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PubMed1978

Iodide organification defect in iodine deficiency endemic goiter.

In 17 goitrous persons in an iodine-deficient area, in 23 nongoitrous inhabitants of the same village, in 10 goitrous persons in Athens, and 8 normal controls the perchlorate discharge test was performed, either in the simple standard form or after pretreatment with either 0.5 or 2.0 mg potassium iodide or 2.5 mg carbimazole. With the simple test or with 0.5 mg potassium iodide, there was no significant discharge in any group studied. With 2.5 mg carbimazole, there was a profound discharge of the trapped iodide in both groups in the iodine-deficient area. With 2.0 mg potassium iodide, however, there was a clear discharge in the two goitrous groups (i.e. the one in the endemic area and the second in Athens), a less pronounced discharge in the controls studied in Athens, and no discharge at all in the nongoitrous inhabitants of the iodine-deficient endemic area. These findings provide evidence for an abnormality present in the patients with endemic goiter, most probably faulty iodine utilization due to impaired organic binding. The nongoitrous persons in the endemic areas, on the other hand, seem to be even more efficient in handling the trapped iodide than the controls studied in Athens. These findings may provide an explanation for previous observations that in endemic areas only part of the population develop a goiter, whereas the others adapt successfully to iodine deficiency without significantly enlarging their glands.

Child↗
PubMed1981

Congenital goiter and the development of metastatic follicular carcinoma with evidence for a leak of nonhormonal iodide: clinical, pathological, kinetic, and biochemical studies and a review of the literature.

We report a large kindred of patients with congenital goiter, followed for 15 yr, in which two siblings (one male and one female) developed metastatic follicular thyroid carcinoma. These two patients were evaluated by iodine kinetic analysis. None of the classical defects of T4 biosynthesis was present in either patient. Rather, both patients had extremely rapid rates of iodine turnover, with elevated 131I uptake and excessive spillage of iodide in the urine. Serum iodoalbumin was present, probably as a nonspecific result of glandular hyperplasia. Iodine kinetic analysis after the ingestion of potassium perchlorate and methimazole was compatible with a leak of nonhormonal iodide from the thyroid. It is not possible to determine whether this iodide leak is the primary pathogenetic defect or is secondary to another unidentified abnormality. The unprecedented development of metastatic thyroid cancer in patients with congenital goiter occurred, in both instances years after subtotal thyroidectomy without thyroid hormone replacement therapy, suggesting a role for TSH in the genesis of human thyroid cancer. On the basis of our study of these patients and a review of the literature, we conclude that TSH is likely to be a factor in the induction of human follicular thyroid carcinoma.

Adenocarcinoma↗
PubMed1983

Thyroid hormone and immunological studies in endemic goiter.

Iodized oil (1 ml im) was given to 58 goitrous patients from a mildly iodine-deficient area in Greece. Goiter size, urinary iodine, and serum T4, T3RU, T3, rT3, TSH, thyroxine-binding globulin (TBG), and thyroid autoantibodies were measured before and 1, 3, and 6 months after the injection. Goiter size decreased. Serum T4 remained relatively constant, but TBG decreased and therefore T3RU and FTI increased. Serum T3 and rT3 initially decreased (P less than 0.001) and then increased at the sixth month (P less than 0.001), both showing roughly parallel changes. Serum TSH, initially normal (1.42 +/- 0.11 (SEM) mU/liter), decreased to 0.65 +/- 0.01 and 0.76 +/- 0.05 mU/liter at the third and sixth month (difference from baseline P less than 0.001). Thyroid autoantibodies, both against thyroglobulin and the microsomal antigen, were undetectable before treatment, but became positive in 42.8% of the patients 3 and 6 months later. Three patients developed transient hyperthyroidism. This occurred 3 or 6 months after treatment, and was associated with high titers of thyroid autoantibodies. These results indicate that: 1) transient hyperthyroidism may occur after the administration of iodized oil, possibly because of thyroid tissue necrosis and leakage of hormones, and 2) serum TBG decreases after iodized oil, a finding not previously reported and one whose cause is not known.

Adult↗
PubMed1983

Association of thyroid-stimulating immunoglobulins and thyrotropin-releasing hormone responsiveness in women with euthyroid goiter.

