Although the follow-up is very short, SN biopsy only in node-negative breast cancer patients had no negative impact on the axillary failure rate and resulted in negligible morbidity.
In hyperthyroidism, patients with GD exhibited increased systemic arterial stiffness, paralleled by increased levels of NT-ProBNP, a marker of volume overload. The decreased subendocardial perfusion in hyperthyroidism seemed to be mainly due to increased heart rates. The observed unfavorable hemodynamic alterations in hyperthyroidism may serve to explain increased cardiovascular event rates in patients with GD.
Primary hyperparathyroidism (PHP) during pregnancy is a very rare event that increases maternal and perinatal morbidity and mortality. We present a case in which hypocalcemic tetany of the neonatal infant - caused by transient hypoparathyroidism in the child - finally revealed asymptomatic maternal PHP. An apparently healthy 30-year-old woman had an uneventful pregnancy and delivery. On the 15th postpartal day, the newborn developed hypocalcemic tetany. After receiving supplementation of calcium and vitamin D, the child developed without further pathological findings. Laboratory and radiological studies in the mother led to a diagnosis of maternal PHP. An adenoma of the right lower parathyroid gland was subsequently removed. The search for the cause of hypocalcemia in a newborn should not focus on the patient alone. Examining the apparently healthy mother and approaching the case in a multidisciplinary fashion may benefit both the child and the mother.
Objective: The aim of our study was to evaluate retrospectively the results of routine calcitonin measurements in patients with nodular thyroid disease over a period of 3 years. Methods: From 1/1999 to 12/2001 calcitonin was determined in 3,899 patients with evidence of thyroid nodules. When calcitonin was elevated, pentagastrin testing was performed. Pentagastrin stimulation was considered positive when the stimulated calcitonin value exceeded 100 pg/ml. Meticulous pathological evaluation included immunohistochemistry. Molecular genetic analysis was carried out in patients with medullary thyroid carcinoma (MTC) and C-cell hyperplasia. Results: Thirty-nine patients (12 females, 27 males) underwent surgery. MTC was diagnosed in seven females and five males. Tumor stages were T1 in nine patients, and T2 in three, one of the latter having lymph node metastasis (Nib). In addition, papillary microcarcinoma was found in two patients. Molecular genetic analysis showed evidence of familial medullary thyroid carcinoma (FMTC) in three patients. Twenty-five (4 females, 21 males) of the remaining 27 patients were found to have C-cell hyperplasia; three also had papillary carcinoma (pT4 in one, microcarcinoma in two). Conclusions: Patients who were operated on because of markedly elevated basal calcitonin levels or a positive stimulation test had either MTC or C-cell hyperplasia. The prevalence of MTC was 0.3%, accounting for 34% of all thyroid malignancies diagnosed during this period. Of those 12 patients, three had hereditary MTC. Eighteen of 25 patients genetically analyzed presented non-neoplastic C-cell hyperplasia and did not harbor any ÄETgermline mutation.
Autoimmune thyroid diseases are thought to be mediated by pro-inflammatory cytokines such as TNFalpha and IL-6. Serum levels of cytokines may indicate activity levels of immune functions. We investigated serum levels of IL-6 and of the soluble receptor of TNFalpha in patients with newly diagnosed onset of Graves' hyperthyroidism. The predominantly female group consisted of 39 patients, mean fT4 was 47.6 pg/ml (normal values 7.5=19.0 pg/ml). After diagnosis, all patients were treated with anti-thyroid drugs. Soluble Tumour Necrosis Factor Receptor I (TNF-RI) serum levels were found significantly increased (mean 3.7+/-1.3 ng/ml; p<0,01) compared to a matched group of apparent healthy individuals (mean sTNF-RI 1.8+/-0.5 ng/ml) and to a matched group of patients with treated Graves' disease (mean sTNF-RI 1.9+/-0.6 ng/ml). When IL-6 was assessed only 4 of the 39 patients exhibited increased serum levels. Our finding may indicate that sTNF-RI and possibly its ligand, TNFalpha, could play an important role in the onset of the acute stage of Graves' disease.
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