A group of cancers with very different phenotypes make up thyroid carcinoma. The identification of genetic, epigenetic and non-genetic factors that contribute to the heterogeneity of these cancers has been advancing as a result of recent advancements in biological technologies. In this review article, we talk about new findings that are making it easier to find new therapeutic targets and expanding our knowledge of the biology of thyroid cancer. The underlying biology and phenotypic characteristics of various thyroid cancer subtypes are examined. We focus on genetic and epigenetic factors, characteristics of cancer stemness and tumor microenvironments in our discussion of recent findings regarding the heterogeneity of thyroid cancer and the crucial mechanisms that contribute to the heterogeneity.
There are various definitions of the term in the literature: Thyroid Carcinoma Occult". According to the most recent online version of the Merriam- Webster dictionary, "occult carcinoma" means "not manifest or detectable by clinical methods alone" as well as "not present in macroscopic amounts." The phrase "occult primary malignancy" is defined as "unknown primary malignancy that is symptomless, which first manifests itself as metastases or secondary paraneoplastic phenomena" in the 2002 edition of the McGraw-Hill Concise Dictionary of Modern Medicine.
Recently reported that 3-T1AM metabolism produces inactive 3-iodothyroacetic acid. In this way, we demonstrated that 3-T1AM's rapid cardiac and thermogenic effects depend on the ethylamine side chain. No iodinated T0AM is produced when 3-T1AM is used as a substrate by Dio1 and Dio3 enzymes, as evidenced by in vitro data. As a result, we were curious about the possibility that deiodination might also function as an inactivation mechanism for 3-T1AM. Due to the fact that T0AM did not cause bradycardia or anapyrexia in mice upon single or repeated administration, our in vivo experiments demonstrate that it does not possess the metabolic, cardiovascular, or thermoregulatory properties of 3-T1AM. Additionally, T0AM did not affect TH homeostasis because it did not affect TH-regulated genes or serum or liver TH concentrations. Previous research has demonstrated that T3 regulates hepatic trace element metabolism (such as Se). By administering T0AM and 3-T1AM, we set out to see if these effects might be at least partially mediated by TAMs. According to our investigations, the major trace element storage, metabolism and transport proteins as well as Se status in serum, liver and kidneys were unaffected by T0AM's repeated administration. Therefore, in our paradigm, T0AM exhibits very little biological activity in comparison to reports of 3-T1AM, which is physiologically more active.
Thyronamine (T0AM) and 3-iodothyronamine (T1AM) are novel endogenous signaling molecules that appear to counteract the actions of traditional thyroid hormone (T3) despite sharing a lot of structural similarities with thyroid hormones. Decarboxylation and some or all deiodination would be required for their proposed biosynthesis from thyroid hormones. Iodine is depleted from substrates by deiodinases (Dio1, Dio2 and Dio3). We investigated whether deiodinases convert thyronamines because thyronamine biosynthesis relies on deiodinases' capacity to accept thyronamines as substrates. Preparations of isozyme-specific deiodinase were incubated with thyronamines. A brand-new approach made use of tandem mass spectrometry (LC-MS/MS) and liquid chromatography was used to analyze the deiodination products.
Introduction: Autoimmune Thyroid diseases are multi-factorial diseases with a genetic susceptibility and environmental factors. A potential role of the protein tyrosine phosphatase non-receptor type 22(PTPN22) gene, the interferon induced helicase domain 1 (IFIH1) gene, the Thyroid-stimulating hormone receptor (TSH-R) gene polymorphisms on autoimmune Thyroid diseases(AITDs) in children has not been established equivocally yet.
