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Volume 28(4); December 2013
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Review Articles
Adrenal gland
The Molecular Pathogenesis of Pituitary Adenomas: An Update
Xiaobing Jiang, Xun Zhang
Endocrinol Metab. 2013;28(4):245-254.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.245
  • 3,859 View
  • 41 Download
  • 37 Crossref
AbstractAbstract PDFPubReader   

Pituitary tumors represent the most common intracranial neoplasms accompanying serious morbidity through mass effects and inappropriate secretion of pituitary hormones. Understanding the etiology of pituitary tumorigenesis will facilitate the development of satisfactory treatment for pituitary adenomas. Although the pathogenesis of pituitary adenomas is largely unknown, considerable evidence indicates that the pituitary tumorigenesis is a complex process involving multiple factors, including genetic and epigenetic changes. This review summarized the recent progress in the study of pituitary tumorigenesis, focusing on the role of tumor suppressor genes, oncogenes and microRNAs.

Citations

Citations to this article as recorded by  
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    Neuropsychiatric Disease and Treatment.2021; Volume 17: 3769.     CrossRef
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    World Neurosurgery.2020; 137: 252.     CrossRef
  • Sellar Tumors
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    Surgical Pathology Clinics.2020; 13(2): 305.     CrossRef
  • Genomic and molecular characterization of pituitary adenoma pathogenesis: review and translational opportunities
    Mazin Elsarrag, Parantap D. Patel, Ajay Chatrath, Davis Taylor, John A. Jane
    Neurosurgical Focus.2020; 48(6): E11.     CrossRef
  • Metabolic profiling reveals distinct metabolic alterations in different subtypes of pituitary adenomas and confers therapeutic targets
    Jie Feng, Hua Gao, Qi Zhang, Yang Zhou, Chuzhong Li, Sida Zhao, Lichuan Hong, Jinjin Yang, Shuyu Hao, Wan Hong, Zhengping Zhuang, Guowang Xu, Yazhuo Zhang
    Journal of Translational Medicine.2019;[Epub]     CrossRef
  • Quantitative Analysis of Proteome in Non-functional Pituitary Adenomas: Clinical Relevance and Potential Benefits for the Patients
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    Frontiers in Endocrinology.2019;[Epub]     CrossRef
  • circOMA1-Mediated miR-145-5p Suppresses Tumor Growth of Nonfunctioning Pituitary Adenomas by Targeting TPT1
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  • Differential Expression of HMGA1 and HMGA2 in pituitary neuroendocrine tumors
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  • Double Pituitary Adenomas with Synchronous Somatotroph and Corticotroph Clinical Presentation of Acromegaly and Cushing's Disease
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  • Association of ApoE haplotype with clinical evidence of pituitary adenoma
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  • Next-generation sequencing of microRNAs reveals a unique expression pattern in different types of pituitary adenomas
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  • Growth hormone and prolactin-staining tumors causing acromegaly: a retrospective review of clinical presentations and surgical outcomes
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  • Study of major genetic factors involved in pituitary tumorigenesis and their impact on clinical and biological characteristics of sporadic somatotropinomas and non-functioning pituitary adenomas
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    Brazilian Journal of Medical and Biological Research.2018;[Epub]     CrossRef
