A recent study by Crudele et al. reported on the association between surrogate indices of liver fibrosis and risk of gynecological cancers among dysmetabolic women. To put this study in context, notions regarding sex dimorphism in nonalcoholic fatty liver disease (NAFLD) are discussed. Additionally, meta-analytic reviews regarding the risk of extrahepatic cancers are reviewed. Next, I discuss the relationship of metabolic dysfunction-associated fatty liver disease (MAFLD) with extrahepatic cancers, notably including the breast and cancers of the female reproductive systems in humans. The pathomechanisms potentially accounting for this association include genetics, deregulated sex hormones, chronic subclinical inflammatory state, dysmetabolic milieu, oxidative stress, gut dysbiosis, environmental pollution, and altered immune surveillance.
{"title":"Is liver fibrosis a risk factor for gynecological cancers?","authors":"A. Lonardo","doi":"10.20517/mtod.2023.56","DOIUrl":"https://doi.org/10.20517/mtod.2023.56","url":null,"abstract":"A recent study by Crudele et al. reported on the association between surrogate indices of liver fibrosis and risk of gynecological cancers among dysmetabolic women. To put this study in context, notions regarding sex dimorphism in nonalcoholic fatty liver disease (NAFLD) are discussed. Additionally, meta-analytic reviews regarding the risk of extrahepatic cancers are reviewed. Next, I discuss the relationship of metabolic dysfunction-associated fatty liver disease (MAFLD) with extrahepatic cancers, notably including the breast and cancers of the female reproductive systems in humans. The pathomechanisms potentially accounting for this association include genetics, deregulated sex hormones, chronic subclinical inflammatory state, dysmetabolic milieu, oxidative stress, gut dysbiosis, environmental pollution, and altered immune surveillance.","PeriodicalId":91001,"journal":{"name":"Metabolism and target organ damage","volume":"72 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140438257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Dustin Baldwin, Ahmed M. Ali, Maria S. Altieri, Eric J. DeMaria
Roux-en-Y gastric bypass (RYGB)-associated marginal ulceration (MU) poses significant challenges for both patients and clinicians. Persistent symptoms such as epigastric pain, nausea, and reduced oral intake complicate the clinical landscape. MU can lead to severe complications, including anastomotic strictures, bleeding, and perforations. The etiology of MU is intricate, likely stemming from a combination of technical and patient-related factors. Technical considerations involve ischemia, tension on the anastomosis causing tissue ischemia, anastomotic technique, gastric pouch size, foreign bodies, and gastrogastric fistulas. Patient factors encompass smoking, nonsteroidal anti-inflammatory drugs (NSAIDs), Helicobacter pylori (H. pylori), and uncontrolled medical comorbidities. Diagnosis primarily relies on upper endoscopy. Initial treatment typically involves proton pump inhibitors (PPI) and sucralfate. Should these measures prove insufficient, the addition of misoprostol and the implementation of endoscopic techniques, such as oversewing or stenting across the ulcer, may be considered to facilitate healing. Ultimately, if medical and endoscopic interventions fail, surgical options become imperative. These include transthoracic truncal vagotomy and revisional procedures such as resection of the ulcer with redo gastrojejunal anastomosis, resection of the ulcer and pouch with esophagojejunal anastomosis, or resection and reversal to normal anatomy. Surgical interventions demand expertise and should be conducted at qualified, high-volume centers. To support clinicians in comprehending the nuances of MU, we conducted a literature review, presenting a summary of our findings. Additionally, we propose an algorithm delineating the escalation of treatments for MU, ranging from medical to endoscopic to surgical therapies. This concise review aims to assist clinicians in both the prevention and treatment of marginal ulceration.