The underlying reason for reaction diseases is that the loss of immune tolerance to tissue-specific antigenic peptides that results in immunologic response directed against one's own body's cells. Still not fully understood, complex immune mechanisms together with the dysfunction of the immune system may be concerned within the autoimmune diseases pathological process. Among the foremost common chronic autoimmune endocrine disorders in kids, there are autoimmune thyroid diseases (AITDs) that include Graves' disease (GD) and Hashimoto's thyroiditis (HT) further as kind sort diabetes (T1D). In kids with autoimmune thyroiditis immune reactions are directed against the cells of the thyroid. In GD the thyrotrophin receptor (TSH-R) is activated with antibodies inflicting the over activity of the thyroid gland, whereas in HT body substance and cell-mediated thyroid injury end up in the destruction of thyroid cells and hypothyroidism as a consequence. In diabetic patients, an inappropriate immune response ends up in auto reactive T-cell infiltration and production of tissue-specific autoantibodies that cause the destruction and dysfunction of the hypoglycemic agent secreting pancreatic beta cells and hypoglycemic agent deficiency. The mechanisms resulting in the development of those diseases remain unknown, but various information indicates that except for the environmental factors there's a powerful genetic susceptibility to the response diseases. The connectedness of genetic factors is obvious from the agglomeration of AITDs or T1D among families, especially monozygotic and dizygotic twins. Several genes could be concerned within the modulation of the system and a few of them were recently found to influence response endocrine disorders development. Moreover, recent studies have incontestable that some genetic risk factors for pathology square measure shared between diseases, causative to the event of quite one autoimmune disease. Current publications showed an association between response diseases and body 10p15 region for IL2RA (interleukin 2 receptor-α), more than 2q33 region for CTLA-4 (cytotoxic T-lymphocyte antigen-4), and body 2q24 region for IFIH1 (interferon elicited with helicase C domain 1). The foremost frequent variety of human ordering variation is single ester polymorphisms (SNPs) providing powerful tools for a range of medical genetic studies. though bound polymorphic variants of genes cryptography IL2AR, CTLA-4, or IFIH1 are reportable to implicate T1D and ATDs development in adults, there square measure solely few studies that specialize in kids. Interleukin 2 (IL2) could be a lymphocyte protein taking part in a crucial role in modulation of immune physiological condition as a necessary self-tolerance regulator. Its action is mediated by a quaternary receptor signal advanced (IL2R) containing α, β, and atypical receptors. The alpha subunit of the IL2 receptor, IL2Rα (also called CD25), encoded by the interleukin 2 receptor α cistron (IL2RA), plays a key role in mediating lymphokine 2 immunoregulatory operate. The expression of IL2RA has been represented at high levels on the surface of the regulative T cells (Tregs), a population of T cells with a capability to inhibit auto reactive T cells. Additional studies indicated IL2RA's essential role in sensitizing lymph cells for elicited death that's crucial for his or her operate as a suppressor for T cell immune responses to auto-, alloantigens, further as tumor antigens and antigens account from pathogens. SNPs of genes influencing Treg to operate, like IL2RA, might cause associate degree accumulated risk of disease.
Aim: To estimate the association of polymorphisms of protein tyrosine phosphatase non-receptor type 22 genes, the interferon induced helicase domain 1 gene, Thyroid-stimulating hormone receptor gene with the predisposition to Graves’ disease (GD) and Hashimoto’s Thyroiditis (HT) in children.
Methods: The study was performed in 142 patients with GD, 57 with HT and 160 healthy volunteers. The three single nucleotide polymorphisms (SNPs): rs2476601 - PTPN22 in the protein tyrosine phosphatase non-receptor type 22 gene, rs1990760 - IFIH1 in the interferon induced helicase domain 1 gene, rs179247 - TSHR in the Thyroid-stimulating hormone receptor gene were genotyped by Taq-Man SNP genotyping assay using the real-time PCR. Furthermore, the interaction between rs1990760, rs2476601, rs179247 polymorphisms and the status of thyroglobulin antibody (TgAb), Thyroid peroxidase antibody (TPOAb) and TSH receptor antibody (TRAb) were analyzed.
rs2476601: Our study revealed that rs2476601-A alleles were more frequent (18% in men and 20% in women) in GD patients in comparison to healthy subjects (11% in men and 10% in women). P-value=0.009 with OR=2.13 and 95% confidence interval for OR: 1.2–4.0, what means that risk for development of GD is over two times higher for A allele in comparison to G allele. Moreover rs2476601 A alleles were more frequent (25% in men and 21% in women) in HT patients in comparison to healthy subjects (11% in men and 10% in women). P-value=0.008 with OR=2.48 and 95% confidence interval for OR: 1.3–5.0, what means that risk for development of HT is two and a half times higher for A allele in comparison to G allele.
