Browse
You are looking at 61 - 70 of 1,475 items for
Department of Diabetes & Endocrinology, Skåne University Hospital, Malmö, Sweden
Search for other papers by Bushra Shahida in
Google Scholar
PubMed
Department of Diabetes & Endocrinology, Skåne University Hospital, Malmö, Sweden
Search for other papers by Tereza Planck in
Google Scholar
PubMed
Search for other papers by Tania Singh in
Google Scholar
PubMed
Department of Ophthalmology, Skåne University Hospital, Malmö, Sweden
Search for other papers by Peter Åsman in
Google Scholar
PubMed
Department of Diabetes & Endocrinology, Skåne University Hospital, Malmö, Sweden
Search for other papers by Mikael Lantz in
Google Scholar
PubMed
Graves’ disease (GD) and Graves’ ophthalmopathy (GO) are complex autoimmune diseases. This study delved into the impact of cigarette smoke extract (CSE), simvastatin, and/or diclofenac on peripheral blood mononuclear cells (PBMCs). Specifically, we explored alterations in IL-1B, IL-6, PTGS2 expression, B- and T-lymphocyte proliferation, and Immunoglobulin G (IgG) production. We also assessed IGF1’s influence on B- and T-lymphocyte proliferation. PBMCs from Graves’ patients were exposed to CSE with/without simvastatin and/or diclofenac. Gene and protein expression was compared with untreated PBMCs. B- and T-lymphocyte proliferation was assessed following IGF1 treatment. PBMCs exposed to CSE exhibited increased expression of IL-1B (6-fold), IL-6 (10-fold), and PTGS2 (5.6-fold), and protein levels of IL-1B (4-fold), IL-6 (16-fold) and PGE2 (3.7-fold) compared with untreated PBMCs. Simvastatin and/or diclofenac downregulated the expression of PTGS2 (0.5-fold), IL-6 (0.4-fold), and IL-1B (0.6-fold), and the protein levels of IL-1B (0.6-fold), IL-6 (0.6-fold), and PGE2 (0.6-fold) compared with untreated PBMCs. CSE exposure in PBMCs increased the proliferation of B and T lymphocytes by 1.3-fold and 1.4-fold, respectively, compared with untreated. CSE exposure increased IgG (1.5-fold) in supernatant from PBMCs isolated from Graves’ patients. IGF1 treatment increased the proliferation of B and T lymphocytes by 1.6-fold. Simvastatin downregulated the proliferation of B and T lymphocytes by 0.7-fold. Our study shows that CSE significantly upregulated the expression and release of the inflammatory markers PTGS2, IL-6 and IL-1B,the IgG levels, and the proliferation of B and T lymphocytes. Additionally, IGF1 increased the proliferation of B and T lymphocytes. Finally, these effects were decreased by diclofenac and/or simvastatin treatment.
Search for other papers by Ayana Suzuki in
Google Scholar
PubMed
Search for other papers by Mitsuyoshi Hirokawa in
Google Scholar
PubMed
Search for other papers by Izumi Otsuka in
Google Scholar
PubMed
Search for other papers by Akihiro Miya in
Google Scholar
PubMed
Search for other papers by Akira Miyauchi in
Google Scholar
PubMed
Search for other papers by Takashi Akamizu in
Google Scholar
PubMed
Papillary thyroid carcinoma (PTC) with marked cystic formation (CPTC) is not a subtype of PTC, and its clinical characteristics have not been fully investigated. This study aimed to clarify the clinical and pathological characteristics of CPTC and propose important indicators for its clinical management. Thirty-three CPTC nodules with cystic areas occupying >50% of their volume were examined. Two matched controls (MCs) were prepared, one with tumor diameter matched for whole tumor diameter (WTD) of CPTCs and the other with tumor diameter matched for solid area diameter (SAD) of CPTCs. The mean age of patients with CPTC was 55.2 years significantly older than that in SAD-MCs. Of the CPTCs, 69.7% were classified as highly suspicious by ultrasonography, and the prevalence was lower than that in WTD-MCs (88.9%) and SAD-MCs (91.5%). Total thyroidectomy was performed in 69.7% of CPTC cases, which was significantly less frequent than that in WDT-MCs (91.7%) and similar to that in SAD-MCs (76.1%). Histologically, CPTCs exhibited two characteristic findings: invasion from the solid area into the surrounding normal thyroid tissue and granulation tissue around the cystic wall. The frequencies of the cases with pathological lateral node metastasis, extrathyroidal extension, and Ki-67 labeling index ≥5% in CPTCs were significantly lower than those in WTD-MCs and relatively similar to those in SAD-MCs. In the surgical strategy and prognosis of CPTC, the evaluation of tumor size should be based on SAD rather than on WTD. We advocate measuring not only WTD but also SAD in CPTC.
