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Requirement
A 26-year-old woman presented with painful, stiff knees of 4 weeks duration. She had a 6-year history of Raynaud's phenomenon. On examination, she had bilateral effusions in both knee joints, but all other joints were normal. She had no skin lesions, muscle tenderness, proteinuria or fever. The results of relevant investigations are shown in Table C10.1. On the basis of these, a diagnosis of Systemic Lupus Erythematosus (SLE) was made and the patient treated with aspirin for her painful knees. She improved over 4 weeks and then remained symptom-free for 5 years. During this time, her antinuclear antibody remained positive at 1/80, her DNA-binding activity varied from 40 to 80%, and her C3 and C4 levels were occasionally low. Later, she developed a bilateral, butterfly rash across her cheeks, blotchy rash on her hands and thighs, consistent with active vasculitis and also presented with proteinuria, hematuria and glomerular nephritis. Her Raynaud's phenomenon concurrently became much worse. Following treatment with prednisolone, the skin manifestations gradually disappeared and the steroids were tailed off.
This patient presented with arthritis and Raynaud's phenomenon. She is unusual in that the arthritis of SLE usually involves small joints, but it is important to note that she remained perfectly well without treatment for 5 years, despite persistently abnormal serology.
Explain the immunological basis of her disease condition and the significance of her elevated levels of antinuclear antibodies (ANA).
Explain as to what caused her glomerular nephritis, vasculitis and bilateral skin rash.
How would you categorize the type of hypersensitivity reactions causing the above disease?
Explain how prednisolone helped to treat the symptoms.
Explain the biochemical mechanism of action of aspirin in its interaction with cyclooxygenase. Which class of macromolecules are affected by this interaction (inhibition) and state briefly a major side effect that may develop as a result of extensive aspirin therapy.
Case 2
A 29-year-old woman presented with a long history of increased sweating and palpitations, fatigue, abnormal heat sensitivity, with emaciation and weight loss. On examination, she was a nervous, agitated woman with an obvious, diffuse, non-tender, smooth, palpable enlargement of her thyroid. She had a fine tremor of her fingers and a resting pulse rate of 150/minute. She also showed signs of exophthalmos. A maternal aunt had suffered from 'thyroid disease'.
On investigation, she had a raised serum T3 of 4.8nmol/l (NR 0.8-2.4) and a T4 of 48nmol/l (NR 9-23). Measurement of her thyroid-stimulating hormone showed that this was low normal, 0.4mU/l (NR 0.4-5mU/l). The biochemical findings pointed to primary thyroid disease rather than pituitary over activity. Biopsy eliminated toxic multinodular goiter. Circulating antibodies to thyroid peroxidase (titer 1/3000; 200iu/ml) were detected by agglutination. Thyroid stimulating immunoglobulin (TSI) levels were markedly elevated. A diagnosis of autoimmune thyrotoxicosis (Graves' disease) was made. She was treated with an antithyroid drug, methimazole and 131I therapy, to control her thyrotoxicosis, and later underwent a thyroidectomy followed by replacement therapy with levothyroxine.
Discuss the immunological basis of the disease.
What is the cause of thyrotoxicosis and hyperthyroidism?
How would you categorize the hypersensitivity reactions causing the disease?
Discuss the significance of ruling out toxic multinodular goiter in arriving at a differential diagnosis.
Describe the biochemical pathway or steps involved in synthesis of thyroid hormone.
Solution
Case study -1
1. Explain the immunological basis of her disease condition and the significance of her elevated levels of antinuclear antibodies (ANA).
The patient is suffering from SLE (Systemic Lupus Erythematosus). It is an autoimmune disease. It is relapsing, remitting multisystem in nature. The disease acts against the nucleus of the own cell body and causes inflammation and organ damage. There is a production of antinuclear antibodies . These antigens from an antibody –nuclear antigen immune complex. This deposits in tissues causing inflammation and tissue injury. There is an increase in cell death and there is a defective clearance of the dead cell material.
There is inappropriate activation of B lymphocytes. T cells in SLE Patients also show abnormal signalling and secretion of cytokinines , which causes inflammation.
The disease is characterised by production of self-destructive antibody. These antibodies target the nucleus . Hence called as an antinuclear antibody. The levels of these are on a higher side in SLE.