Thyroid-stimulating immunoglobulins (TSI) were measured, using a highly sensitive cytochemical bioassay, in plasma from 26 euthyroid women with idiopathic diffuse or multinodular goiter selected on the basis of their serum TSH responses to TRH stimulation. Thirteen were chosen because they were previously identified to have impairment in TRH responsiveness and were compared with 13 consecutive patients who had normal responses to TRH. TSI were present in a significantly greater number of those who had subnormal TRH responses (11:13) compared to those who had normal responses (3:13) P less than 0.005. Although serum T4, T3, and basal TSH values were all within the normal range, mean serum T4 and T3 values were significantly higher and basal TSH significantly lower in the 14 patients who had TSI than in the 12 in whom TSI was absent. The coexistence of impaired TRH responsiveness and TSI was associated with a family history of thyroid disease. The data suggest that TSI in patients with euthyroid goiter cause a modest increase in thyroid secretion sufficient to blunt the TSH response to TRH but not to cause clinical hyperthyroidism.

Adult↗
PubMed1984

Transient impairment of thyroid function in newborn from an area of endemic goiter.

Thyroid function was studied in newborn from 3 areas of Sicily in which iodine intake is normal (area A), moderately decreased (area B), and severely decreased (area C). In the latter 2 areas, there is a high incidence of goiter and in area C endemic cretinism is present. TSH and T4 were measured in the cord serum of 5673 newborn from area A, 2096 from area B, and 184 from area C. The mean TSH value was significantly higher in areas C (P less than 0.001) and B (P less than 0.005) when compared to area A; moreover, in both endemic goiter areas the mean cord serum T4 was significantly reduced (P less than 0.01). All infants with cord serum TSH levels above 50 microU/ml were recalled because of the suspicion of congenital hypothyroidism. Such values were found in 41 of the 7953 infants (0.52%) with an increasing frequency from area A (9:5673 = 0.16%) to area B (14:2096 = 0.67%) to area C (18:184 = 9.78%). At the time of the recall examination [mean age, 32 +/- 8 (SD) days], 3 of the 41 recalled infants had died. Of the remaining 38 infants, 3 patterns evolved: 1) 23 had normal serum TSH and T4 values and were not studied further (false positives). 2) Eleven had elevated serum TSH and normal T4 values. They were reevaluated again after 3-6 weeks: all had normal values (transient hyperthyropinemia ). 3) Four infants had both high serum TSH and low serum T4 values (2 from area A and 2 from area C). They were diagnosed as having congenital hypothyroidism and treated with T4. At 10-13 months of age, after treatment withdrawal, the 2 infants from area A had permanent congenital hypothyroidism due to thyroid agenesis whereas the 2 infants from area C were euthyroid (transient congenital hypothyroidism). The present studies indicate, therefore, that in newborn from areas of iodine deficiency there is a higher frequency of elevated TSH levels and low T4 values than is found in areas where iodine intake is normal. This frequency is correlated to the degree of the iodine deficiency. The data suggest that the impairment of thyroid function at birth may be a transient phenomenon. The duration and the severity of the transient neonatal hypothyroidism, however, is greatly variable and its evolution unpredictable.

Congenital Hypothyroidism↗
PubMed1987

Relationships between serum thyrotropin, serum free thyroxine (T4), and 3,5,3'-triiodothyronine (T3) and the daily T4 and T3 production rates in euthyroid patients with multinodular goiter.

Serum TSH, as measured by a sensitive assay, and serum free T4 and T3, as measured by an ultrafiltration technique, were compared in 14 euthyroid patients with multinodular goiter and 14 normal subjects. T4 and T3 turnover studies also were performed, using the single injection, noncompartmental approach. The goitrous patients had serum free T3 levels within the normal range, but their median serum T3 level was increased compared to that in the normal subjects [goitrous patients, 5.48 pmol/L (range, 4.41-9.03); normal subjects, 4.12 pmol/L (range, 2.58-5.78); P less than 0.01]. The T3 production rate (PR) also was elevated in the patients (median, 39.4 nmol/day X 70 kg; range, 28.7-70.5) compared to that in the normal subjects 31.1 nmol/day X 70 kg; range, 24.4-45.2); P less than 0.05). No differences were found between the two groups with regard to serum free T4 levels or T4 PRs. Serum TSH levels in the patients were reduced (median, 0.20 mU/L; range, less than 0.05-1.6) compared to those in normal subjects (1.8 mU/L; range, 0.36-5.1; P less than 0.01). A significant inverse correlation was found between serum TSH levels and free T3 levels (r = 0.70; P less than 0.001), whereas serum TSH did not correlate with serum free T4 or the PR of T4 or T3. Our data suggest that clinically and biochemically euthyroid patients with multinodular goiter have slight T3 hyperproduction, and TSH secretion in the patients studied was more closely related to serum free T3 levels than to serum free T4 levels or the T3 or T4 PR.

