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PubMed1998

Diagnosis and radioablation treatment of toxic multinodular goiter in a hemodialysis patient.

Toxic multinodular goiter is rare in hemodialysis patients. In addition, establishing the diagnosis of hyperthyroidism in the elderly patient with renal failure is difficult because abnormal thyroid function tests can erroneously be attributed to euthyroid sick syndrome. Treatment of hyperthyroidism in dialysis patients by radioiodine ablation involves careful calculation of 131I dose, determination of interval between 131I administration and its removal by hemodialysis, and minimization of radiation hazards during dialytic removal of 131I. We described the clinical presentation of an elderly dialysis patient with toxic multinodular goiter and discussed our diagnostic and therapeutic approaches. The patient's recovery after 131I ablation was complete and uneventful.

Aged↗
PubMedDate not supplied

Parathyroid adenoma after radioactive iodine therapy for multinodular goiter.

The development of hyperparathyroidism after radioactive iodine (RAI) therapy has been reported in 38 cases in the literature. However, the development of a parathyroid adenoma after RAI therapy for a hyperfunctioning multinodular goiter has not been reported. This report describes the pathologic and operative finding on a patient with both hyperthyroidism and hyperparathyroidism, which was diagnosed after previous RAI therapy for a toxic, multinodular goiter.

Adenoma↗
PubMed1977

[Diagnostic and therapeutic aspects of endothoracic goiter (author's transl)].

Among mediastinal tumors requiring operative treatment endothoracic goiters have to be considered as common cause (13.7%) in differential diagnostic aspects next to dysontogenetic and neurogenic tumors. Final diagnosis is best established by chest x-rays in two directions, perhaps with additional barium swallow and a scintigraphy (131I or technetium). Angiography is of no valuable further information concerning tumor identification or operability. The disadvantage refers to unwanted iodine load in case of thyroid malignancy. The operative approach for real mediastinal goiter necessitates partial or total sternotomy or occasionally lateral thoracotomy.

Diagnosis, Differential↗
PubMed1993

Levothyroxine suppressive therapy in the medical management of nontoxic benign multinodular goiter.

The aim of this investigation was to evaluate the efficacy of levothyroxine suppressive therapy in the medical management of nontoxic benign multinodular goiter. We studied 104 patients with multiple (2 to 5, mean = 2.5 +/- 0.7), solid (96%) or predominantly solid (4%), nonfunctional (68%) or hypofunctional (32%) thyroid nodules. The benign (colloid) nature of 94% of the nodules was confirmed by fine-needle aspiration biopsy. All the patients received suppressive (2.2 micrograms per Kg body weight) daily oral doses of levothyroxine for 6 months. To confirm the effectiveness of the suppressive therapy, TSH levels were measured by an ultrasensitive immunometric assay at 3 and 6 month of treatment. For each patient, the volume of each nodule before and after levothyroxine therapy was evaluated by high-resolution ultrasonography. After 3 and 6 months of treatment, TSH levels were suppressed (lower than 0.1 mIU/l) in 75 patients and detectable in 29. At the end of the study, the volume of all the nodules was decreased by 50% or more (responder group) in 20/75 (27%) of the patients with suppressed TSH levels, and in 3/29 (10%) of those with detectable TSH values. In the latter group the proportion of patients in which one or more nodule(s) showed an increase in volume (48%) was significantly higher (p < 0.0005) than in patients with suppressed TSH (29%). We can conclude that an effective TSH suppressive therapy is an useful tool in the treatment of nontoxic benign multinodular goiter.

Adult↗
PubMed1996

Molecular aspects of the pathogenesis of nodular goiters, thyroid nodules and adenomas.

