Newly diagnosed type 1 diabetes mellitus in a human immunodeficiency virus-infected patient with antiretroviral therapy-induced immune reconstitution inflammatory syndrome: a case report.

BACKGROUND: Diabetes that develops in human immunodeficiency virus (HIV)-infected patients who receive antiretroviral therapy (ART) is usually type 2 diabetes mellitus (T2DM); however, autoimmune diabetes, such as type 1 diabetes mellitus (T1DM) can also develop in this population. After treatment with ART, patients might experience clinical deterioration following an increase in the CD4 cell count, which is termed immune reconstitution inflammatory syndrome (IRIS). Here, we describe an HIV-infected patient on ART who developed T1DMat due to IRIS, highlighting the clinical complexity in diagnosis and treatment. CASE PRESENTATION: A 36-year-old man infected with HIV had a nadir CD4 cell count of 15.53/µL before medication, which increased to 429.09/µL after 9 months of regular ART. The fasting serum glucose at 9 months was between 96 mg/dL and 117 mg/dL. After 11 months of ART, the patient was admitted to hospital for diabetic ketoacidosis (DKA) and Graves' disease (GD). Noninsulin antidiabetics (NIADs) were prescribed following the resolution of DKA. However, poor glycemic control was noted despite well-titrated NIADs. Further investigation demonstrated poor pancreatic beta cell function and elevated anti-glutamic acid decarboxylase (anti-GAD) and anti-tyrosine phosphatase-like insulinoma antigen 2 (anti-IA2) titers. According to the results, he was diagnosed with T1DM and received multiple daily injections(MDI) of insulin. The regimen of MDI was insulin degludec as basal insulin and insulin aspart as prandial insulin. After MDI therapy, his glycemic control was improved. CONCLUSION: In this case, T1DM was ascribed to IRIS. Although this phenomenon has been demonstrated in previous case reports, further study is necessary to realize the mechanism of this association. Therefore, we emphasize that when HIV-infected patients on ART experience an unstable blood glucose level and abnormal thyroid function, physicians should consider T1DM and GD associated with ART-induced IRIS to reduce the subsequent complications and more serious endocrine dysfunction.

Office-based salivary gland ductal irrigation in patients with chronic sialoadenitis: A preliminary study.

BACKGROUND/PURPOSE: To evaluate the therapeutic responsiveness of office-based salivary gland ductal irrigation in patients with chronic sialoadenitis. METHODS: Between August 2017 and April 2019, 55 patients comprising the following three disease groups were enrolled: Sjogren's syndrome: 39 patients; postradiotherapy sialoadenitis: ten patients; and post-RAI sialoadenitis: six patients. Quantitative salivary scintigraphy was recorded, and a formulated questionnaire including the Summated Xerostomia Inventory was utilized to assess acute/chronic symptoms. All patients received at least three serial salivary gland ductal irrigations with a one-month interval in our outpatient department. RESULTS: The general response rates for each disease groups are as follows: Sjogren's syndrome: 61.5% (24/39); postradiotherapy: 60% (6/10); and post-RAI: 83.3% (5/6). Among the patients with Sjogren's syndrome, the parotid scintigraphic Tmin showed a significant positive correlation with the responsiveness of salivary irrigation (P = 0.046), whereas the treatment tended to be irresponsive in patients who previously took medicine for their related discomfort (P = 0.009). In the postradiotherapy and post-RAI groups, no significant factors were found to be associated with the responsiveness of irrigation. CONCLUSION: Simple salivary ductal irrigation without complex equipment can be performed as an outpatient procedure to alleviate glandular swelling or xerostomia in patients with Sjogren's syndrome, postradiotherapy sialoadenitis or post-RAI sialoadenitis, and it can be considered an alternative management approach for patients refractory to conventional strategies.

The development of a novel cancer immunotherapeutic platform using tumor-targeting mesenchymal stem cells and a protein vaccine.

