The Experts below are selected from a list of 279 Experts worldwide ranked by ideXlab platform
Carmen C Solorzano - One of the best experts on this subject based on the ideXlab platform.
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Toxic Nodular Goiter and cancer a compelling case for thyroidectomy
Annals of Surgical Oncology, 2013Co-Authors: Joshua J Smith, Xi Chen, David F Schneider, Ratnam Nookala, James T Broome, Rebecca S Sippel, Herbert Chen, Carmen C SolorzanoAbstract:Recent American Thyroid Association guidelines call for thyroidectomy or 131I (Recommendation 31) in managing hyperthyroidism due to Toxic Nodular Goiter (TNG). Concern for concomitant malignancy favors surgery. A 3 % thyroid cancer incidence in TNG patients has been reported, yet recent studies suggest this rate is underestimated. This multi-institutional study examined cancer incidence in TNG patients referred to surgery. Patients referred for thyroidectomy at three tertiary-care institutions were included (2002–2011). Patients with concurrent indeterminate or malignant diagnosis by fine-needle aspiration (FNA) were excluded. Cancer incidence in TNG patients was determined. Fisher’s exact and chi-square tests and nonparametric t tests were used. Among 2,551 surgically treated patients, 164 had TNG (6.4 %). Median age at presentation was 49.7 years, and 86 % were female. Overall cancer incidence was 18.3 % (30 of 164), and rates were not significantly different between institutions. A significantly greater cancer rate was noted in Toxic multiNodular Goiter versus single Toxic nodule patients (21 vs. 4.5 %, P 0.05). No significant cancer association was noted with age, preoperative dominant nodule size, lymphocytic thyroiditis or preoperative FNA (P > 0.05). These data demonstrate a higher than expected incidental cancer rate in TNG patients compared to historical reports (18.3 vs. 3 %). This higher cancer incidence may alter the risk/benefit analysis regarding TNG treatment. This information should be provided to TNG patients before decision making regarding treatment.
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Cancer after Thyroidectomy: A Multi-Institutional Experience with 1,523 Patients
Journal of the American College of Surgeons, 2013Co-Authors: J. Joshua Smith, Xi Chen, David F Schneider, James T Broome, Rebecca S Sippel, Herbert Chen, Carmen C SolorzanoAbstract:Background The incidence of thyroid cancer in patients treated operatively for thyroid disease has been historically low ( Study Design A total of 2,551 patients underwent thyroidectomy at 3 high-volume institutions. Indeterminate/malignant fine-needle aspiration diagnosis was excluded (n = 1,028). Cancer cases were compared among 1,523 patients with Graves' disease (n = 264), Nodular Goiter (n = 1,095), and Toxic Nodular Goiter (n = 164). Fisher's exact test, chi-square test, Wilcoxon rank sum, Kruskal-Wallis nonparametric t -tests, and multivariable logistic regression were used. Results Overall, 238 (15.6%) cancers were recorded: Graves' disease (6.1%), Nodular Goiter (17.5%), and Toxic Nodular Goiter (18.3%). Cancer rates were significantly different among these groups (p 0.5 cm; 39% >1 cm). Most patients underwent total thyroidectomy (80%). Conclusions These data confirm higher than expected incidental thyroid cancer rates (15.6%) in the largest multi-institutional surgical series to date. Nodular thyroids, males, and young patients were more likely to harbor incidental carcinoma. These data support consideration of initial total thyroidectomy as the preferred approach for patients referred to the surgeon with bilateral Nodular disease.
Mark E. Peterson - One of the best experts on this subject based on the ideXlab platform.
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Animal models of disease: feline hyperthyroidism: an animal model for Toxic Nodular Goiter.
