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Artificial intelligence (AI) is revolutionizing healthcare by enhancing diagnostics, optimizing treatment plans, and improving patient outcomes through data analysis and predictive modeling. Within the field of reproductive endocrinology and infertility, machine learning algorithms trained on large datasets can analyze images, laboratory results, and genetic information to optimize in vitro fertilization outcomes. A comprehensive search of the electronic databases PubMeD and MEDLINE was conducted, and search results were narrowed to publications after the year 2020 yielding 54 publications included in this review; select seminal publications from before the year 2020 were also included. This review summarizes the most recent evidence demonstrating the design, implementation, and validation of AI in assisted reproductive technologies. The summarized findings are categorized by application of AI to the embryology laboratory and to clinical workflows as well as highlighting ethical concerns regarding the use of such tools. AI-powered tools have been deployed in fertility clinics and embryology laboratories to enhance gamete selection and as drivers of quality improvement. Despite the promise of AI, challenges such as data bias, ethical concerns, and regulatory hurdles persist. As AI continues to evolve, its integration into reproductive medicine holds the potential to improve success rates and expand the accessibility of infertility treatments.
Adenomyosis is a chronic reproductive condition that impairs fertility and is characterized by endometrial tissue invading the myometrium. Despite advances in MRI and 3D ultrasound for diagnosis, there is still no consensus on optimal fertility management. The choice between uterus-sparing surgery and direct IVF, including the ideal timing for each approach, remains a subject of ongoing debate. This narrative review analyzed relevant studies retrieved from PubMed, Scopus, and Web of Science, focusing on uterine morphology, hormonal and surgical therapeutic responses, and IVF/ICSI outcomes in women with adenomyosis. Infertility in adenomyosis is associated with JZ remodeling, inflammation, hypercontractility, and impaired endometrial receptivity. Poor prognostic markers include JZ thickness ≥8.5 mm, uterine volume 90-130 mL, and MUSA direct features. These features are linked to lower live birth rates (aRR=0.62; 95% CI 0.43-0.88; P=0.007) and higher miscarriage risk (aRR=2.88; 95% CI 1.49-5.57; P=0.002), with larger uterine volume (>130 cm3) and thicker JZ significantly correlating with pregnancy failure and reduced cumulative live birth in Kaplan-Meier analyses. Assessment of JZ morphology, uterine volume, and MUSA features is crucial for individualized treatment planning in women with adenomyosis and infertility. Based on observational data, a pragmatic approach may include: 1) medical therapy with GnRH agonists for 3-6 cycles for uterine volumes 100-200 mL and JZmax 8.5-16 mm, followed by IVF; 2) consideration of uterus-sparing surgery for volumes >200 mL and JZmax >16 mm in highly selected patients, then IVF with an ultra-long protocol; and 3) direct IVF for volumes <100 mL and JZmax <8.5 mm, preferably using an ultra-long protocol with a freeze-all and HRT-FET strategy. These proposals are intended as a clinically oriented framework derived from current observational evidence rather than as formal guideline recommendations.
Insulin resistance (IR) is a condition where insulin-targeted tissues (muscle, liver, and adipose tissue) fail to normally respond to insulin action, leading to impaired insulin signaling and hyperglycemia. It is common in individuals with obesity and diagnosed with type 2 diabetes mellitus (T2DM), with the most prevalent disorders being polycystic ovarian syndrome and coronary artery disease. IR is also associated with cardiovascular risk factors such as hypertension and dyslipidemia. Current methods for detecting and measuring insulin sensitivity include the oral glucose tolerance test, insulin tolerance test, hyperinsulinemic-euglycemic clamp. Therapies for treating and preventing IR includes physical activity, diet modifications, and medications like Glucagon-like peptide-1 receptor agonists, gliclazide and metformin. This review aims at deciphering the molecular mechanisms and factors contributing to IR, potential clinical practices for measuring IR, medications for treating T2DM and the physical activity and dietary measures for controlling IR.