An ideal anticancer strategy should target only the malignant cells but spare the normal ones. In this regard, we established a platform, consisting of an antigen-delivering vehicle and a protein vaccine, for developing an immunotherapeutic approach with the potential for eliminating various cancer types. Mesenchymal stem cells (MSCs) have been demonstrated capable of targeting tumors and integrating into the stroma. Moreover, we have developed a protein vaccine PE(ΔIII)-E7-KDEL3 which specifically recognized E7 antigen and elicited immunity against cervical cancer. Taking advantage of tumor-homing property of MSCs and PE(ΔIII)-E7-KDEL3, we used E6/E7-immortalized human MSCs (KP-hMSCs) as an E7 antigen-delivering vehicle to test if this protein vaccine could effectively eliminate non-E7-expressing tumor cells. Animals which received combined treatment of KP-hMSCs and PE(ΔIII)-E7-KDEL3 demonstrated a significant inhibition of tumor growth and lung-metastasis when compared to PE(ΔIII)-E7-KDEL3 only and KP-hMSCs only groups. The efficiency of tumor suppression correlated positively to the specific immune response induced by PE(ΔIII)-E7-KDEL3. In addition, this combined treatment inhibited tumor growth via inducing apoptosis. Our findings indicated that KP-hMSCs could be used as a tumor-targeting device and mediate antitumor effect of PE(ΔIII)-E7-KDEL3. We believe this strategy could serve as a platform for developing a universal vaccine for different cancer types.

Clinical significance of hepatic function in Graves disease with type 2 diabetic mellitus: A single-center retrospective cross-sectional study in Taiwan.

Graves disease (GD) and type 2 diabetes mellitus (T2DM) both impair liver function; we therefore explored the possibility of a relationship among diabetic control, thyroid function, and liver function. This retrospective, cross-sectional study compared serum liver function biomarkers of primary GD patients in a single center between 2016 and 2020, derived from clinical databases, and clarified the correlation of liver function in GD patients with or without T2DM. Furthermore, the diabetes mellitus group was divided into glycated hemoglobin A1C (HbA1C) <6.5% group and ≥6.5% group to further analyze the effect by disease control in patients. Statistical differences between groups were assessed using independent t tests to clarify the association of serum biomarkers between GD with T2DM. Pearson test was applied to assess within-group statistical correlation of serum biomarkers. The correlation of factors in each group was demonstrated by using the Kendall tau-b method and stepwise regression analysis. A total of 77 patients were included in the study. In the study population, glutamate pyruvate transaminase (GPT) was significantly correlated with thyroid-stimulating hormone, and HbA1C was significantly correlated with alkaline phosphatase (ALK-P), glutamate oxaloacetate transaminase (GOT), and GPT. An examination of GOT, GPT, free thyroxine (FT4), and HbA1C levels revealed a significant difference between the non-T2DM and T2DM groups. GPT also exhibited a significant correlation with triiodothyronine in the T2DM group. The T2DM group was further divided into groups: HbA1C <6.5% and ≥6.5%. The results demonstrated that ALK-P, GOT, GPT, and FT4 levels were significantly different between the groups. A significant correlation between ALK-P and thyroid-stimulating hormone and between GOT and FT4 was also identified in the HbA1C <6.5% group. Our single-center study revealed that diabetes affects liver function in patients with GD. For patients with T2DM, when liver function becomes impaired, thyroid function control deteriorates. GPT was correlated with triiodothyronine but not with FT4, which indicated the impairment of deiodination in the liver. This phenomenon was not observed in the non-T2DM population. The early detection of abnormal liver function in patients with GD and T2DM may help limit the development of comorbidities and improve disease management.

Is the level of serum lactate dehydrogenase a potential biomarker for glucose monitoring with type 2 diabetes mellitus?

