Pub Date : 2025-02-01DOI: 10.1016/j.disamonth.2025.101863
Neel Vora, Parth Patel, Mohammed Dheyaa Marsool Marsool, Ali Dheyaa Marsool Marsool, Rayyan Sunasra, Parva Ladani, Shefali Pati, Dhruvi Khoont, Priyadarshi Prajjwal, Raunak Ranjan
Alzheimer's disease is a progressive neurodegenerative disorder that primarily affects the elderly population; and is characterized by the gradual loss of memory, cognition, and ability to carry out daily activities. However, a growing body of research indicates that there exists a subtype of Alzheimer's disease known as Atypical Alzheimer's disease. Atypical Alzheimer's disease is a rare form of dementia that differs from the typical presentation of Alzheimer's disease, such as variations in the age of onset, distribution of brain pathology, and clinical symptoms. The patients affected have a younger age of onset and have predominantly visual, language, executive function, motor, and behavioral dysfunction. The diagnosis requires a comprehensive neurological evaluation with specific attention to cognitive and behavioral changes while ruling out other potential causes of dementia. Emerging biomarkers including CSF profiles, amyloid and tau PET imaging, and advanced neuroimaging techniques offer promising avenues for improving diagnostic accuracy and understanding disease mechanisms. In this article, we focus on atypical presentations seen in the posterior cortical variant, frontal variant, progressive aphasic variant, corticobasal syndrome and look at the specific biomarkers used in the diagnosis of each variant along with focusing on the treatment of the disease. We also aim to provide an understanding of Atypical Alzheimer's disease, its clinical features, the biomarkers helping in diagnosing the disease, the current treatment guidelines, and the current scientific advancements in the field.
{"title":"Atypical Alzheimer's dementia: Addressing the subtypes, epidemiology, atypical presentations, diagnostic biomarkers, and treatment updates.","authors":"Neel Vora, Parth Patel, Mohammed Dheyaa Marsool Marsool, Ali Dheyaa Marsool Marsool, Rayyan Sunasra, Parva Ladani, Shefali Pati, Dhruvi Khoont, Priyadarshi Prajjwal, Raunak Ranjan","doi":"10.1016/j.disamonth.2025.101863","DOIUrl":"https://doi.org/10.1016/j.disamonth.2025.101863","url":null,"abstract":"<p><p>Alzheimer's disease is a progressive neurodegenerative disorder that primarily affects the elderly population; and is characterized by the gradual loss of memory, cognition, and ability to carry out daily activities. However, a growing body of research indicates that there exists a subtype of Alzheimer's disease known as Atypical Alzheimer's disease. Atypical Alzheimer's disease is a rare form of dementia that differs from the typical presentation of Alzheimer's disease, such as variations in the age of onset, distribution of brain pathology, and clinical symptoms. The patients affected have a younger age of onset and have predominantly visual, language, executive function, motor, and behavioral dysfunction. The diagnosis requires a comprehensive neurological evaluation with specific attention to cognitive and behavioral changes while ruling out other potential causes of dementia. Emerging biomarkers including CSF profiles, amyloid and tau PET imaging, and advanced neuroimaging techniques offer promising avenues for improving diagnostic accuracy and understanding disease mechanisms. In this article, we focus on atypical presentations seen in the posterior cortical variant, frontal variant, progressive aphasic variant, corticobasal syndrome and look at the specific biomarkers used in the diagnosis of each variant along with focusing on the treatment of the disease. We also aim to provide an understanding of Atypical Alzheimer's disease, its clinical features, the biomarkers helping in diagnosing the disease, the current treatment guidelines, and the current scientific advancements in the field.</p>","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":" ","pages":"101863"},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-28DOI: 10.1016/j.disamonth.2024.101850
Nancy Friedman, Ross Friedman
{"title":"Foreword: Ecstasy, Molly, MDMA: What health practitioners need to know about this common recreational drug.","authors":"Nancy Friedman, Ross Friedman","doi":"10.1016/j.disamonth.2024.101850","DOIUrl":"https://doi.org/10.1016/j.disamonth.2024.101850","url":null,"abstract":"","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":" ","pages":"101850"},"PeriodicalIF":3.8,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143069383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-16DOI: 10.1016/j.disamonth.2025.101852
