On the clinical importance of thyroid microsomal and thyroglobulin antibody determination

1987 ◽  
Vol 116 (1_Suppl) ◽  
pp. S325-S329 ◽  
Author(s):  
W. A. Scherbaum

Abstract. Among the various autoantibody tests applied in research and clinical practice, the determination of thyroid microsomal (TMAb) and thyroglobulin antibodies (TgAb) still retains its strong value in the screening for thyroid autoimmunity. The presence in the serum of TMAb is almost invariably associated with thyroid autoimmune disease or focal thyroiditis. The appearance of TMAb together with elevated serum-TSH in subclinical autoimmune thyroiditis strongly suggests progression to overt hypothyroidism. Pregnant women with positive TMAb and/or TgAb run an increased risk for post-partum painless thyroiditis with transient thyrotoxicosis and subsequent hypothyroidism. After delivery also a relapse of previously unrecognized Graves' thyrotoxicosis may occur. Thyroid antibody determination is not a valuable tool to discriminate autoimmune thyroiditis from thyroid malignancies. TMAb and TgAb determination helps to recognize individuals with thyroid autoimmunity among patients with non-thyroid autoimmune diseases such as Addison's disease and Type I diabetes mellitus.

1974 ◽  
Vol 75 (2) ◽  
pp. 274-285 ◽  
Author(s):  
A. Gordin ◽  
P. Saarinen ◽  
R. Pelkonen ◽  
B.-A. Lamberg

ABSTRACT Serum thyrotrophin (TSH) was determined by the double-antibody radioimmunoassay in 58 patients with primary hypothyroidism and was found to be elevated in all but 2 patients, one of whom had overt and one clinically borderline hypothyroidism. Six (29%) out of 21 subjects with symptomless autoimmune thyroiditis (SAT) had an elevated serum TSH level. There was little correlation between the severity of the disease and the serum TSH values in individual cases. However, the mean serum TSH value in overt hypothyroidism (93.4 μU/ml) was significantly higher than the mean value both in clinically borderline hypothyroidism (34.4 μU/ml) and in SAT (8.8 μU/ml). The response to the thyrotrophin-releasing hormone (TRH) was increased in all 39 patients with overt or borderline hypothyroidism and in 9 (43 %) of the 21 subjects with SAT. The individual TRH response in these two groups showed a marked overlap, but the mean response was significantly higher in overt (149.5 μU/ml) or clinically borderline hypothyroidism (99.9 μU/ml) than in SAT (35.3 μU/ml). Thus a normal basal TSH level in connection with a normal response to TRH excludes primary hypothyroidism, but nevertheless not all patients with elevated TSH values or increased responses to TRH are clinically hypothyroid.


2005 ◽  
Vol 113 (07) ◽  
pp. 404-408 ◽  
Author(s):  
K. Vondra ◽  
J. Vrbíková ◽  
B. Bendlová ◽  
K. Dvorakova ◽  
I. Sterzl ◽  
...  

2018 ◽  
Vol 24 (9_suppl) ◽  
pp. 230S-239S ◽  
Author(s):  
Asmaa M. Zahran ◽  
Omnia El-Badawy ◽  
Ismail L. Mohamad ◽  
Deiaaeldin M. Tamer ◽  
Safwat M. Abdel-Aziz ◽  
...  

Hyperglycemia alone may not explain the increased risk of cardiovascular diseases (CVDs) in patients with type 1 diabetes (T1D) compared with type 2. This study emphases on the evaluation of some platelet activity markers in patients with T1D, with relevance to some metabolic disorders as hyperlipidemia and hyperglycemia. This study was performed on 35 patients with T1D and 20 healthy controls. All participants were subjected to full history taking, clinical examination and assay of glycated hemoglobin (HbA1c), and lipid profile. The expression of CD62P and CD36 on platelets and the frequency of platelet–monocyte, and platelet–neutrophil aggregates were assessed by flow cytometry. Patients showed significantly higher expression of CD62P and CD36 than the control group. Platelets aggregates with monocytes were also higher among patients than the control group. Levels of CD36+ platelets, CD62P+ platelets, and platelet–monocyte aggregates revealed significant correlations with the levels of HbA1c, total cholesterol, low-density lipoprotein, and triglycerides. Hyperlipidemia and hyperglycemia accompanying T1D have a stimulatory effect on platelet activation which probably makes those patients vulnerable to CVD than nondiabetics.