Introduction: Type 2 diabetes mellitus (T2DM) is a metabolic disorder due to defects in insulin secretion or insulin resistance leading to the dysfunction and damage of various organs. To improve the clinical evaluation of short-term blood glycemic variability monitoring, it is critical to identify another blood cell status and nutritional status biomarker that is less susceptible to interference. This study identifies the significance of serum lactate dehydrogenase (LDH) level among T2DM patients treated in outpatient clinics and investigates the relationship of LDH level with other variables. Methods: This study comprised 72 outpatients with T2DM over 20 years of age. Blood samples were collected followed by a hematological analysis of serum glycated albumin (GA), LDH, fasting blood glucose, glycosylated hemoglobin, C-peptide, and insulin antibodies (insulin Ab). Results: Serum LDH level was significantly correlated with GA (p < 0.001), C-peptide (p = 0.04), insulin Ab (p = 0.03), and thyroid-stimulating hormone (TSH) levels (p = 0.04). Hence, we performed a linear regression analysis of hematological markers. GA (p < 0.001, r2 = 0.45) and insulin Ab (p < 0.001, r2 = 0.40) were significantly associated with LDH level. Then, we classified patients into low (<200 U/L) and high (≥200 U/L) serum LDH level groups, respectively. GA (p < 0.001), C-peptide (p = 0.001), and TSH (p = 0.03) showed significant differences in patients with high LDH levels compared with those in patients with low LDH levels. Conclusion: In conclusion, we suggested that LDH level was independent of long-term but associated with short-term blood glucose monitoring. The results indicated that changes in serum GA induced cell damage and the abnormal elevation of the serum level of LDH may occur simultaneously with glycemic variability. It has been reported that many biomarkers are being used to observe glucose variability in T2DM. However, LDH could provide a more convenient and faster evaluation of glycemic variability in T2DM.

Effect of metformin monotherapy and dual or triple concomitant therapy with metformin on glycemic control and lipid profile management of patients with type 2 diabetes mellitus.

Background: In this study, we aimed to compare the effects of metformin-based dual therapy versus triple therapy on glycemic control and lipid profile changes in Taiwanese patients with type 2 diabetes mellitus (T2DM). Methods: In total, 60 patients were eligible for participation in this study. Patients received at least 24 months of metformin monotherapy, dual therapy, or triple therapy with metformin plus linagliptin (a dipeptidyl peptidase 4 (DPP-4) inhibitor) or dapagliflozin (a sodium-glucose cotransporter-2 (SGLT2) inhibitor). Blood samples were collected from each patient, followed by evaluation of changes in their blood glucose control and lipid profile-related markers. Results: A combination of metformin and DPP4 and SGLT2 inhibitor therapy more effectively reduced low-density lipoprotein cholesterol (LDL-C) (p = 0.016) than metformin monotherapy. A combination of metformin and DPP4 and SGLT2 inhibitor therapy more effectively improved total cholesterol (Chol, p = 0.049) and high-density lipoprotein cholesterol (HDL-C) than metformin monotherapy (p = 0.037). Metformin plus linagliptin dual therapy was more effective than metformin monotherapy in reducing glycosylated hemoglobin (HbA1C, p = 0.011). Patients who received a combination of linagliptin and empagliflozin showed a significant reduction in their fasting blood glucose (p = 0.019), HbA1c (p = 0.036), and Chol (p = 0.010) compared with those who received linagliptin dual therapy. Furthermore, patients who received metformin plus dapagliflozin and saxagliptin showed significantly reduced Chol (p = 0.011) and LDL-C (p = 0.035) levels compared with those who received metformin plus dapagliflozin. Conclusion: In conclusion, dual therapy with metformin and linagliptin yields similar glycemic control ability to triple therapy. Among metformin combination triple therapy, triple therapy of empagliflozin and linagliptin might have a better glycemic control ability than dual therapy of linagliptin. Moreover, Triple therapy of dapagliflozin and saxagliptin might have a better lipid control ability than dual therapy of dapagliflozin.

Normoxically overexpressed hypoxia inducible factor 1-alpha is involved in arsenic trioxide resistance acquisition in hepatocellular carcinoma.