Search for other papers by M Cherenko in
Google Scholar
PubMed
Search for other papers by N M Appelman-Dijkstra in
Google Scholar
PubMed
Search for other papers by A L Priego Zurita in
Google Scholar
PubMed
Search for other papers by N R Biermasz in
Google Scholar
PubMed
Search for other papers by O M Dekkers in
Google Scholar
PubMed
Search for other papers by F A Klok in
Google Scholar
PubMed
Search for other papers by N Reisch in
Google Scholar
PubMed
Search for other papers by A Aulinas in
Google Scholar
PubMed
Search for other papers by B Biagetti in
Google Scholar
PubMed
Search for other papers by S Cannavo in
Google Scholar
PubMed
Search for other papers by L Canu in
Google Scholar
PubMed
Search for other papers by M Detomas in
Google Scholar
PubMed
Search for other papers by F Devuyst in
Google Scholar
PubMed
Search for other papers by H Falhammar in
Google Scholar
PubMed
Search for other papers by R A Feelders in
Google Scholar
PubMed
Search for other papers by F Ferrau in
Google Scholar
PubMed
Search for other papers by F Gatto in
Google Scholar
PubMed
Search for other papers by C Grasselli in
Google Scholar
PubMed
Search for other papers by P van Houten in
Google Scholar
PubMed
Search for other papers by C Hoybye in
Google Scholar
PubMed
Search for other papers by A M Isidori in
Google Scholar
PubMed
Search for other papers by A Kyrilli in
Google Scholar
PubMed
Search for other papers by P Loli in
Google Scholar
PubMed
Search for other papers by D Maiter in
Google Scholar
PubMed
Search for other papers by E Nowak in
Google Scholar
PubMed
Search for other papers by R Pivonello in
Google Scholar
PubMed
Search for other papers by O Ragnarsson in
Google Scholar
PubMed
Search for other papers by R V Steenaard in
Google Scholar
PubMed
Search for other papers by N Unger in
Google Scholar
PubMed
Search for other papers by A van de Ven in
Google Scholar
PubMed
Search for other papers by S M Webb in
Google Scholar
PubMed
Search for other papers by D Yeste in
Google Scholar
PubMed
University of Glasgow, Office for Rare Conditions, Glasgow, UK
University of Glasgow, Developmental Endocrinology Research Group, Royal Hospital for Children, Glasgow, UK
Search for other papers by S F Ahmed in
Google Scholar
PubMed
Search for other papers by A M Pereira in
Google Scholar
PubMed
Background
Patients with Cushing syndrome (CS) are at increased risk of venous thromboembolism (VTE).
Objective
The aim was to evaluate the current management of new cases of CS with a focus on VTE and thromboprophylaxis.
Design and methods
A survey was conducted within those that report in the electronic reporting tool (e-REC) of the European Registries for Rare Endocrine Conditions (EuRRECa) and the involved main thematic groups (MTG’s) of the European Reference Networks for Rare Endocrine Disorders (Endo-ERN) on new patients with CS from January 2021 to July 2022.
Results
Of 222 patients (mean age 44 years, 165 females), 141 patients had Cushing disease (64%), 69 adrenal CS (31%), and 12 patients with ectopic CS (5.4%). The mean follow-up period post-CS diagnosis was 15 months (range 3–30). Cortisol-lowering medications were initiated in 38% of patients. One hundred fifty-four patients (69%) received thromboprophylaxis (including patients on chronic anticoagulant treatment), of which low-molecular-weight heparins were used in 96% of cases. VTE was reported in six patients (2.7%), of which one was fatal: two long before CS diagnosis, two between diagnosis and surgery, and two postoperatively. Three patients were using thromboprophylaxis at time of the VTE diagnosis. The incidence rate of VTE in patients after Cushing syndrome diagnosis in our study cohort was 14.6 (95% CI 5.5; 38.6) per 1000 person-years.