One of the most significant results of recent molecular thyroid research on the pathogenesis of nodular goiters may be the finding that not only thyroid adenomas but also many thyroid nodules are clonal in origin and thus are true benign tumors. Both clonal and polyclonal nodules may coexist within the same nodular goiter. Since clonal nodules may secondarily acquire a heterogeneous phenotype, they can become morphologically indistinguishable from polyclonal lesions. The molecular mechanisms that generate thyroid nodules and adenomas are still poorly understood. Certainly, the recent detection of activating mutations in the TSH receptor and the Gs alpha gene in a subset of toxic thyroid adenomas and nodules may explain the generation of hyperfunction in these tumors, but there is strong evidence that these mutations are not the unique and primary cause of tumor formation. In this respect the concept of natural occurring heterogeneity of thyroid growth and function can provide a plausible explanation for the early stages of nodular transformation: If a thyrocyte has a high intrinsic growth potential or if it is affected by overexpression of a protooncogene or a growth factor or hit by an oncogene or other molecular events, the cell will outgrow and form a tumor. The inborn qualities of proliferating cells or the sequence of various genetic alterations in proliferating cells will in turn determine the phenotype and function of the tumor.

Adenoma↗
PubMed2005

VATS with a supraclavicular window for huge substernal goiter: an alternative technique for preventing recurrent laryngeal nerve injury.

A careless attempt to remove a huge substernal goiter using the cervical approach can lead to recurrent laryngeal nerve injury, which has been consistently reported after the surgery. We present an alternative and less invasive technique combining video-assisted thoracoscopic surgery (VATS) with a supraclavicular approach. This technique seems to offer improved exposure and reliable control of the neuro-vascular structures in the anterior mediastinum when resecting a huge substernal goiter that may prevent nerve injury.

Aged↗
PubMed1990

Effect of Somatostatin on TSH levels in non-toxic sporadic goiter.

Somatostatin (SS-14; growth hormone-release inhibiting hormone) was infused into eight patients with non-toxic sporadic goiter and into eleven normal control subjects. Each patient was given 150 microgram(s) of somatostatin as an intravenous bolus and 350 microgram(s) by infusion over a period of 60 minutes. Somatostatin did not lower the basal TSH levels as compared to the pre-infusion levels in this type of goiter, but produced a decrease in the TSH response to TRH during and after the infusion.

Adult↗
PubMed1986

Congenital goiter sustaining normal level of serum triiodothyronine.

We attempted to elucidate the deficient site of thyroid hormone biosynthesis in the thyroid gland and the mechanism of sustaining normal T3 level in sera of a patient with congenital goiter. TY, a 8-yr-old boy, first noted the onset of a diffuse goiter at the age of 2. There was no clinical evidence of hypothyroidism except for the slight impairment of intellectual development and the awkward physical activity. BMR, T3-RSU and T4 showed low values (-13%, 20.8% and 2.2 micrograms/dl), but serum T3 was normal (180 ng/dl). Serum TSH was 18 microU/ml. The intrathyroidal T3 and T4 were slightly low. Thyroidal 131I uptake was high, but KSCN discharge test was negative. Percent distribution of 131I labelled amino acids in the pancreatin digested thyroid homogenate was 17.4% in MIT, 33.4% in DIT and 11.3% in T3 and T4. Thyroid iodide peroxidase activities in mitochondrial and microsomal fractions were slightly low (19.6 and 26.8 (normal: 32 +/- 3.0 and 37.4 +/- 9.5) mumoles/mg protein). The activity was not increased by the addition of hematin. Thyroglobulin was found to be normal. A biological half life of 131I labelled T4 was shorter (3.5 days) than that of the normal. Electron microscopic examination exhibited the increment and expansion of endoplasmic reticulum in the follicular cell. Low iodide peroxidase activity of this patient may correlate to low T3 and T4 level in the thyroid cell. Moreover, shortened biological half life of T4 implies that normal T3 level in serum is sustained by the accelerated conversion of T4 to T3 in peripheral tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1995

Prenatal diagnosis and management of fetal goiter caused by maternal Grave's disease.

We present a case of maternal Grave's disease associated with fetal goitrous hyperthyroidism. Fetal goiter was diagnosed by ultrasound and diagnosis of fetal hyperthyroidism was established by umbilical blood sampling. Fetus was successfully treated by increasing maternal propylthiouracil dosage. Fetal thyroid status was normal at birth. Role of sonography and umbilical blood sampling in management of fetal goiter complicated with maternal Grave's disease is discussed.