与 Roux-en-Y 胃旁路术（RYGB）相关的边缘溃疡（MU）给患者和临床医生都带来了巨大的挑战。上腹部疼痛、恶心和口腔摄入量减少等持续性症状使临床情况变得更加复杂。MU 可导致严重的并发症，包括吻合口狭窄、出血和穿孔。MU 的病因错综复杂，可能源于技术和患者相关因素的综合作用。技术因素包括缺血、造成组织缺血的吻合口张力、吻合技术、胃袋大小、异物和胃胃瘘。患者因素包括吸烟、服用非甾体类抗炎药（NSAID）、幽门螺旋杆菌（H. pylori）和未得到控制的并发症。诊断主要依靠上内镜检查。初始治疗通常包括质子泵抑制剂（PPI）和蔗糖酸盐。如果这些措施被证明效果不佳，则可考虑加用米索前列醇，并采用内窥镜技术，如在溃疡处进行缝合或支架植入，以促进溃疡愈合。最后，如果药物和内窥镜干预无效，则必须选择手术治疗。这包括经胸迷走神经切断术和翻修手术，如切除溃疡并重新进行胃空肠吻合术、切除溃疡和胃袋并进行食管空肠吻合术，或切除溃疡并翻修至正常解剖结构。手术干预需要专业技术，应在合格、高产量的中心进行。为了帮助临床医生理解 MU 的细微差别，我们进行了文献综述，并对研究结果进行了总结。此外，我们还提出了一种算法，划分了从内科治疗到内窥镜治疗再到外科治疗的MU治疗升级过程。这篇简明扼要的综述旨在帮助临床医生预防和治疗边缘溃疡。
{"title":"Marginal ulceration after Roux-en-Y gastric bypass - literature review and management algorithm","authors":"Dustin Baldwin, Ahmed M. Ali, Maria S. Altieri, Eric J. DeMaria","doi":"10.20517/mtod.2023.33","DOIUrl":"https://doi.org/10.20517/mtod.2023.33","url":null,"abstract":"Roux-en-Y gastric bypass (RYGB)-associated marginal ulceration (MU) poses significant challenges for both patients and clinicians. Persistent symptoms such as epigastric pain, nausea, and reduced oral intake complicate the clinical landscape. MU can lead to severe complications, including anastomotic strictures, bleeding, and perforations. The etiology of MU is intricate, likely stemming from a combination of technical and patient-related factors. Technical considerations involve ischemia, tension on the anastomosis causing tissue ischemia, anastomotic technique, gastric pouch size, foreign bodies, and gastrogastric fistulas. Patient factors encompass smoking, nonsteroidal anti-inflammatory drugs (NSAIDs), Helicobacter pylori (H. pylori), and uncontrolled medical comorbidities. Diagnosis primarily relies on upper endoscopy. Initial treatment typically involves proton pump inhibitors (PPI) and sucralfate. Should these measures prove insufficient, the addition of misoprostol and the implementation of endoscopic techniques, such as oversewing or stenting across the ulcer, may be considered to facilitate healing. Ultimately, if medical and endoscopic interventions fail, surgical options become imperative. These include transthoracic truncal vagotomy and revisional procedures such as resection of the ulcer with redo gastrojejunal anastomosis, resection of the ulcer and pouch with esophagojejunal anastomosis, or resection and reversal to normal anatomy. Surgical interventions demand expertise and should be conducted at qualified, high-volume centers. To support clinicians in comprehending the nuances of MU, we conducted a literature review, presenting a summary of our findings. Additionally, we propose an algorithm delineating the escalation of treatments for MU, ranging from medical to endoscopic to surgical therapies. This concise review aims to assist clinicians in both the prevention and treatment of marginal ulceration.","PeriodicalId":91001,"journal":{"name":"Metabolism and target organ damage","volume":"333 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140476731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Milluzzo, L. Manuella, Lucia Frittitta, Laura Sciacca
The worldwide growing prevalence of diabetes and cancer led to an increase in subjects affected by both these diseases that share several of the involved risk factors and have a complex, multifactorial etiopathogenesis. Cancer therapies could have harmful effects on several organs, particularly in subjects also affected by diabetes and its related comorbidities. Moreover, cancer diagnosis often monopolizes the attention of both patients and caregivers, thus reducing the attention to pre-existent diseases. Retinopathy is one of the most frequent microvascular complications of diabetes, accounting for about 5% of legal blindness worldwide. The retinal neurovascular unit is dysfunctional in diabetes and could represent a frail site when cancer therapies are administered. Nevertheless, the short- and long-term effects of the different anticancer molecules on retinal tissue, especially in diabetic subjects, are poorly known, and no specific recommendations on their prevention and management are available. In this review, we summarised the current data on this topic, focusing on the different cancer class drugs involved in retinal damage: anti-oestrogen, classical cytolytic chemotherapy (alkylating agents, taxanes, topoisomerase inhibitors, and antimetabolites), mitogen-activated protein kinase, tyrosine-kinase, and vascular endothelial growth factor inhibitors are the cancer drugs associated with retinal damage and visual disturbance. However, further studies are necessary to improve knowledge on the molecular and clinical relation between cancer therapies and retinopathy, in order to provide clinicians with evidence-based protocols to optimise the management of these conditions and minimise vision loss occurrence, impaired quality of life, and public health expense.