Conclusion
Thirty percent of patients with CS did not receive preoperative thromboprophylaxis during their active disease stage, and half of the VTE cases even occurred during this stage despite thromboprophylaxis. Prospective trials to establish the optimal thromboprophylaxis strategy in CS patients are highly needed.
Significance statement
The incidence rate of venous thromboembolism in our study cohort was 14.6 (95% CI 5.5; 38.6) per 1000 person-years. Notably, this survey showed that there is great heterogeneity regarding time of initiation and duration of thromboprophylaxis in expert centers throughout Europe.
Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK
Department of Endocrinology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
School of Nursing and Midwifery, Institute of Clinical Sciences, University of Birmingham, UK
Search for other papers by Sherwin Criseno in
Google Scholar
PubMed
Department of Endocrinology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
Search for other papers by Helena Gleeson in
Google Scholar
PubMed
Search for other papers by Andrew A Toogood in
Google Scholar
PubMed
Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK
Department of Endocrinology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
Search for other papers by Neil Gittoes in
Google Scholar
PubMed
Search for other papers by Anne Topping in
Google Scholar
PubMed
Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK
Department of Endocrinology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
Search for other papers by Niki Karavitaki in
Google Scholar
PubMed
Objective
We conducted a survey of UK endocrine clinicians between June 2022 and August 2022 to understand current practices regarding GH treatment discontinuation in adults with growth hormone deficiency.
Design and methods
Using Survey Monkey®, a web-based multiple-choice questionnaire was disseminated to the UK Society for Endocrinology membership. It consisted of 15 questions on demographics, number of patients receiving GH and current practice on GH treatment discontinuation.
Results
In total, 102 endocrine clinicians completed the survey. Of these, 65 respondents (33 endocrinologists and 32 specialist nurses) indicated active involvement in managing patients with growth hormone deficiency. In total, 27.7% of clinicians were routinely offering a trial of GH discontinuation to adults receiving long-term GH therapy. Only 6% had a clinical guideline to direct such practice. In total, 29.2% stated that GH discontinuation should be routinely offered as an option to patients on long-term treatment, whilst 60% were not clearly in favour or against this approach but stated that it should probably be considered, and 9.2% were against. During the GH withdrawal period, most clinicians monitor signs and symptoms (75.4%), measure IGF-1 (84.6%), and complete a quality-of-life assessment (89.2%).
Conclusion
The practice of offering a trial of GH discontinuation in growth hormone deficiency adults on long-term GH therapy is highly variable, reflecting the lack of high-quality evidence. Around a quarter of clinicians offer GH withdrawal for a number of reasons, but only a few have a local clinical guidance. A further 60% of clinicians stated they would probably consider such an approach. Methodologically sound studies underpinning the development of safe and cost-effective guidance are needed.
Significance statement
In this UK survey of endocrine clinicians managing adults with growth hormone deficiency on long-term GH therapy, we explored for the first-time current practice and views on offering GH treatment discontinuation. In total, 27.7% of clinicians were routinely offering this option for a variety of reasons. Only 6% have local clinical guideline available to direct their practice on this. The majority of clinicians (60%), were not clearly in favour or against this approach but indicated it should probably be considered. In the absence of robust evidence on consequences of GH withdrawal, clinicians proposed monitoring of various clinical, biochemical and quality-of-life parameters during the period of discontinuation. Methodologically sound studies that will underpin the development of a safe, cost-effective guidance are needed.