BACKGROUND: The aim of this study was to examine the underlying signaling mechanisms of arsenic trioxide (ATO)-mediated anticancer effects and the responsible biomarker(s) for the acquired resistance in human heptatocellular carcinoma (HCC). MATERIALS AND METHODS: The therapeutic effects of ATO were examined using 2 characteristically distinct HCC cell lines, Hep-J5 (overexpressing HIF-1α/GRP78) and SK-Hep-1 (the matched control). ATO-mediated proliferation inhibition, oxidative stress, and apoptosis were analyzed using flowcytometric analysis and western blotting. The role of HIF-1α and GRP78 in HCC resistance to ATO treatment was determined using RNA silencing and inhibitor approaches. RESULTS: SK-Hep-1 cells, lacking both HIF-1α and GRP78 expressions were responsive to ATO-induced apoptosis via an oxidative-nitrosative mechanism. Intracellular glutathione depletion and lipid peroxidation have been identified as the early cascade of events preceding apoptosis via cytochrome c release and the severe drop of mitochondrial membrane potential (MMP). Conversely, Hep-J5 cells, with normoxic coexpression of HIF-1α and GRP78, were resistant to ATO-induced apoptosis. GRP78-silenced Hep-J5 cells remained resistant to ATO treatment. In contrast, ATO resistance in Hep-J5 cells was overcome by the addition of YC-1, a HIF-1α inhibitor. CONCLUSIONS: HIF-1α was identified as the major positive modifier for ATO resistance acquisition in HCC, and it represents a prime molecular target for overcoming ATO resistance.

Increased cellular apoptosis susceptibility (CSE1L/CAS) protein expression promotes protrusion extension and enhances migration of MCF-7 breast cancer cells.

Microtubules are part of cell structures that play a role in regulating the migration of cancer cells. The cellular apoptosis susceptibility (CSE1L/CAS) protein is a microtubule-associated protein that is highly expressed in cancer. We report here that CSE1L regulates the association of α-tubulin with ß-tubulin and promotes the migration of MCF-7 breast cancer cells. CSE1L was associated with α-tubulin and ß-tubulin in GST (glutathione S-transferase) pull-down and immunoprecipitation assays. CSE1L-GFP (green fluorescence protein) fusion protein experiments showed that the N-terminal of CSE1L interacted with microtubules. Increased CSE1L expression resulted in decreased tyrosine phosphorylation of α-tubulin and ß-tubulin, increased α-tubulin and ß-tubulin association, and enhanced assembly of microtubules. Cell protrusions or pseudopodia are temporary extensions of the plasma membrane and are implicated in cancer cell migration and invasion. Increased CSE1L expression increased the extension of MCF-7 cell protrusions. In vitro migration assay showed that enhanced CSE1L expression increased the migration of MCF-7 cells. Our results indicate that CSE1L plays a role in regulating the extension of cell protrusions and promotes the migration of cancer cells.

Recent Advances in Salivary Scintigraphic Evaluation of Salivary Gland Function.

Saliva plays an important role in supporting upper gastrointestinal tract function and oral well-being. Salivary dysfunction mainly manifests with a decrease in salivary flow. Among varieties of quantitative methods, salivary scintigraphy is a relatively noninvasive, well-tolerated, reproducible, and objective approach for functional evaluation of salivary disorders, yet the lack of precise quantitative reference values and no standardized protocol limit its generalized utilization. In this article, we review the scintigraphic performance between the visual analysis and quantitative methods in predicting Sjögren's syndrome and verify the potential aspects of the application in interpreting different disease entities and phases of functional salivary disorders.

The investigation of mitogen-activated protein kinase phosphatase-1 as a potential pharmacological target in non-small cell lung carcinomas, assisted by non-invasive molecular imaging.