Jerrold B Leikin
{"title":"Foreword: Hallucinogenic amphetamine, cannabis and opioid issues for the primary care practitioner.","authors":"Jerrold B Leikin","doi":"10.1016/j.disamonth.2025.101852","DOIUrl":"https://doi.org/10.1016/j.disamonth.2025.101852","url":null,"abstract":"","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":" ","pages":"101852"},"PeriodicalIF":3.8,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143015797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-14DOI: 10.1016/j.disamonth.2024.101851
Andrew M Farrar, Isabelle H Nordstrom, Kaitlyn Shelley, Gayane Archer, Kaitlyn N Kunstman, Joseph J Palamar
3,4-methylenedioxymethamphetamine (MDMA; commonly referred to as "ecstasy" or "molly") is a substituted amphetamine drug that is used recreationally for its acute psychoactive effects, including euphoria and increased energy, as well as prosocial effects such as increased empathy and feelings of closeness with others. Acute adverse effects can include hyperthermia, dehydration, bruxism, and diaphoresis. Post-intoxication phenomena may include insomnia, anhedonia, anxiety, depression, and memory impairment, which can persist for days following drug cessation. MDMA acts as a releasing agent for monoamine neurotransmitters, including dopamine (DA), norepinephrine (NE) and serotonin (5-HT), by interfering with vesicular storage and transporter function, thus increasing extracellular levels of DA, NE, and 5-HT. Medical intervention in response to adverse events is complicated by the fact that illicitly-acquired MDMA is frequently adulterated, contaminated, or outright replaced with other psychoactive drugs such as synthetic cathinones ("bath salts") or methamphetamine, often unknown to the person using the drug. This review provides background on the legal status of MDMA and its use patterns, including proposals for its use as an adjunct in psychotherapy. It also discusses the pharmacological properties, mental and physical health effects, and interactions of MDMA with other drugs, with special focus on harm reduction strategies. This information will help healthcare providers assess adverse health effects related to MDMA/ecstasy use in order to facilitate appropriate treatment strategies and improve patient outcomes.
{"title":"Ecstasy, molly, MDMA: What health practitioners need to know about this common recreational drug.","authors":"Andrew M Farrar, Isabelle H Nordstrom, Kaitlyn Shelley, Gayane Archer, Kaitlyn N Kunstman, Joseph J Palamar","doi":"10.1016/j.disamonth.2024.101851","DOIUrl":"https://doi.org/10.1016/j.disamonth.2024.101851","url":null,"abstract":"<p><p>3,4-methylenedioxymethamphetamine (MDMA; commonly referred to as \"ecstasy\" or \"molly\") is a substituted amphetamine drug that is used recreationally for its acute psychoactive effects, including euphoria and increased energy, as well as prosocial effects such as increased empathy and feelings of closeness with others. Acute adverse effects can include hyperthermia, dehydration, bruxism, and diaphoresis. Post-intoxication phenomena may include insomnia, anhedonia, anxiety, depression, and memory impairment, which can persist for days following drug cessation. MDMA acts as a releasing agent for monoamine neurotransmitters, including dopamine (DA), norepinephrine (NE) and serotonin (5-HT), by interfering with vesicular storage and transporter function, thus increasing extracellular levels of DA, NE, and 5-HT. Medical intervention in response to adverse events is complicated by the fact that illicitly-acquired MDMA is frequently adulterated, contaminated, or outright replaced with other psychoactive drugs such as synthetic cathinones (\"bath salts\") or methamphetamine, often unknown to the person using the drug. This review provides background on the legal status of MDMA and its use patterns, including proposals for its use as an adjunct in psychotherapy. It also discusses the pharmacological properties, mental and physical health effects, and interactions of MDMA with other drugs, with special focus on harm reduction strategies. This information will help healthcare providers assess adverse health effects related to MDMA/ecstasy use in order to facilitate appropriate treatment strategies and improve patient outcomes.</p>","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":" ","pages":"101851"},"PeriodicalIF":3.8,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143015796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-13DOI: 10.1016/j.disamonth.2025.101853