Search for other papers by Xiaonan Guo in
Google Scholar
PubMed
Search for other papers by Wenjing Hu in
Google Scholar
PubMed
Search for other papers by Xiaorui Lyu in
Google Scholar
PubMed
Search for other papers by Hanyuan Xu in
Google Scholar
PubMed
Search for other papers by Huijuan Zhu in
Google Scholar
PubMed
Search for other papers by Hui Pan in
Google Scholar
PubMed
Search for other papers by Linjie Wang in
Google Scholar
PubMed
Search for other papers by Hongbo Yang in
Google Scholar
PubMed
Search for other papers by Fengying Gong in
Google Scholar
PubMed
Objective
Patients with growth hormone deficiency (GHD) with inadequate growth hormone levels are often correlated with nonalcoholic fatty liver disease (NAFLD). However, the potential mechanism of how GHD influences liver function remains obscure. In the present study, we aim to perform hepatic metabolomics in Lewis dwarf rats, which were the standard congenital isolated GH-deficient rat, to evaluate the characterizations of hepatic metabolic profiles and explore their relations with liver functions.
Methods
Lewis dwarf homozygous (dw/dw) rats at 37 weeks (five females and five males), and Lewis dwarf heterozygous (dw/+) rats at 37 weeks (five females and five males) were analyzed in our study. Body lengths and weights, liver weights, serum alanine transaminase (ALT), and serum aspartate transaminase (AST) were measured. ELISA and RT-qPCR were used to assess IGF-1 levels in serum and liver, respectively. The non-targeted metabolomics was performed in the livers of dw/+ and dw/dw rats. Differential metabolites were selected according to the coefficient of variation (CV), variable importance in the projection (VIP) > 1, and P < 0.05. Hierarchical clustering of differential metabolites was conducted, and the KEGG database was used for metabolic pathway analysis.
Results
The body weights, body lengths, liver weights, and IGF-1 levels in the serum and liver of dw/dw rats were significantly decreased compared with dw/+ rats. Dw/dw rats exhibited more obvious hepatic steatosis accompanied by higher serum ALT and AST levels. Hepatic metabolomics showed that a total of 88 differential metabolites in positive ion mode, and 51 metabolites in negative ion mode were identified. Among them, lysophosphatidylcholine (LPC) 16:2, LPC 18:3, LPC 22:6, fatty acid esters of hydroxy fatty acids (FAHFA)18:1 were significantly decreased, while palmitoyl acid, dehydrocholic acid, and 7-ketolithocholic acid were significantly increased in dw/dw rats compared with dw/+ rats. These seven differential metabolites were significantly associated with phenotypes of rats. Finally, KEGG pathway analysis showed that the arginine and proline metabolism pathway and bile secretion pathway were mainly clustered.
Conclusion
Lewis dw/dw rats with congenital isolated growth hormone deficiency (IGHD) showed liver steatosis and abnormal liver function, which could be potentially associated with the distinctive hepatic metabolic profiles.
Search for other papers by Svjatoslavs Kistkins in
Google Scholar
PubMed
Search for other papers by Othmar Moser in
Google Scholar
PubMed
Search for other papers by Vitālijs Ankudovičs in
Google Scholar
PubMed
Search for other papers by Dmitrijs Blizņuks in
Google Scholar
PubMed
Search for other papers by Timurs Mihailovs in
Google Scholar
PubMed
Search for other papers by Sergejs Lobanovs in
Google Scholar
PubMed
Search for other papers by Harald Sourij in
Google Scholar
PubMed
Search for other papers by Andreas F H Pfeiffer in
Google Scholar
PubMed
Faculty of Medicine, University of Latvia, Riga, Latvia
Search for other papers by Valdis Pīrāgs in
Google Scholar
PubMed
The increasing prevalence of ‘diabesity’, a combination of type 2 diabetes and obesity, poses a significant global health challenge. Unhealthy lifestyle factors, including poor diet, sedentary behaviour, and high stress levels, combined with genetic and epigenetic factors, contribute to the diabesity epidemic. Diabesity leads to various significant complications such as cardiovascular diseases, stroke, and certain cancers. Incretin-based therapies, such as GLP-1 receptor agonists and dual hormone therapies, have shown promising results in improving glycaemic control and inducing weight loss. However, these therapies also come with certain disadvantages, including potential withdrawal effects. This review aims to provide insights into the cross-interactions of insulin, glucagon, and GLP-1, revealing the complex hormonal dynamics during fasting and postprandial states, impacting glucose homeostasis, energy expenditure, and other metabolic functions. Understanding these hormonal interactions may offer novel hypotheses in the development of ‘anti-diabesity’ treatment strategies. The article also explores the question of the antagonism of insulin and glucagon, providing insights into the potential synergy and hormonal overlaps between these hormones.