  • Detection of circulating tumor cells in patients with pituitary tumors
    Gao Hua, He Yanjiao, Liu Qian, Wang Jichao, Zhang Yazhuo
    BMC Cancer.2018;[Epub]     CrossRef
  • Plurihormonal ACTH-GH Pituitary Adenoma: Case Report and Systematic Literature Review
    Elena Roca, Pier Paolo Mattogno, Teresa Porcelli, Luigi Poliani, Francesco Belotti, Alberto Schreiber, Filippo Maffezzoni, Marco Maria Fontanella, Francesco Doglietto
    World Neurosurgery.2018; 114: e158.     CrossRef
  • The role of galectin-3 in the tumorigenesis and progression of pituitary tumors
    Bo Diao, Ying Liu, Guo‑Zheng Xu, Yi Zhang, Jun Xie, Jie Gong
    Oncology Letters.2018;[Epub]     CrossRef
  • Programmed cell senescence: role of IL-6 in the pituitary
    Melanie Sapochnik, Mariana Fuertes, Eduardo Arzt
    Journal of Molecular Endocrinology.2017; 58(4): R241.     CrossRef
  • Selective molecular biomarkers to predict biologic behavior in pituitary tumors
    Aydin Sav, Fabio Rotondo, Luis V. Syro, Meric A. Altinoz, Kalman Kovacs
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  • MicroRNA-200b inhibits pituitary tumor cell proliferation and invasion by targeting PKCα
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  • Increased expression of the microRNA 106b~25 cluster and its host gene MCM7 in corticotroph pituitary adenomas is associated with tumor invasion and Crooke’s cell morphology
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  • Bromocriptine Induces Autophagy-Dependent Cell Death in Pituitary Adenomas
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  • Biomarkers of pituitary carcinomas
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    Expert Review of Endocrinology & Metabolism.2016; 11(3): 253.     CrossRef
  • MicroRNAs in the pituitary
    Erica Gentilin, Ettore degli Uberti, Maria Chiara Zatelli
    Best Practice & Research Clinical Endocrinology & Metabolism.2016; 30(5): 629.     CrossRef
  • Molecular markers in pituitary tumors
    Asha M. Robertson, Anthony P. Heaney
    Current Opinion in Endocrinology, Diabetes & Obesity.2016; 23(4): 324.     CrossRef
  • MicroRNA-106b promotes pituitary tumor cell proliferation and invasion through PI3K/AKT signaling pathway by targeting PTEN
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  • Isolated double adrenocorticotropic hormone-secreting pituitary adenomas: A case report and review of the literature
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    Samuel A. Wells
    Clinical Cancer Research.2016; 22(20): 4981.     CrossRef
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  • Epidrug mediated re-expression of miRNA targeting the HMGA transcripts in pituitary cells
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  • Pituitary Adenoma and the Chemokine Network: A Systemic View
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  • Brief Review of Articles in 'Endocrinology and Metabolism' in 2013
    Won-Young Lee
    Endocrinology and Metabolism.2014; 29(3): 251.     CrossRef
  • Epigenetics of pituitary tumours
    William E. Farrell
    Current Opinion in Endocrinology, Diabetes & Obesity.2014; 21(4): 299.     CrossRef
  • The Role of Genetic and Epigenetic Changes in Pituitary Tumorigenesis
    Hidenori FUKUOKA, Yutaka TAKAHASHI
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Close layer
Bone Metabolism
Recent Progress in Osteocyte Research
Paola Divieti Pajevic
Endocrinol Metab. 2013;28(4):255-261.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.255
  • 3,381 View
  • 22 Download
  • 11 Crossref
AbstractAbstract PDFPubReader   