Adult↗
PubMed1988

Autonomous growth, but not autonomous function, in embryonic human thyroids: a clue to understanding autonomous goiter growth?

Thyroid glands from six 8- to 10-week-old fetuses obtained at the time of legal abortion were cryopreserved in liquid nitrogen and transplanted into nude nu/nu mice. Histological and autoradiographic studies of the grafts labeled with [3H]thymidine and [125I]iodine showed proliferation and functional differentiation of the fetal thyroid tissue. Despite T4-mediated suppression of host TSH secretion, up to 36% of the follicular cell nuclei incorporated the thymidine label, reflecting autonomous proliferation, while iodine organification was almost entirely obliterated. Methimazole-induced TSH hypersecretion readily stimulated both growth and function of the transplanted tissue. Thus, during early development, the human thyroid largely depends on TSH for function, but not for growth. Similar findings were obtained in newborn mice, in whom 58% of the thyroid follicular cells proliferated autonomously, i.e. in the absence of TSH. The number of autonomously proliferating cells gradually declined with increasing age to about 1% in 60-day-old animals and, as reported previously, in xenotransplanted normal human thyroid tissue, whereas the number of autonomously proliferating cells was previously found to be several times higher in xenotransplanted human multinodular goiters. We, therefore, hypothesize that the rapidly and autonomously replicating cells that initiate nodule formation in human multinodular goiters reflect the persistence in the adult gland of cells with fetal growth potential.

Age Factors↗
PubMed1990

Coexistence of autoantibody to human thyrotropin (TSH) and autoanti-idiotypic antibody to antihuman TSH antibody in a case with simple goiter.

A 70-yr-old woman with simple goiter showed normal serum levels of T4, T3, free T4, TSH receptor antibody (TRAb) and increased TBG. Discrepancy in serum hTSH level was observed by different assay methods. Coexistence of both autoantibodies for hTSH and for anti-hTSH antibody were demonstrated by the reaction of the patient's antibody with both 125I-hTSH and 125I-anti-hTSH (monoclonal antibody; mAb). These two autoantibodies belong to the polyclonal immunoglobulin G (IgG). The autoantibody for hTSH recognized only beta-subunit of hTSH. Neither stimulating type of TRAb in Graves' disease nor blocking type of TRAb in primary hypothyroidism interfered with the binding of the patient's antibody to 125I-hTSH or 125I-anti-hTSH. Anti-idiotypic antibody (anti-ID antibody) for anti-hTSH antibody was purified by anti-hTSH antibody affinity chromatography. The binding reaction of 125I-anti-hTSH (mAb) with this anti-ID antibody could be inhibited by the unlabeled hTSH. This anti-ID antibody might represent the internal image of the nonbiological active site of TSH molecule, because of absence of thyroid stimulating activity. Goiter in this patient may have occurred by the unbound TSH with IgG (free TSH) and the bound TSH with IgG, because TSH levels in both the whole serum and the IgG free serum (the unbound TSH with IgG) were decreased significantly by T4 treatment. Coexistence of these antibodies may participate in the autoimmune mechanism of an idiotype-anti-idiotype network.

Aged↗
PubMed1991

The lack of nocturnal serum thyrotropin surge in patients with nontoxic nodular goiter may predict the subsequent occurrence of hyperthyroidism.