Department of Clinical Research, University of Southern Denmark, Odense, Denmark
Search for other papers by Maria Houborg Petersen in
Google Scholar
PubMed
Search for other papers by Jacob Volmer Stidsen in
Google Scholar
PubMed
Department of Sports Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark
Search for other papers by Martin Eisemann de Almeida in
Google Scholar
PubMed
Search for other papers by Emil Kleis Wentorf in
Google Scholar
PubMed
Search for other papers by Kurt Jensen in
Google Scholar
PubMed
Search for other papers by Niels Ørtenblad in
Google Scholar
PubMed
Department of Clinical Research, University of Southern Denmark, Odense, Denmark
Search for other papers by Kurt Højlund in
Google Scholar
PubMed
Aim
We investigated whether a high-intensity interval training (HIIT) protocol could restore beta-cell function in type 2 diabetes compared with sedentary obese and lean individuals.
Materials and methods
In patients with type 2 diabetes, and age-matched, glucose-tolerant obese and lean controls, we examined the effect of 8 weeks of supervised HIIT combining rowing and cycling on the acute (first-phase) and second-phase insulin responses, beta-cell function adjusted for insulin sensitivity (disposition index), and serum free fatty acid (FFA) levels using the Botnia clamp (1-h IVGTT followed by 3-h hyperinsulinemic–euglycemic clamp).
Results
At baseline, patients with type 2 diabetes had reduced insulin sensitivity (~40%), acute insulin secretion (~13-fold), and disposition index (>35-fold), whereas insulin-suppressed serum FFA was higher (⁓2.5-fold) compared with controls (all P < 0.05). The HIIT protocol increased insulin sensitivity in all groups (all P < 0.01). In patients with type 2 diabetes, this was accompanied by a large (>200%) but variable improvement in the disposition index (P < 0.05). Whereas insulin sensitivity improved to the degree seen in controls at baseline, the disposition index remained markedly lower in patients with type 2 diabetes after HIIT (all P < 0.001). In controls, HIIT increased the disposition index by ~20–30% (all P < 0.05). In all groups, the second-phase insulin responses and insulin-suppressed FFA levels were reduced in response to HIIT (all P < 0.05). No group differences were seen in these HIIT-induced responses.
Conclusion
HIIT combining rowing and cycling induced a large but variable increase in beta-cell function adjusted for insulin sensitivity in type 2 diabetes, but the disposition index remained severely impaired compared to controls, suggesting that this defect is less reversible in response to exercise training than insulin resistance.
Trial registration
ClinicalTrials.gov (NCT03500016).
Search for other papers by Huiyuan Zhai in
Google Scholar
PubMed
Search for other papers by Dongxu Wang in
Google Scholar
PubMed
Search for other papers by Yong Wang in
Google Scholar
PubMed
Search for other papers by Hongwei Gu in
Google Scholar
PubMed
Search for other papers by Juan Jv in
Google Scholar
PubMed
Search for other papers by Liangliang Yuan in
Google Scholar
PubMed
Search for other papers by Chao Wang in
Google Scholar
PubMed
Search for other papers by Leiyao Chen in
Google Scholar
PubMed
Chronic inflammation induced by obesity plays a crucial role in the pathogenesis of insulin resistance. The infiltration of macrophages into adipose tissues contributes to adipose tissue inflammation and insulin resistance. Kaempferol, a flavonoid present in various vegetables and fruits, has been shown to possess remarkable anti-inflammatory properties. In this study, we used leptin receptor-deficient obese mice (db/db) as an insulin-resistant model and investigated the effects of kaempferol treatment on obesity-induced insulin resistance. Our findings revealed that the administration of kaempferol (50 mg/kg/day, for 6 weeks) significantly reduced body weight, fat mass, and adipocyte size. Moreover, it effectively ameliorated abnormal glucose tolerance and insulin resistance in db/db mice. In the adipose tissue of obese mice treated with kaempferol, we observed a reduction in macrophage infiltration and a downregulation of mRNA expression of M1 marker genes TNF-α and IL-1β, accompanied by an upregulation of Arg1 and IL-10 mRNA expression. Additionally, kaempferol treatment significantly inhibited the STING/NLRP3 signaling pathway in adipose tissue. In vitro experiments, we further discovered that kaempferol treatment suppressed LPS-induced inflammation through the activation of NLRP3/caspase 1 signaling in RAW 264.7 macrophages. Our results suggest that kaempferol may effectively alleviate inflammation and insulin resistance in the adipose tissue of db/db mice by modulating the STING/NLRP3 signaling pathway.