rs1990760: Rs1990760 T alleles were more frequent in GD male patients in comparison to healthy males (69% vs. 42%). P-value=0.003 with OR=3.00 and 95% confidence interval for OR: 1.5–6.2, what means that risk for development of GD is three times higher for T allele in comparison to C allele, when considering male group. In case of HT patients rs1990760 T alleles were also more frequent in males compared to healthy subjects (65% vs. 42%). P-value=0.086 with OR=2.47 and 95% confidence interval for OR: 0.9–7.5, what means that risk for development of HT is nearly two and a half times higher for T allele in comparison to C allele. Results for female group were non-significant from the statistical point of view, hence are not discussed here.
rs179247: Our study revealed that rs179247 A alleles were more frequent (47% both in men and women) in GD patients in comparison to healthy subjects (37% in men and 38% in women). P-value=0.039 with OR=1.51 and 95% confidence interval for OR: 1.0–2.3, what means that risk for development of GD is over two times higher for A allele in comparison to G allele.
Conclusions: rs2476601: A/G polymorphism in protein tyrosine phosphatase non-receptor type 22 gene could contribute to development of AITDs in children and an allele is the main risk factor. rs1990760: C/T polymorphism in the interferon induced helicase domain 1 gene could contribute to development of AITDs in children and T allele is the main risk factor. rs179247: A/G polymorphism in Thyroid-stimulating hormone receptor gene could contribute to development of AITDs in children and an allele is the main risk factor.
Background: Massive substernal goiters are frequently noted in developing countries, but are not as frequently treated in developed countries. Management of massive Thyroid goiters is frequently referred to tertiary university hospitals. In the following study, we present our recent community hospital based experience managing such cases using a trans-cervical approach.
Objective: To assess a community hospital based experience managing massive substernal Thyroid goiters. To assess our clinical outcomes using a trans-cervical or a collar neck incision for accessing and surgically removing such massive tumors. Setting: Southern California Permanente Medical Group, community hospital setting.
Method: Retrospective review over the past 6 years (2006-2011) of all cases of massive substernal Thyroid goiters surgically treated. Chart review was performed and identified were age, sex, diagnosis, extent of goiter, treatment, disease status, survival (months), size of Thyroid (grams), complications (hypocalcemia, vocal cord injury) and estimated blood lose (ml). A comparison was made between pre- and post-operative function (breathing, speech and swallowing).
We retrospectively reviewed the case notes, imaging records, and operation records of all patients who had undergone thyroidectomy between 2000 and 2003 at the United Christian Hospital in Hong Kong. We defined SSG as either the lower extent of the goiter having transgressed the fourth thoracic vertebra2 or at least 50% of the mass3 residing within the thorax. Large thyroid masses with inferior borders at the thoracic inlet were not included in this study. Patients were investigated with a standard preoperative protocol that included routine thyroid function tests, chest X-ray, and computed tomographic (CT) scans of the neck and thorax. Thyrotoxic patients were rendered euthyroid prior to surgery. The possibility of sternotomy was explained, and informed consent was obtained. Computed tomographic scan delineated the extent of the SSG; the degree and level of tracheal compression or deviation provided by CT scan is imperative to the selection of optimal methods of intubation by the anesthetist. Fibreoptic endoscope guided tracheal intubation was performed when there was evidence of significant tracheal displacement or compression. Lung function tests were performed at the discretion of the anesthetist or pulmonary physician. Flow-volume loop studies were helpful in the diagnosis of extra thoracic airway compression, but they were not critical in the decision to proceed with surgery. Preoperative vocal cord examination was routinely evaluated by flexible laryngoscope and was repeated postoperatively in patients who experienced any degree of voice change. If vocal cord palsy was discovered, out-patient endoscopic monitoring of vocal cord status was carried out regularly as flexible laryngoscopes were available.
After having been anaesthetized, the patients were placed in a supine position with the neck extended and were draped to expose the nipple line so that partial sternotomy could be employed at any time. A collar incision was used, and the strap muscle was transected when necessary to improve accessibility. The thyroid gland was mobilized by capsular dissection, with the superior thyroid vessels controlled individually. Parathyroid glands were either preserved or auto grafted into the sternomastoid muscle if devascularisation was suspected. The middle and inferior thyroid veins were also carefully ligated to avoid bleeding due to avulsion, as they were often distended and obstructed by the SSG. The thoracic component of the SSG was then manually retracted to the cervical region. The recurrent laryngeal nerve was often not identifiable until the SSG was liberated from the thorax. Manubrium resection or median sternotomy was rarely needed. Drainage was often employed to avert seroma formation in the resulting cavity.