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2. Explain as to what caused her glomerular nephritis, vasculitis and bilateral skin rash.
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In SLE the bilateral skin rash occurs due to acute cutaneous lupus. This causes a rash on the sun exposed area. The bilateral skin rash is the best-known example of the effect of SLE on skin.
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Glomerular nephritis occurs during the flare of the disease. The cell damage is extensive. Hence it is necessary to keep a check on the routine urine analysis. Nephritis develops very late.
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Vasculitis mainly develops due to complex interplay among the immune cells, endothelial cells , auto antibodies which are deposited in cell and the immune complex deposition. All these factors cause vasculitis.
3. How would you categorise the type of hypersensitivity reactions causing the above disease?
SLE is known as an autoimmune chronic inflammatory condition. It is type III hypersensitivity response. Patients with SLE have B cells activation with mainly immature B cells are in dominance.
4. Explain how prednisolone helped to treat the symptoms.
The above-mentioned medicine Prednisolone is a steroid. It prevents the release of antibodies which deposit in cells to cause inflammation. Hence in case of SLE, it is utilised to reduce the inflammation. It makes the life of the patient better.
5. Explain the biochemical mechanism of action of aspirin in its interaction with cyclooxygenase. Which class of macromolecules are affected by this interaction (inhibition) and state briefly a major side effect that may develop as a result of extensive aspirin therapy?
There are two types of cyclooxygenase. COX-1 and COX-2. Aspirin works on both of them. These COX produce prostaglandins which act as pro-inflammatory. Aspirin acts on COX-2 and modifies it to produce lipoxins. This acts as anti-inflammatory.4-benzenesulfonamide 5 is the macromolecule involved in this interaction
Aspirin has many common and rare side effects. The common side effects include excessive acid secretion from stomach, nausea, stomach cramps. Due to extensive use of aspirin, there can be symptoms like rupture of stomach walls, bleeding intestine walls, decrease blood platelets, brain haemorrhage, seizures etc.
Case study -2
1. Discuss the immunological basis of the disease.
Graves Disease is an autoimmune disorder which is characterised by the infiltration of immune effectors cells and thyroid antigen-specific T cells into the thyroid stimulating hormone receptor in the tissues. Example- orbits causing exophthalmos. Also, the antibodies produced activate thyroid stimulating hormone receptor leading to overproduction of thyroid. It also causes thyroid hyperplasia.
2. What is the cause of thyrotoxicosis and hyperthyroidism?
Graves Disease is the most common cause of thyrotoxicosis. Graves Disease is autoimmune in nature. Due to this antibodies are produced which stimulate the thyroid gland to produce excessive of thyroid hormone causing thyrotoxicosis . Hyperthyroidism is also caused due to the same factor.
3. How would you categorise the hypersensitivity reactions causing the disease?
It is a type II hypersensitivity reaction . In this, the antibodies produced as a result of person’s immune system response to bind to own antigen on the own cell surface. This causes a B cell response.
4. Discuss the significance of ruling out toxic multinodular goitre in arriving at a differential diagnosis.
Toxic nodular goitre is mainly caused by iodine deficiency. Once its presence is ruled out , we can be convinced that patient does not have an iodine deficiency. In multinodular goitre the T4 is low. In our case T4 is high. Hence once toxic multinodular goitre is ruled out and we were able to reach a differential diagnosis.
5. Describe the biochemical pathway or steps involved in the synthesis of thyroid hormone.
Biochemical pathway in synthesis of thyroid hormone
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Iodine Transport-Iodide is actively transported from the blood. It reaches the follicular lumen.
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Thyroglobulin synthesis- This is a protein which has a large number of tyrosine amino acids. This goes on to become individual thyroid molecules. Then thyroglobulin after getting synthesised in follicular epithelium cell is then secreted into follicular lumen.
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Thyroid Peroxidase-It first generated I2 by oxidising I- . Then the I2 is organised. Singly and doubly bond iodinated species of tyrosine is formed. These are Monoiodotyrosine( MIT) and Diiodotyrosine(DIT). Then Thyroid Peroxidase combines with MIT and DIT which reduces to generate T3 AND T4. T3 and T4 are transported in circulation.
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