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INTRODUCTION: The global incidence of thyroid cancer (TC) has increased in the last decades. While improvements in diagnosis may contribute, overdiagnosis is also a possibility. This review focuses on the epidemiology, risk factors, and immune microenvironment associated with differentiated TC (DTC). AREAS COVERED: A search was conducted in Scielo, Scopus, and EMBASE databases, involving 72 articles. TC is the most common endocrine neoplasm, with DTC form being predominant. Its incidence has globally risen, particularly among women aged over 45. Endogenous risk factors for DTC include genetic disorders, race, age, female gender, obesity, and type 2 diabetes mellitus. Environmental risks involve ionizing radiation, whether through therapeutic treatment or environmental contamination from nuclear accidents, iodine deficiency, endocrine disruptors, residence in volcanic areas, environmental pollution, and stress. The use of anti-obesity medications remains controversial. The tumor's immune microenvironment is the histological space where tumor cells interact with host cells, crucial for understanding aggressiveness. Immunotherapy emerges as a promising intervention. EXPERT OPINION: Recent advances in DTC management offer transformative potential, requiring collaborative efforts for implementation. Emerging areas like precision medicine, molecular profiling, and immunotherapy present exciting prospects for future exploration, shaping the next era of diagnostic and therapeutic strategies in thyroid cancer research.
The global incidence of thyroid cancer (TC) has significantly increased, attributed partly to improved diagnosis and potentially to overdiagnosis. This review focuses on the epidemiology, risk factors, and immune microenvironment associated with differentiated TC (DTC). DTC is the most common endocrine neoplasm, and predominantly affects women over 45 years old. Endogenous risk factors include genetic disorders, race, age, female gender, obesity, and type 2 diabetes mellitus (T2DM). Environmental risks encompass ionizing radiation, iodine deficiency, endocrine disruptors, volcanic residence, pollution, and stress. The use of glucagon-like peptide 1 agonists remains controversial. The tumor's immune microenvironment is crucial for understanding aggressiveness, with immunotherapy showing promise. Understanding both macro and microenvironmental factors is crucial for devising effective prevention and treatment strategies for DTC.
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INTRODUCTION: Neuroendocrine tumors [NETs] exhibit a wide range of clinical presentations, including the production of various hormones. Calcitonin, a sensitive marker for medullary thyroid cancer [MTC], is nonspecific and may be elevated in extra-thyroidal NETs. CASE REPORT: We present the case of a 64-year-old female patient who underwent total thyroidectomy due to a nodule in the isthmus, with a fine-needle aspiration biopsy indicating follicular neoplasia. Pathological examination revealed macro- and micro-nodular thyroid hyperplasia, along with a parathyroid adenoma. During postoperative follow-up, a progressive elevation of calcitonin was observed, reaching 64.2 pg/ml, while carcinoembryonic antigen levels remained normal. Since no MTC foci were found upon reviewing the thyroidectomy specimen, an investigation into the origin of the elevated calcitonin was initiated. Serum chromogranin A and specific neuronal enolase levels were within normal ranges. Tc-99m HYNIC-TOC scintigraphy yielded negative results. Additionally, an upper gastrointestinal endoscopy revealed a submucosal lesion in the second portion of the duodenum, with a biopsy confirming a grade 1 NET. The patient underwent Whipple surgery and hepatic metastasectomy. Postoperatively, a decrease in baseline serum calcitonin levels was observed. Seven years after surgery, she continues specialized monitoring with no biochemical or imaging evidence of disease. CONCLUSION: Serum calcitonin contributes to the diagnosis and monitoring of anterior intestine NETs.
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Hepatocrinology explores the intricate relationship between liver function and the endocrine system. Chronic liver diseases such as liver cirrhosis can cause endocrine disorders due to toxin accumulation and protein synthesis disruption. Despite its importance, assessing endocrine issues in cirrhotic patients is frequently neglected. This article provides a comprehensive review of the epidemiology, pathophysiology, diagnosis, and treatment of endocrine disturbances in liver cirrhosis. The review was conducted using the PubMed/Medline, EMBASE, and Scielo databases, encompassing 172 articles. Liver cirrhosis is associated with endocrine disturbances, including diabetes, hypoglycemia, sarcopenia, thyroid dysfunction, hypogonadotropic hypogonadism, bone disease, adrenal insufficiency, growth hormone dysfunction, and secondary hyperaldosteronism. The optimal tools for diagnosing diabetes and detecting hypoglycemia are the oral glucose tolerance test and continuous glucose monitoring system, respectively. Sarcopenia can be assessed through imaging and functional tests, while other endocrine disorders are evaluated using hormonal assays and imaging studies. Treatment options include metformin, glucagon-like peptide-1 analogs, sodium-glucose co-transporter-2 inhibitors, and insulin, which are effective and safe for diabetes control. Established standards are followed for managing hypoglycemia, and hormone replacement therapy is often necessary for other endocrine dysfunctions. Liver transplantation can address some of these problems.
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Diabetes Mellitus , Hipoglicemia , Sarcopenia , Humanos , Automonitorização da Glicemia , Sarcopenia/diagnóstico , Sarcopenia/etiologia , Sarcopenia/terapia , Glicemia/metabolismo , Cirrose Hepática/complicações , Cirrose Hepática/diagnóstico , Cirrose Hepática/terapia , Sistema Endócrino/metabolismo , Diabetes Mellitus/epidemiologia , Insulina/uso terapêutico , Hipoglicemia/complicaçõesRESUMO
BACKGROUND: Obesity is a multifactorial chronic disease with a high, increasing worldwide prevalence. Genetic causes account for 7% of the cases in children with extreme obesity. DATA SOURCES: This narrative review was conducted by searching for papers published in the PubMed/MEDLINE, Embase and SciELO databases and included 161 articles. The search used the following search terms: "obesity", "obesity and genetics", "leptin", "Prader-Willi syndrome", and "melanocortins". The types of studies included were systematic reviews, clinical trials, prospective cohort studies, cross-sectional and prospective studies, narrative reviews, and case reports. RESULTS: The leptin-melanocortin pathway is primarily responsible for the regulation of appetite and body weight. However, several important aspects of the pathophysiology of obesity remain unknown. Genetic causes of obesity can be grouped into syndromic, monogenic, and polygenic causes and should be assessed in children with extreme obesity before the age of 5 years, hyperphagia, or a family history of extreme obesity. A microarray study, an analysis of the melanocortin type 4 receptor gene mutations and leptin levels should be performed for this purpose. There are three therapeutic levels: lifestyle modifications, pharmacological treatment, and bariatric surgery. CONCLUSIONS: Genetic study technologies are in constant development; however, we are still far from having a personalized approach to genetic causes of obesity. A significant proportion of the affected individuals are associated with genetic causes; however, there are still barriers to its approach, as it continues to be underdiagnosed. Video Abstract (MP4 1041807 KB).