The association between Graves' disease and thrombocytopenia is rare and the mechanisms involved are protean. Though a common autoimmune basis can be hypothesized to explain both the conditions, the failure of the platelet count to recover until the toxicosis is controlled suggests alternative explanations. We report a case of a 50- year- old female who was diagnosed to have chronic immune thrombocytopenic purpura (ITP) and was started on steroids. When the platelet count was normalizing, she developed Graves ' thyrotoxicosis and her platelet count plummeted down despite an increase in steroid dosage. Once her thyrotoxic status improved after radio-iodine ablation her platelet counts rose significantly to near normal levels. This case exemplifies the possible non-immune mechanisms involved in the causation of thrombocytopenia during thyrotoxicosis and the need for testing thyroid functions in cases of autoimmune diseases like ITP especially when response to conventional treatment is poor.

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Thyroid hormones regulate the activity of some key enzymes in lipoprotein transport. In the present study, lipid profile of patients with sub clinical hypothyroidism and overt hypothyroidism who presented at G.B.Pant Hospital, New Delhi, India was reviewed for a period of one year. Serum TSH, T4 and T3 were assayed using ELISA based kits. The concentration of serum total cholesterol, HDL- cholesterol and triglycerides were measured on Auto analyzer by standard methods. Data collected was subjected to standard statistical analysis. The patients of hypothyroidism had significantly higher levels of serum cholesterol as compared to the euthyroid controls (p < 0.05). The HDL levels were comparatively lower in the hypothyroid patients. It can be concluded that hypothyroidism is associated with dyslipidemia i.e. increased Total cholesterol and LDL- cholesterol levels and decreased HDL-cholesterol levels. Lipid disorders are probably responsible for the development of atherosclerosis in hypothyroid patients in Indian population.

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Graves ' ophthalmopathy is the most frequent extrathyroidal manifestation of Graves ' disease. The manifestations of Graves ' ophthalmopathy are secondary to an increase in the volume of orbital content. The clinical features include Lid lag and lid retraction, conjunctival erythema and Chemosis, proptosis, restrictive extraocular myopathy and optic neuropathy. Disease activity can be assessed by using the Clinical Activity Score (CAS). Graves' ophthalmopathy is thought to develop as a consequence of autoimmunity to cross reacting thyroid and orbital autoantigens. Investigations include Thyroid Function Tests, Anti TSH receptor, Anti-thyroid peroxidase antibody assay and MRI of orbit. Treatment options for severe active eye disease consist of Glucocorticoids or other immunosuppressive therapy and radiotherapy. Rehabilitative surgical procedures are done after the resolution of active eye disease. They include orbital decompression, strabismus surgery and surgery for lid retraction.

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Highly Active Anti Retroviral Therapy (HAART) for the treatment of HIV causes a paradoxical deterioration of the clinical status after it's initiation, due to the reactivation of immune response to a latent or sub-clinical process. This phenomenon is called Immune Reconstitution Syndromes (1RS). We report a 48-year old man with HIV infection who was started on combination antiretroviral therapy. Three years after the initiation of therapy, he developed symptoms and signs of thyrotoxicosis. He was diagnosd to have Graves ' disease and was started on beta blockers and Neomercazole. Radioactive iodine was given after a good clinical and biochemical improvement. He became hypothyroid and currently doing well on replacement therapy. Immune reconstitution syndrome Grave's disease may appear months or even years after the initiation of antiretroviral therapy. As there is a high chance of relapse with anti-thyroid drugs, radioiodine ablation probably is more appropriate treatment in this condition after initial stabilization of thyrotoxicosis with anti-thyroid drugs

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Full text not available  [PDF]

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