Prevalence of diaphragmatic muscle weakness and dyspnoea in Graves' disease and their reversibility with carbimazole therapy.
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OBJECTIVES: Dyspnoea is a common complaint among patients with thyrotoxicosis. However, its causative mechanisms have not been identified. We assessed the role of thoracic diaphragmatic muscle weakness in dyspnoea among patients with active Graves' disease. METHODS: Twenty-seven patients (19 female, 8 male) with active Graves' disease were assessed for the clinical severity of dyspnoea, functional (pressure generating capacity) and anatomical aspects (thickness and excursion) of the diaphragm at presentation. The severity of dyspnoea was assessed using a visual analogue scale (VAS) and the 6 min walk test. Lung function tests, diaphragmatic strength (sniff oesophageal pressure, SniffP(oeso)), maximum inspiratory and expiratory pressures, diaphragmatic thickness and movements on real time ultrasonography were evaluated during normal and deep respiration. Twenty of the 27 patients were reassessed after achieving euthyroidism with carbimazole therapy at a mean interval of 5+/-2 months. RESULTS: Reevaluation after carbimazole therapy revealed a significant reduction in dyspnoea on the VAS (59+/-26 to 23+/-13%). Patients covered a similar distance during the 6 min walk before and after euthyroidism. Significant improvement was observed in the vital capacity (2.57+/-0.62 to 2.94+/-0.60 l), forced expiratory volume in the first second (2.21+/-0.49 to 2.45+/-0.47 l), total lung capacity (3.57+/-1.19 to 4.1+/-1.12 l), diaphragmatic movement during deep respiration (5.5+/-1.0 to 6.6+/-1.1 cm) and SniffP(oeso) (68.7+/-23 to 93.1+/-25.2 cmH(2)O). There was no significant change in the distance walked in 6 min, tidal volume, lung diffusion capacity and diaphragmatic thickness. There was no significant correlation between the net change in dyspnoea score and net change in lung function tests, diaphragmatic movement and SniffP(oeso). CONCLUSIONS: Significant functional weakness of diaphragm muscle is present in patients with active Graves' disease. This weakness is more marked during a maximal respiratory manoeuvre, indicating a diminished diaphragmatic reserve which could be the cause of dyspnoea observed on exertion among patients with thyrotoxicosis. (+info)
Thyrotoxic periodic paralysis in a white woman.
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A 24 year old white woman presented with sudden onset of flaccid quadriparesis and hypokalaemia. She was later found to be thyrotoxic. Paralysis resolved with potassium supplements, and after initiation of antithyroid medication she had no further episodes of hypokalaemic paralysis. To the best of the authors' knowledge, and after a Medline search, thyrotoxic periodic paralysis has not been described previously in a white woman. (+info)
Successful radioiodine treatment in a 3 year old child with Graves' disease following antithyroid medication induced neutropenia.
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A 3 year old child with Graves' disease and mitral valve prolapse became neutropenic on carbimazole therapy. She was switched to propylthiouracil but the neutropenia recurred. She was treated with radioiodine but required two doses of 113 MBq and then 198 MBq five months later before becoming hypothyroid. The mitral valve prolapse resolved when she was euthyroid on thyroxine replacement. Antithyroid drugs, surgery, and radioiodine all have a place in the management of the thyrotoxic child. (+info)
Cholestatic jaundice caused by sequential carbimazole and propylthiouracil treatment for thyrotoxicosis.
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A 36-year-old Chinese man presented to the Queen Mary Hospital in August 1999 with a 2-week history of jaundice due to propylthiouracil treatment for thyrotoxicosis. He had previously received carbimazole but had developed an urticarial skin rash after 2 weeks of treatment. The patient developed liver failure and fulminant pneumonitis shortly after hospital admission. Despite receiving treatment with broad-spectrum antibiotics and intravenous immunoglobulin, he died 11 days after the onset of the respiratory symptoms. Postmortem examination using electron microscopy showed typical glycogen bodies within the cytoplasm of the hepatocytes, which corresponded to eosinophilic cytoplasmic inclusion bodies visible under light microscopy. Immunohistochemical studies of the inclusion bodies were positive for carcinoembryonic antigen and albumin, and negative for fibrinogen, complement protein C3, immunoglobulins G, M, and A, alpha-fetoprotein, and alpha-1-antitrypsin. This is the first report of a patient who received two sequential antithyroid drugs and developed predominate cholestasis with unique histological features. Extreme caution should be taken when a patient develops allergy to one type of antithyroid drug, because cross-reactivity may develop to the other type. (+info)
Hypokalaemic thyrotoxic periodic paralysis in an Asian man in the United Kingdom.
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A large number of ethnic Chinese and other oriental populations are living in the West because of the modern day migration of people. Hypokalaemic periodic paralysis attributable to thyrotoxicosis is a common presentation in an Asian emergency department. It is uncommon in the white communities. There is a difference in the genetic type in the different racial groups. Thyrotoxic features are often masked or absent. Life may be threatened because of severe hypokalaemia and therefore a prompt diagnosis of this condition in the certain ethnic group presenting with weakness and hypokalaemia is essential. Thyroid function studies are mandatory in these cases. (+info)
Paroxysmal kinesigenic dyskinesia manifestation of hyperthyroidism.
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Sporadic paroxysmal kinesigenic dyskinesia (PKD) secondary to thyrotoxicosis is an extremely rare entity. A 36-year-old female presented with the features of PKD. Her investigations revealed thyrotoxicosis. Her dyskinesia did not respond to carbamazepine but remitted with the anti-thyroid drug, neomercazole. Perhaps hyperthyroidism-related PKD is a result of a metabolic disturbance of the basal ganglia circuits rather than a permanent and irreversible change. (+info)
Reactions of 1-methyl-2-mercaptoimidazole with hypochlorous acid and superoxide.
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Reactions of thioureylene antithyroid drugs (1-methyl-2-mercaptoimidazole and carbimazole) with hypochlorous acid (HOCl) and superoxide were followed optically and products were analyzed by mass spectrometry. 1-methyl-2-mercaptoimidazole (MMI) and carbimazole reacted rapidly with HOCl with a rate constant of 1 x 10(7) and 7 x 10(6) M(-1)s(-1), respectively. The characteristic spectrum assigned to MMI disulfide appeared immediately after addition of HOCl, followed by a slow conversion to a final spectrum. The conversion was dependent upon the ratio of HOCl to MMI and both antithyroid drugs uptake 3 moles HOCl for complete conversion. A similar sequence of spectral changes was also observed when the HOCl was replaced by myeloperoxidase (MPO)/H2O2/Cl- system. The final oxidation product of MMI and carbimazole with HOCl and superoxide was 1-methylimidazole. (+info)
Pyoderma gangraenosum associated with autoimmune thyreopathy and hyperandrogenic syndrome.
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An unusual clinical appearance and course of pyoderma gangraenosum (PG) in a 35-year-old woman is presented. Signs of both the ulcerative and vegetative forms of PG were expressed. The association of two systemic diseases, the autoimmune thyreopathy and the hyperandrogenic syndrome were observed in a female. The recommended conventional therapy for PG: corticosteroids, antibiotics, cyclosporine and cyclophosphamide yielded a poor response, whereas after thyroidectomy and reaching an euthyroid state the symptoms receded. This close association of PG and autoimmune thyreopathy supports the autoimmune concept of PG. (+info)