Cases reported "Hypothyroidism"

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1/24. Transient elevation of triiodothyronine caused by triiodothyronine autoantibody associated with acute Epstein-Barr-virus infection.

    A unique 16-year old female patient presented after acute Epstein-Barr virus (EBV) infection with severe primary hypothyroidism. Her thyroid test results were thyrotropin level (TSH) of 198 mU/L (normal, 0.4-4 mU/L), free thyroxine [FT(4)], 2.5 pmol/L (normal, 10-25 pmol/L), total triiodothyronine (TT(3)) > 19.5 nmol/L (normal, 1.3-2.7 nmol/L), and free triiodothyronine (FT(3)), 0.77 pmol/L (normal, 3.3-6.3 pmol/L). She had high titers of thyroglobulin and thyroid peroxidase autoantibodies. in vitro triiodothyronine (T(3))-binding measured by radioimmunoprecipitation was 86% (normal, up to 8.5%) and thyroxine (T(4))-binding 8.2% (normal, 6.4%). Serum immunoglobulin g (IgG) absorption, achieved by protein-G sepharose beads, decreased TT(3) toward normal. Levothyroxine treatment normalized the low baseline FT(4) and FT(3) values, and suppressed TSH to normal. However, TT(3) remained highly elevated and returned to normal after 20 months, while T(3 )binding gradually decreased. Thus, her severe hypothyroidism was masked by this unusual phenomenon. Thirty-four patients with EBV infection (15 with acute disease and 19 with previous infection) were tested for thyroid hormone levels. EBV antibodies (early antigen immunoglobulin m [IgM] and IgG and anti-Epstein-Barr virus nuclear antigen [EBNA] IgG) were measured by enzyme-linked immunosorbent assay (ELISA). In 15 patients with acute EBV the mean TT(3) level was 2.47 /- 0.39 nmol/L (5 had TT(3) values above normal) compared to a mean TT(3) of 1.70 /- 0.53 nmol/L in 19 subjects with previous infection (p < 0.0005; only 1 had a TT(3) result above normal), with no differences in FT(4) and TSH concentrations between the two groups. Acute EBV infection may be associated with transient mild to severe TT(3) elevation as a result of assay interference by anti-T(3) autoantibodies.
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2/24. Full-blown hypothyroidism associated with vitiligo and acropachy. Report of one case.

    During the first two years after the onset of hypothyroidism, a patient with spontaneous primary myxedema developed thyroid acropachy. Fifteen years before the diagnosis of thyroid disease, he had patchy vitiligo of the face. There were high serum levels of antibodies against thyroglobulin (anti-Tg) and microsomal antigen (anti-M) were present, while the serum levels of antibodies against the second antigen of the colloid and the cell-surface antigen fell within the normal range. Moreover, antibodies to gastric parietal cells, adrenocortical cells or pancreatic islets in the serum were not present. Concerning the immuno-genetic pattern of our patient, his HLA system did not appear to confirm the well documented prevalence in whites with autoimmune disorders of an antigen specificity positive for the locus DR3.
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3/24. Down's syndrome and autoimmunity.

    A patient with Down's syndrome (DS) with multiple autoimmune phenomena is described. She suffered from hypothroidism, a celiac-like enteropathy and hemolytic anemia, and displayed cellular immunity directed against peripheral nerve antigen and basic myeloprotein and serum autoantibodies to many other tissue antigens. Her mother did not suffer from any overt autoimmune disease, but similar autoantibodies were found in her serum. It is suggested that DS resembles other autoimmune diseases, especially that which occurs in the NZB mice. The resemblance is based on the assumption that in both cases genetic and/or viral factors cause T-cell dysfunction which leads on the one hand to increased susceptibility to infections and leukemias, to autoimmune phenomena and to depressed cellular immunity, and on the other hand to increased B--cell reactivity.
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4/24. Immune complex glomerulonephritis mediated by thyroid antigens.