{"title":"Cancer drugs and diabetic retinopathy: a dangerous, underestimated association","authors":"A. Milluzzo, L. Manuella, Lucia Frittitta, Laura Sciacca","doi":"10.20517/mtod.2023.43","DOIUrl":"https://doi.org/10.20517/mtod.2023.43","url":null,"abstract":"The worldwide growing prevalence of diabetes and cancer led to an increase in subjects affected by both these diseases that share several of the involved risk factors and have a complex, multifactorial etiopathogenesis. Cancer therapies could have harmful effects on several organs, particularly in subjects also affected by diabetes and its related comorbidities. Moreover, cancer diagnosis often monopolizes the attention of both patients and caregivers, thus reducing the attention to pre-existent diseases. Retinopathy is one of the most frequent microvascular complications of diabetes, accounting for about 5% of legal blindness worldwide. The retinal neurovascular unit is dysfunctional in diabetes and could represent a frail site when cancer therapies are administered. Nevertheless, the short- and long-term effects of the different anticancer molecules on retinal tissue, especially in diabetic subjects, are poorly known, and no specific recommendations on their prevention and management are available. In this review, we summarised the current data on this topic, focusing on the different cancer class drugs involved in retinal damage: anti-oestrogen, classical cytolytic chemotherapy (alkylating agents, taxanes, topoisomerase inhibitors, and antimetabolites), mitogen-activated protein kinase, tyrosine-kinase, and vascular endothelial growth factor inhibitors are the cancer drugs associated with retinal damage and visual disturbance. However, further studies are necessary to improve knowledge on the molecular and clinical relation between cancer therapies and retinopathy, in order to provide clinicians with evidence-based protocols to optimise the management of these conditions and minimise vision loss occurrence, impaired quality of life, and public health expense.","PeriodicalId":91001,"journal":{"name":"Metabolism and target organ damage","volume":"21 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139597410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A prominent endocrine disorder linked to unhealthy lifestyle behaviors and increased visceral adiposity is Male Obesity Secondary Hypogonadism (MOSH). The pathogenesis of MOSH remains under investigation. However, recent evidence supports a direct role of leptin in affecting Leydig cells, reducing testosterone production, and increasing appetite. Conversely, testosterone deficiency is associated with comorbidities like hypertension, diabetes, and nonalcoholic fatty liver disease. A recently published study entitled “Relationship between sex hormones, markers of adiposity and inflammation in male patients with severe obesity undergoing bariatric surgery” describes evidence supportive of an inverse association between testosterone and serum leptin as well as levels of c-reactive protein (CRP) and IL-6, as well as a correlation between body mass index and CRP. The same study also provides novel insight retrieved from their in vitro findings, which reveal that testosterone exposure influences the expression of genes associated with adiposity, like fatty acid binding protein 4, peroxisome proliferation-activated receptor γ (PPARγ), leptin, and adiponectin, as well as von Willebrand factor, in human-derived adipocytes. Overall, the latest evidence highlights the importance of early identification of hypogonadism in obese males and the potential benefits of testosterone supplementation in alleviating complications associated with obesity, particularly chronic inflammation. These observations underscore the need for a holistic approach to managing severe obesity, addressing hormonal and inflammatory factors to reduce its overall burden on health.
