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07.03.08
Hashimoto’s thyroiditis:
1. Enlargement of the thyroid gland (goitre)
2. Lack of essential substances in diet (iodine)
3. Histologically:
• Destruction of thyroid follicle epithelium
• Diffuse infiltration of the thyroid by lymphocytes
• The normally flattened thyroid epithelial cells are replaced by plump
Hurthie cells
4. Hashimoto’s thyroiditis auto – Ab:
• Anti – thyroglobulin Ab against thyroglobulin Ag
• Anti – microsomal Ab against peroxidase Ag
5. Thyroglobulin:
• T3: Tri – iodothyronine
• T4: thyroxin
6. Immunologic pathogenesis:
• Ab may cooperate with normal lymphocytes to produce tissue damage
• In test tube, normal lymphocytes of human can cooperate with thyroid
Ab to damage thyroid cells (Ag) or lyses carrier cells coated with
thyroglobulin or thyroid microsomes
• This finding support the view that Ab – dependent cell mediated
lymphocytotoxicity (ADCC) is responsible for the induction of
pathologic changes in thyroid
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• Anti – microsomal Ab against peroxidase Ag
• Anti – human thyroid stimulating immunoglobulin Ab (TSI)
against TSH receptor Ag
7. Laboratory diagnosis:
• Thyroid function test:
o Increase level of T3 and T4
o Lower level of TSH
8. Histologically:
• Hyper secretion of the gland with little inflammation or no
inflammation
• The thyroid follicular lining cells are cuboids instead of flat
• The colloid near the epithelium has a scalloped appearance
•
Laboratory diagnosis of Hashimoto’s and Graves’ disease:
1. Indirect immuno-fluorescence technique to detect auto – Ab against
thyroglobulin and microsomal Ag
2. Substrate (Ag): thyroid gland from rats or mice
• Auto – Ab: patient serum (diluted)
• Fluorescence is seen in either:
o In the colloid area (thyroglobulin Ab) of thyroid epithelium
o In the cytoplasm (microsomal Ab) of thyroid epithelium
3. Agglutination reaction to detect auto – Ab against thyroglobulin and
microsomal Ag
• Latex agglutination or hemagglutination reaction
• Latex beads or erythrocytes are coated with specific Ag
• Patient’s serum: contain auto – Ab
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MYASTHENIA GRAVIS
Diagnosis:
1. RIA for detecting anti – ACH receptor Ab:
• Place labelled 125I (α-bungarotoxin) toxin in test tube
• Add preparation of human ACH receptor (Ag) complexes
• Incubate and allow to react
• Add patient’s serum (anti – ACH receptor Ab)
• Incubate
• Add specific human anti – globulin Ab (specific second Ab against
no 4)
• Incubate
• Final link: α-bungarotoxin – human ACH receptor – serum contain
anti – ACH receptor – anti globulin Ab specific
• Precipitation of the labelled toxin – receptor Ag – Ab – anti Ab =
complexes occur
• The precipitate is counted for radioactivity to estimate the Ab
content of the sample
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GOOD PASTURE’S SYNDROME
Symptoms:
1. Haemoptysis (coughing up blood from the lung)
2. Haematuria (blood in urine) developing renal failure
Laboratory diagnosis:
1. Kidney biopsy (histology) glomerulonephritis, proliferation of parietal
layer of Bowman’s capsule, crescent shape
2. Direct immunofluorescence (kidney biopsy), a diffuse linear deposition of
IgG is seen along the glomerular capillary walls
3. RIA: detection of Ab to glomerular basement membrane
Laboratory diagnosis:
1. Stained blood smear with giemsa, immature, large platelet can be found in
peripheral blood
2. Assays for auto – Ab against platelets (Ag) in serum by RIA
3. Assay for presence of auto – Ab on surface of platelets by flow cytometry
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LEUKAEMIA
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• Myeloperoxidase positive – positive for myeloid, negative for
lymphoid
• TdT negative (anti – TdT)
Diagnosis of CLL:
1. Examination of peripheral blood smears
• Absolute lymphocyte count always greater than (10X109 litre)
• Normal small lymphocytes later stages appearance of nucleoli
2. Bone marrow not required for diagnosis
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