Adult↗
PubMed2006

Negative-pressure pulmonary edema after resection of mediastinum thyroid goiter.

Negative-pressure pulmonary edema (NPPE) is an uncommon but life-threatening complication of acute or chronic upper airway obstruction; however, there are few reports of NPPE after giant goiter resection. We report a case with severe NPPE induced by the resection of a mediastinum thyroid goiter. The patient was successfully treated by non-invasive positive airway ventilation (NPPV).

Adenocarcinoma, Papillary↗
PubMed2004

Correlation between serum leptin levels and insulin sensitivity in diffuse toxic goiter.

OBJECTIVE: The aim of this survey was to assess the correlation between leptin and insulin sensitivity (IS) in cases of diffuse toxic goiter. DESIGN, PATIENTS, MEASUREMENTS: This is a descriptive study on patients with diffuse toxic goiter (DTG) assessing their body mass index (BMI), serum leptin concentrations, circulating insulin (area under the curve (AuC) of insulin), average insulin level, thyroid hormones, thyroid stimulating hormone (TSH), glycemia and IS (using a hyperinsulinemic-euglycemic clamp and the homeostasis model for assessment of insulin resistance (HOMA-IR) before and after euthyroidism induced with metimazol. RESULTS: The average patient age was 35 years old (range 31-40 years), height was 157 cm (range 151-160 cm), glycemia was 4.3 +/- 0.3 mmol/L and TSH 0.1 +/- 0.1 microU/mL. Average leptin level was 11.3 +/- 2.8 ng/dL, the average insulin level was 10.13 +/- 3.7 mIU/mL and the AuC for insulin was 50.6 +/- 18 microIU x min/mL. No correlation was found between leptin and BMI, thyroid hormones and glycemia. While controlling for the BMI effect, a correlation was found between leptin and TSH (r = -0.77, p = 0.042), as well as between leptin and insulinemia (r = 0.93, r2 = 0.86, p = 0.001) independently from the state of thyroid function. There was a tendency for a high correlation between leptin and the insulin AuC (hyperthyroidism: r = 0.89, p = 0.056; euthyroidism: r = 0.99, p = 0.056). A negative correlation was found between IS and the insulin AuC (rho = -0.58, p = 0.18). There was a high tendency for correlation between leptin and IS when the BMI effect (HOMA-IR: r = 0.70, p = 0.12; PHE: r = -0.55, p = 0.26) was taken into consideration. CONCLUSIONS: There is a high tendency for a negative correlation between leptin and IS when the BMI effect is controlled. There is a high tendency for a positive correlation between leptin and insulin and TSH.

Adult↗
PubMed2000

Mapping a dominant form of multinodular goiter to chromosome Xp22.

Multinodular goiter (MNG) is a common disorder characterized by a nodular enlargement of the thyroid gland and occurring with a female&rcolon;male ratio of 5&rcolon;1. This article reports the analysis of an Italian three-generation pedigree MNG, including 10 affected females and 2 affected males. After linkage to candidate regions previously implicated in various forms of goiter was excluded, a novel MNG locus was searched. Because no male-to-male transmission was present in the study pedigree, an X-linked autosomal dominant pattern of inheritance was hypothesized. Therefore, 18 markers spaced at 10-cM intervals on the X chromosome were examined. A significant LOD score was observed in the Xp22 region, where marker DXS1226 generated a maximum LOD score of 4.73 at a recombination fraction of 0. Analysis of six flanking microsatellites confirmed these data, and haplotype inspection delimited a 9.6-cM interval lying between DXS1052 and DXS8039.

Chromosome Mapping↗
PubMed2001

Overexpression of epidermal growth factor and epidermal growth factor-receptor mRNAs in dyshormonogenetic goiters.