    Hypothyroidism, microscopic hematuria, and proteinuria developed in an 11-year-old girl. A renal biopsy specimen showed increased mesangial cells and matrix with focal glomerular basement membrane thickening. Three years later, a pronounced increase in proteinuria was detected. Elevated levels of antibody to thyroid microsomal antigen and thyroglobulin were found in the serum. A renal biopsy specimen showed a pronounced increase in mesangial cells and matrix with generalized glomerular basement membrane thickening. Electron microscopic studies demonstrated granular deposits in the capillary walls and mesangium. Immunofluorescent studies revealed granular deposits of IgG, IgM, and C3, primarily on the glomerular basement membrane. By indirect immunofluorescence, granular glomerular basement membrane and mesangial staining were detected with antibody specific for thyroglobulin and thyroid microsomal antigen. These observations suggest development of immune complex glomerulonephritis mediated by thyroid antigens.
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5/24. association between human leukocyte antigen (HLA) and interferon- induced thyroid diseases in four patients with HCV-related chronic hepatitis.

    OBJECTIVES: The interferon-alpha (IFN-alpha) therapy for HCV hepatitis may exacerbate or induce underlying thyroid disorders. Besides viral factors, the human leukocyte antigen (HLA) may be an independent risk factor. methods: We evaluated fifteen patients with HCV chronic hepatitis during a period of 40 months. At the enrollment, all the patients were negative for thyroid disorders, excluding one patient with subclinical hypothyroidism. Eleven patients received IFN-alpha therapy. The HLA system was examined in every patient, evaluating antigens (n=40) of locus A, B and Cw and alleles (n=19) of locus DRB1* and DQB1*. The HLA system was also examined in healthy subjects (n=107) as a control group. RESULTS: The HCV genotype distribution in patients was: 1b=20%, 2a=60%, 3a=20%. Four IFN-treated patients presented clinical thyroid disorders, including autoimmune hypothyroidism (n=2), transient thyrotoxicosis (n=1) and subacute thyroiditis (n=1). The HLA susceptibility to thyroid disorders (antigen/allele frequency) in the whole group of patients was not different in respect to controls and normal Italian population. The patients with HCV chronic hepatitis that developed thyroid diseases after IFN- treatment had a double and specific association with the HLA system (Mantel-Haenszel X(c)(2)=4.706, p<0.05). CONCLUSIONS: This case report suggests that HLA system examination is an important and promising diagnostic aspect that may be considered in order to evaluate the appearance of thyroid disorders during the IFN-alpha treatment for HCV-related chronic hepatitis.
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6/24. Exacerbation of hypothyroidism following tumor necrosis factor-alpha infusion.

    A 46-year-old woman with chronic thyroiditis who had been receiving thyroid hormone treatment for 10 yr developed severe hypothyroidism (FT4 0.37 ng/dl, FT3 1.38 pg/ml, TSH 151.00 microU/ml) following tumor necrosis factor-alpha (TNF) infusion for the treatment of a complicated cutaneous T-cell lymphoma. Indirect immunofluorescence staining of thyroid follicular cells showed aberrant expression of HLA class II antigens. The mechanisms underlying the exacerbation of the hypothyroidism may be an augmentation of immunological processes in the thyroid and a direct action of TNF on the synthesis and secretion of thyroid hormone.
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7/24. Severe hypothyroidism induced by thyroid metastasis of colon adenocarcinoma: a case report and review of the literature.

    An 85-year-old man who had undergone a right hemicolectomy for colon cancer presented with severe hypothyroidism and hoarseness 21 months after the operation. The serum thyrotropin (TSH) was markedly elevated to 118.14 microIU/mL and serum free thyroxine (fT4) level was markedly suppressed to 0.34 ng/dL. Symptoms of hoarseness and neck swelling were already evident 4 months prior at which time tests for normal thyroid function were performed. The patient was referred due to aggravated pain on his diffusely enlarged hard goiter. An enlarged thyroid with some calcification was noticed in the neck ultrasonography with multiple cervical lymphadenopathies. Core biopsy of the thyroid gland showed invasion of poorly differentiated adenocarcinoma cells. Immunohistochemical studies showed positive staining only for carcinoembryonic antigen (CEA). There were multiple lung parenchymal nodules and adrenal masses at the time of evaluation. The patient was started on palliative chemotherapy with thyroid hormone replacement and gradually became euthyroid. From these findings and the clinical observations, thyroid metastasis with hypothyroidism developing acutely from metastatic colon adenocarcinoma was diagnosed.
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8/24. A case of transient elevation of the serum carcinoembryonic antigen and associated with severe malnutrition and low T3, T4 syndrome.