TSH secretion, with particular regard to the nocturnal TSH surge, was evaluated in 115 subjects with non-toxic nodular goiter. All patients were clinically and biochemically euthyroid. After 18-36 months of follow-up (mean, 24 months), hyperthyroidism occurred in 21 (18%; group 1), while the remaining 94 remained euthyroid (82%; group II). The analysis of hormonal data at the time of first observation showed that the 2 groups had similar total and free T4 and T3 serum concentrations. Morning serum TSH values in group I were lower than those in group II patients (0.6 +/- 0.1 vs. 1.1 +/- 0.1 mU/L; P less than 0.001); this difference was even more striking for the nocturnal values (0.6 +/- 0.1 vs. 2.2 +/- 0.2 mU/L; P less than 0.0001); nocturnal values were significantly lower than morning values in group II, but not in group I. The mean peak TSH value after TRH was also significantly reduced in group I (5.5 +/- 0.4 vs. 9.2 +/- 0.7 mU/L; P less than 0.001). Morning TSH values in group II did not differ from those in controls (1.3 +/- 0.1 mU/L), whereas nocturnal and TRH stimulated peak TSH values were slightly but significantly lower. The nocturnal serum TSH values in control subjects were 62-390% higher than morning values. The nocturnal TSH surge was abolished in 18 of 21 (86%) group I patients and in 7 of 94 (8%) group II patients. TRH testing resulted in an absent or blunted TSH responses in 5 subjects in group I and 6 in group II. Analysis by the Galen and Gambino predictive model; comparing the abolition of the nocturnal TSH surge and the abnormal TRH test as predictors of the subsequent occurrence of hyperthyroidism, showed that the former had higher sensitivity (86% vs. 24%) and predictivity (72% vs. 45%). In conclusion, the results of the present study demonstrate that the evaluation of the nocturnal TSH surge may be useful in identifying patients with nontoxic nodular goiter in whom hyperthyroidism may eventually occur. Patients who lack the nocturnal serum TSH surge are more prone to develop thyroid hyperfunction; their thyroid status should, therefore, be more carefully and frequently monitored.

Adult↗
PubMed1993

A nonsense mutation causes human hereditary congenital goiter with preferential production of a 171-nucleotide-deleted thyroglobulin ribonucleic acid messenger.

Defective or impaired thyroglobulin (Tg) synthesis usually results in congenital goitrous hypothyroidism, virtual absence of Tg in thyroid tissue, and the presence of an elevated concentration of iodoalbumin. The final result of these abnormalities is a decreased rate of T3 and T4 synthesis. We have previously reported two siblings with this syndrome that was attributable to decreased levels of thyroid tissue Tg mRNA, resulting in decreased translation of a fully mature Tg. Further molecular studies in this family are the subject of this report. The Tg mRNA from normal and goitrous thyroid tissue was first reverse transcribed and divided into five overlapping portions from positions 57-8448, and the resulting cDNAs were amplified by polymerase chain reaction and analyzed by agarose gel electrophoresis. The amplification of nucleotides (nt) 4502-5184 from control thyroid tissue Tg mRNA showed a predominant fragment of 683 basepairs (bp) and a minor fragment of 512 bp. This latter fragment contained a 171-nt deletion that mapped between positions 4567 and 4737 of the Tg mRNA. In contrast, the fragment predominantly present in the congenital goiter was 512 bp. The sequencing of the 683-bp fragment revealed that the responsible mutation is a cytosine to thymine transition, creating a stop codon at position 1510. This results in loss of a TaqI restriction site. The point mutation is, thus, removed from a portion of the transcripts by the preferential accumulation in the goiter of a 171-nt-deleted Tg mRNA. The reading frame is maintained and is potentially fully translatable into a Tg polypeptide chain shorter by 57 residues. The presence of the deleted Tg mRNA in normal thyroid tissue, albeit at a low level, strongly suggests that the deleted mRNA sequence corresponds to a complete exon. Our studies suggest that the shorter, alternatively spliced Tg mRNA predominates in the goitrous tissue and probably has a shorter half-life. This would explain the tissue's low Tg mRNA levels, previously reported. Moreover, translation of the mutated transcript would generate a severely truncated Tg polypeptide with limited ability to generate thyroid hormone, resulting in congenital goitrous hypothyroidism.

Amino Acid Sequence↗
PubMed1994

Analysis of cytokine gene expression in Graves' disease and multinodular goiter.