The last decade has seen an exponential increase in our understanding of osteocytes function and biology. These cells, once considered inert by-standers trapped into the mineralized bone, has now risen to be key regulators of skeletal metabolism, mineral homeostasis, and hematopoiesis. As tools and techniques to study osteocytes improved and expanded, it has become evident that there is more to these cells than initially thought. Osteocytes are now recognized not only as the key responders to mechanical forces but also as orchestrators of bone remodeling and mineral homeostasis. These cells are the primary source of several important proteins, such as sclerostin and fibroblast growth factor 23, that are currently target as novel therapies for bone loss (as the case for antisclerostin antibodies) or phosphate disorders. Better understanding of the intricate cellular and molecular mechanisms that govern osteocyte biology will open new avenue of research and ultimately indentify novel therapeutics to treat bone and mineral disorders. This review summarizes novel findings and discusses future avenues of research.

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Close layer
Obesity and Metabolism
Clinical Application of Glucagon-Like Peptide 1 Receptor Agonists for the Treatment of Type 2 Diabetes Mellitus
Young Min Cho, Rhonda D. Wideman, Timothy J. Kieffer
Endocrinol Metab. 2013;28(4):262-274.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.262
  • 4,995 View
  • 79 Download
  • 37 Crossref
AbstractAbstract PDFPubReader   

Glucagon-like peptide 1 (GLP-1) is secreted from enteroendocrine L-cells in response to oral nutrient intake and elicits glucose-stimulated insulin secretion while suppressing glucagon secretion. It also slows gastric emptying, which contributes to decreased postprandial glycemic excursions. In the 1990s, chronic subcutaneous infusion of GLP-1 was found to lower blood glucose levels in patients with type 2 diabetes. However, GLP-1's very short half-life, arising from cleavage by the enzyme dipeptidyl peptidase 4 (DPP-4) and glomerular filtration by the kidneys, presented challenges for clinical use. Hence, DPP-4 inhibitors were developed, as well as several GLP-1 analogs engineered to circumvent DPP-4-mediated breakdown and/or rapid renal elimination. Three categories of GLP-1 analogs, are being developed and/or are in clinical use: short-acting, long-acting, and prolonged-acting GLP-1 analogs. Each class has different plasma half-lives, molecular size, and homology to native GLP-1, and consequently different characteristic effects on glucose metabolism. In this article, we review current clinical data derived from each class of GLP-1 analogs, and consider the clinical effects reported for each category in recent head to head comparison studies. Given the relatively brief clinical history of these compounds, we also highlight several important efficacy and safety issues which will require further investigation.

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Thyroid
The Diagnosis and Management of Hyperthyroidism in Korea: Consensus Report of the Korean Thyroid Association
Jae Hoon Moon, Ka Hee Yi
Endocrinol Metab. 2013;28(4):275-279.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.275
  • 4,975 View
  • 59 Download
  • 53 Crossref
AbstractAbstract PDFPubReader   

Hyperthyroidism is one of the causes of thyrotoxicosis and the most common cause of hyperthyroidism in Korea is Graves disease. The diagnosis and treatment of Graves disease are different according to geographical area. Recently, the American Thyroid Association and the American Association of Clinical Endocrinologists suggested new management guidelines for hyperthyroidism. However, these guidelines are different from clinical practice in Korea and are difficult to apply. Therefore, the Korean Thyroid Association (KTA) conducted a survey of KTA members regarding the diagnosis and treatment of hyperthyroidism, and reported the consensus on the management of hyperthyroidism. In this review, we summarized the KTA report on the contemporary practice patterns in the diagnosis and management of hyperthyroidism, and compared this report with guidelines from other countries.

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Editorial
Obesity and Metabolism
Noninvasive Markers for the Diagnosis of Nonalcoholic Fatty Liver Disease
Sang Yong Kim
Endocrinol Metab. 2013;28(4):280-282.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.280
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Original Articles
Obesity and Metabolism
Association of Serum Adipocyte-Specific Fatty Acid Binding Protein with Fatty Liver Index as a Predictive Indicator of Nonalcoholic Fatty Liver Disease
Won Seon Jeon, Se Eun Park, Eun-Jung Rhee, Cheol-Young Park, Ki-Won Oh, Sung-Woo Park, Won-Young Lee
Endocrinol Metab. 2013;28(4):283-287.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.283
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  • 33 Download
  • 15 Crossref
AbstractAbstract PDFPubReader   
Background

Adipocyte-specific fatty acid-binding protein (A-FABP) is a cytoplasmic protein expressed in macrophages and adipocytes and it plays a role in insulin resistance and metabolic syndrome. Recently, the fatty liver index (FLI) was introduced as an indicator of nonalcoholic fatty liver disease (NAFLD). In this study, we aimed to investigate the relationship between baseline serum A-FABP levels and FLI after 4 years in apparently healthy subjects.

Methods

A total of 238 subjects without a past history of alcoholism or hepatitis were recruited from a medical check-up program. The NAFLD state was evaluated 4 years later in the same subjects using FLI. Fatty liver disease was diagnosed as diffusely increased echogenicity of the hepatic parenchyma compared to the kidneys, vascular blurring, and deep-echo attenuation. NAFLD was defined as subjects with fatty liver and no history of alcohol consumption (>20 g/day).