Donald E Greydanus, Ahsan Nazeer, Dilip R Patel
The subject of substance use disorders in the pediatric population remains a disturbing conundrum for clinicians, researchers and society in general. Many of our youth are at risk of being damaged and even killed by drug addictions that result from the collision of rapidly developing as well as vulnerable central nervous systems encountering the current global drug addiction crisis. A major motif of this chemical calamity is opioid use disorder in adolescents and young adults that was stimulated by the 19th century identification of such highly addictive drugs as morphine, heroin and a non-opiate, cocaine. This analysis focuses on the pervasive presence of opioid drugs such as heroin and fentanyl that has become a major tragedy in the 21st century arising from an overall substance use and misuse phenomenon rampant in global society. Themes covered in this article include the history of addictive drugs in humans, diagnostic terms in use, the role of neurobiology in drug addiction, and current psychopharmacologic approaches to opioid overdose as well as addiction. Our youth are continuously confronted by dangers of high-risk behaviors including death and injury from opioid use disorders due to their central nervous system neuroplasticity as well as the widespread availability of these harmful chemicals. Healthcare professionals should actively assist our youth who unknowingly and even innocently encounter this deadly menace in the 21st century.
{"title":"Opioid use and abuse in adolescents and young adults; dealing with science, laws and ethics: Charming the COBRAS.","authors":"Donald E Greydanus, Ahsan Nazeer, Dilip R Patel","doi":"10.1016/j.disamonth.2025.101853","DOIUrl":"https://doi.org/10.1016/j.disamonth.2025.101853","url":null,"abstract":"<p><p>The subject of substance use disorders in the pediatric population remains a disturbing conundrum for clinicians, researchers and society in general. Many of our youth are at risk of being damaged and even killed by drug addictions that result from the collision of rapidly developing as well as vulnerable central nervous systems encountering the current global drug addiction crisis. A major motif of this chemical calamity is opioid use disorder in adolescents and young adults that was stimulated by the 19th century identification of such highly addictive drugs as morphine, heroin and a non-opiate, cocaine. This analysis focuses on the pervasive presence of opioid drugs such as heroin and fentanyl that has become a major tragedy in the 21st century arising from an overall substance use and misuse phenomenon rampant in global society. Themes covered in this article include the history of addictive drugs in humans, diagnostic terms in use, the role of neurobiology in drug addiction, and current psychopharmacologic approaches to opioid overdose as well as addiction. Our youth are continuously confronted by dangers of high-risk behaviors including death and injury from opioid use disorders due to their central nervous system neuroplasticity as well as the widespread availability of these harmful chemicals. Healthcare professionals should actively assist our youth who unknowingly and even innocently encounter this deadly menace in the 21st century.</p>","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":" ","pages":"101853"},"PeriodicalIF":3.8,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: While an association between cannabis use and the risk of atherosclerotic cardiovascular diseases (ASCVD) has been reported numerous times, it remains inconclusive as to whether this link is causal in nature. We sought to consolidate data from observational studies to explore the association between ever use of cannabis and ASCVD outcomes, including myocardial infarction, stroke, and a combined measure of any adverse cardiovascular events in comparison to non-users or controls.
Methods: We performed a systematic literature search on PubMed, Scopus, ScienceDirect, and Cochrane Library for relevant studies from inception until April 2024. Statistical analyses utilized RevMan 5.4 with a random effects model. The study protocol has been registered with PROSPERO (CRD42024530366).