BACKGROUND: Invasiveness and metastasis are the most common characteristics of non small cell lung cancer (NSCLC) and causes of tumour-related morbidity and mortality. Mitogen-activated protein kinases (MAPKs) signalling pathways have been shown to play critical roles in tumorigenesis. However, the precise pathological role(s) of mitogen-activated protein kinase phosphatase-1 (MKP-1) in different cancers has been controversial such that the up-regulation of MKP-1 in different cancers does not always correlate to a better prognosis. In this study, we showed that the induction of MKP-1 lead to a significant retardation of proliferation and metastasis in NSCLC cells. We also established that rosiglitazone (a PPARgamma agonist) elevated MKP-1 expression level in NSCLC cells and inhibited tumour metastasis. METHODS: Both wildtype and dominant negative forms of MKP-1 were constitutively expressed in NSCLC cell line H441GL. The migration and invasion abilities of these cells were examined in vitro. MKP-1 modulating agents such as rosiglitazone and triptolide were used to demonstrate MKP-1's role in tumorigenesis. Bioluminescent imaging was utilized to study tumorigenesis of MKP-1 over-expressing H441GL cells and anti-metastatic effect of rosiglitazone. RESULTS: Over-expression of MKP-1 reduced NSCLC cell proliferation rate as well as cell invasive and migratory abilities, evident by the reduced expression levels of MMP-2 and CXCR4. Mice inoculated with MKP-1 over-expressing H441 cells did not develop NSCLC while their control wildtype H441 inoculated littermates developed NSCLC and bone metastasis. Pharmacologically, rosiglitazone, a peroxisome proliferator activated receptor-gamma (PPARgamma) agonist appeared to induce MKP-1 expression while reduce MMP-2 and CXCR4 expression. H441GL-inoculated mice receiving daily oral rosiglitazone treatment demonstrated a significant inhibition of bone metastasis when compared to mice receiving sham treatment. We found that rosiglitazone treatment impeded the ability of cell migration and invasion in vitro. Cells pre-treated with triptolide (a MKP-1 inhibitor), reversed rosiglitazone-mediated cell invasion and migration. CONCLUSION: The induction of MKP-1 could significantly suppress the proliferative and metastatic abilities of NSCLC both in vitro and in vivo. Therefore, MKP-1 could be considered as a potential therapeutic target in NSCLC therapy and PPARgamma agonists could be explored for combined chemotherapy.

Preprandial single oral dose of sitagliptin does not affect circulating ghrelin and gastrin levels in normal subjects.

AIMS: To determine the effect of an oral dose of sitagliptin on the secretion of ghrelin and gastrin hormones. METHODS: Ten healthy volunteers were recruited in this study. A baseline blood sample was drawn before oral dosing with a 100-mg tablet of sitagliptin. Two blood samples were obtained 0.5 and 1 h after dosing. Three additional postprandial blood samples were drawn at 0.5, 1, and 2 h. Radioimmunoassay was used for determining hormonal levels. A Student's t test, Pearson correlation analysis, and multivariate approach to repeated-measures analysis of variance were used for statistics. RESULTS: After sitagliptin dosing, but before the meal, there was no significant change in circulating ghrelin, gastrin, insulin, and glucose levels. Only after meal loading was there a progressive and persistent decline in ghrelin levels until the end of the study, while a rapid and temporary rise in gastrin, insulin, and glucose levels at 0.5 h was observed. The levels of gastrin, insulin, and glucose then declined progressively. CONCLUSIONS: Preprandial oral dose of sitagliptin does not affect circulating ghrelin, gastrin, insulin, and glucose concentrations in normal subjects. Decreased ghrelin and increased gastrin and insulin levels occurred only after meal loading. These results support the theory that sitagliptin might not cause appetite-enhanced body weight gain and insulin-induced hypoglycemia.

The establishment and application of sialoscintigraphic reference values from patients with obstructive sialadenitis.

AIM: To evaluate feasibility of establishing a clinically applicable reference value through those unaffected salivary gland on sialoscintigraphic data obtained from patients presented with obstructive sialadenitis affected a single gland. MATERIALS AND METHODS: Ninety-one patients suffered from single salivary gland swelling, pain/tenderness and received sialoscintigraphic examinations were retrospectively enrolled. The quantitative data parameters, including the uptake ratio, maximal accumulation, maximal excretion, time to maximal (Tmax) and time to minimal (Tmin) activity of the affected and unaffected glands, were calculated for analysis. Data were also obtained and recorded for comparison from 50 patients who fulfill the American-European criteria for the diagnosis of Sjogren's syndrome. RESULTS: The maximal excretion appeared to be the best indicator for distinguishing affected and unaffected glands of obstructive diseases, for parotid and submandibular glands (P = 0.0002 and P < 0.0001, respectively). The area under the receiver-operating characteristic curve (AUC) is 0.82 for submandibular glands. In patients with Sjogren's syndrome, the maximal excretion and Tmin were the best parameters, for parotid (P = 0.002 and P < 0.0001, respectively) and submandibular glands (P < 0.0001 and P = 0.002, respectively). Uptake ratio was a good parameter for submandibular gland (P < 0.0001). The AUC of maximal excretion and uptake ratio for submandibular glands is 0.81 and 0.77, respectively. CONCLUSION: Quantitative data obtained from the unaffected glands of patients with obstructive sialadenitis could be used as reference values for the functional evaluation of salivary gland disorders with maximal excretion as one of the reliable parameters.

