Aim:This study aimed to evaluate the benefits of Arnica montana on post-operative blood loss and seroma production in women undergoing unilateral total mastectomy by administering Arnica Montana 1000 Korsakovian dilution (1000 K).Materials and Methods:From 2012 to 2014, 53 women were randomly assigned to A. montana or placebo and were followed up for 5 days. The main end point was the reduction in blood and serum volumes collected in drainages. Secondary end points were duration of drainage, a self-evaluation of pain, and the presence of bruising or hematomas.Results:The per-protocol analysis revealed a lower mean volume of blood and serum collected in drainages with A. montana (−94.40 ml; 95% confidence interval [CI]: 22.48-211.28; P = 0.11). A regression model including treatment, volume collected in the drainage on the day of surgery, and patient weight showed a statistically significant difference in favor of A. montana (−106.28 ml; 95% CI: 9.45-203.11; P = 0.03). Volumes collected on the day of surgery and the following days were significantly lower with A. montana at days 2 (P = 0.033) and 3 (P = 0.0223). Secondary end points have not revealed significant differences.Conclusions:A. montana 1000 K could reduce post-operative blood and seroma collection in women undergoing unilateral total mastectomy. Larger studies are needed with different dilutions of A. montana to further validate these data.
Amiodarone-induced thyrotoxicosis occurs in 2-12.1% of patients on chronic amiodarone treatment. In most cases its pathogenesis is related to iodine overload in the presence of preexisting thyroid abnormalities, such as multinodular or diffuse goiter or autonomous nodule. A minority of patients show apparently normal glands or pictures of non-autoimmune thyroiditis. However, there is recent evidence of a direct toxic effect of amiodarone, with consequent release of iodothyronines into the circulation. We report a patient with amiodarone-induced thyrotoxicosis with toxic thyroid effects demonstrated by electron microscopy in a fine-needle aspiration biopsy. There were three main pathologic findings: multilamellar lysosomal inclusions, intramitchondrial glycogen inclusions--both ultrastructural findings indicating thyroid cell damage--and a microscopic morphological pattern of thyroid cell hyperfunction. No inflammatory changes were found. Plasma thyroglobulin levels were high. The patient proved to be a non responder to simultaneous administration of methimazole (starting dose 30 mg/day) and potassium perchlorate (1000 mg/day for 40 days), while still taking amiodarone, thus providing evidence against a possible pathogenetic role of iodine overload. Dexamethasone (starting dose 3 mg/day) was added to methimazole. After three months euthyroidism had been restored and plasma thyroglobulin level substantially decreased. Subsequent subclinical hypothyroidism developed, which persisted after stopping antithyroid treatment and required substitution treatment with levothyroxine. In view of the primary role of lysosome function in the proteolysis of thyroglobulin molecules and of the energy-requiring carrier-mediated transport of monoiodotyrosine across the lysosomal membrane for iodine salvage and reutilization, we suggest that the pathological lysosomal and mitochondrial changes observed could be an ultrastructural marker for subsequent hypothyroidism in amiodarone-induced thyrotoxicosis. Our observations suggest the usefulness of ultrastructural thyroid evaluation and serial plasma thyroglobulin determinations to thoroughly evaluate the underlying pathogenetic mechanisms in amiodarone-associated thyrotoxicosis with apparently normal thyroid glands. Moreover, more knowledge of its pathogenesis could improve both prognostic stratification and treatment guides.
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