Aging is accompanied by a decline in physiological function and increased vulnerability to disease, with mitochondrial dysfunction and epigenetic alterations recognized as key hallmarks. Nicotinamide riboside (NR), a vitamin B3 precursor to NAD+, and high-intensity interval training (HIIT) have both been proposed to ameliorate aging-related mitochondrial decline, but their effects on skeletal muscle epigenetic aging are not fully elucidated. Here, we assessed the impact of 5-month NR supplementation and 4-6 weeks HIIT on epigenetic age acceleration (EAA, via seven epigenetic clocks) in human skeletal muscle across three independent studies. NR supplementation was associated with reduced muscle EAA, particularly when measured with the PCHannum, MEAT, and DunedinPACE clocks, while HIIT produced opposite effects in some clocks, notably increasing pace of aging by DunedinPACE. Correlation analyses revealed that changes in skeletal muscle mitochondrial content correlated with changes in MEAT-derived EAA after NR and 6 weeks of HIIT. Together, these findings indicate that skeletal muscle epigenetic aging can be modulated by NR and HIIT interventions but in opposing directions, highlighting a potential link between mitochondrial abundance and epigenetic clocks. Further studies are warranted to clarify how NR and exercise regulate epigenetic aging. These results offer new insights into development of strategies for promoting epigenetic outcomes and healthy aging.
Real-time continuous glucose monitoring (RT-CGM) is widely used in patients with type 1 diabetes (T1D) to improve glycemic control by reducing postprandial glucose peaks and hypoglycemic episodes. In addition, traditional biomarkers such as glycated hemoglobin (HbA1c), glycated albumin, and fructosamine provide retrospective estimates of glucose regulation over varying timeframes. This study aimed to evaluate the correlation between these biomarkers and glycemic metrics obtained from two types of RT-CGM systems: an implantable sensor (Eversense E3) and subcutaneously inserted sensors (Dexcom G6 and Guardian 4). We analyzed data from 35 patients with T1D: 13 used the Eversense E3 system, and 22 used Dexcom G6 or Guardian 4. Mean blood glucose (MBG) and time in range (TIR) were assessed at multiple time points and correlated with HbA1c, glycated albumin, and fructosamine levels. In the Eversense group, no significant correlation was observed between CGM-derived metrics and any of the biomarkers. Conversely, in the Dexcom/Guardian group, MBG and TIR demonstrated significant correlations with all biomarkers, showing large effect sizes for HbA1c and fructosamine, and medium for glycated albumin. These findings suggest that the Dexcom G6 and Guardian 4 systems more reliably reflect established biochemical markers of mid- to long-term glucose control, while Eversense may be less consistent in this regard. This highlights the importance of sensor selection when interpreting CGM data for clinical or research applications in diabetes management.
Amylin is a peptide hormone co-secreted with insulin from pancreatic β-cells that plays a crucial role in glucose homeostasis. Amylin by inhibiting glucagon secretion, slowing gastric emptying, and reducing food intake improves blood glucose and insulin sensitivity. However, emerging evidence suggests that amylin may also contribute to β-cell dysfunction and the development of insulin resistance (IR) in type 2 diabetes (T2D). This review explores the dual roles of amylin in T2D pathogenesis and management, highlighting its therapeutic and pathogenic implications. High amylin levels are associated with amyloid fibril formation, β-cell cytotoxicity, and progression of T2D complications. Conversely, amylin analogues have been shown to improve glycemic control, promote weight loss, and enhance energy balance via dual activation of amylin and calcitonin receptors in the hypothalamus. Experimental and clinical data demonstrate that both detrimental and protective effects of amylin are depending on concentration, duration, and receptor interaction. Amylin and its analogues exhibit paradoxical actions in T2D, acting as both pathogenic and protective effects. While preclinical and limited clinical studies support their role in improving metabolic control, concerns about amyloidogenic toxicity persist. Therefore, further robust clinical trials are needed to clarify amylin's long-term safety and optimize its therapeutic potential in T2D management.