Results

Baseline serum A-FABP levels were significantly associated with FLI after adjustment for age and sex (P<0.001). The subjects with higher A-FABP levels had a higher mean FLI (P for trend=0.006). After adjusting for age and sex, serum A-FABP levels at baseline were shown to be significantly associated with FLI as a marker of development of NAFLD after 4 years (odds ratio, 2.68; 95% confidence interval, 1.24 to 5.80 for highest tertile vs. lowest tertile; P=0.012).

Conclusion

This study demonstrated that higher baseline serum A-FABP levels were associated with FLI as a predictive indicator of NAFLD after 4 years of follow-up in healthy Korean adults.

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    Erdem Akbal, Erdem Koçak, Ömer Akyürek, Seyfettin Köklü, Hikmetullah Batgi, Mehmet Şenes
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    An-Ning Yang, Hui-Ping Zhang, Yue Sun, Xiao-Ling Yang, Nan Wang, Guangrong Zhu, Hui Zhang, Hua Xu, Sheng-Chao Ma, Yue Zhang, Gui-Zhong Li, Yue-Xia Jia, Jun Cao, Yi-Deng Jiang
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    Min-Kyung Lee, Eun-Jung Rhee, Min Chul Kim, Byung Sub Moon, Jeong In Lee, Young Seok Song, Eun Na Han, Hyo Sun Lee, Yoonjeong Son, Se Eun Park, Cheol-Young Park, Ki-Won Oh, Sung-Woo Park, Won-Young Lee
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    Won-Young Lee
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    Sang Yong Kim
    Endocrinology and Metabolism.2013; 28(4): 280.     CrossRef
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Adrenal gland
Effects of Chronic Restraint Stress on Body Weight, Food Intake, and Hypothalamic Gene Expressions in Mice
Joo Yeon Jeong, Dong Hoon Lee, Sang Soo Kang
Endocrinol Metab. 2013;28(4):288-296.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.288
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  • 139 Download
  • 125 Crossref
AbstractAbstract PDFPubReader   
Background

Stress affects body weight and food intake, but the underlying mechanisms are not well understood.

Methods

We evaluated the changes in body weight and food intake of ICR male mice subjected to daily 2 hours restraint stress for 15 days. Hypothalamic gene expression profiling was analyzed by cDNA microarray.

Results

Daily body weight and food intake measurements revealed that both parameters decreased rapidly after initiating daily restraint stress. Body weights of stressed mice then remained significantly lower than the control body weights, even though food intake slowly recovered to 90% of the control intake at the end of the experiment. cDNA microarray analysis revealed that chronic restraint stress affects the expression of hypothalamic genes possibly related to body weight control. Since decreases of daily food intake and body weight were remarkable in days 1 to 4 of restraint, we examined the expression of food intake-related genes in the hypothalamus. During these periods, the expressions of ghrelin and pro-opiomelanocortin mRNA were significantly changed in mice undergoing restraint stress. Moreover, daily serum corticosterone levels gradually increased, while leptin levels significantly decreased.

Conclusion

The present study demonstrates that restraint stress affects body weight and food intake by initially modifying canonical food intake-related genes and then later modifying other genes involved in energy metabolism. These genetic changes appear to be mediated, at least in part, by corticosterone.

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Close layer
Obesity and Metabolism
Glycogen Synthase Kinase 3 Inactivation Induces Cell Senescence through Sterol Regulatory Element Binding Protein 1-Mediated Lipogenesis in Chang Cells
You-Mie Kim, Insun Song, Yong-Hak Seo, Gyesoon Yoon
Endocrinol Metab. 2013;28(4):297-308.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.297
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AbstractAbstract PDFPubReader   
Background

Enhanced lipogenesis plays a critical role in cell senescence via induction of expression of the mature form of sterol regulatory element binding protein 1 (SREBP1), which contributes to an increase in organellar mass, one of the indicators of senescence. We investigated the molecular mechanisms by which signaling molecules control SREBP1-mediated lipogenesis and senescence.

Methods

We developed cellular models for stress-induced senescence, by exposing Chang cells, which are immortalized human liver cells, to subcytotoxic concentrations (200 µM) of deferoxamine (DFO) and H2O2.

