PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 6438696

[Thyroid diagnosis today].

S F Grebe·H Müller
View original source ↗Export metadata ↓

Abstract

For functional diagnostics the FT4 index is calculated from the T4 and T3U values. Hyperthyroidism is suggested or borderline values are found; the T3 test is carried out. An index of free iodine hormones (IFIH) can be calculated. (formula; see text) Hypothyroidism and borderline cases require TSH evaluation or even a TRH test. T4 and T3 autoantibodies can cause high or low values in spite of euthyroidism or hypothyroidism. Differences in FT4 values are found if the kits used were not made by the same manufacturer. These values help to determine hyperthyroidism in pregnancy. The FT3 value is better than the TT3 value in determining T3 hyperthyroidism in borderline cases. Autonomy can be guaranteed by the 123 I short test or the 20-min 99 m Tc uptake test before and after administration of T4. Location diagnostics by scintigraphy after administration of 99m Tc or radioiodine determine localization, size, shape, and distribution of functioning thyroid tissue and metastases by iodine accumulation. This is imaging of biochemical processes. By ultrasonography, a physical method, cysts, disintegration cysts or parenchymal nodes can be recognized. X-ray films of the trachea can determine stenosis caused by a struma. In addition to the exact proof of an intrathoracal struma (front and back mediastine), a retrotracheal or retroesophageal thyroid gland can be seen on CT. RIA determination of the tumor markers calcitonin and TG supports the diagnosis of medullar and follicular or papillary thyroid carcinoma.

Explore related subjects

AutoantibodiesCalcitoninHumansRadioimmunoassayTechnetiumThyroglobulinThyroid DiseasesThyroid Function TestsThyroid GlandThyroid HormonesThyroid NeoplasmsThyrotropin-Releasing HormoneEnglish AbstractJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S F Grebe, H Müller. 1984. [Thyroid diagnosis today].. https://pubmed.ncbi.nlm.nih.gov/6438696/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2022

Integration of Infant Metabolite, Genetic, and Islet Autoimmunity Signatures to Predict Type 1 Diabetes by Age 6 Years.

CONTEXT: Biomarkers that can accurately predict risk of type 1 diabetes (T1D) in genetically predisposed children can facilitate interventions to delay or prevent the disease. OBJECTIVE: This work aimed to determine if a combination of genetic, immunologic, and metabolic features, measured at infancy, can be used to predict the likelihood that a child will develop T1D by age 6 years. METHODS: Newborns with human leukocyte antigen (HLA) typing were enrolled in the prospective birth cohort of The Environmental Determinants of Diabetes in the Young (TEDDY). TEDDY ascertained children in Finland, Germany, Sweden, and the United States. TEDDY children were either from the general population or from families with T1D with an HLA genotype associated with T1D specific to TEDDY eligibility criteria. From the TEDDY cohort there were 702 children will all data sources measured at ages 3, 6, and 9 months, 11.4% of whom progressed to T1D by age 6 years. The main outcome measure was a diagnosis of T1D as diagnosed by American Diabetes Association criteria. RESULTS: Machine learning-based feature selection yielded classifiers based on disparate demographic, immunologic, genetic, and metabolite features. The accuracy of the model using all available data evaluated by the area under a receiver operating characteristic curve is 0.84. Reducing to only 3- and 9-month measurements did not reduce the area under the curve significantly. Metabolomics had the largest value when evaluating the accuracy at a low false-positive rate. CONCLUSION: The metabolite features identified as important for progression to T1D by age 6 years point to altered sugar metabolism in infancy. Integrating this information with classic risk factors improves prediction of the progression to T1D in early childhood.

Autoantibodies↗
PubMed2022

Heterogeneity of Acetylcholine Receptor Autoantibody-Mediated Complement Activity in Patients With Myasthenia Gravis.

BACKGROUND AND OBJECTIVES: Autoantibodies targeting the acetylcholine receptor (AChR), found in patients with myasthenia gravis (MG), mediate pathology through 3 mechanisms: complement-directed tissue damage, blocking of the acetylcholine binding site, and internalization of the AChR. Clinical assays, used to diagnose and monitor patients, measure only autoantibody binding. Consequently, they are limited in providing association with disease burden, understanding of mechanistic heterogeneity, and monitoring therapeutic response. The objective of this study was to develop a cell-based assay that measures AChR autoantibody-mediated complement membrane attack complex (MAC) formation. METHODS: An HEK293T cell line-modified using CRISPR/Cas9 genome editing to disrupt expression of the complement regulator genes (CD46, CD55, and CD59)-was used to measure AChR autoantibody-mediated MAC formation through flow cytometry. RESULTS: Serum samples (n = 155) from 96 clinically confirmed AChR MG patients, representing a wide range of disease burden and autoantibody titer, were tested along with 32 healthy donor (HD) samples. AChR autoantibodies were detected in 139 of the 155 (89.7%) MG samples through a cell-based assay. Of the 139 AChR-positive samples, autoantibody-mediated MAC formation was detected in 83 (59.7%), whereas MAC formation was undetectable in the HD group or AChR-positive samples with low autoantibody levels. MAC formation was positively associated with autoantibody binding in most patient samples; ratios (mean fluorescence intensity) of MAC formation to AChR autoantibody binding ranged between 0.27 and 48, with a median of 0.79 and an interquartile range of 0.43 (0.58-1.1). However, the distribution of ratios was asymmetric and included extreme values; 16 samples were beyond the 10-90 percentile, with high MAC to low AChR autoantibody binding ratio or the reverse. Correlation between MAC formation and clinical disease scores suggested a modest positive association (rho = 0.34, p = 0.0023), which included a subset of outliers that did not follow this pattern. MAC formation did not associate with exposure to immunotherapy, thymectomy, or MG subtypes defined by age-of-onset. DISCUSSION: A novel assay for evaluating AChR autoantibody-mediated complement activity was developed. A subset of patients that lacks association between MAC formation and autoantibody binding or disease burden was identified. The assay may provide a better understanding of the heterogeneous autoantibody molecular pathology and identify patients expected to benefit from complement inhibitor therapy.

Autoantibodies↗
PubMed1998

Antiglycolipid antibodies in motor neuropathies.

In peripheral neuropathies with monoclonal gammopathy, mainly IgM, it appears clear from clinical, electrophysiological, and experimental data, that the target glycolipid or glycolipid epitope for the IgM is related to the type of neuropathy--purely sensory, predominantly sensory, or uniquely motor. Investigations have focused on chronic peripheral neuropathies associated with polyclonal IgM reactivity to glycolipids. Although IgM anti-GM1 antibodies are present in normal controls, there is a subgroup of motor neuropathies with high titer anti-GM1 antibodies, mainly multifocal neuropathies with conduction blocks (MMNCB). Another subgroup of MMNCB may include IgM anti-SGPG antibodies that do not cross-react with MAG. The importance of the fine structure of the epitope has to be considered in view of the pathogenicity of the antibody. It may bear consequences on its binding properties on the neuronal surfaces and on its biological implications.

Autoantibodies↗