Author(s):  
Fernando A. Munoz ◽  
Cindy Chin ◽  
Samantha A. Kops ◽  
Katie Kowalek ◽  
Michael D. Seckeler

AbstractObjectivesType I diabetes mellitus (T1DM) is one of the most common chronic diseases of childhood. Diabetic ketoacidosis (DKA) in this population contributes to significant healthcare utilization, including emergency room visits, hospitalizations, and ICU care. Comorbid psychiatric illnesses (CPI) are additional risks for increased healthcare utilization. While CPI increased risk for DKA hospitalization and readmission, there are no data evaluating the relationship between CPI and hospital outcomes. We hypothesized that adolescents with T1DM and CPI admitted for DKA have increased length of stay (LOS) and higher charges compared to those without CPI.MethodsRetrospective review of 2000–2012 Healthcare Cost and Utilization Project’s (HCUP) Kids’ Inpatient Databases (KID). Patients 10–21 years old admitted with ICD-9 codes for DKA or severe diabetes (250.1–250.33) with and without ICD-9 codes for depression (296–296.99, 311) and anxiety (300–300.9). Comparisons of LOS, mortality, and charges between groups (No CPI, Depression and Anxiety) were made with one way ANOVA with Bonferroni correction, independent samples Kruskal-Wallis test with Bonferroni correction and χ2.ResultsThere were 79,673 admissions during the study period: 68,573 (86%) No CPI, 8,590 (10.7%) Depression and 12,510 (15.7%) Anxiety. Female patients comprised 58.2% (n=46,343) of total admissions, 66% of the Depression group, and 71% of the Anxiety group. Patients with depression or anxiety were older and had longer LOS and higher mean charges (p<0.001 for both).ConclusionComorbid depression or anxiety are associated with significantly longer LOS and higher charges in adolescents with T1DM hospitalized for DKA. This study adds to the prior findings of worse outcomes for patients with both T1DM and CPI, emphasizing the importance of identifying and treating these comorbid conditions.


1994 ◽  
Vol 40 (3) ◽  
pp. 31-35
Author(s):  
Ye. G. Starostina ◽  
G. R. Galstyan ◽  
I. I. Dedov

The treatment options for insulin-dependent (T1DM) and insulin-independent (T2DM) diabetes mellitus are significantly different, although they have a number of common goals (eliminating the symptoms of hyperglycemia, minimizing the risk of hypoglycemia, and preventing micro- and macroangiopathies). The main method for the correction of hyperglycemia in T2DM is the normalization of body weight (BW) with a low-calorie diet and increased physical activity. With T1DM, the genesis of which is associated not with excess BW, but with autoimmune death of p-cells and insulin deficiency, insulin replacement therapy is the main treatment method, and dietary restrictions for T1DM patients, according to modern views, are auxiliary and should be prescribed only to the extent in which their insulin therapy is different from the physiological secretion of insulin. The fundamental principles of traditional diet therapy for T1DM have been critically reviewed in recent years. The most important requirement of traditional dietetics is the so-called "calorie balance"; hence, with an excess BW, a hypocaloric diet is usually recommended, with a deficiency of BW, a diet with a high calorie content, and with normal BW, one that guarantees the maintenance of BW. However, it has recently been proven that with normal BW, the lowest rates of morbidity and mortality are by no means always observed. In contrast, the highest expected life expectancy was found in individuals with relatively small excess BW. Based on this, patients with T1DM are unlikely to strive at all costs for a true "ideal weight". A diet with a reduced number of calories compared to a healthy person with the same physical activity cannot provide a patient with T1DM with a normal weight of sufficient physical performance. A deficiency of carbohydrates leads to an insufficient supply of energy to the body. In adults, this is manifested by a decrease in working capacity, in children - by a lag in physical development. In addition, insufficient intake of carbohydrates is accompanied by the emptying of glycogen depots in the liver and an increased risk of hypoglycemia. With a deficiency of carbohydrates, endogenous fats begin to be consumed as an energy source, which leads to acetonuria.