Menopause brings a series of endocrine changes that significantly increase the risk of developing metabolic syndrome (MetS), a condition characterized by central obesity, dyslipidemia, hypertension, and insulin resistance. In this context, the gut microbiota has gained relevance as a key modulating factor in the pathophysiology of MetS in postmenopausal women. The decline in estrogen levels affects microbial diversity and composition, promoting a dysbiotic environment marked by the loss of beneficial bacteria, such as Akkermansia muciniphila and Bifidobacterium spp., and an increase in proinflammatory, lipopolysaccharide (LPS)-producing microorganisms, such as Proteobacteria and Escherichia coli. This imbalance leads to increased intestinal permeability and endotoxin translocation, triggering systemic low-grade inflammation associated with various MetS components. Clinical studies have identified correlations between specific microbial taxa, metabolites such as imidazole propionate and phenylacetylglutamine, and clinical markers of metabolic dysfunction. In this scenario, dietary intervention emerges as an effective therapeutic tool. Dietary patterns like the Mediterranean diet - rich in polyphenols, fiber, and monounsaturated fats - have shown beneficial effects on gut microbiota modulation, enhancing short-chain fatty acid production, reducing inflammation, and improving metabolic homeostasis. Likewise, the DASH diet and plant-based dietary patterns have demonstrated potential in the prevention and management of MetS in postmenopausal women. In conclusion, the interaction between gut microbiota, metabolism, and postmenopausal hormonal changes represents a critical axis in the development of MetS. Personalized dietary approaches aimed at restoring eubiosis may offer an effective strategy to improve metabolic health in this vulnerable population.
Premature ovarian insufficiency (POI) is a critical condition affecting young women before the median age of menopause and consisting of spontaneous oligo-amenorrhea for at least four months associated with follicle stimulating hormone (FSH) levels ≥25 UI/L detected before 40 years of age. Several causes like genetic abnormalities, autoimmune diseases, drugs and/or pelvic surgery may favor this condition that is associated with a deeper clinical impact on women's health compared to physiological menopause. Specifically, cardiovascular and musculoskeletal systems as well as brain could be especially affected by the early loss of ovarian hormones. Therefore, appropriate treatment is necessary to adequately narrow the biological gap with the average age of menopause. Hormone replacement therapy (HRT) is the treatment of choice, regardless of the presence of neurovegetative symptoms. Transdermal high dosage of natural estradiol is generally preferred to guarantee the preservation of cardio-metabolic and bone health. When contraception is required, oral estroprogestins (EPs) maybe considered. A referral to reproductive experts for fertility preservation techniques should be considered case by case.
Currently, worldwide millions of individuals, athletes, and non-athletes, of different ages and probably of all social genders (cisgender males and females, male to female (MtF) and female to male (FtM) transgenders, etc.), are current or former androgenic anabolic steroids (AAS) abusers. AAS abuse is associated with seriously increased short- and long-term risks for general, reproductive and sexual health. Indeed, to improve the knowledge and health of the population at risk of AAS misuse and standardize the current clinical practice concerning the health risks of such abuse, it is essential to also prevent, detect, diagnose, and treat all reproductive and sexual sequelae of non-therapeutic AAS assumption. The main AAS-related pathways and factors influencing reproduction and sexuality in humans, the possible reproductive and sexual signs and symptoms associated with AAS abuse and to AAS withdrawal, and the major concerns in the diagnosis and management of such clinical conditions are reported. The scientific literature has mainly evaluated male AAS abusers, but, we tried to describe/hypothesize all the possible reproductive and sexual side effects and concerns of AAS abuse also in other genders.
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Sarcopenic obesity is closely related to metabolic dysfunction-associated steatotic liver disease (MASLD), but the independent contributions of lean mass and fat mass components to MASLD are not well understood. Our study aimed to evaluate the relationship between the dual-energy X-ray absorptiometry (DXA)-derived soft tissue components and the extent of liver steatosis in patients with MASLD. A cross-sectional study of 118 obese/overweight patients aged 33-78 years, with type 2 diabetes mellitus (T2DM) or prediabetes and MASLD, on oral antidiabetic medication was conducted. Sex-stratified correlation analysis was performed between DXA-derived lean mass and fat mass parameters, (e.g., relative muscle mass [RMM], lean mass/ fat mass [LM/FM] and appendicular lean mass [ALM]), as well as between each of those parameters and the hepatic steatosis index (HSI). Multiple linear regression models were fitted with android fat percentage as the dependent variable, and lean mass indices as independent variables. The models were adjusted for age, sex, the HOMA index, triglyceride and ALT levels. Accordingly, ROC curves were plotted with HSI=36 as a classifier of steatosis. A significant negative correlation was detected between android fat % and RMM (r=-0,96, P≤0.001), between android fat percentage and ALM /BMI (r=-0.70, P≤0.001), between android fat percentage and ALM /height2 (r=-0.28, P≤0.001); between HSI and RMM (r=-0.50, P≤0.001); and between HSI and ALM/BMI (r=-0.39, P≤0.001). The significant positive correlations were as follows: android fat percentage and BMI (r=0.53, P≤0.001); android fat % and ALT (r=0.25, P=0.04); HSI and android fat percentage (r=0.59, P≤0.001); HSI and gynoid fat % (r=0.39, P≤0.001). The AUCs for android fat percentage in the models calculated from LM/FM were as follows: adjusted for the HOMA index, age and sex group, ROC=0.748 (95% CI 0.66-0.83); adjusted for ALT and sex group, ROC=0.743 (95% CI 0.66-0.83). The AUC for android fat percentage in the model calculated from RMM: adjusted for triglycerides, ALT and sex group, ROC=0.741 (95% CI 0.65-0.83). Our findings demonstrate that an increase in android fat distribution and a decrease in lean mass are positively associated with MASLD. The regression models support the utility of DXA-derived indices as practical, indirect markers of liver steatosis for clinical application in patients with TDM2 and MASLD.