A novel cell-based therapy for contusion spinal cord injury using GDNF-delivering NIH3T3 cells with dual reporter genes monitored by molecular imaging.

UNLABELLED: This aim of our study was to evaluate a novel cell-based therapy for contusion spinal cord injury (SCI) using embryonic-derived NIH3T3 cells, which endogenously express glial cell line-derived neurotrophic factor (GDNF). METHODS: Proliferation and differentiation of transplanted NIH3T3 cells and their anti-apoptotic effects were examined after their engraftment into the spinal cords of Long-Evans rats subjected to acute SCI at the T10 vertebral level by a New York University impactor device. NIH3T3 cells were initially engineered to contain dual reporter genes, namely thymidine kinase (T) and enhanced green fluorescence protein (G), for in vivo cell tracking by both nuclear and fluorescence imaging modalities. RESULTS: Planar and fluorescence imaging demonstrated that transplanted NIH3T3-TG cells at the L1 vertebral level migrated 2 cm distal to the injury site as early as 2 h, and the signals persisted for 48 h after SCI. The expression of GDNF by NIH3T3-TG cells was then confirmed by immunohistochemical analysis both in vitro and in vivo. GDNF-secreting NIH3T3-TG transplant provided anti-apoptotic effects in the injured cord over the period of 3 wk. Finally, NIH3T3-TG cells cultured under neuronal differentiation medium exhibited both morphologic and genetic resemblance to neuronal cells. CONCLUSION: GDNF-secreting NIH3T3-TG cells in combination with molecular imaging could be a platform for developing therapeutic tools for acute SCI.

Utility of 18F-FDG PET/CT uptake patterns in Waldeyer's ring for differentiating benign from malignant lesions in lateral pharyngeal recess of nasopharynx.

UNLABELLED: Focally increased (18)F-FDG uptake in the lateral pharyngeal recess (LPR) of the nasopharynx due to a benign or malignant lesion is not an uncommon finding on PET images. The aim of this study was to evaluate whether, on PET/CT images, (18)F-FDG uptake occurs with characteristic patterns and intensities in various regions of Waldeyer's ring that can improve our ability to differentiate benign from malignant lesions. METHODS: Data generated from the (18)F-FDG PET/CT images of 1,628 subjects in our cancer-screening program were analyzed. Increased uptake in the LPR was observed in 80 subjects (4.9%) presenting with benign lesions, including 53 subjects without and 27 subjects with symptoms of upper airway discomfort. In addition, 30 healthy controls and 21 patients with newly diagnosed nasopharyngeal carcinoma were recruited for this study. Visual uptake, measurements of the lesions' standardized uptake value (SUV), and any abnormalities on PET/CT were evaluated. The receiver-operating-characteristic curve and area under the curve were applied to evaluate the discriminating power. RESULTS: Increased (18)F-FDG uptake (SUV, mean +/- SD) was found in the LPR, with a statistically significant (P < 0.001) difference between benign lesions (3.0 +/- 1.16) and malignant lesions (7.03 +/- 3.83). However, associated increased uptake exclusively in the palatine tonsil, lingual tonsil, and submandibular gland was found in both asymptomatic and symptomatic subjects. The ratio of LPR uptake to palatine tonsil uptake (N/P ratio) in benign lesions (0.81 +/- 0.37) was significantly (P < 0.001) lower than that in malignant lesions (2.30 +/- 1.62). Higher incidences of asymmetric (18)F-FDG LPR uptake, cervical lymph node uptake, and asymmetric wall thickening of the LPR on CT were observed in patients with nasopharyngeal carcinoma. When an SUV of less than 3.9 and an N/P ratio of less than 1.5 were used as cutoff points in subjects showing the combination of symmetric uptake in the LPR and normal or symmetric wall thickening, and detectable lymph node uptake, the area under the curve for benign lesions on PET/CT was 0.932 +/- 0.042 (95% confidence interval, 0.86-0.98), with a sensitivity of 90.4% and a specificity of 93.8%. CONCLUSION: The intensity and patterns of (18)F-FDG uptake in various regions of Waldeyer's ring along with CT scan findings provide a feasible modality to differentiate benign from malignant nasopharyngeal lesions.