Results: Our analysis incorporated data from 17 studies involving a total of 1,902,481 individuals aged between 18 and 74 years, with a mean follow-up duration of 8.5 years. Upon pooled analysis, no statistically significant association was found between cannabis use and the risk of myocardial infarction compared to non-users, with an RR of 1.25 (95% CI: 0.91-1.71, p = 0.17). Similarly, while the risk of stroke showed no significant association with cannabis use (RR: 1.38, 95% CI: 0.88 to 2.16, p = 0.16), a statistically significant association was observed between ever use of cannabis and the composite of any adverse cardiovascular events (RR: 1.48, 95% CI: 1.16-1.90, p = 0.002).
Conclusion: The evident statistical correlations between cannabis use and adverse cardiovascular outcomes underscore its potential as a risk factor for cardiovascular disease, suggesting plausibility for a causal relationship between cannabis use and ASCVD. With rising trends in medical cannabis use and cannabis use disorder across age demographics, heightened risk awareness and informed decision-making regarding cannabis consumption are critical priorities in healthcare and public health initiatives.
{"title":"Cannabis use and atherosclerotic cardiovascular disease outcomes: A meta-analysis of multinational cohort data.","authors":"Sneha Annie Sebastian, Yash Shah, Camelia Arsene, Geetha Krishnamoorthy","doi":"10.1016/j.disamonth.2024.101849","DOIUrl":"https://doi.org/10.1016/j.disamonth.2024.101849","url":null,"abstract":"<p><strong>Background: </strong>While an association between cannabis use and the risk of atherosclerotic cardiovascular diseases (ASCVD) has been reported numerous times, it remains inconclusive as to whether this link is causal in nature. We sought to consolidate data from observational studies to explore the association between ever use of cannabis and ASCVD outcomes, including myocardial infarction, stroke, and a combined measure of any adverse cardiovascular events in comparison to non-users or controls.</p><p><strong>Methods: </strong>We performed a systematic literature search on PubMed, Scopus, ScienceDirect, and Cochrane Library for relevant studies from inception until April 2024. Statistical analyses utilized RevMan 5.4 with a random effects model. The study protocol has been registered with PROSPERO (CRD42024530366).</p><p><strong>Results: </strong>Our analysis incorporated data from 17 studies involving a total of 1,902,481 individuals aged between 18 and 74 years, with a mean follow-up duration of 8.5 years. Upon pooled analysis, no statistically significant association was found between cannabis use and the risk of myocardial infarction compared to non-users, with an RR of 1.25 (95% CI: 0.91-1.71, p = 0.17). Similarly, while the risk of stroke showed no significant association with cannabis use (RR: 1.38, 95% CI: 0.88 to 2.16, p = 0.16), a statistically significant association was observed between ever use of cannabis and the composite of any adverse cardiovascular events (RR: 1.48, 95% CI: 1.16-1.90, p = 0.002).</p><p><strong>Conclusion: </strong>The evident statistical correlations between cannabis use and adverse cardiovascular outcomes underscore its potential as a risk factor for cardiovascular disease, suggesting plausibility for a causal relationship between cannabis use and ASCVD. With rising trends in medical cannabis use and cannabis use disorder across age demographics, heightened risk awareness and informed decision-making regarding cannabis consumption are critical priorities in healthcare and public health initiatives.</p>","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":" ","pages":"101849"},"PeriodicalIF":3.8,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Erdheim-Chester disease (ECD) is an extremely rare non-Langerhans cell disorder that is believed to include both inflammatory and neoplastic characteristics. It is caused due to genetic mutations in proto-oncogenes like BRAF and MEK, while immunological pathways have an essential role in the onset and progression of the disease. Despite its rarity, ECD poses significant diagnostic and therapeutic challenges due to its heterogeneous clinical presentation and limited understanding of its underlying pathophysiology. Multiple organs can be affected, with the most frequent being long bones, central nervous system and retro-orbital abnormalities, pericardial and myocardial infiltration, interstitial lung disease, retroperitoneal fibrosis, and large blood vessel aberrations. Here, in this review, we comprehensively underline the current knowledge of ECD, including its epidemiology, clinical manifestations, genetics, pathophysiology, diagnostic modalities, and treatment options. By synthesizing existing literature and highlighting areas of ongoing research, this review aims to provide clinicians and researchers with a comprehensive understanding of ECD and guide future directions for improved patient care and outcomes.