{"title":"Exploring the role of testosterone upon adiposity and cardiovascular risk markers in men with severe obesity","authors":"Eleni Armeni","doi":"10.20517/mtod.2023.40","DOIUrl":"https://doi.org/10.20517/mtod.2023.40","url":null,"abstract":"A prominent endocrine disorder linked to unhealthy lifestyle behaviors and increased visceral adiposity is Male Obesity Secondary Hypogonadism (MOSH). The pathogenesis of MOSH remains under investigation. However, recent evidence supports a direct role of leptin in affecting Leydig cells, reducing testosterone production, and increasing appetite. Conversely, testosterone deficiency is associated with comorbidities like hypertension, diabetes, and nonalcoholic fatty liver disease. A recently published study entitled “Relationship between sex hormones, markers of adiposity and inflammation in male patients with severe obesity undergoing bariatric surgery” describes evidence supportive of an inverse association between testosterone and serum leptin as well as levels of c-reactive protein (CRP) and IL-6, as well as a correlation between body mass index and CRP. The same study also provides novel insight retrieved from their in vitro findings, which reveal that testosterone exposure influences the expression of genes associated with adiposity, like fatty acid binding protein 4, peroxisome proliferation-activated receptor γ (PPARγ), leptin, and adiponectin, as well as von Willebrand factor, in human-derived adipocytes. Overall, the latest evidence highlights the importance of early identification of hypogonadism in obese males and the potential benefits of testosterone supplementation in alleviating complications associated with obesity, particularly chronic inflammation. These observations underscore the need for a holistic approach to managing severe obesity, addressing hormonal and inflammatory factors to reduce its overall burden on health.","PeriodicalId":91001,"journal":{"name":"Metabolism and target organ damage","volume":"55 21","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139447037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The investigation of the relationship between hyperuricemia and hypertension is a captivating field in hypertension research. The final product of purine metabolism is uric acid (UA), and the elevation of serum UA (SUA) levels directly contributes to the development of hypertension. Numerous studies have substantiated that hyperuricemia is a significant risk factor for hypertension. Furthermore, initial clinical trials have demonstrated that therapeutic interventions aimed at reducing SUA levels lower blood pressure (BP) in individuals with hypertension attributed to hyperuricemia. Recent research has demonstrated that hyperuricemia can facilitate the onset of hypertension via multiple mechanisms, including oxidative stress, inflammation, diminished nitric oxide (NO) synthesis, activation of reactive oxygen species (ROS), insulin resistance, vascular smooth muscle proliferation, and renal impairment. Given the interconnectedness between hyperuricemia and hypertension, it is advantageous to identify potential therapeutic approaches for timely intervention in order to impede the advancement of hypertension in individuals with hyperuricemia. This article reviews the research progress on the pathogenesis of hyperuricemia-induced hypertension.
调查高尿酸血症与高血压之间的关系是高血压研究中一个引人入胜的领域。嘌呤代谢的最终产物是尿酸（UA），血清尿酸（SUA）水平的升高直接导致高血压的发生。大量研究证实，高尿酸血症是高血压的重要危险因素。此外，初步临床试验表明，旨在降低 SUA 水平的治疗干预措施可降低因高尿酸血症导致的高血压患者的血压（BP）。最新研究表明，高尿酸血症可通过多种机制促进高血压的发生，包括氧化应激、炎症、一氧化氮（NO）合成减少、活性氧（ROS）激活、胰岛素抵抗、血管平滑肌增生和肾功能损害。鉴于高尿酸血症和高血压之间的相互联系，找出潜在的治疗方法以便及时干预，从而阻止高尿酸血症患者的高血压进展，是非常有利的。本文回顾了有关高尿酸血症诱发高血压发病机制的研究进展。
{"title":"The relationship between hyperuricemia and hypertension: a short review of current evidence","authors":"Zhiwei Wang, Guiping Yao, Bing Yan, Chenghao Zhanghuang","doi":"10.20517/mtod.2023.41","DOIUrl":"https://doi.org/10.20517/mtod.2023.41","url":null,"abstract":"The investigation of the relationship between hyperuricemia and hypertension is a captivating field in hypertension research. The final product of purine metabolism is uric acid (UA), and the elevation of serum UA (SUA) levels directly contributes to the development of hypertension. Numerous studies have substantiated that hyperuricemia is a significant risk factor for hypertension. Furthermore, initial clinical trials have demonstrated that therapeutic interventions aimed at reducing SUA levels lower blood pressure (BP) in individuals with hypertension attributed to hyperuricemia. Recent research has demonstrated that hyperuricemia