The significance of FDG uptake in bilateral thyroid glands.

AIM: To evaluate the significance of bilateral fluorodeoxyglucose (FDG) uptake in the thyroid glands. METHODS: Bilateral thyroid FDG uptake, defined as visualization of thyroid glands, was found in 66 (3.4%) of 1925 subjects who underwent our FDG PET cancer-screening program. Additionally, 16 of the 41 patients with Graves' disease and hyperthyroidism (GD(H)) and six of the 20 subjects with Graves' disease and euthyroidism (GD(E)), who had FDG uptake in thyroid glands, were enrolled in this study. RESULTS: Among the 66 subjects, 22 were normal variant, 39 subjects had chronic thyroiditis (35 subjects presented with diffuse goitre and four with multinodular goitre), and five subjects had multinodular goitre (MNG) without chronic thyroiditis. Fourteen of 22 (63.6%) of the subjects with the normal variant had a visual uptake intensity less than that of the liver, while 30 of 39 (76.9%) of the subjects with chronic thyroiditis and 14 of 22 (63.6%) of the subjects with Graves' disease had visual uptake intensity greater than or equal to liver uptake. Two of the five subjects with MNG with focally intense uptake were proven to have thyroid carcinoma. Bilateral loser uptake in thyroids associated with thymus and symmetrical skeletal muscle uptake were found in GD(H). The standard uptake value (SUV) (mean+/-SD) in subjects with chronic thyroiditis (2.76+/-1.24) were higher, while those with GD(H) (1.59+/-0.36) were lower than that of the normal variant (1.99+/-0.63). Subjects with hypothyroidism (3.04+/-1.39) had higher SUV levels than those subjects with euthyroidism (2.44+/-1.11). In addition, patients with GD(H) had lower levels than those with GD(E) (2.0+/-0.38). CONCLUSION: (1) Bilateral thyroidal uptake of FDG can be found in normal variants and subjects with various thyroid disorders, showing varieties of uptake patterns. (2) Diffuse intense uptake and higher SUV levels are a clue to a diagnosis of chronic thyroiditis, especially for those with hypothyroidism. (3) Focally intense uptake suggests the possibility of a thyroid carcinoma. (4) Sparse uptake associated with the thymus and symmetrical skeletal muscle uptake and lower SUV level raise the possibility of Graves' disease with hyperthyroidism.

The Concomitant Association of Thyroid Disorders and Myasthenia Gravis.

