Thyrotoxicosis: Papi G

Papi G. · No affiliation provided · Recenti Prog Med. · Pubmed #16499167 No free full text.

Abstract: 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.

Papi G, Papi G, Pearce EN, Braverman LE, Betterle C, Roti E. · Department of Internal Medicine, Endocrinology Unit, ASL Modena, Italy. · Am J Med. · Pubmed #15808130 No free full text.

Abstract: 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.

Papi G, Papi G, Pearce EN, Braverman LE, Betterle C, Roti E. · Department of Internal Medicine, Endocrinology Unit, ASL Modena, Italy. · Am J Med. · Pubmed #15808130 No free full text.

Abstract: 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.

Papi G, Carapezzi C, Corsello SM. · Dipartimento di Medicina Interna, AUSL Modena, Ospedale Ramazzini, Carpi, Italy. · Minerva Endocrinol. · Pubmed #11961503 No free full text.

Abstract: Thyrotoxicosis is a well defined clinical entity, determined by an increase of plasma levels of thyroid hormones (T3 and T4). A number of causes of thyrotoxicosis are known, and it is therefore very important for the treatment to establish its etiology. In fact, metimazole or propylthiouracil are indicated for the thyrotoxic states caused by thyroid gland's hyperfunction (hyperthyroidism), but are not effective when thyrotoxicosis is determined by a follicular damage and disruption with leakage of preformed thyroid hormones, or in case of thyrotoxicosis factitia. Besides medical therapy, other two therapeutic options are available for the treatment of thyrotoxicosis: radioiodide administration (131I) and surgery. The physician can decide the best therapy on the basis of the following factors: etiology of thyrotoxicosis; patient's age and needs; presence/absence of concomitant diseases or pregnancy; presence of ophthalmopathy; goiter's size; advantages and disadvantages of each therapeutic option. A problem of particular regard is when and if to treat subclinical thyrotoxicosis (low TSH values, and normal plasma levels of thyroid hormones). On the basis of the natural history and of its consequences on the cardiovascular system and skeletal integrity, the authors propose to begin therapy whether subclinical thyrotoxicosis develop in the following four subgroups of subjects: patients with nodular goiter; women in post-menopause; patients with cardiac diseases; patients with osteoporosis.

Papi G, Corrado S, Carapezzi C, Corsello SM. · Department of Internal Medicine, AUSL, Modena, Italy. · Int J Clin Pract. · Pubmed #12918902 No free full text.

Abstract: We describe the case of a 30-year-old woman who, five months after giving birth, was referred with a solitary nodule in her anterior neck. Laboratory analysis, ultrasonography, pertechnetate (Tc99m) thyroid scan and cytological examination of fine needle aspiration biopsy performed on the nodule led us to diagnose postpartum thyroiditis (PPT). Twenty-eight months after parturition, overt hyperthyroidism developed, with raised thyroperoxidase and thyroid stimulating hormone receptor antibody titres, diffuse high uptake of Tc99m at thyroid scan, and high vascular flow throughout the gland at Color-Power imaging. The diagnosis of Graves' disease (GD) was established. The differential diagnosis of thyrotoxicosis in the postpartum period, and the possible aetiological relationships between PPT and GD are discussed. To our knowledge, this is the first published report of a PPT presenting as a cold nodule, and evolving to GD.