2019 ◽  
Vol 35 (4) ◽  
Author(s):  
Muneera Fadhil Ridha ◽  
Munib Ahmed Al Zubaidi

Background & Objective: As an autoimmune disease, Type-1 diabetes mellitus (DM) may be associated with other autoimmune disorders, the presence of thyroid antibodies could be negatively impact the diabetic control. Our objective was to investigate thyroid autoimmunity in a cohort of children and adolescents with Type-1 diabetes and the Influence of the presence of thyroid autoimmune abnormalities on the control of diabetes in group of Iraqi pediatric patients with Type-I D.M. Methods: This study was conducted at the Medical City Complex, Children Welfare Hospital, Baghdad, Iraq. This study was carried out from the first of January 2016 till the end of September 2017. Data were analyzed from 150 patients with Type-1 diabetes, aged 1–18 years who were treated and are coming for regular follow up in the diabetic clinic. Thyroid functions tests, Antibodies to thyroglobulin (anti-TG) and thyroperoxidase (anti-TPO) were measured, documented and correlated with diabetic control according to glycated haemoglobin (HbA1c) level. Results: In the total of 150 patients, positive Antibodies to thyroglobulin (anti TG) were more in ≤3 years duration group of Diabetes mellitus( DM) and negative anti TG was less in the >3 years duration of DM group with statistically significant results (p=0.043), Regarding the distribution of thyroid antibodies (AB) according to HbA1c group, there was progressive positive anti thyroperoxidase (anti TPO) titer with glycemic status, good glycemic control had the lowest positive anti TPO titer and poor glycemic control group had the highest positive anti TPO titer and the result was statistically significant (p=0.048). Conclusions: Thyroid autoimmunity may be associated with poor diabetic control and elevated TSH levels, indicating subclinical hypothyroidism that my affect the diabetic control. doi: https://doi.org/10.12669/pjms.35.4.192 How to cite this:Ridha MF, Al-Zubaidi MA. Thyroid auto immune antibodies in children with type I Diabetes mellitus in relation to diabetes control. Pak J Med Sci. 2019;35(4):---------. doi: https://doi.org/10.12669/pjms.35.4.192 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


2019 ◽  
Author(s):  
Nsrein Ali ◽  
Hamid Reza Rezvani ◽  
Diana Motei ◽  
Sufyan Suleman ◽  
Walid Mahfouf ◽  
...  

AbstractCoping with diabetes requires frequent and even today mostly invasive blood glucose-based monitoring. Partly due to this invasive nature and the associated reduced skin wound healing and increased risk of infection, non-invasive glucose monitoring technologies would represent considerable progress. Edited keratinocytes may enable such a function.To address this hypothesis, we conducted a proteomic screen in the skin by making use of the experimental in vivo mouse model of type I diabetes alongside controls. We identified Trisk 95 as the only protein whose expression is induced in response to high blood glucose. A luciferase reporter assay demonstrated that induction of Trisk 95 expression occurs not only at the protein level but also transcriptionally. This induction was associated with a marked elevation in the Fluo-4 signal, suggesting a role for intracellular calcium changes in the signalling cascade. Strikingly, these changes lead concurrently to fragmentation of the mitochondria. As judged from the knockout findings, both the calcium flux and the mitochondrial phenotype were dependent on Trisk 95 function, since the phenotypes in question were abolished.The data demonstrate that the skin represents an organ that reacts robustly and thus mirrors changes in systemic blood glucose levels. The findings are also consistent with a channelling model of Trisk 95 that serves as an insulin-independent but glucose-responsive biomarker taking part in releasing calcium from the cellular stores in the skin. The skin cells may thus provide a novel mean for glucose monitoring when analysing changes in labelled Trisk 95 and calcium. By that, this study is the first proof of the concept of our registered patent (No. PCT FI2016/050917), which proposes the use of cells as biosensors for developing personalized health-monitoring devices.


