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Posts archive for: March, 2006
  • thyroid hormone actions (and oestrogen)

    Thyroid hormones and their effects: a new perspective.
    Hulbert AJ

    Comparison of the mechanisms of nongenomic actions of thyroid hormone and steroid hormones.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=11117200&tool=ExternalSearch

    Flavonoid effects on transport, metabolism and action of thyroid hormones.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15255309&query_hl=1&itool=pubmed_docsum]
    Z Arztl Fortbild Qualitatssich. 2004 May;98 Suppl 5:17-24. Review. German.
    PMID: 15255309 [PubMed - indexed for MEDLINE]

    Chronic daily ethanol and withdrawal: 5. Diurnal effects on plasma thyroid hormone levels.
    Endocrine. 2003 Dec;22(3):329-34.

    Insight into the physiological actions of thyroid hormone receptors from genetically modified mice.
    J Endocrinol. 2002 Dec

  • Effects of Binding Proteins; Blood Tests

    Below is page4, pls read the whole artilce for more on blood tests

    http://www.medscape.com/viewarticle/524956_4

    Effects of Binding Proteins
    Various hormone binding proteins are present at a range of concentrations in all serum or plasma samples.
    Measurement of total hormone concentration requires displacement of the hormone from its binding site. Unless the protein binding of both labelled and unlabelled ligands is inhibited or removed, an equilibrium will form between the binding proteins, the labelled and unlabelled ligand and the analytical antibody, producing false Results.[42]

    Assays may be affected by changes in specific binding proteins, whether due to congenital variations, increased synthesis or decreased clearance.
    GH binding protein can interfere with the measurement of GH to different extents in different immunoassays,[63] as can corticotrophin releasing hormone (CRH) binding protein in CRH assays.[64]
    Changes in cortisol binding globulin may affect the measurement of progesterone, oestradiol, GH and cortisol itself.
    The use of free T4 assays has largely overcome the problem of interpreting T4 Results when thyroxine binding globulin varies.[65]

    A number of drugs, including phenytoin, carbamazepine and salicylate, compete with thyroid hormone binding to serum binding proteins and may increase free T4.
    Frusemide affects free T4 assays by the same mechanism when samples for thyroid hormone measurement are taken from intravenous sites where frusemide has been administered.[66,67]
    In vivo administration of heparin liberates FFAs, which displace thyroid hormones from their binding proteins and so increase free T4 when measured by equilibrium Methods.[40]
    The presence of paraproteins in serum may also result in nonspecific binding of either analyte or reagent[68] or interference in nephelometric assays.[69-72]
    Binding proteins may also be increased artefactually when an individual assumes an upright position after a period of recumbency and this may also result from the use of a tourniquet on blood collection.[31]

    also read other pages

  • Hashimoto Encephalopathy

    http://www.medscape.com/viewarticle/524449?src=mp
    Serum Levels of Thyroid Antibodies Clue to Hashimoto Encephalopathy

    NEW YORK (Reuters Health) Feb 27 - Testing for serum levels of thyroid peroxidase and thyroglobulin antibodies might improve the diagnosis of steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), also known as "Hashimoto encephalopathy," researchers report.

    Little is known about the pathophysiology and characteristics of SREAT, a syndrome that might be present even though the regular tests to evaluate the cause of an encephalopathy (such as serum sensitive thyroid-stimulating hormone levels, erythrocyte sedimentation rates, cerebrospinal fluid profiles, and neuroimaging results) appear normal.

    "These patients do not fit the typical criteria that most of us were trained to look for to diagnose an autoimmune disorder," co-author Dr. Brad Boeve, from the Mayo Clinic College of Medicine in Rochester, Minnesota, told Reuters Health. "Doctors must learn to systematically check for thyroid antibodies and other markers of autoimmunity."

    Although high serum levels of thyroid peroxidase antibodies are often found in patients with SREAT, it is a common marker for most autoimmune neurologic disorders. Because misdiagnosis of SREAT is common and the syndrome is treatable with steroid therapy, detecting abnormal blood levels of thyroid antibodies might save lives.

    "The primary goal of our study is to raise awareness that some patients who at first are diagnosed with an untreatable or fatal form of encephalopathy might actually be saved with steroid therapy," Dr. Boeve said.

    To better characterize SREAT, Dr. Boeve and his team retrospectively analyzed clinical, laboratory and radiologic data of 20 patients diagnosed with SREAT between 1995 to 2003. The findings are published in the February issue of the Archives of Neurology.

    By definition, all patients presented serum thyroid antibodies and improved significantly when given high-dose corticosteroid therapy. Fifteen returned to their baseline status and five still had mild symptoms.

    The authors note that all patients had been given an incorrect diagnosis at presentation, most commonly viral encephalitis, Creutzfeldt-Jakob disease, or a degenerative dementia.

    The most frequent clinical features of these patients were: tremor in 80%, transient aphasia in 80%, myoclonus in 65%, gait ataxia in 65%, seizures in 60%, and sleep abnormalities in 55%.

    The most frequent laboratory abnormalities included increased liver enzyme levels, increased serum sensitive thyroid-stimulating hormone levels, and increased erythrocyte sedimentation rate.

    These results provide additional symptoms to better characterize SREAT and identify patients who might benefit from steroid therapy, according to the authors.

    Arch Neurol 2006;63:197-202.

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