The Journal of endocrinology, 2014Co-Authors: Mark E. PetersonAbstract:Since first discovered just 35 years ago, the incidence of spontaneous feline hyperthyroidism has increased dramatically to the extent that it is now one of the most common disorders seen in middle-aged to senior domestic cats. Hyperthyroid cat Goiters contain single or multiple autonomously (i.e. TSH-independent) functioning and growing thyroid nodules. Thus, hyperthyroidism in cats is clinically and histologically similar to Toxic Nodular Goiter in humans. The disease in cats is mechanistically different from Graves' disease, because neither the hyperfunction nor growth of these nodules depends on extrathyroidal circulating stimulators. The basic lesion appears to be an excessive intrinsic growth capacity of some thyroid cells, but iodine deficiency, other nutritional goitrogens, or environmental disruptors may play a role in the disease pathogenesis. Clinical features of feline Toxic Nodular Goiter include one or more palpable thyroid nodules, together with signs of hyperthyroidism (e.g. weight loss despite an increased appetite). Diagnosis of feline hyperthyroidism is confirmed by finding the increased serum concentrations of thyroxine and triiodothyronine, undetectable serum TSH concentrations, or increased thyroid uptake of radioiodine. Thyroid scintigraphy demonstrates a heterogeneous pattern of increased radionuclide uptake, most commonly into both thyroid lobes. Treatment options for Toxic Nodular Goiter in cats are similar to that used in humans and include surgical thyroidectomy, radioiodine, and antithyroid drugs. Most authorities agree that ablative therapy with radioiodine is the treatment of choice for most cats with Toxic Nodular Goiter, because the animals are older, and the disease will never go into remission.
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Comments regarding "Subclinical hyperthyroidism in cats: a spontaneous model of subclinical Toxic Nodular Goiter in humans?".
Thyroid : official journal of the American Thyroid Association, 2008Co-Authors: Duncan C. Ferguson, Margarethe Hoenig, Elaine M. Kaptein, Mark E. PetersonAbstract:We would like to comment on some of the points made by Wakeling et al. in their manuscript entitled ‘‘Subclinical Hyperthyroidism in Cats: A Spontaneous Model of Subclinical Toxic Nodular Goiter in Humans?’’ (1). The authors state: ‘‘The purpose of this study was to determine whether a relationship exists between TSH concentration and thyroid histopathology in biochemically euthyroid cats (as assessed by tT4 [serum total T4 concentration] thereby providing further evidence for the existence of subclinical hyperthyroidism in cats.’’ We certainly support the idea that the histopathological changes associated with spontaneous feline hyperthyroidism provide a model of Toxic Nodular Goiter (Plummer’s disease), and have contributed to the literature in this regard (2–4). Undoubtedly, there is a prodromal period for this disease associated with clinically and biochemically undetectable hyperthyroidism. However, the authors of this manuscript have chosen a ‘‘healthy’’ population dominated by cats with chronic renal disease which we propose confounds the interpretation of their data. The concern rises from the observation in human patients with chronic kidney disease, both before as well as following kidney transplantation, that there is an increased frequency of Goiter and thyroid adenomas (as well as hypothyroidism, probably due to increased serum iodine levels). In one study (5) of patients with chronic renal disease, the incidence of abnormal thyroid structures (nodules or abnormal echogenicity on ultrasound) in patients before or chronically after transplantation was 63=70% with 13=17% having Goiter. The control group with normal renal function had 29%=16%, respectively. Despite the increased tendency for nodules, the thyroid volume was not significantly altered in the chronic kidney disease patients. A second concern is the reliance on the heterologous canine TSH assay to characterize thyroid hyperfunction in these cats. The commercially available canine TSH assay does detect gross elevations of TSH in the cat, such as during methimazole therapy. The assay has a sensitivity limit of 0.03 ng=mL that translates to about 0.1 ng=mL (very close to 1 mU=L) when corrected for 36% crossreactivity to recombinant feline TSH (6,7). Therefore, as was true for firstgeneration human TSH assays, on a case-by-case basis, a normal concentration cannot be reliably distinguished from an undetectable value. The authors quote from ‘‘unpublished data’’ (now published in reference 8) from 90 cats that the reference range for healthy senior cats is 7 years of age had detectable TSH. The authors note: ‘‘However, it is likely that not all cats with TSH
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Etiopathology of feline Toxic Nodular Goiter
The Veterinary clinics of North America. Small animal practice, 1994Co-Authors: Hans Gerber, H J Peter, Duncan C. Ferguson, Mark E. PetersonAbstract:The etiopathology of feline Toxic Nodular Goiter is discussed in the context of human Nodular Goiter pathogenesis. This article reviews the thyroid heterogeneity, growth regulation, functional and growth autonomy, nodule and tumor formation, and the evolution of Toxic Nodular Goiter in the human being. The history, morphologic findings, xenotransplantation and cell culture studies, evidence for and against circulating thyroid stimulators, and epizootiologic studies of the feline disease are also summarized.
Harriet M. Syme - One of the best experts on this subject based on the ideXlab platform.
