more research, but there is no mechanism for a refund unless I die within the first year of the 3-year cycle, provide incorrect credit card digits, or accidentally duplicate payments.

The renewal fee is just part of the issue.

I also received an alert about the requirement for more "narcotics prescribing education" thanks to the Medication Access and Training Expansion Act (MATE). 

The requirement seems counterintuitive because opioid prescribing has decreased for the 10th consecutive year, according to the AMA Overdose Epidemic Report. The continuing rise in overdose deaths is largely due to illegitimate manufacturing of synthetic opioids. 

I've written zero outpatient narcotics prescriptions in the past 6 years, and I've written very few in my 33 years of practice. My use is limited to intravenous morphine for flash pulmonary edema or refractory angina, but unless you graduated from a training program within 5 years of the June 2023 mandate or are boarded in addiction medicine, there is no way to escape the 8-hour education requirement.

The problem is that these courses are never just 8 hours in duration. After signing up for one such CME course that cost $150, I was still dying of boredom and at risk for DVT 4 days later. That's how long it took to sit through.

Instead of the 30 seconds it should have taken to review the simple instructions to deliver Narcan, there were scores of screens followed by juvenile quizlets and cartoons. All but about 2 hours out of the 4 days is now relegated to that category of "hours of my life that I can never get back." Additionally, none of that mandatory "education" will change my prescribing habits one whit. 

Of course, I would always be truthful when asked to check the box on the DEA renewal application attesting to my having completed the required education. On the outside chance that you plan to check the yes box without completing the relevant courses, those found guilty of such false claims could be fined up to $250,000 and subject to "not more than four years in prison," or both. Yikes! 

Larry Houck, a former DEA investigator, explained that "[t]here are lot of people who are coming up for renewal and log on but still don't know this is a requirement." Neither ignorance nor complacency is an acceptable defense. 

The only good thing that came of those 4 long days of opioid education was a motivation to drive change in our current licensing and educational experience. Why not use this opportunity to reform the DEA-physician/prescriber relationship? 

The educational requirements should be curtailed for those of us who do not provide outpatient narcotic prescriptions even if we use inpatient opioids. Meds with low abuse potential should be rescheduled to minimize who gets caught in the broad net of the education requirement. 

We should reduce overregulation of the legitimate prescribers by lowering, instead of increasing, licensing fees. We should change to a single license number that covers every state. In this digital age, there is no legitimate excuse to prevent this from happening. 

After all, the settlements from opioid manufacturers and distributors will in time total $50 billion. It seems that at least some of the responsibilities of the DEA could shift to states, cities, and towns. 

My friend Siamak Karimian, MD, who provides locum services in multiple states, pays for seven active DEA licenses every 3 years. He pointed out the hypocrisy in the current regulatory system: "It's funny that you can have only one DEA or state license and work for the government in all other states or territories with no limits, including the VA, Indian healthcare systems, or prison systems."

All other prescribers require a separate DEA number for every state. Ultimately, you'd think tracking prescriptions for a single DEA number should be far simpler than tracking someone with seven. 

Competent physicians not guilty of criminal overprescribing seem to be the last to be considered in nearly every healthcare endeavor these days. It would be refreshing if they would reduce our fees and prevent this waste of our time. 

And while we are at it, perhaps a more fitting punishment is due for Richard Sackler and all the Purdue Pharma–affiliated family members. The Sacklers will pay out $6 billion in exchange for immunity against civil litigation. That doesn't seem like much when they are worth $11 billion. 

Perhaps they should be made to take an 8-hour course on opioid prescribing, annually and in perpetuity. Let's see them complete a few quizlets and sit through screens of instruction on how to administer Naloxone. Of course, that would be a mild punishment for those who manufactured a drug that killed hundreds of thousands. But it would be a start. 

https://www.medscape.com/viewarticle/dea-training-mandate-8-hours-my-life-id-back-2024a1000avg

Auto-brewery syndrome 2

While some people might have experienced the feeling of "being drunk" the morning after they consumed excessive amounts of alcohol, is it possible to feel intoxicated without ever drinking an alcoholic beverage?

Although it’s extremely rare, experts say it can happen.

The phenomenon is called auto-brewery syndrome, or ABS, according to Dr. Douglas Dieterich, M.D., director of the Institute for Liver Medicine at the Mount Sinai Health System in New York City.

The syndrome occurs when a patient’s gut gets colonized by a fungus that metabolizes carbohydrates and sugar into alcohol through fermentation, the doctor told Fox News Digital.

Before diagnosing a patient with ABS, Dieterich said that doctors "should always rule out other causes and make sure the patient is not drinking surreptitiously."

Here's a deeper dive.

A real-life case of auto-brewery syndrome

In one recent case study published in the Canadian Medical Association Journal, a 50-year-old woman had not consumed alcohol. Yet she continually had symptoms associated with intoxication, including the smell of alcohol on her breath, slurred speech and elevated blood alcohol levels during several emergency department visits.

The woman had a history of recurrent urinary tract infections that were treated with several courses of antibiotics, along with medications to reduce stomach acid.

Eventually the patient was diagnosed with auto-brewery syndrome, according to the published report.

"ABS carries paramount medical, legal, social and financial consequences for patients and their loved ones," Dr. Rahel Zewude, lead author of the study and an infectious diseases and microbiology fellow at University of Toronto in Canada, told Fox News Digital.