{"title":"Erdheim-Chester disease: Comprehensive insights from genetic mutations to clinical manifestations and therapeutic advances.","authors":"Rishabh Chaudhary, Anand Kumar, Alpana Singh, Vipul Agarwal, Mujeeba Rehman, Arjun Singh Kaushik, Siddhi Srivastava, Sukriti Srivastava, Vikas Mishra","doi":"10.1016/j.disamonth.2024.101845","DOIUrl":"https://doi.org/10.1016/j.disamonth.2024.101845","url":null,"abstract":"<p><p>Erdheim-Chester disease (ECD) is an extremely rare non-Langerhans cell disorder that is believed to include both inflammatory and neoplastic characteristics. It is caused due to genetic mutations in proto-oncogenes like BRAF and MEK, while immunological pathways have an essential role in the onset and progression of the disease. Despite its rarity, ECD poses significant diagnostic and therapeutic challenges due to its heterogeneous clinical presentation and limited understanding of its underlying pathophysiology. Multiple organs can be affected, with the most frequent being long bones, central nervous system and retro-orbital abnormalities, pericardial and myocardial infiltration, interstitial lung disease, retroperitoneal fibrosis, and large blood vessel aberrations. Here, in this review, we comprehensively underline the current knowledge of ECD, including its epidemiology, clinical manifestations, genetics, pathophysiology, diagnostic modalities, and treatment options. By synthesizing existing literature and highlighting areas of ongoing research, this review aims to provide clinicians and researchers with a comprehensive understanding of ECD and guide future directions for improved patient care and outcomes.</p>","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":" ","pages":"101845"},"PeriodicalIF":3.8,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142933455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-02DOI: 10.1016/j.disamonth.2024.101848
Anna Gaddy, Mohamed Elrggal, Hector Madariaga, Adam Kelly, Edgar Lerma, Gates Colbert
Diabetic kidney disease is a leading cause of kidney failure worldwide and is easily detectable with screening examination. Diabetes causes hyperfiltration and activation of the renin-angiotensin aldosterone system by hemodynamic changes within the nephron, which perpetuates damaging physiology. Diagnosis is often clinical after detection of heavy proteinuria in a patient with diabetes,but can be confirmed by observation of histologic stages on kidney biopsy. Mainstays of treatment include angiotensin conversion or receptor blockade, mineralocorticoid receptor blockade, and tight glucose control. Newer agents favored in diabetic kidney disease are sodium glucose-cotransporters and glucagon-like peptide 1 receptor agonists, both for glycemic control and for various methods of reversing damaging physiology.
{"title":"Diabetic Kidney Disease.","authors":"Anna Gaddy, Mohamed Elrggal, Hector Madariaga, Adam Kelly, Edgar Lerma, Gates Colbert","doi":"10.1016/j.disamonth.2024.101848","DOIUrl":"https://doi.org/10.1016/j.disamonth.2024.101848","url":null,"abstract":"<p><p>Diabetic kidney disease is a leading cause of kidney failure worldwide and is easily detectable with screening examination. Diabetes causes hyperfiltration and activation of the renin-angiotensin aldosterone system by hemodynamic changes within the nephron, which perpetuates damaging physiology. Diagnosis is often clinical after detection of heavy proteinuria in a patient with diabetes,but can be confirmed by observation of histologic stages on kidney biopsy. Mainstays of treatment include angiotensin conversion or receptor blockade, mineralocorticoid receptor blockade, and tight glucose control. Newer agents favored in diabetic kidney disease are sodium glucose-cotransporters and glucagon-like peptide 1 receptor agonists, both for glycemic control and for various methods of reversing damaging physiology.</p>","PeriodicalId":51017,"journal":{"name":"Dm Disease-A-Month","volume":" ","pages":"101848"},"PeriodicalIF":3.8,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142928722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}