Results

In this model of stress-induced cell senescence using DFO and H2O2, the phosphorylation profile of glycogen synthase kinase 3α (GSK3α) and β corresponded closely to the expression profile of the mature form of SREBP-1 protein. Inhibition of GSK3 with a subcytotoxic concentration of the selective GSK3 inhibitor SB415286 significantly increased mature SREBP1 expression, as well as lipogenesis and organellar mass. In addition, GSK3 inhibition was sufficient to induce senescence in Chang cells. Suppression of GSK3 expression with siRNAs specific to GSK3α and β also increased mature SREBP1 expression and induced senescence. Finally, blocking lipogenesis with fatty acid synthase inhibitors (cerulenin and C75) and siRNA-mediated silencing of SREBP1 and ATP citrate lyase (ACL) significantly attenuated GSK3 inhibition-induced senescence.

Conclusion

GSK3 inactivation is an important upstream event that induces SREBP1-mediated lipogenesis and consequent cell senescence.

Citations

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Close layer
Obesity and Metabolism
Association between Cardiac Autonomic Neuropathy, Diabetic Retinopathy and Carotid Atherosclerosis in Patients with Type 2 Diabetes
Chan-Hee Jung, Ae-Rin Baek, Kyu-Jin Kim, Bo-Yeon Kim, Chul-Hee Kim, Sung-Koo Kang, Ji-Oh Mok
Endocrinol Metab. 2013;28(4):309-319.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.309
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AbstractAbstract PDFPubReader   
Background

It is not clear whether microangiopathies are associated with subclinical atherosclerosis in type 2 diabetes mellitus (T2DM). We investigated the relation of cardiac autonomic neuropathy (CAN) and other microangiopathies with carotid atherosclerosis in T2DM.

Methods

A total of 131 patients with T2DM were stratified by mean carotid intima-media thickness (CIMT) ≥ or <1.0 mm and the number of carotid plaques. CAN was assessed by the five standard cardiovascular reflex tests according to the Ewing's protocol. CAN was defined as the presence of at least two abnormal tests or an autonomic neuropathy points ≥2. Diabetic microangiopathies were assessed.

Results

Patients with CAN comprised 77% of the group with mean CIMT ≥1.0 mm, while they were 29% of the group with CIMT <1.0 mm (P=0.016). Patients with diabetic retinopathy (DR) comprised 68% of the group with CIMT ≥1.0 mm, while they were 28% of the group without CIMT thickening (P=0.003). Patients with CAN comprised 51% of the group with ≥2 carotid plaques, while they were 23% of the group with ≤1 carotid plaque (P=0.014). In multivariable adjusted logistic regression analysis, the patients who presented with CAN showed an odds ratio [OR] of 8.6 (95% confidence interval [CI], 1.6 to 44.8) for CIMT thickening and an OR of 2.9 (95% CI, 1.1 to 7.5) for carotid plaques. Furthermore, patients with DR were 3.8 times (95% CI, 1.4 to 10.2) more likely to have CIMT thickening.

Conclusion

These results suggest that CAN is associated with carotid atherosclerosis, represented as CIMT and plaques, independent of the traditional cardiovascular risk factors in T2DM. CAN or DR may be a determinant of subclinical atherosclerosis in T2DM.

Citations

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    Hyun-Kyung Chung
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    Won-Young Lee
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Close layer
Obesity and Metabolism
A Novel Mutation in the Von Hippel-Lindau Tumor Suppressor Gene Identified in a Patient Presenting with Gestational Diabetes Mellitus
Yun Hyi Ku, Chang Ho Ahn, Chan-Hyeon Jung, Jie Eun Lee, Lee-Kyung Kim, Soo Heon Kwak, Hye Seung Jung, Kyong Soo Park, Young Min Cho
Endocrinol Metab. 2013;28(4):320-325.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.320
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AbstractAbstract PDFPubReader   
Background

Von Hippel-Lindau (VHL) disease is an autosomal dominantly inherited, multisystemic tumor syndrome caused by mutations in the VHL gene. To date, more than 1,000 germline and somatic mutations of the VHL gene have been reported. We present a novel mutation in the VHL tumor suppressor gene that presented with gestational diabetes mellitus.