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subclinical hyperthyroidism in cats a spontaneous model of subclinical Toxic Nodular Goiter in humans
Thyroid, 2007Co-Authors: Jennifer Wakeling, Ken C. Smith, Tim Scase, Rachel Kirkby, Jonathan Elliott, Harriet M. SymeAbstract:Introduction and Objectives: Hyperthyroidism in cats, caused by Nodular hyperplasia or adenomas, is clinically and histologically similar to Toxic Nodular Goiter in humans. Subclinical hyperthyroidism in humans is defined as low thyrotropin (TSH) in conjunction with within-reference-range thyroid hormone concentrations, but has not previously been defined in cats. The objective of this study was to test the hypothesis that euthyroid senior cats with low TSH have histological evidence of thyroid Nodular hyperplasia and/or adenoma. Design: Thyroid glands removed postmortem from four groups of cats (n = 73) were examined histologically and scored in a blinded fashion. Clinically euthyroid senior (>7 years) cats were divided into two groups dependent on their TSH concentration—TSH below the limit of quantification (LOQ) of the assay (<0.03 ng/mL; n = 15; UndetectableTSH group) and TSH above the LOQ (≥0.03 ng/mL; n = 31; DetectableTSH group)—using archived plasma samples, collected 0–6 months antemortem. Thyro...
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Subclinical hyperthyroidism in cats: a spontaneous model of subclinical Toxic Nodular Goiter in humans?
Thyroid : official journal of the American Thyroid Association, 2007Co-Authors: Jennifer Wakeling, Ken C. Smith, Tim Scase, Rachel Kirkby, Jonathan Elliott, Harriet M. SymeAbstract:Introduction and Objectives: Hyperthyroidism in cats, caused by Nodular hyperplasia or adenomas, is clinically and histologically similar to Toxic Nodular Goiter in humans. Subclinical hyperthyroidism in humans is defined as low thyrotropin (TSH) in conjunction with within-reference-range thyroid hormone concentrations, but has not previously been defined in cats. The objective of this study was to test the hypothesis that euthyroid senior cats with low TSH have histological evidence of thyroid Nodular hyperplasia and/or adenoma. Design: Thyroid glands removed postmortem from four groups of cats (n = 73) were examined histologically and scored in a blinded fashion. Clinically euthyroid senior (>7 years) cats were divided into two groups dependent on their TSH concentration—TSH below the limit of quantification (LOQ) of the assay (
M E Peterson - One of the best experts on this subject based on the ideXlab platform.
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comments regarding subclinical hyperthyroidism in cats a spontaneous model of subclinical Toxic Nodular Goiter in humans
Thyroid, 2008Co-Authors: Duncan C. Ferguson, Margarethe Hoenig, Elaine M. Kaptein, M E PetersonAbstract:We would like to comment on some of the points made by Wakeling et al. in their manuscript entitled ‘‘Subclinical Hyperthyroidism in Cats: A Spontaneous Model of Subclinical Toxic Nodular Goiter in Humans?’’ (1). The authors state: ‘‘The purpose of this study was to determine whether a relationship exists between TSH concentration and thyroid histopathology in biochemically euthyroid cats (as assessed by tT4 [serum total T4 concentration] thereby providing further evidence for the existence of subclinical hyperthyroidism in cats.’’ We certainly support the idea that the histopathological changes associated with spontaneous feline hyperthyroidism provide a model of Toxic Nodular Goiter (Plummer’s disease), and have contributed to the literature in this regard (2–4). Undoubtedly, there is a prodromal period for this disease associated with clinically and biochemically undetectable hyperthyroidism. However, the authors of this manuscript have chosen a ‘‘healthy’’ population dominated by cats with chronic renal disease which we propose confounds the interpretation of their data. The concern rises from the observation in human patients with chronic kidney disease, both before as well as following kidney transplantation, that there is an increased frequency of Goiter and thyroid adenomas (as well as hypothyroidism, probably due to increased serum iodine levels). In one study (5) of patients with chronic renal disease, the incidence of abnormal thyroid structures (nodules or abnormal echogenicity on ultrasound) in patients before or chronically after transplantation was 63=70% with 13=17% having Goiter. The control group with normal renal function had 29%=16%, respectively. Despite the increased tendency for nodules, the thyroid volume was not significantly altered in the chronic kidney disease patients. A second concern is the reliance on the heterologous canine TSH assay to characterize thyroid hyperfunction in these cats. The commercially available canine TSH assay does detect gross elevations of TSH in the cat, such as during methimazole therapy. The assay has a sensitivity limit of 0.03 ng=mL that translates to about 0.1 ng=mL (very close to 1 mU=L) when corrected for 36% crossreactivity to recombinant feline TSH (6,7). Therefore, as was true for firstgeneration human TSH assays, on a case-by-case basis, a normal concentration cannot be reliably distinguished from an undetectable value. The authors quote from ‘‘unpublished data’’ (now published in reference 8) from 90 cats that the reference range for healthy senior cats is 7 years of age had detectable TSH. The authors note: ‘‘However, it is likely that not all cats with TSH <0.03 ng=mL have subclinical hyperthyroidism, particularly cats with severe concurrent illness and young cats.’’ Of the 59 cats for which there was histopathological data, 41 had chronic kidney disease and 13 were young cats. Therefore, 54=59 or 91.5% of the cases fit the categorization over which they raise concern. The authors continue: ‘‘In particular, it is known that kidney disease suppresses thyroid hormone production in cats and that the degree of suppression of tT4 is related to the severity of the concurrent disease (25).’’ As one of us was an author on this study (9), we would state that while the depression of serum total T4 concentration was observed, no measurement of thyroid hormone production per se was undertaken. The authors state that because creatinine was similar in the normal TSH and high TSH groups, and body weight and liver enzymes were similar, there were no differences in the populations. Aside from the effects of a chronic illness, uremia per se will be a major contributor to altering thyroid hormone metabolism, in part through alteration of serum T4 binding. No free T4 measurements were provided in the current study to evaluate this possibility, but the subsequent publication by the authors (8) supports this hypothesis in cats: the median free T4 concentration in the group with chronic kidney disease was only slightly higher than that of normal euthyroid population while the median total T4 concentration
Duncan C. Ferguson - One of the best experts on this subject based on the ideXlab platform.
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comments regarding subclinical hyperthyroidism in cats a spontaneous model of subclinical Toxic Nodular Goiter in humans
Thyroid, 2008Co-Authors: Duncan C. Ferguson, Margarethe Hoenig, Elaine M. Kaptein, M E PetersonAbstract:We would like to comment on some of the points made by Wakeling et al. in their manuscript entitled ‘‘Subclinical Hyperthyroidism in Cats: A Spontaneous Model of Subclinical Toxic Nodular Goiter in Humans?’’ (1). The authors state: ‘‘The purpose of this study was to determine whether a relationship exists between TSH concentration and thyroid histopathology in biochemically euthyroid cats (as assessed by tT4 [serum total T4 concentration] thereby providing further evidence for the existence of subclinical hyperthyroidism in cats.’’ We certainly support the idea that the histopathological changes associated with spontaneous feline hyperthyroidism provide a model of Toxic Nodular Goiter (Plummer’s disease), and have contributed to the literature in this regard (2–4). Undoubtedly, there is a prodromal period for this disease associated with clinically and biochemically undetectable hyperthyroidism. However, the authors of this manuscript have chosen a ‘‘healthy’’ population dominated by cats with chronic renal disease which we propose confounds the interpretation of their data. The concern rises from the observation in human patients with chronic kidney disease, both before as well as following kidney transplantation, that there is an increased frequency of Goiter and thyroid adenomas (as well as hypothyroidism, probably due to increased serum iodine levels). In one study (5) of patients with chronic renal disease, the incidence of abnormal thyroid structures (nodules or abnormal echogenicity on ultrasound) in patients before or chronically after transplantation was 63=70% with 13=17% having Goiter. The control group with normal renal function had 29%=16%, respectively. Despite the increased tendency for nodules, the thyroid volume was not significantly altered in the chronic kidney disease patients. A second concern is the reliance on the heterologous canine TSH assay to characterize thyroid hyperfunction in these cats. The commercially available canine TSH assay does detect gross elevations of TSH in the cat, such as during methimazole therapy. The assay has a sensitivity limit of 0.03 ng=mL that translates to about 0.1 ng=mL (very close to 1 mU=L) when corrected for 36% crossreactivity to recombinant feline TSH (6,7). Therefore, as was true for firstgeneration human TSH assays, on a case-by-case basis, a normal concentration cannot be reliably distinguished from an undetectable value. The authors quote from ‘‘unpublished data’’ (now published in reference 8) from 90 cats that the reference range for healthy senior cats is 7 years of age had detectable TSH. The authors note: ‘‘However, it is likely that not all cats with TSH <0.03 ng=mL have subclinical hyperthyroidism, particularly cats with severe concurrent illness and young cats.’’ Of the 59 cats for which there was histopathological data, 41 had chronic kidney disease and 13 were young cats. Therefore, 54=59 or 91.5% of the cases fit the categorization over which they raise concern. The authors continue: ‘‘In particular, it is known that kidney disease suppresses thyroid hormone production in cats and that the degree of suppression of tT4 is related to the severity of the concurrent disease (25).’’ As one of us was an author on this study (9), we would state that while the depression of serum total T4 concentration was observed, no measurement of thyroid hormone production per se was undertaken. The authors state that because creatinine was similar in the normal TSH and high TSH groups, and body weight and liver enzymes were similar, there were no differences in the populations. Aside from the effects of a chronic illness, uremia per se will be a major contributor to altering thyroid hormone metabolism, in part through alteration of serum T4 binding. No free T4 measurements were provided in the current study to evaluate this possibility, but the subsequent publication by the authors (8) supports this hypothesis in cats: the median free T4 concentration in the group with chronic kidney disease was only slightly higher than that of normal euthyroid population while the median total T4 concentration
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Comments regarding "Subclinical hyperthyroidism in cats: a spontaneous model of subclinical Toxic Nodular Goiter in humans?".