Results: 9 cases were identified which met study criteria. The average age at diagnosis was 59.1 yrs. (43-86 yrs.). There were 2 males and 7 females. There were 6 multi-nodular goiters and 3 goiters with papillary Thyroid carcinoma present. With regard to extent of goiter – 4 cases extended under the arch of the aorta, 5 cases extended to the mid-arch, and all compressed the trachea to some extent. All surgically underwent total Thyroidectomy, mediastinal dissection via trans-cervical approach and neck dissections in 3 cases. All patients are alive and cancer free or disease free at 26.3 months. The average size of the gland was 184 grams (100-353 grams). With regard to complications there were 2 cases of vocal cord paralysis, 2 cases of vocal cord paresis and 6 cases requiring long term calcium supplementation. The average blood lose surgically was 167 ml (50-500 ml). All patients had returned to normal breathing, speech and swallowing function post-operatively.
Conclusion: Massive substernal goiters can be surgically removed via a trans-cervical approach, thus avoiding sternotomy. A thoracic surgeon was available at all times to assist with our cases. Our community hospital based series although not large is a good representation of what potential outcomes might be in a non-tertiary setting. All patients improved post-operatively with regarding to breathing, speech and swallowing. A higher complication rate of recurrent laryngeal nerve was noted in cancer cases due to tumor invasion. Long term follow up of our patients is needed to fully confirm these studies findings.
Objective: Hypothyroidism is an endocrine disorder. In hypothyroidism patient has an underactive Thyroid (“hypo-” means “under” or “below normal”). In patients with hypothyroidism, the Thyroid does not make enough Thyroid hormone to keep the body maintain its normal balance. Common causes of hypothyroidism are autoimmune disease, surgical removal of the Thyroid, and radiation treatment. The objective of this literature review is to present the evidence based nursing practice for patients with hypothyroidism.
Methodology: The literature review was done from the period of January to November 2015 from various online databases such as PUBMED, CINAHL and Allied Health Literature. Key words used: ‘Hypothyroidism’, ‘adults’, and ‘Nursing Care’ using Boolean (AND, OR) words. The final reference list consists of 20 relevant articles ranging from 2010 to 2015, which include qualitative and quantitative researches, literature reviews, peer reviews, and index articles.
This CPG adheres to the 2010 AACE Protocol for Standardized Production of Clinical Practice Guidelines published in Endocrine Practice (5). This updated protocol describes a more transparent methodology of rating the clinical evidence and synthesizing recommendation grades. The protocol also stipulates a rigorous multilevel review process. The process was begun by developing an outline for reviewing the principal clinical aspects of hypothyroidism. Computerized and manual searches of the medical literature and various databases, primarily including Medline, were based on specific section titles, thereby avoiding inclusion of unnecessary detail and exclusion of important studies.
AACE, American Association of Clinical Endocrinologists; ATA, American Thyroid Association; CPG, Clinical Practice Guideline; RAI, radioactive iodine; T3, triiodothyronine; T4, thyroxine; TPOAb, anti–thyroid peroxidase antibodies; TRIAC, 3,5,3¢-triiodothyroacetic acid; TSH, thyrotropin; TSHRAb, TSH receptor antibodies.
Compilation of the bibliography was a continual and dynamic process. Once the principal clinical aspects of hypothyroidism were defined, questions were formulated with the intent to then develop recommendations that addressed these questions. The grading of recommendations was based on consensus among the authors. The final document was approved by the American Association of Clinical Endocrinologists (AACE) and American Thyroid Association (ATA), and was officially endorsed by the American Association of Diabetes Educators (AADE), American Association of Endocrine Surgeons (AAES), American Academy of Otolaryngology—Head and Neck Surgery (AAOHNS), American College of Endocrinology (ACE), Italian Association of Clinical Endocrinologists (AME), American Society for Metabolic & Bariatric Surgery (ASMBS), The Endocrine Society of Australia (ESA), International Association of Endocrine Surgeons (IAES), Korean Thyroid Association (KTA), Latin American Thyroid Society (LATS), and Ukranian Association of Endocrine Surgeons (UAES).