Hepatology is experiencing major shifts in disease etiologies and raising demand for multidisciplinary care. However, a globally harmonized framework defining core training content remains lacking. We aimed to develop a globally informed expert consensus framework for the content of core hepatology training, in order to provide a structured foundation for curriculum development. A two-round modified Delphi using the RAND/UCLA Appropriateness Method (RAM) was conducted. A comprehensive list of curriculum items was developed from international training standards, refined by a steering committee, and rated by a stratified international panel. Consensus was determined using medians and a disagreement index (DI), which classified curriculum items as essential, desirable, or optional. 456 experts completed Round 1, of whom 78.7% also completed Round 2. Consensus was strongest for foundational knowledge and core diagnostic skills, including interpretation of abnormal liver function and liver screening test results, and non-invasive fibrosis assessment (both DI=0). Management of major liver diseases was consistently prioritized as essential. Procedures with the highest endorsement for independent performance were paracentesis, transient elastography, variceal screening, and endoscopic variceal therapy. Consensus was limited for conventional ultrasonography and advanced interventions, reflecting regional variability in resources and scope of practice. Most experts (79.1%) supported formal training in research methodology, and the median recommended fellowship length was 24 months. Subgroup differences were mainly observed in selected resource-dependent or highly specialized items. This global consensus offers a priority-stratified outline of core hepatology training content providing a practical foundation for curriculum development and staged implementation across diverse health systems. Our study provides a consensus-based, priority-stratified framework for core hepatology training content that may inform curriculum development and local adaptation, given the growing global burden of liver disease and the heterogeneity of training standards. This framework may support curriculum mapping and local adaptation for trainees, program directors, professional societies, and policymakers, including in settings where structured hepatology training pathways are still evolving. In practical terms, these findings may assist educators and institutions in reviewing and refining national curricula and training structures. However, specific implementation decisions, including accreditation requirements and procedural training standards, will need to be adapted to local regulatory and resource contexts. Recognizing that these recommendations are based on expert consensus rather than outcome data and may be variably implementable in resource-limited settings, the next steps are pilot implementation in diverse settings, evaluation of trainee and patient outcomes, and iterative revision, supported by coordinated efforts from societies, governments, and training institutions.
Novel therapies targeting apolipoprotein C3 (apoC3) have recently emerged as promising treatment options for hypertriglyceridemia and have been evaluated in phase II and III randomized clinical trials. This study aimed to perform an updated meta-analysis to assess the effects of apoC3 inhibitors on triglyceride and apoC3 concentrations, as well as their impact on the risk of acute pancreatitis. We conducted a meta-analysis of randomized, placebo-controlled trials evaluating apoC3-targeting therapies, including antisense oligonucleotides and small interfering RNA. Outcomes of interest included changes in triglyceride and apoC3 levels and the incidence of acute pancreatitis. The analysis was performed in accordance with PRISMA recommendations. Fourteen randomized trials comprising 3,422 participants met the inclusion criteria. Treatment with apoC3 inhibitors resulted in significant reductions in triglyceride levels compared with placebo (mean difference -58.7%; 95% CI -62.3 to -55.1; I2=93.8%). Similarly, apoC3 concentrations were markedly decreased (mean difference -75.3%; 95% CI -80.3 to -70.3; I2=94.7%). In addition, these therapies were associated with a significantly lower risk of acute pancreatitis (odds ratio 0.20; 95% CI 0.10 to 0.40; I2=0%). ApoC3-targeting therapies significantly reduce triglyceride and apoC3 levels in patients with hypertriglyceridemia and are associated with a reduced incidence of acute pancreatitis, supporting their potential role as an effective therapeutic strategy in this high-risk population.