can facilitate the onset of hypertension via multiple mechanisms, including oxidative stress, inflammation, diminished nitric oxide (NO) synthesis, activation of reactive oxygen species (ROS), insulin resistance, vascular smooth muscle proliferation, and renal impairment. Given the interconnectedness between hyperuricemia and hypertension, it is advantageous to identify potential therapeutic approaches for timely intervention in order to impede the advancement of hypertension in individuals with hyperuricemia. This article reviews the research progress on the pathogenesis of hyperuricemia-induced hypertension.","PeriodicalId":91001,"journal":{"name":"Metabolism and target organ damage","volume":"19 17","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139389433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mohd Danish Ansari, Haya Majid, Anas Khan, Yasmin Sultana
Metabolic bone disease (MBD)encompasses various conditions that adversely impact bone health, such as osteoporosis, primary hyperparathyroidism, osteomalacia, and fluorosis disease. Effectively managing these disorders requires early detection and a focus on maintaining healthy nutritional habits. Dietary adjustments serve as a cornerstone, but supplementation of essential minerals like calcium, phosphate, and vitamin D is often necessary to support bone reabsorption and regeneration, and reduce fracture risk. Despite the effectiveness of these measures in many cases, hereditary bone diseases pose distinctive challenges due to genetic factors. Emerging technologies that provide higher-resolution insights into bone architecture and quality are now complementing traditional diagnostic tools like dual-energy X-ray absorptiometry (DXA). Moreover, the therapeutic landscape has transformed with the introduction of newer agents that not only halt bone loss but also stimulate bone formation. These agents promise better outcomes with reduced side effects, catering to a wider patient population. However, the management of MBDs remains multifaceted, necessitating individualized approaches based on the patient’s clinical profile. As the global prevalence of MBDs, especially osteoporosis, continues to soar, it becomes imperative for clinicians to stay abreast with the evolving paradigms. This review serves as a bridge between historical knowledge and recent discoveries, offering a holistic perspective on the challenges and opportunities in the domain of MBDs.
代谢性骨病（MBD）包括对骨骼健康产生不利影响的各种疾病，如骨质疏松症、原发性甲状旁腺功能亢进症、骨软化症和氟中毒症。要有效控制这些疾病，就必须及早发现并注重保持健康的营养习惯。饮食调整是基础，但通常还需要补充钙、磷酸盐和维生素 D 等必需矿物质，以支持骨骼的再吸收和再生，降低骨折风险。尽管这些措施在许多情况下都很有效，但由于遗传因素，遗传性骨病带来了独特的挑战。新兴技术能够提供更高分辨率的骨骼结构和质量洞察力，是对双能 X 射线吸收测量法（DXA）等传统诊断工具的补充。此外，随着不仅能阻止骨质流失，还能刺激骨质形成的新型药物的推出，治疗领域也发生了变化。这些药物有望取得更好的疗效，同时减少副作用，满足更多患者的需求。然而，骨质疏松症的治疗仍然是多方面的，需要根据患者的临床特征采取个性化的方法。随着骨质疏松症（尤其是骨质疏松症）在全球的发病率不断飙升，临床医生必须跟上不断发展的治疗模式。本综述是历史知识与最新发现之间的桥梁，从整体角度探讨了骨质疏松症领域的挑战与机遇。
{"title":"Clinical frontiers of metabolic bone disorders: a comprehensive review","authors":"Mohd Danish Ansari, Haya Majid, Anas Khan, Yasmin Sultana","doi":"10.20517/mtod.2023.38","DOIUrl":"https://doi.org/10.20517/mtod.2023.38","url":null,"abstract":"Metabolic bone disease (MBD)encompasses various conditions that adversely impact bone health, such as osteoporosis, primary hyperparathyroidism, osteomalacia, and fluorosis disease. Effectively managing these disorders requires early detection and a focus on maintaining healthy nutritional habits. Dietary adjustments serve as a cornerstone, but supplementation of essential minerals like calcium, phosphate, and vitamin D is often necessary to support bone reabsorption and regeneration, and reduce fracture risk. Despite the effectiveness of these measures in many cases, hereditary bone diseases pose distinctive challenges due to genetic factors. Emerging technologies that provide higher-resolution insights into bone architecture and quality are now complementing traditional diagnostic tools like dual-energy X-ray absorptiometry (DXA). Moreover, the therapeutic landscape has transformed with the introduction of newer agents that not only halt bone loss but also stimulate bone formation. These agents promise better outcomes with reduced side effects, catering to a wider patient population. However, the management of MBDs remains multifaceted, necessitating individualized approaches based on the patient’s clinical profile. As the global prevalence of MBDs, especially osteoporosis, continues to soar, it becomes imperative for clinicians to stay abreast with the evolving paradigms. This review serves as a bridge between historical knowledge and