Methods

A 30-year-old woman presented with gestational diabetes mellitus. She sequentially showed multiple pancreatic cysts, spinal cord hemangioblastoma, cerebellar hemangioblastoma, and clear cell type renal cell carcinomas. Also, her father and brother had brain hemangioblastomas. Each of the three exons of the VHL gene was individually amplified by polymerase chain reaction and direct sequencing was performed using an ABI 3730 DNA analyzer.

Results

DNA sequence analysis to determine the presence of VHL mutation in her family revealed del291C, a novel frameshift mutation.

Conclusion

We found a novel mutation in the VHL tumor suppressor gene that presented with gestational diabetes mellitus.

Citations

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  • Retinal hemangioblastoma in a patient with Von Hippel-Lindau disease: A case report and literature review
    Yikeng Huang, Weiwen Hu, Xionggao Huang
    Frontiers in Oncology.2022;[Epub]     CrossRef
  • Updates on the Role of Molecular Alterations and NOTCH Signalling in the Development of Neuroendocrine Neoplasms
    Claudia von Arx, Monica Capozzi, Elena López-Jiménez, Alessandro Ottaiano, Fabiana Tatangelo, Annabella Di Mauro, Guglielmo Nasti, Maria Lina Tornesello, Salvatore Tafuto
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    Won-Young Lee
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Close layer
Case Reports
Obesity and Metabolism
Recurrent Insulin Autoimmune Syndrome Caused by α-Lipoic Acid in Type 2 Diabetes
Sang Mook Bae, Myoung Nam Bae, Eun Young Kim, Il Kyu Kim, Min Woo Seo, Jin Kyeong Shin, Sung Rae Cho, Gui Hwa Jeong
Endocrinol Metab. 2013;28(4):326-330.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.326
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  • 49 Download
  • 17 Crossref
AbstractAbstract PDFPubReader   

Insulin autoimmune syndrome (IAS) is characterized by spontaneous hypoglycemia caused by insulin autoantibodies in the absence of exogenous insulin administration. Some drugs containing sulfhydryl compounds are known to initiate the onset of IAS. A 67-year-old female who had diabetes for 5 years visited the outpatient clinic at our institution due to diabetic peripheral polyneuropathy. She was prescribed α-lipoic acid (ALA), which contains two sulfur atoms. Two weeks later, she complained of recurrent hypoglycemic symptoms. We detected a high level of insulin and high titers of insulin autoantibodies. Her human leukocyte antigen (HLA) genotype included the DRB1*0406 allele, which indicates a high level of susceptibility to IAS. She was treated with prednisolone. After this episode, she experienced two more hypoglycemic events after taking ALA for diabetic neuropathy in other hospitals. As ALA can be used to treat diabetic peripheral polyneuropathy, physician discretion is advised based on the possibility of IAS due to ALA in diabetic patients.

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Thyroid
Rhabdomyolysis and Acute Kidney Injury Associated with Hypothyroidism and Statin Therapy
Pyoung Ahn, Hyun-Jun Min, Sang-Hyun Park, Byoung-Mu Lee, Myung-Jin Choi, Jong-Woo Yoon, Ja-Ryong Koo
Endocrinol Metab. 2013;28(4):331-334.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.331
  • 3,723 View
  • 37 Download
  • 9 Crossref
AbstractAbstract PDFPubReader   

Rhabdomyolysis is a syndrome involving the breakdown of skeletal muscle that causes myoglobin and other intracellular proteins to leak into the circulatory system, resulting in organ injury including acute kidney injury. We report a case of statin-induced rhabdomyolysis and acute kidney injury that developed in a 63-year-old woman with previously undiagnosed hypothyroidism. Untreated hypothyroidism may have caused her hypercholesterolemia requiring statin treatment, and it is postulated that statin-induced muscle injury was aggravated by hypothyroidism resulting in her full-blown rhabdomyolysis. Although this patient was successfully treated with continuous venovenous hemofiltration and L-thyroxin replacement, rhabdomyolysis with acute kidney injury is a potentially life-threatening disorder. Physicians must pay special attention to the possible presence of subclinical hypothyroidism when administering statins in patients with hypercholesterolemia.