    A patient with a transient elevation of the serum carcinoembryonic antigen (CEA) associated with a benign disease was reported. The elevation of CEA was noted in the patient with low T3, T4 syndrome associated with malnutrition due to malabsorption syndrome induced by post-gastrectomy and chronic pancreatitis. Mild liver dysfunction and diabetes mellitus were also noted. The CEA level decreased as T3, T4 level and malnutrition were improved by administration of a massive digestive enzyme preparation. This inverse correlation between the serum CEA and serum T3, T4 levels suggested that high levels of the serum CEA can be found in the patient with malnutrition.
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9/24. Imparied cyclic-AMP response to thyrotrophin in congenital hypothyroidism with thyroglobulin deficiency.

    A 19 year old man had congenital hypothyroidism and severely retarded development. His thyroid gland was not enlarged and laboratory findings included low serum concentration of T4 (2.8 microgram/100 ml) and T3 (16 ng/100 ml) with a high level of TSH (52 microU/ml) that rose to 192 microU/ml after TRH. 131I uptake by the thyroid was normal (41.5% at 24 h) and did not show a normal increase after exogenous TSH administration (49.5% at 24 h). The perchlorate discharge test was negative and no antibodies against thyroid antigens were found. Studies on the biopsy specimen revealed low iodide trapping by the thyroid slices and no formation of cyclic amp after TSH was added to the medium. The endogenous TSH of the patient was biologically active increasing cyclic adenosine monophosphate c-AMP concentration in normal thyroid slices. No thyroglobulin was found in the thyroid tissue either by immunological or ultracentrifugational methods. An increased proportion of iodoalbumin was present in the serum. We postulate that the fundamental defect in this gland is an impaired generation of c-AMP by the defective thyroid cell and deficiency of thyroglobulin formation resulting in inadequate thyroxine and triiodothyronine synthesis.
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10/24. Qualitative and quantitative defects of thyroglobulin resulting in congenital goiter. Absence of gross gene deletion of coding sequences in the TG gene structure.

    Seven subjects belonging to three families (ME, MA, MO), with congenital goiter and various degrees of thyroid hypofunction, were investigated from the standpoints of clinical, biochemical, and molecular biology. In two of these families (ME, MA), 6 individuals had low serum levels of Tg-related antigens with a minor increase after bovine TSH (bTSH) stimulation. A large proportion of the tracer was incorporated into serum albumin, and Tg antigens in the thyroid extracts were barely detectable by RIA. (0.19 mg/g tissue; normal, 70-90 mg/g). Gel filtration (CL6B sepharose gel) showed absence of a normal Tg peak, and SDS agarose gel electrophoresis indicated complete absence of Tg dimer and monomer. immunoelectrophoresis confirmed the absence of Tg-related antigens. Thus, in these patients a quantitative defect of Tg gene expression was characterized. By contrast, in the MO family a high basal serum concentration of immunoreactive Tg was present, with an exaggerated response to bTSH. Thyroid extracts revealed elevated TPO activity and normal levels of Tg-related antigens. Tg was also eluted in the gel filtration columns with the same mobility as standard 19S Tg. immunoelectrophoresis against rabbit and human Tg was abnormal, with two precipitin arcs being detected. The Tg molecule after hydrolysis yielded only DIT and MIT, with poor formation of iodothyronines. Microscopic studies revealed a pronounced lack of colloid in the follicular lumina, and overdistended endoplasmic reticulum cisternae.(ABSTRACT TRUNCATED AT 250 WORDS)
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