recent discoveries, offering a holistic perspective on the challenges and opportunities in the domain of MBDs.","PeriodicalId":91001,"journal":{"name":"Metabolism and target organ damage","volume":" 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139143493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Metabolic bone disease: from basic science to clinical frontier","authors":"Ling-Feng Zeng","doi":"10.20517/mtod.2023.39","DOIUrl":"https://doi.org/10.20517/mtod.2023.39","url":null,"abstract":"","PeriodicalId":91001,"journal":{"name":"Metabolism and target organ damage","volume":"57 8","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139208410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Batoul Jaafar, Jessica Abou Chaaya, Shahed Ammar, Ibrahim Salti
Acute pancreatitis rarely occurs in pregnancy, with hypertriglyceridemia being the fourth leading cause during pregnancy. Hypertriglyceridemia, of which Familial Chylomicronemia Syndrome is the most severe form, ranks among the four principal causes of pancreatitis in pregnancy. Total Plasma exchange (TPE) has been found to be an effective and safe intervention both as a therapeutic and a prophylactic act. A 22-year-old female with FCS presented at the 21st week of gestation with acute hypertriglyceridemia pancreatitis. Despite medical management, she was then started on TPE at the two-week follow-up after serum triglyceride level was out of control. The triglyceride dropped from 55.0 % to 77.5 % during these sessions. Despite these interventions, pancreatitis recurred in week 34. An emergency C-section was carried out after a drop in the fetal heart rate. Postpartum triglycerides dropped by 57 % but remained above 1,000 mg/dl. FCS is difficult to manage during pregnancy, and it frequently fails to respond to various pharmacologic lines. TPE can help prolong a pregnancy, but it is not a definite treatment. Novel therapies for hypertriglyceridemia in pregnancy await additional safety testing.
{"title":"Acute pancreatitis in pregnancy and familial chylomicronemia syndrome: case report and literature review","authors":"Batoul Jaafar, Jessica Abou Chaaya, Shahed Ammar, Ibrahim Salti","doi":"10.20517/mtod.2023.12","DOIUrl":"https://doi.org/10.20517/mtod.2023.12","url":null,"abstract":"Acute pancreatitis rarely occurs in pregnancy, with hypertriglyceridemia being the fourth leading cause during pregnancy. Hypertriglyceridemia, of which Familial Chylomicronemia Syndrome is the most severe form, ranks among the four principal causes of pancreatitis in pregnancy. Total Plasma exchange (TPE) has been found to be an effective and safe intervention both as a therapeutic and a prophylactic act. A 22-year-old female with FCS presented at the 21st week of gestation with acute hypertriglyceridemia pancreatitis. Despite medical management, she was then started on TPE at the two-week follow-up after serum triglyceride level was out of control. The triglyceride dropped from 55.0 % to 77.5 % during these sessions. Despite these interventions, pancreatitis recurred in week 34. An emergency C-section was carried out after a drop in the fetal heart rate. Postpartum triglycerides dropped by 57 % but remained above 1,000 mg/dl. FCS is difficult to manage during pregnancy, and it frequently fails to respond to various pharmacologic lines. TPE can help prolong a pregnancy, but it is not a definite treatment. Novel therapies for hypertriglyceridemia in pregnancy await additional safety testing.","PeriodicalId":91001,"journal":{"name":"Metabolism and target organ damage","volume":"16 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139279049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kyle Rodrigues, Rawdat Hussain, Sarah Cooke, Gary Zhang, Deqiang Zhang, Lei Yin, Xin Tong
Acetaminophen (APAP) is the most widely used analgesic in the world. APAP overdose can cause severe hepatotoxicity and therefore is the most common cause of drug-induced liver injury. The only approved treatment for APAP overdose is N-acetyl-cysteine (NAC) supplementation. However, the narrow efficacy window of the drug severely limits its clinical use, prompting the search for other therapeutic options to counteract APAP toxicity. Recent research has pointed to fructose as a novel nutraceutical for APAP-induced liver injury. This review summarizes the current understanding of the molecular mechanisms underlying APAP-induced liver injury, introduces how fructose supplementation could prevent and treat APAP liver toxicity with a focus on the ChREBPα-FGF21 pathway, and proposes possible future directions of study.
