Solitary fibrous tumor of the thyroid gland associated with papillary thyroid carcinoma.
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Aged↗
Biomedical subjects
Giampaolo Papi
Publications and source records attributed to Giampaolo Papi.
Primary spindle cell lesions of the thyroid gland; an overview.
Spindle cell lesions of the thyroid gland (T-SCL) are not encountered routinely in clinical practice or in the context of thyroid pathology. They commonly are classified as primary or secondary to metastatic disease. Primary T-SCL can be derivedfromfollicular, C-cell (parafollicular), or mesenchymal components and may be the result of reactive or neoplastic processes, including post-fine-needle aspiration spindle cell nodules, Riedel thyroiditis, solitary fibrous tumor, leiomyoma, peripheral nerve sheath tumor, hyalinizing trabecular tumor, spindle epithelial tumor with thymus-like differentiation, follicular dendritic cell tumor, medullary carcinoma, papillary carcinoma, anaplastic carcinoma, sarcoma, squamous cell carcinoma, and carcinoma showing thymus-like differentiation. Because T-SCL may represent the expression of benign and highly malignant neoplasms, distinction among these processes is crucial because it dictates therapy and defines prognosis. The present article reviews the clinical, imaging, pathologic, and immunohistochemical characteristics of primary T-SCL.
Adenocarcinoma, Papillary↗
A clinical and therapeutic approach to thyrotoxicosis with thyroid-stimulating hormone suppression only.
Subclinical hyperthyroidism is defined as normal serum free thyroxine (T4) and triiodothyronine (T3) concentrations and persistently suppressed thyroid stimulating hormone (TSH) concentrations. The most common cause of subclinical hyperthyroidism is the use of suppressive doses of L-thyroxine for treatment of hypothyroidism or, less commonly, diffuse nontoxic goiter or thyroid carcinoma (exogenous subclinical hyperthyroidism). Endogenous subclinical hyperthyroidism may be caused by a variety of thyroid disorders that result in overproduction and release of thyroid hormones from the gland with normal/high 24-hour thyroid radioiodine uptake or by inflammation in the thyroid resulting in release of excess thyroid hormones and low 24-hour thyroid radioiodine uptake. Several groups have investigated whether persistent endogenous or exogenous subclinical hyperthyroidism, like overt hyperthyroidism, causes symptoms, adverse effects on the cardiovascular and the skeletal systems, and increased mortality, whether endogenous subclinical hyperthyroidism evolves to overt thyrotoxicosis, and whether or not it should be treated. The present report reviews the most important and recent studies of subclinical hyperthyroidism and attempts to draw conclusions based upon the literature and the authors' experience.
Bone and Bones↗
[Current issues in the treatment of thyrotoxicosis].
Overt thyrotoxicosis is defined as elevated serum free thyroxine (FT4) and free triiodothyronine (FT3), and suppressed thyrotropin (TSH) concentrations. Thyrotoxicosis with TSH suppression only (TTSO), and normal thyroid hormone concentrations, is also defined as mild thyrotoxicosis. Both overt thyrotoxicosis and TTSO may be caused by the same thyroid disorders. The most common cause of thyrotoxicosis is the use of excessive doses of L-thyroxine for the treatment of hypothyroidism, non-toxic goiter or thyroid carcinoma (exogenous thyrotoxicosis). Less commonly, the cause of thyrotoxicosis is endogenous. The endogenous thyrotoxicosis may be due to either overproduction and release of thyroid hormones from the gland with normal/high 24-hour thyroid radioiodine uptake (e.g., Graves disease and toxic nodular goiter), or release of excess thyroid hormones due to follicle disruption with low/absent 24-hour thyroid radioiodine uptake (e.g., sub-acute de Quervain thyroiditis). The present report briefly reviews the current problems regarding the clinical and therapeutical approach to thyrotoxicosis, and in particular the TTSO.
Humans↗
Progression of subacute (de Quervain's) thyroiditis into Hashimoto's thyroiditis.
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Acute Disease↗
Current concepts on Riedel thyroiditis.
Riedel thyroiditis (RT) is an uncommon form of chronic thyroiditis in which the thyroid gland is replaced by fibrous tissue. The etiologic mechanisms underlying RT are unclear: the prevailing view is that it is part of a generalized fibroinflammatory process also involving other organs. The clinical manifestations of RT are protean, often resembling malignancy owing to goiter of remarkably hard consistency. Physical examination, laboratory analysis, cytology, and imaging features are not useful for differentiating between RT and neoplastic diseases or the fibrous variant of Hashimoto thyroiditis in the presurgical evaluation of patients. Histologic examination is necessary to establish the final diagnosis of RT. The present article reviews the most recent concepts about etiologic mechanisms, pathogenesis, diagnosis, and management of RT
Cytodiagnosis↗
Achondroplasic and GH-deficiency dwarfism. Diego Velasquez (1656).
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Achondroplasia↗