Autoimmune thyroid disease (AITD), a common organ specific autoimmune disorder is seen mostly in women between 30-50 yrs of age. Thyroid autoimmunity can cause several forms of thyroiditis ranging from hypothyroidism (Hashimoto's thyroiditis) to hyperthyroidism (Graves'Disease). Prevalence rate of autoimmune mediated hypothyroidism is about 0.8 per 100 and 95% among them are women. Graves' disease is about one tenth as common as hypothyroidism and tends to occur more in younger individuals. Both these disorders share many immunologic features and the disease may progress from one state to other as the autoimmune process changes. Genetic, environmental and endogenous factors are responsible for initiation of thyroid autoimmunity. At present the only confirmed genetic factor lies in HLA complex (HLA DR-3) and the T cell regulatory gene (CTLA 4). A number of environmental factors like viral infection, smoking, stress & iodine intake are associated with the disease progression. The development of antibodies to thyroid peroxidase (TPO) thyroglobulin (TG) and Thyroid stimulating hormone receptor (TSH R) is the main hallmark of AITD. Circulating T Lymphocytes are increased in AITD and thyroid gland is infiltrated with CD4+ and CD8+ T Cells. Wide varieties of cytokines are produced by infiltrated immune cells, which mediate cytotoxicity leading to thyroid cell destruction. Circulating antibodies to TPO and TG are measured by immunofluorescense, hemagglutination, ELISA & RIA. TSHR antibodies of Graves' disease can be measured in bioassays or indirectly in assays that detect antibody binding to the receptor.
Summary Chromosomal abnormalities in 55 AML patients from Orissa (India) were studied. Of them, 12 patients had only abnormal metaphases (AA), 41 patients had both normal and abnormal metaphases (AN) and the rest 2 patients exhibited only normal metaphases (NN). Basing on the number of chromosome all the patients were classified into 5 sub-groups like (1) normal diploidy with 46 chromosomes in 2 patients, (2) pseudodiploidy group with 46 chromosomes and some structural abnormalities in 4 patients, (3) hypodiploid group with Ͻ46 chromosomes in 37 patients, (4) hyperdiploidy-A group with 47 to 50 chromosomes in 8 patients and hyperdiploidy-B group with Ͼ50 chromosomes in 4 patients. Primary translocations like t(8, 21), t(1, 14), t(9, 22) were detected in 8, 1 and 7 patients respectively. In addition, secondary aberrations were also observed in 36 patients. These secondary aberrations were mostly unstable and nonclonal ones which were present singly or in various combinations. Maximum number of patients achieved complete remmission (CR) from AN subgroup (46.3%) hyperdiploidy-B group (100%), patients with t(8; 21) translocation (75%), patients with trisomy 22 and patients with no secondary aberrations. This study suggests that hyperdiploidy, t(8, 21), trisomy 8, presence of both normal and abnormal metaphases and absence of secondary aberrations are the favourable prognosticators while presence of only abnormal metaphases, presence of more than one secondary aberration, t(9, 22) translocation, hypodiploidy and monosomy 7 are unfavourable prognosticators.
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