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Thyroid
Papillary Thyroid Carcinoma: Four Cases Required Caution during Long-Term Follow-Up
Hea Min Yu, Jae Min Lee, Kang Seo Park, Tae Sun Park, Heung Young Jin
Endocrinol Metab. 2013;28(4):335-340.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.335
  • 3,617 View
  • 28 Download
  • 3 Crossref
AbstractAbstract PDFPubReader   

Due to the increased prevalence of papillary thyroid carcinoma (PTC), difficult cases and unexpected events have become more common during long-term follow-up. Herein we reported four cases that exhibited poor progress during long-term follow-up. All the cases were diagnosed with PTC and treated with total thyroidectomy before several years, and the patients had been newly diagnosed with recurrent and metastatic PTC. These four cases included recurred PTC with invasion of large blood vessels, a concomitant second malignancy, malignant transformation, and refractoriness to treatment. Physicians should closely monitor patients to promptly address unforeseen circumstances during PTC follow-up, including PTC recurrence and metastasis. Furthermore, we suggest that the development of a management protocol for refractory or terminal PTC is also warranted.

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  • Induction of epithelial-mesenchymal transition in thyroid follicular cells is associated with cell adhesion alterations and low-dose hyper-radiosensitivity
    Ankit Mathur, Vijayakumar Chinnadurai, Param Jit Singh Bhalla, Sudhir Chandna
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  • Thyroglobulin Level in Fine-Needle Aspirates for Preoperative Diagnosis of Cervical Lymph Node Metastasis in Patients with Papillary Thyroid Carcinoma: Two Different Cutoff Values According to Serum Thyroglobulin Level
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    Won-Young Lee
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Thyroid
Co-Occurrence of Papillary Thyroid Carcinoma and Mucosa-Associated Lymphoid Tissue Lymphoma in a Patient with Long-Standing Hashimoto Thyroiditis
Yoon Jeong Nam, Bo Hyun Kim, Seong Keun Lee, Yun Kyung Jeon, Sang Soo Kim, Woo Jin Jung, Dong Hwahn Kahng, In Ju Kim
Endocrinol Metab. 2013;28(4):341-345.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.341
  • 4,123 View
  • 60 Download
  • 12 Crossref
AbstractAbstract PDFPubReader   

Papillary thyroid carcinoma (PTC) is a common affliction of the thyroid gland, accounting for 70% to 80% of all thyroid cancers, whereas mucosa-associated lymphoid tissue (MALT) lymphoma of the thyroid gland is uncommon. The simultaneous occurrence of both malignancies is extremely rare. We report the case of a patient with both PTC and MALT lymphoma in the setting of Hashimoto thyroiditis. An 81-year-old female patient was first admitted with goiter and hoarseness, which was attributed to an ultrasonographic thyroid nodule. Subsequent fine-needle aspirate, interpreted as suspicious of papillary thyroid cancer, prompted total thyroidectomy. MALT lymphoma was an incidental postsurgical finding, coexisting with PTC in the setting of Hashimoto thyroiditis. Although the development of MALT lymphoma is very rare, patients with longstanding Hashimoto thyroiditis should undergo careful surveillance for both malignancies.

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    Qiong Wu, Yu-xin Jiang, Jun-chao Guo, Yu Xiao, Xiao Yang, Rui-na Zhao, Xing-jian Lai, Shen-ling Zhu, Xiao-yan Zhang, Bo Zhang
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    Saul Levy-Blitchtein, Stefany Plasencia-Rebata, Domingo Morales Luna, Juana del Valle Mendoza
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    Jun Suk Byun, Hye Yoon Lee, Ki Won Chun, Dae Sung Yoon
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    Won-Young Lee
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    Shaakir Hasan, Aruna Turaka
    Journal of Radiotherapy in Practice.2014; 13(4): 490.     CrossRef
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    Byung Soo Kong, Yoon Hee Cho, Eun Jig Lee, Rajesh Mohanraj
    PLoS ONE.2014; 9(11): e113242.     CrossRef
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Endocrinol Metab : Endocrinology and Metabolism