PURPOSE: Diabetic kidney disease (DKD) in type 1 diabetes has been shown to be strongly associated with insulin resistance, but this has not been previously explored using the euglycemic-hyperinsulinemic clamp. Therefore, we investigated insulin sensitivity in people with type 1 diabetes with and without DKD using M/I-values (mean glucose disposal rates [GDR]/mean plasma insulin) and compared GDRs to estimated GDR (eGDR)-formulae. METHODS: In this pilot study, we studied 17 adult individuals with type 1 diabetes (ten with and seven without DKD) using euglycemic-hyperinsulinemic clamps and assessed correlations between GDR and eGDR values. RESULTS: M/I-values were 62.5% lower in individuals with type 1 diabetes and DKD compared to those without DKD, albeit not statistically significant (0.16 ± 0.08 vs. 0.10 ± 0.08 mg/kg/min per mIU/L, P = 0.154). In the whole group (n = 17) eGDR by Williams et al. demonstrated the highest correlation with GDR (r = 0.35, P = 0.167), while eGDR by Januszewski et al. had the highest correlation in the DKD group (n = 10, r = 0.46, P = 0.177). CONCLUSION: Our pilot study suggests the possibility of increased insulin resistance in people with type 1 diabetes and DKD.
Papillary thyroid carcinoma (PTC) has classically been considered a sporadic carcinoma. However, a subgroup with familial clustering has been observed, which appears to present a poorer prognosis than the sporadic form. The aim of this study is to analyze the recurrence rates and prognostic factors for familial PTC (FPTC) treated with curative intent. Multicenter national study, endorsed by the Spanish Association of Surgeons. Study population: patients with FPTC (families who have at least 2 first-degree relatives with a confirmed PTC) who meet cure criteria after the treatment. Study endpoints: recurrence rate and risk factors for recurrence. Statistical analysis: Cox regression analysis and survival analysis. The study included 252 cases with a mean follow-up of 90±68,9 months, recurrence in 26.9% (N.=68) and a disease-free survival of 183,46±7,8 months. In the multivariate analysis, the independent factors for the risk of recurrence were: 1) the number of patients with FPTC in the family (OR 1.165); 2) the multifocality (OR 2.525); 3) the vascular invasion (OR 2.770); and 4) TNM staging system (OR 5.128). In the reanalysis that included the American Thyroid Association (ATA) risk of recurrence, this variable was highly predictive of recurrence (OR 12.048). FPTC presents a high recurrence rate, which is related to the number of cases of FPTC in the family, the presence of multifocality and vascular invasion, the TNM staging system and the ATA recurrence risk assessment.
A uniform definition distinguishing metabolically healthy obesity (MHO) from metabolically unhealthy obesity (MUO) is lacking. MUO is characterized by higher liver and visceral fat than MHO. Epicardial fat tissue (EFT) is an index of cardiac adiposity strongly associated with risk of cardiovascular events. This study aimed to further define the MHO/MUO status by evaluating EFT and hepatic steatosis/fibrosis indices in adults presenting visceral obesity. In this monocentric, observational study, 56 patients (48 females; 43.8±13.1 years) were recruited. Clinical characteristics, anthropometric measurements, and metabolic parameters were evaluated. Hepatic fibrosis and steatosis were assessed by Fibroscan (502Touch, Echosense). EFT thickness was assessed by transthoracic echocardiography (GE Vivid E95 system). EFT thickness values of 9.5 mm in men and 7.5 mm in women were used as predictors of the metabolic syndrome (MetS). Patients with MUO had significantly higher steatosis/fibrosis indices and EFT values than the MHO group (P<0.001). EFT values above the cut-off were found in 82.1% of MUO, but also in 42.9% of MHO. At ROC analysis, the specificity and sensitivity of the EFT cut-off point to predict MUO phenotype combined with hypertension, 60-min post load plasma glucose, and adiponectin, were 98.6% and 92.0%, respectively. As EFT thickness values above the predictive threshold for MetS were found in about half of MHO, the MHO/MUO classification may not correctly identify the cardiovascular risk of MHO. Further clinical evidence is needed to confirm EFT thickness as potential additional marker for MHO/MUO phenotypic differentiation.