Search for other papers by Xiao-Shan Huang in
Google Scholar
PubMed
Search for other papers by Ning Dai in
Google Scholar
PubMed
Search for other papers by Jian-Xia Xu in
Google Scholar
PubMed
Search for other papers by Jun-Yi Xiang in
Google Scholar
PubMed
Search for other papers by Xiao-Zhong Zheng in
Google Scholar
PubMed
Search for other papers by Tian-Yu Ke in
Google Scholar
PubMed
Search for other papers by Lin-Ying Ma in
Google Scholar
PubMed
Search for other papers by Qi-Hao Shi in
Google Scholar
PubMed
Search for other papers by Shu-Feng Fan in
Google Scholar
PubMed
Objective
Hashimoto’s thyroiditis is an inflammatory disease, and research suggests that a low-carbohydrate diet may have potential anti-inflammatory effects. This study aims to utilize Dixon-T2-weighted imaging (WI) sequence for a semi-quantitative assessment of the impact of a low-carbohydrate diet on the degree of thyroid inflammation in patients with Hashimoto’s thyroiditis.
Methods
Forty patients with Hashimoto’s thyroiditis were recruited for this study and randomly divided into two groups: one with a normal diet and the other with a low-carbohydrate diet. Antibodies against thyroid peroxidase (TPOAb) and thyroglobulin (TgAb) were measured for all participants. Additionally, thyroid water content was semi-quantitatively measured using Dixon-T2WI. The same tests and measurements were repeated for all participants after 6 months.
Results
After 6 months of a low-carbohydrate diet, patients with Hashimoto’s thyroiditis showed a significant reduction in thyroid water content (94.84 ± 1.57% vs 93.07 ± 2.05%, P < 0.05). Concurrently, a decrease was observed in levels of TPOAb and TgAb (TPOAb: 211.30 (92.63–614.62) vs 89.45 (15.9–215.67); TgAb: 17.05 (1.47–81.64) vs 4.1 (0.51–19.42), P < 0.05). In contrast, there were no significant differences in thyroid water content or TPOAb and TgAb levels for patients with Hashimoto’s thyroiditis following a normal diet after 6 months (P < 0.05).
Conclusion
Dixon-T2WI can quantitatively assess the degree of thyroid inflammation in patients with Hashimoto’s thyroiditis. Following a low-carbohydrate diet intervention, there is a significant reduction in thyroid water content and a decrease in levels of TPOAb and TgAb. These results suggest that a low-carbohydrate diet may help alleviate inflammation in patients with Hashimoto’s thyroiditis.
Search for other papers by Lu Yang in
Google Scholar
PubMed
Search for other papers by Xingguo Jing in
Google Scholar
PubMed
Search for other papers by Hua Pang in
Google Scholar
PubMed
Search for other papers by Lili Guan in
Google Scholar
PubMed
Search for other papers by Mengdan Li in
Google Scholar
PubMed
In this review, we discuss the definition, prevalence, and etiology of sporadic multiglandular disease (MGD), with an emphasis on its preoperative and intraoperative predictors. Primary hyperparathyroidism (PHPT) is the third-most common endocrine disorder, and multiglandular parathyroid disease (MGD) is a cause of PHPT. Hereditary MGD can be definitively diagnosed with detailed family history and genetic testing, whereas sporadic MGD presents a greater challenge in clinical practice, and parathyroidectomy for MGD is associated with a higher risk of surgical failure than single gland disease (SGD). Therefore, it is crucial to be able to predict the presence of sporadic MGD in a timely manner, either preoperatively or intraoperatively. Various predictive methods cannot accurately identify all cases of sporadic MGD, but they can greatly optimize the management of MGD diagnosis and treatment and optimize the cure rate. Future research will urge us to investigate more integrative predictive models as well as increase our understanding of MGD pathogenesis.