1987 ◽  
Vol 116 (1_Suppl) ◽  
pp. S27-S34 ◽  
Author(s):  
Ian Todd ◽  
Ricardo Pujol-Borrell ◽  
Antonino Belfiore ◽  
Gian Franco Bottazzo

Abstract. The occurrence of HLA Class II expression by thyroid (and other endocrine) epithelia in autoimmune diseases suggests that these cells may facilitate their own destruction by immunogenically presenting autoantigens. This is supported by the findings that Class II+ thyrocytes can specifically stimulate virus-specific and autoreactive T cell clones, and that Class II expression by thyrocytes correlates with the occurrence of thyroid autoantibodies. A variety of factors may contribute to the regulation of Class II expression by thyrocytes: this is induced by interferon (IFN-gamma), and is enhanced by thyroid stimulating hormone (TSH) and by tumour necrosis factor (TNF). Conversely, epidermal growth factor (EGF) suppresses the induction of Class II in thyrocytes. This complex regulation is reflected in differences in HLA-D subregion expression between patients (DR > DP > DQ). The immune-based mechanisms of thyrocyte Class II regulation are clearly applicable to the on-going disease in an infiltrated thyroid, but the possibility of nonimmune Class II induction deserves attention, particularly in identifying factors which might contribute to the initial autoimmune attack. The possible involvement of such mechanisms in autoimmunity is supported by findings in Type I diabetes in which Class II+ islet beta cells can be found in the absence of infiltration. Further evidence is provided by the observation that a proportion of thyrocytes transformed with SV40 DNA constitutively express Class II molecules. Finally, the 'activated' state of capillary endothelial cells in organs subject to autoimmune attack suggests that they may play an important role in facilitating the autoreactive infiltration of the tissues.


2020 ◽  
Vol 30 (Supplement_5) ◽  
Author(s):  
K Giannakou ◽  
I Bolanou ◽  
S Chrysostomou

Abstract Background Type I Diabetes mellitus (DT1) is a multifactorial disease with various genetic and environmental factors involved in its pathophysiology. Several nutritional factors such as the timing of exposure to solid foods may increase the risk of DT1. The aim of this systematic review was to investigate the association between the time of introducing solid food into infant's nutrition during the first year of life and the risk of developing DT1. Methods PubMed and Science Direct were searched from inception to October 2019 for observational studies that investigated the above association. No restrictions on language or publication date were applied. Specific inclusion and exclusion criteria were set for the selection of articles. Title and abstract screening were performed by two independent researchers and data were extracted from shortlisted articles. Results In total, 76 studies were screened, and 7 articles met the inclusion criteria. The analysis shows that early exposure (before or during 3 or 4 months) and subsequent exposure (during or after 6 or 7 months) was associated with an increased risk of developing DT1 and/or pancreatic islet autoimmunity, compared to an intermediate exposure period (4-6 months, 4-5 months or 3-6 months). Conclusions The evidence suggests that an interim exposure period of genetically predisposed infants to DT1 from 4 to 5 months of age may reduce the risk of developing DT1 in later life as compared to early or later exposure. However, due to the limitations of the studies, further investigation is required to inform DT1 prevention practices. Key messages There is some evidence indicating that early exposure and later exposure to solid food may increase the risk of developing DT1 in children with a genetic predisposition. Due to the methodological heterogeneity across the studies included, more reliable data from large prospective studies and randomized clinical trials are needed.


2013 ◽  
Vol 24 (2) ◽  
pp. 108-128 ◽  
Author(s):  
H V WRIGHT ◽  
D J WILLIAMS

Thyrotoxicosis affects approximately 1:500 women of reproductive age. Untreated or poorly controlled thyrotoxicosis in pregnancy is associated with significant maternal and perinatal morbidity. Recognition and diagnosis of new onset thyrotoxicosis in pregnancy can be challenging as many of the symptoms can be misattributed to physiological adaptation of normal pregnancy. Women with hyperemesis gravidarum (HG) often have biochemical, but not clinical evidence of thyrotoxicosis, which does not need treatment with anti-thyroid drugs (ATDs). For women with clinical thyrotoxicosis, uncertainty regarding the risks of teratogenicity due to ATDs has led to new guideline recommendations for their use in pregnancy. Women with autoimmune diseases such as type I diabetes and who have thyroid peroxidase antibodies (TPOAb) are at an increased risk of developing postpartum thyroiditis, which can result in permanent hypothyroidism. This review summarises the management of thyrotoxicosis in pregnancy and highlights controversial areas for which conclusive evidence is still lacking.


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