The gut microbiota plays a crucial role in the human body and has an impact on the physiological function of the host. In particular, changes in the gut microbiota are especially pronounced in patients with type 2 diabetes. There is ample evidence that glucose-lowering drugs exert their therapeutic effects precisely through their interactions with the gut microbiota, but there is a lack of summarization. An overall comparison of the effects of each hypoglycemic agent on the gut flora can provide new inspiration for combinations. In this paper, we selected several representative glucose-lowering drugs, such as metformin, sodium-dependent glucose transporters 2 inhibitors (dapagliflozin), glucagon-like peptide-1 receptor agonists (semaglutide, liraglutide), and the traditional Chinese medicine (berberine), and illustrated how they can affect the disease process by regulating metabolic homeostasis, immune response, and gut barrier. We found that each of these four hypoglycemic agents can have conflicting effects on the gut flora depending on the timing and mode of administration. Meanwhile, the potential impact of gut microbiota on drug safety is explored, and an outlook for the optimization of future type 2 diabetes treatment regimens is presented.
Obesity has reached epidemic proportions globally, with its prevalence nearly tripling since 1975. It is now recognized as a chronic, relapsing disease associated with increased morbidity and mortality due to its strong relationship with several cardio-renal-metabolic conditions. This narrative review aims to explore the major obesity-related complications - namely obstructive sleep apnea syndrome (OSAS), metabolic dysfunction-associated steatotic liver disease (MASLD), dyslipidemia, and chronic kidney disease (CKD) - highlighting their pathophysiological mechanisms, clinical consequences, and current therapeutic strategies. Obesity contributes to OSAS by increasing upper airway collapsibility and to MASLD through ectopic fat accumulation, insulin resistance, and inflammatory responses. Dyslipidemia in obesity is characterized by elevated triglycerides, small dense LDL particles, and low HDL-C, driven by chronic inflammation and insulin resistance. CKD progression, particularly obesity-related glomerulopathy (ORG), is also mediated by metabolic and hemodynamic derangements, including renin-angiotensin-aldosterone system activation and glomerular hyperfiltration. Therapeutic interventions such as lifestyle modification, pharmacological therapy - including glucagon-like peptide-1 receptor agonists (GLP-1RAs) and sodium-glucose cotransporter-2 inhibitors (SGLT-2is) - and bariatric surgery have shown efficacy not only in promoting weight loss but also in improving the clinical course of these obesity-related conditions. In particular, Very Low Energy Ketogenic Therapy (VLEKT) is emerging as a promising approach in improving metabolic parameters, hepatic steatosis, and cardiovascular risk factors. A comprehensive and multidisciplinary approach to obesity is essential, focusing not only on weight loss but also on mitigating associated complications. Effective management can significantly improve patients' quality of life and reduce the long-term burden of obesity on healthcare systems.
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Advanced and progressive thyroid cancer (TC) such as radioiodine-refractory thyroid cancer (RAIR-TC), presents a significant clinical challenge due to its poorer prognosis and limited therapeutic options. Lenvatinib is an oral multi-targeted tyrosine kinase approved as first line for the treatment of RAIR-TC. We provide a comprehensive review of lenvatinib in the management of advanced thyroid cancer including RAIR-TC, poorly differentiated (PDTC), anaplastic (ATC) and medullary thyroid carcinoma (MTC). A search was carried out on PubMed up to July 2024 to identify all relevant studies. The research was performed using the terms "thyroid neoplasms" (MeSH Terms) AND "lenvatinib" (MeSH Terms). Lenvatinib demonstrated beneficial outcomes in treating RAIR-TC with most patients achieving either partial response or stable disease, which led to its approval by regulatory agencies worldwide. In PDTC, lenvatinib demonstrated potential therapeutic usefulness, whereas its efficacy as a monotherapy in ATC has yielded less consistent outcomes. However, in ATC the combination of lenvatinib with immune check point inhibitors (such as pembrolizumab) seem promising. In MTC, the available data is limited to phase II studies. Adverse effects of any grade occur in almost all lenvatinib-treated patients and mostly have a time specific sequence of occurrence. Therapy discontinuations due to adverse events are not uncommon, and in some cases, drug-related fatalities may occur. Lenvatinib demonstrated clinical efficacy and safety in both clinical trials and real-world studies for the treatment of patients with different types of thyroid cancer.