Thyroid malignancy has been induced by long-term endogenous thyrotropin (TSH) stimulation in experimental animals, leading to local and distant metastasis. It has been postulated that constant and prolonged endogenous TSH stimulation in dyshormonogenetic thyroid tissues could result in thyroid neoplasia. The possible role of growth factors and oncogenes in goitrogenesis and favoring neoplasia has also been mentioned. Overexpression of certain growth factors and/or their receptors, and of oncogenes implicated in growth promotion may play a significant role in the relatively frequent finding of thyroid malignancy in congenital goiters. In this study the expression of epidermal growth factor (EGF), epidermal growth factor receptor (EGF-R), transforming growth factor-beta (TGF-beta), c-myc, and p53 mRNAs was determined in 14 thyroid tissue samples: 6 from patients with thyroid peroxidase (TPO) gene mutations, 4 with thyroglobulin (Tg) gene defects and 4 normal thyroid tissues. EGF mRNA overexpression was seen in 7 of 10 dyshormonogenetic tissues (3.5 to 12.0 arbitrary optical densitometry units [AODU]) and considered significantly higher (p < 0.01) when compared to normal thyroid tissues (0.25 to 0.32 AODU). Moreover, overexpression of EGF-R mRNA was present in 6 of 10 dyshormonogenetic tissues (2.23 to 13.03 AODU) and considered significantly higher (p < 0.01) when compared to normal thyroid tissues (0.42 to 0.65 AODU). There was no difference in c-myc, p53, and TGF-beta mRNAs expression between dyshormonogenetic and normal tissues. The overexpression of EGF and EGF-R mRNAs found in dyshormonogenetic tissues may suggest that this growth factor may play a role in cellular proliferation and contribute to goiter formation.

Cell Division↗
PubMed2002

Levels of soluble human leukocyte antigen class 1 are increased in Graves' disease and toxic multinodular goiter and correlate with the levels of triiodothyronine.

Soluble human leukocyte antigens class 1 (sHLA-1) are postulated to play a role in immunomodulation. Thyroid hormones and thyroid stimulating hormone influence expression of major histocompatibility complex (MHC) class 1 genes. We hypothesized similar changes in sHLA-1 with changes in the thyroid hormone. We measured serum levels of sHLA-1 in 140 normal controls, 11 patients with toxic multinodular goiter and 26 patients with active Graves' disease. On follow-up 1 year after treatment for Graves' disease, we repeated the measurement of the levels of sHLA-1 in 21 patients. Levels of sHLA-1 were markedly elevated in the group of patients with active Graves' disease compared to the normal controls (p = 0.00016). The levels of sHLA-1 were also elevated significantly in patients with toxic multinodular goiter compared to normal controls (p = 0.034). There is no significant difference between genders and the two races tested among patients with Graves' disease in contrast to controls. Free triiodothyronine (T(3)) levels positively correlated with the levels of sHLA-1 (r = 0.61). On follow-up after treatment for Graves' disease, levels of sHLA-1 decreased by 62% with p = 0.0006 (active Graves vs. follow-up). We conclude that there is a definite association between thyroid hormones and sHLA-1 levels.

Adult↗
PubMed2003

Treatment of recurrent nodular goiters with percutaneous ethanol injection: a clinical study of twelve patients.

Twelve patients who had previously undergone thyroid surgery received percutaneous ethanol injection (PEI) treatment because of recurrent nodular goiter (3 with a toxic [TN], 2 with a nontoxic cystic [NCN], and 7 with a nontoxic solid nodule [NSN]). Two of the 12 had recurrent nerve palsy contralateral to the nodule. Each patient received a mean total dose of 0.88 mL of ethanol per milliliter of nodular volume. Ethanol was injected in a mean of 3.5 sessions for solid and 3 sessions for NCN. In most cases, a slight to moderate burning pain was experienced during and for 12-48 hours after PEI treatment, and one patient experienced temporary hoarseness. One patient with TN and 2 patients with NSN became hypothyroid, 7 patients with nontoxic nodules remained euthyroid, 1 with TN became euthyroid, and a previously hyperthyroid patient with TN became subclinically hyperthyroid 1-year posttherapy. The nodule shrank by more than 50% of the pretreatment volume in all patients (8.6 +/- 2.6 vs. 2.9 +/- 1.2 mL in TN, and 12.3 +/- 4.9 vs. 4.16 +/- 2.54 mL in nontoxic nodules, pretreatment vs. 1 year posttreatment volume, respectively). With regard to the increased risk of reoperation, PEI treatment can be proposed for patients with recurrent nodular goiter requiring surgery.