{"title":"Fructose as a novel nutraceutical for acetaminophen (APAP)-induced hepatotoxicity","authors":"Kyle Rodrigues, Rawdat Hussain, Sarah Cooke, Gary Zhang, Deqiang Zhang, Lei Yin, Xin Tong","doi":"10.20517/mtod.2023.28","DOIUrl":"https://doi.org/10.20517/mtod.2023.28","url":null,"abstract":"Acetaminophen (APAP) is the most widely used analgesic in the world. APAP overdose can cause severe hepatotoxicity and therefore is the most common cause of drug-induced liver injury. The only approved treatment for APAP overdose is N-acetyl-cysteine (NAC) supplementation. However, the narrow efficacy window of the drug severely limits its clinical use, prompting the search for other therapeutic options to counteract APAP toxicity. Recent research has pointed to fructose as a novel nutraceutical for APAP-induced liver injury. This review summarizes the current understanding of the molecular mechanisms underlying APAP-induced liver injury, introduces how fructose supplementation could prevent and treat APAP liver toxicity with a focus on the ChREBPα-FGF21 pathway, and proposes possible future directions of study.","PeriodicalId":91001,"journal":{"name":"Metabolism and target organ damage","volume":"8 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136067907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hepatic steatosis is caused by exaggerated hepatic lipid accumulation and is a common histological and radiological finding. Non-alcoholic fatty liver disease (NAFLD), or metabolic dysfunction associated steatotic liver disease (MASLD), is highly associated with metabolic syndrome and represents the most common cause of hepatic steatosis. However, since several comorbidities, lifestyle factors, and drugs can cause hepatic steatosis, MASLD is, to some extent, a diagnosis of exclusion. Nevertheless, initiatives have been taken to encompass positive (instead of negative) criteria for diagnosis - such as the presence of cardiometabolic risk factors together with hepatic steatosis. Nonetheless, before confirming a patient with MASLD, it is essential to map and evaluate other causes of fatty liver disease or steatotic liver disease. Several causes of hepatic steatosis have been identified in studies; however, the study cohorts are scarce and often anecdotal. Additionally, many studies have shown correlation without proving causation, and many are retrospective without reporting relevant patient characteristics and comorbidities - making it difficult to draw conclusions regarding the underlying etiology or present comorbidity of hepatic steatosis. In this narrative review, we aimed to identify and summarize present studies evaluating the impact of the most common and often suggested causes of hepatic steatosis.
{"title":"Non-metabolic causes of steatotic liver disease","authors":"Patrik Nasr, Cecilia Jönsson, Mattias Ekstedt, Stergios Kechagias","doi":"10.20517/mtod.2023.20","DOIUrl":"https://doi.org/10.20517/mtod.2023.20","url":null,"abstract":"Hepatic steatosis is caused by exaggerated hepatic lipid accumulation and is a common histological and radiological finding. Non-alcoholic fatty liver disease (NAFLD), or metabolic dysfunction associated steatotic liver disease (MASLD), is highly associated with metabolic syndrome and represents the most common cause of hepatic steatosis. However, since several comorbidities, lifestyle factors, and drugs can cause hepatic steatosis, MASLD is, to some extent, a diagnosis of exclusion. Nevertheless, initiatives have been taken to encompass positive (instead of negative) criteria for diagnosis - such as the presence of cardiometabolic risk factors together with hepatic steatosis. Nonetheless, before confirming a patient with MASLD, it is essential to map and evaluate other causes of fatty liver disease or steatotic liver disease. Several causes of hepatic steatosis have been identified in studies; however, the study cohorts are scarce and often anecdotal. Additionally, many studies have shown correlation without proving causation, and many are retrospective without reporting relevant patient characteristics and comorbidities - making it difficult to draw conclusions regarding the underlying etiology or present comorbidity of hepatic steatosis. In this narrative review, we aimed to identify and summarize present studies evaluating the impact of the most common and often suggested causes of hepatic steatosis.","PeriodicalId":91001,"journal":{"name":"Metabolism and target organ damage","volume":"60 3","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136381363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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