Iodine-induced thyrotoxicosis was documented in eighty-five cases. Eighty per cent occur in apparently normal thyroid glands; 60% among them occur in males. Amiodarone accounted for 50% of iodine-induced thyrotoxicosis. Mean thyroid hormone levels at diagnosis were: FT1: 21.7 (normal mean: 7.5, arbitrary units); T3: 4.53 nmol 1(-1) (normal: 2.30 nmol 1(-1). Mean 131I- 24-h uptake was 3.5% (normal range in France 25-45%) and was activated by exogenous TSH (mean 27%). The spontaneous cure in nontreated cases was observed within an average 6 months. A phase of biological hypothyroidism (mean FT1: 3.7, T3: 1.23 nmol 1(-1), TSH: 9.6 microU ml-1 (normal TSH range: 1-7 microU ml-1] preceded the return to euthyroidism. Intrathyroid iodine content measured by X-ray fluorescence was high, then fell gradually. Thyroid tissue study showed a large quantity of intrathyroid iodine and the overiodination of thyroglobulin. Histological and electron microscopic studies are reported. Prednisone and in some cases propylthiouracile were found to be effective.
The clinical and pathological findings in four cases of fulminant hepatic failure due to massive infiltration of the liver by acute leukemia or lymphoma are reported. Liver abnormalities were found simultaneously with or led to the discovery of hematologic malignancies, and consisted of marked hepatomegaly and severe hepatocellular insufficiency associated with hyperlactatemia. The blood malignancies were peculiar in their fast cellular growth and large tumor mass. Evolution was rapidly fatal in all these cases. In another patient, marked hepatomegaly and hyperlactatemia revealed the presence of a widespread lymphoma before the appearance of hepatocellular insufficiency. Immediate chemotherapy was instituted, and complete remission without hepatic complication was obtained. It is suggested that malignant hematological diseases with fast cellular growth may present as fulminant hepatic failure. In order to avoid a rapidly fatal outcome secondary to liver failure and metabolic disorders, early recognition of these malignancies is necessary so as to assure prompt administration of appropriate chemotherapy.
We have examined conjunctival biopsies from nine primary and two secondary cases of Sjögren's syndrome. In all cases histopathological examination revealed metaplasia of the conjunctival epithelium associated with a reduced number of goblet cells and a polymorphic inflammatory cell infiltrate of the stroma. Using monoclonal antibodies with texture analysis of stained preparations we have shown that in all cases the lymphocytic infiltrate was predominantly T-cell but with substantial numbers of IgA and IgG secretory B-cells in three cases. The number of Langerhans cells present was reduced in biopsies showing the most marked degree of epithelial metaplasia.
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