Administration, Cutaneous↗
PubMed1992

Goiter and pregnancy: a new insight into an old problem.

Evidence is presented that pregnancy constitutes a goitrogenic stimulus, particularly in conditions with a restricted or even a marginally low iodine intake. In a series of studies carried out in a large cohort of pregnancies in the Brussels area, the authors show that an increase in thyroid volume is observed in a majority of pregnant women, leading to goiter formation at delivery in 9% of the cases. Furthermore, increments in thyroid volume were correlated with biochemical evidences of functional stimulation of the thyroid, such as an elevation in serum TG levels, preferential T3 secretion, and slight increases in basal TSH at delivery. Hence, the association of biochemical features of thyroidal stimulation with volumetric changes in the gland strongly suggests that pregnancy truly induces goitrogenesis rather than vascular swelling ("intumescence") alone, at least in conditions with a low iodine intake. Finally, preliminary data from this laboratory, as well as recently published data from other investigators, suggest that goiter formation during pregnancy can easily be prevented by increasing the iodine supply during pregnancy.

Adult↗
PubMed1997

Incidence and clinical characteristics of thyroid carcinoma after iodine prophylaxis in an endemic goiter country.

Iodized salt prophylaxis has been performed in Austria since 1963. Through this approach, mean urinary iodine excretion has been normalized to 144+/-23.5 microg/g creatinine per day. Thus Tyrol is no longer an endemic goiter area. We have analyzed the impact of iodized salt prophylaxis on thyroid cancer (TC) comparing data from the early 1960s with those corresponding to the period 1986 to 1995, when iodine supply was normalized. The study included 439 patients from Tyrol and Southern Tyrol. The incidence of TC in Tyrol has risen during the past decades from 3.07 between in 1957 and 1970 to 7.8 between 1990 and 1994 (CR/100000/year). We observed a rise in the percentage of differentiated adenocarcinomas (56% to 91.5%) with a predominance of papillary TC (54.4%) along with a decrease of anaplastic TC. In addition to these histological features, a shift to less advanced TNM stages, eg, T1-3, N0-1a, M0, was obvious, increasing from 29% to 72.2%, whereas advanced tumors, ie, T4 or N1b or M1, decreased from 71% to 28%. These changes have significantly improved prognosis. The current 5-year survival rate is 90.7% as compared with a rate of 73% in the 1960s; the values for 7-year survival are 89% and 48%, respectively. The marked effects of age, tumor stages, and histology on prognosis were confirmed with the Kaplan-Meier method. We conclude that together with normalization of iodine supply in an endemic goiter region the epidemiological profile of TC has changed. Even though the incidence of TC has risen, prognosis has significantly improved due to a shift towards differentiated forms of TC that are diagnosed at earlier stages.

Age Factors↗
PubMed1998

Amyloid goiter due to primary systemic amyloidosis: a diagnostic challenge.

We describe a euthyroid patient who presented with a goiter that continued to enlarge despite levothyroxine administration. Three fine-needle aspirations for cytology were nondiagnostic. An open biopsy was complicated by bleeding from the surgical site. Primary systemic amyloidosis was diagnosed on the basis of the goiter histology, bone marrow aspirate, and urine immunoelectrophoresis. The patient received melphalan and steroid treatment and survived for an additional 16 months. This period was complicated by congestive heart failure, generalized seizures, and upper gastrointestinal bleeding. Our case illustrates the difficulties in making the diagnosis and in treatment of primary systemic amyloidosis.

Adult↗