Results: The evidence based nursing suggests that nurses should monitor vital signs of patients with hypothyroidism because fluctuations in metabolic rate are exhibited by changes in blood pressure, heart rate, and body temperature. Also, nurses should watch for the reduction in symptoms related to hypothyroidism such as fatigue, constipation, cold intolerance, lethargy, depression, and menstrual irregularities, it demonstrate that patient is getting therapeutic effect from drug. Nursing intervention should also include watching for the symptoms of hyperthyroidism such as nervousness, insomnia, tachycardia, dysrhythmias, heat intolerance, chest pain, and diarrhea as these symptoms may indicate that the drug is at a toxic level. Moreover, evidence based nursing care recommends to monitor T3, T4, and TSH levels as these levels help determine the effectiveness of pharmacotherapy. Monitoring of blood glucose levels, especially in individuals with Diabetes Mellitus is important as hormone can increases metabolic rate, and glucose utilization may be altered. Most importantly, nurses should provide supportive nursing care to cope with symptoms of hypothyroidism such as constipation, cold intolerance, and fatigue until drug has achieved therapeutic effects as it will decrease the client’s anxiety, which will promote healing and compliance. Nursing intervention also includes monitor weight once a week as weight loss is expected because of increased metabolic rate as these changes help determine the effectiveness of drug therapy. Furthermore, nurses should monitor patients for signs of decreased compliance with therapeutic regimen as it may require early intervention and education about the medical regimen and the disease process.
Conclusion: Evaluation of the effectiveness of drug therapy is an important task for nurses in order to confirm that patient goals and expected outcomes have been met. These outcomes include the patient’s Thyroid hormone levels are normal, the patient demonstrates decreased symptoms of hypothyroidism, the patient is free from significant adverse effects from drug therapy. And the patient demonstrates an understanding of the drug’s action by accurately describing drug side effects and precautions.
Anatomically, Thyroid gland (TG) is located anteriorly in the lower neck, covering the distance from the fifth cervical vertebra till to the first thoracic. Its shape is either H or U and divided into two lobes connected with a median isthmus. Sometimes, the isthmus may be missing and only the two lobes form the gland. Their length is approximately 50-60 mm, while the gland weighs 25-30 g. Also, is highly vascularized and innervated by the autonomic nervous system. Parasympathetic fibers come from the vagus nerves, and sympathetic fibers are distributed from the superior, middle and inferior ganglia of the sympathetic trunk. The produced hormones are Triiodothyronine (T3) and Thyroxin (T4), under regulation of thyroid stimulating hormone (TSH) which is produced in pituitary gland and regulated in turn by thyrotrophin releasing hormone (TRH), finally produced in Hypothalamus. Moreover, Thyroid gland secrets the hormone calcitonin which is implicated in homeostasis of blood calcium level. TG is considered to be the cornerstone of entire endocrine system.
In 2012 there were 1.5 million deaths worldwide directly caused by diabetes. It was the eighth leading cause of death among both sexes and the fifth leading cause of death in women in 2012. Blood glucose levels that are higherthan-optimal, even if below the diagnostic threshold for diabetes, are a major source of mortality and morbidity. The diagnostic criterion for diabetes is fasting plasma glucose ≥ 7.0 mmol/L – a diagnostic point selected on the basis of micro-vascular complications such as diabetic retinopathy. The risk of macro-vascular disease, such as heart attack or stroke, however, starts increasing well before this diagnostic point. To better understand the full impact of blood glucose levels on mortality therefore requires a look at mortality related to blood glucose as a risk factor. The total burden of deaths from high blood glucose1 in 2012 has been estimated to amount to 3.7 million. This number includes 1.5 million diabetes deaths, and an additional 2.2 million deaths from cardiovascular diseases, chronic kidney disease, and tuberculosis related to higher-than-optimal blood glucose. Its magnitude highlights that high blood glucose causes a large burden of mortality beyond those deaths directly caused by diabetes. The largest number of deaths resulting from high blood glucose occur in upper-middle income countries (1.5 million) and the lowest number in low-income countries (0.3 million). After the age of 50, middle-income countries have the highest proportion of deaths attributed to high blood glucose, for both men and women.
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