"Therefore, awareness of this rare syndrome in the medical community, as well as in the general public, can be instrumental in reducing delays in diagnosis."

"ABS carries paramount medical, legal, social and financial consequences for patients and their loved ones."

The woman in the case study saw her physician and visited the emergency department at least seven times over a two-year period. She complained of excessive sleepiness, slurred speech, falls and alcohol smells on her breath.

During her first ED visit, she was diagnosed with alcohol intoxication after having an elevated blood alcohol limit at 39 mmol/L (normal is 2 mmol/L or less) — despite her reports of not consuming alcoholic drinks, which family members verified.

The woman’s liver enzymes were normal and a computed tomography (CT) scan of her head revealed no acute findings, the study said.

Throughout the woman’s various visits to the emergency department, three psychiatrists provided addiction-related care, even though she scored a zero on the CAGE (Cut, Annoyed, Guilty and Eye) screening test, which assesses patients for alcohol use disorder.

(A total score of 2 or higher is considered clinically significant, according to the American Addiction Centers website.)

After experiencing episodes every one to two months, the woman was diagnosed — upon her seventh visit to the ED — with possible auto-brewery syndrome. She was prescribed an antifungal medication called fluconazole and referred to a gastroenterologist.

She completed a one-month course of fluconazole and adhered to a low-carb diet — and her symptoms began to resolve.

After four months, though, symptoms began to come back when she ramped up her carbohydrate intake, the study said.

After another course of fluconazole and a return to a low-carb diet, the symptoms resolved.

A course of probiotics was also prescribed to help foster better gut health.

Several factors contribute to ABS, according to Zewude.

"The disease likely presents when these factors emerge simultaneously alongside a high-carbohydrate diet," she told Fox News Digital.

One of the main factors is disruption of the gut microbiome, which is the population of microorganisms in the gut.

"In ABS, the fungi that ferment alcohol overpopulate our gut ahead of other non-fermenting bacteria," Zewude said.

"This gut microbiome disruption can occur due to frequent or prolonged courses of antibiotics."

Diabetes as well as gastrointestinal illnesses such as Crohn’s, liver disease and ulcerative colitis can also be risk factors for ABS, Zewude said.

Genetic predispositions that affect how the body metabolizes and clears ethanol can also play a role.

One way to test for ABS is to perform an oral glucose challenge in a supervised setting, where a patient first measures their fasting blood alcohol level.

This baseline level should be undetectable if the person had fasted for eight hours and did not consume any alcohol, according to Zewude.

"Diet modification is an extremely important part of reducing or resolving symptoms of auto-brewery disease."

The patient then ingests a high load of glucose, and their alcohol level is measured in 30-minute, one-hour, two-hour, four-hour, eight-hour and 24-hour increments.

"If their alcohol level begins to rise after ingestion of glucose, that can help confirm gut fermentation of alcohol from carbohydrates, which is ABS," Zewude told Fox News Digital.

The test should be conducted in a monitored clinic to ensure that the patient is not consuming alcohol, and to ensure safety in the event that the patient does become intoxicated, the expert advised.

The rare condition requires a multidisciplinary approach that may include a liver specialist or gastroenterologist, primary care physician, infectious diseases specialist and registered dietitian, health experts told Fox News Digital.

It is typically treated with antifungal medications and a low-carb diet, as noted in the case study mentioned earlier.

"Diet modification is an extremely important part of reducing or resolving symptoms of auto-brewery disease," Simone Gmuca, a registered dietitian who works with patients in Douglaston, New York, told Fox News Digital.

"A sugar-free, low-carb diet has been shown to be effective in managing symptoms — the fewer carbohydrates ingested, the less chance that carbohydrate fermentation will occur in the gut," added Gmuca, who was not affiliated with the study.

Patients should avoid simple carbohydrates like breads, pastas, crackers, sugary beverages, potato chips and fruit juices during treatment, the doctor said.

"Increasing lean protein, heart-healthy fats and low-starch vegetables can help promote satiation and reduce the risk of nutrient deficiencies," Gmuca added.

Patients with ABS should also incorporate plenty of lean meats, fish, avocados, olive oil, nuts, seeds and leafy green vegetables into their diet, she recommended.

Although ABS has been described in medical literature for over 50 years, the condition still remains misunderstood — with limited information regarding diagnosis and treatment, according to health experts.

https://www.foxnews.com/health/can-you-become-drunk-without-drinking-alcohol-could-happen

Rahel T. Zewude, Kenneth Croitoru, Ronit Das, Brian Goldman, Isaac I. Bogoch. Auto-brewery syndrome in a 50-year-old woman. CMAJ Jun 2024, 196 (21) E724-E727; DOI: 10.1503/cmaj.231319

KEY POINTS

Auto-brewery syndrome involves endogenous alcohol fermentation by fungi in the gut.

Diagnostic evaluation includes collateral history, ethanol level measurements with an oral glucose challenge, and, potentially, fungal culture and susceptibility testing of gastrointestinal secretions.

Management involves longitudinal, multidisciplinary care involving specialists in primary care, gastroenterology, infectious diseases, and mental health, as well as dietitians, with a strategy of antifungal therapy and a low-carbohydrate diet.

Auto-brewery syndrome may carry substantial social, legal, occupational, and medical consequences for patients, and awareness of this syndrome is essential for clinical diagnosis and management.