Thyroid : official journal of the American Thyroid Association, 2008Co-Authors: Duncan C. Ferguson, Margarethe Hoenig, Elaine M. Kaptein, Mark E. PetersonAbstract:We would like to comment on some of the points made by Wakeling et al. in their manuscript entitled ‘‘Subclinical Hyperthyroidism in Cats: A Spontaneous Model of Subclinical Toxic Nodular Goiter in Humans?’’ (1). The authors state: ‘‘The purpose of this study was to determine whether a relationship exists between TSH concentration and thyroid histopathology in biochemically euthyroid cats (as assessed by tT4 [serum total T4 concentration] thereby providing further evidence for the existence of subclinical hyperthyroidism in cats.’’ We certainly support the idea that the histopathological changes associated with spontaneous feline hyperthyroidism provide a model of Toxic Nodular Goiter (Plummer’s disease), and have contributed to the literature in this regard (2–4). Undoubtedly, there is a prodromal period for this disease associated with clinically and biochemically undetectable hyperthyroidism. However, the authors of this manuscript have chosen a ‘‘healthy’’ population dominated by cats with chronic renal disease which we propose confounds the interpretation of their data. The concern rises from the observation in human patients with chronic kidney disease, both before as well as following kidney transplantation, that there is an increased frequency of Goiter and thyroid adenomas (as well as hypothyroidism, probably due to increased serum iodine levels). In one study (5) of patients with chronic renal disease, the incidence of abnormal thyroid structures (nodules or abnormal echogenicity on ultrasound) in patients before or chronically after transplantation was 63=70% with 13=17% having Goiter. The control group with normal renal function had 29%=16%, respectively. Despite the increased tendency for nodules, the thyroid volume was not significantly altered in the chronic kidney disease patients. A second concern is the reliance on the heterologous canine TSH assay to characterize thyroid hyperfunction in these cats. The commercially available canine TSH assay does detect gross elevations of TSH in the cat, such as during methimazole therapy. The assay has a sensitivity limit of 0.03 ng=mL that translates to about 0.1 ng=mL (very close to 1 mU=L) when corrected for 36% crossreactivity to recombinant feline TSH (6,7). Therefore, as was true for firstgeneration human TSH assays, on a case-by-case basis, a normal concentration cannot be reliably distinguished from an undetectable value. The authors quote from ‘‘unpublished data’’ (now published in reference 8) from 90 cats that the reference range for healthy senior cats is 7 years of age had detectable TSH. The authors note: ‘‘However, it is likely that not all cats with TSH
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Etiopathology of feline Toxic Nodular Goiter
The Veterinary clinics of North America. Small animal practice, 1994Co-Authors: Hans Gerber, H J Peter, Duncan C. Ferguson, Mark E. PetersonAbstract:The etiopathology of feline Toxic Nodular Goiter is discussed in the context of human Nodular Goiter pathogenesis. This article reviews the thyroid heterogeneity, growth regulation, functional and growth autonomy, nodule and tumor formation, and the evolution of Toxic Nodular Goiter in the human being. The history, morphologic findings, xenotransplantation and cell culture studies, evidence for and against circulating thyroid stimulators, and epizootiologic studies of the feline disease are also summarized.