BACKGROUND: Some of the thyroid disorders (TD) and Myasthenia gravis (MG) are autoimmune related disease. The purpose of the study to evaluate the relationship of MG with all morphological and functional thyroid disorders. METHODS: We constructed a population-based cohort study during the period from January 2000-December 2002 by using reimbursement data from the Bureau National Health Insurance (NHI) system in Taiwan. Patients with TD and MG were identified by referring to the ICD-9-CM codes. (ICD-10-CM as reference) .The association of TD with MG occurred only in the same person within the study period. The Q value was used to measure the strength of disease-disease associations. RESULTS: We obtained 520628 TD and 7965 MG records for analysis. Diffuse toxic goiter had highest association rate, followed by nontoxic nodular goiter, simple goiter, chronic lymphocytic thyroiditis, thyroid cancer, and toxic nodular goiter. Female and older patients had a higher rate than their male and younger counterparts, respectively. Functional abnormalities revealed higher incidence of thyrotoxicosis and hypothyroidism in both sexes. We also found the strongest association in men with chronic thyroiditis, diffuse toxic goiter, thyrotoxicosis, acquired hypothyroidism, thyroid cancer, and simple goiter. While an intermediate association was observed in female with diffuse toxic goiter, in a male with toxic and nontoxic nodular/multinodular goiters, in female with thyrotoxicosis, thyroid cancer and acquired hypothyroidism. CONCLUSION: This population based cohort study showed potential association of all types of TD with MG, and observed a higher association rate in female autoimmune TD whereas males showed a higher strength of association.

The impact of different surgical procedures on hypoparathyroidism after thyroidectomy: A population-based study.

The main objective of this study is to investigate the outcome between surgical procedures and the risk of development of hypoparathyroidism followed by surgical procedure in patients with thyroid disorders.We analyzed the data acquired from Taiwan's Bureau of National Health Insurance (BNHI) research database from 1998 to 2011 and found 9316 patients with thyroid surgery. Cox regression model was used to calculate the hazard ratio (HR).A count of 314 cases (3.4%) of hypoparathyroidism was identified. The 9 years cumulated incidence of hypoparathyroidism was the highest in patient undergone bilateral total thyroidectomy (13.5%) and the lowest in the patient with unilateral subtotal thyroidectomy (1.2%). However, in the patients who had undergone unilateral subtotal, the risk was the highest in bilateral total (HR: 11.86), followed by radical thyroidectomy with unilateral neck lymph node dissection (HR: 8.56), unilateral total (HR, 4.39), and one side total and another side subtotal (HR: 2.80).The extent of thyroid resection determined the risk of development of hypoparathyroidism. It is suggested that the association of these factors is investigated in future studies.

Lowered cutoff points of obesity indicators are better predictors of hypertension and diabetes mellitus in premenopausal Taiwanese women.

INTRODUCTION: In previous study, we found that in order to prevent MS in women aged <65 years, the cutoff points of obesity indicators should be lowered. OBJECTIVE: To investigate whether our proposed cutoff points of obesity indicators predict the occurrence of hypertension (HT), diabetes mellitus (DM), and hyperlipidemia in premenopausal women with greater sensitivity and specificity compared to reference cutoff points of obesity that are currently being used. METHODS: Using the database of the "2002 Survey on the Prevalence of Hypertension, Hyperglycemia and Hyperlipidemia in Taiwan" provided by the Bureau of Health Promotion, Taiwan as research material, data from 2270 premenopausal women aged 20-65 years were used for the analyses. The receiver-operating characteristic curves (ROC) of the body-mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), and waist-to-height ratio (WHtR) were used to predict HT, DM, and hyperlipidemia. RESULTS: Obesity is not a good predictor of the occurrence of hyperlipidemia in premenopausal women aged <65 years. However, our proposed cutoff points had greater sensitivity and specificity than did the reference cutoff points. To prevent the risk of HT and DM in premenopausal women, the cutoff points of obesity indicators should be reduced. The proposed values are as follows: a WHR of 0.79; a WC of 74.7 cm; a WHtR of 0.49; and a BMI of 22.3 kg/m(2).

Neurofibroma with increased uptake of [F-18]-fluoro-2 deoxy-D-glucose interpreted as a metastatic lesion.

We report a patient with a solitary spinal neurofibroma in the posterior mediastinum interpreted as a metastatic tumor. A 46-year-old female with rectal cancer who had undergone operation and subsequent adjuvant chemotherapy two years previously was referred to our department for a follow-up whole body FDG-PET study. PET scan revealed a mass with increased uptake of FDG (SUV = 4.6) in the posterior mediastinum. MRI examination showed a dumbbell neurogenic tumor originating from the intercostal nerve at T6 level. A subsequent CT-guided biopsy demonstrated a neurofibroma.