Cytokines have a central role in the generation of an autoimmune response and can directly affect the target organ. In Graves' disease, both the infiltrating mononuclear cells and the thyroid follicular cells produce certain cytokines, but the relative contribution of each is unclear, and there are conflicting data on the exact profile of cytokines expressed within the thyroid. To clarify these issues, we used the method of reverse transcription-polymerase chain reaction amplification to analyze cytokine gene expression by intrathyroidal lymphocytes (ITL) and purified thyroid follicular cells (TFC) from six patients with Graves' disease. All ITL samples were positive for interleukin-1 alpha (IL-1 alpha), IL-1 beta, IL-6, IL-8, IL-10, and tumor necrosis factor-alpha (TNF alpha) messenger ribonucleic acids (mRNAs). Four samples were positive for IL-2 mRNA, and of these, three were also positive for interferon-gamma (IFN gamma). All TFC samples contained IL-6 and IL-8 mRNAs, even after depletion of CD3-positive T-cells. One TFC sample was additionally positive for IL-10 and TNF alpha mRNAs, and in the case of IL-10, this signal was not eliminated by CD3-positive T-cell depletion. IL-4 was not detected in any sample of ITL, TFC, or whole tissue. Semiquantitative analysis showed that the ITL fraction represented the major source of IL-6, IL-8, and TNF alpha mRNAs. By contrast, only three of five multinodular goiter samples were positive for IL-1 alpha mRNA; of these, two were also positive for IL-6, and 1 was positive for IL-8 mRNA. One multinodular goiter sample was positive for IL-8 mRNA alone, but IL-2, IL-4, IL-10, and TNF alpha mRNAS were not detected. These results suggest that although the TFC themselves may express certain cytokines, the ITL population represents the most important source of cytokine production in Graves' thyroid glands. The presence of IL-2, IFN-gamma, and TNF alpha and the absence of IL-4 mRNA in samples of ITL indicate a pattern of cytokine production that most closely resembles that of the TH1 helper T-cell subset. Given the etiological role of thyroid-stimulating antibodies in Graves' disease, the production of which is likely to depend upon TH2 helper T-cell function, it is perhaps surprising that the TH1 subset appears to predominate. It is possible that IL-10 is important in stimulating intrathyroidal autoantibody production, and this cytokine may also play a role in inhibiting cell-mediated thyroid injury in Graves' disease.

Base Sequence↗
PubMed1995

The effects of different doses of oral iodized oil on goiter size, urinary iodine, and thyroid-related hormones.

The prevention of iodine deficiency is still a worldwide concern. This study, conducted in Soja in western Sudan, was carried out to evaluate the effects of a dose of iodized oil sufficient enough to give maximum protection against goiter and provide an acceptable iodine supply without side-effects over a sufficiently long period of time. Adult goitrous subjects (n = 117) were randomly assigned to three groups, A, B, and C, and received a single oral dose of 200, 400, or 800 mg iodine, respectively. Urine and blood samples were collected at the start of the study and monitored for 1 yr. In the 3 groups, mean serum T4 and median urinary iodine and serum TSH values were restored to reference limits, and these were maintained for about 1 yr. In each treatment group, about two thirds of the subjects displayed a reduction in goiter size, and the 400- and 800-mg doses were not more efficient than the 200-mg dose to accomplish normalization of thyroid hormone values. A temporary rise in TSH was noted 1 week after iodine administration in 1, 3, and 10 subjects, respectively, and 1, 0, and 3 subjects showed biochemical signs of thyrotoxicosis during the year after treatment with the 3 different doses. The data indicate that oral administration of 200 mg iodine is effective and acceptable for treating iodine deficiency in adults for 1 yr. Because of the risks of side-effects and the shortage of medical resources, higher doses are not recommended.

Administration, Oral↗
PubMed1997

Randomized, double blind, placebo-controlled trial of low dose iodide in endemic goiter.

Iodine (I) is essential for normal thyroid function, and the majority of subjects tolerate a wide range of dietary levels. However, a subset of individuals upon exposure to normal or elevated levels of I develop thyroid dysfunction and autoimmunity. In this double blind trial, we evaluated efficacy and tolerability of low dose I in adults with euthyroid, diffuse, endemic goiter. Sixty-two subjects were randomly assigned I (0.2 mg/day) or placebo for 12 months. After termination of therapy, both groups were followed for a further 6 months. Thyroid sonography and determinations of thyroid-related hormones, urinary I excretion per 24 h, and thyroid antibodies were carried out at baseline and at 3, 6, 9, 12, 15, and 18 months. Markedly elevated urinary I values were found during therapy in subjects receiving I (32 at baseline vs. 213 micrograms/24 h at 12 months; P = 0.0001) compared to placebo (34 and 33 micrograms/24 h, respectively; P < 0.0001 vs. I). I substantially reduced thyroid volume (29 vs. 18 mL at 12 months; -38%; P = 0.0001), and at 18 months, the therapeutic effect was sustained. In the placebo group, no significant changes were observed. High microsomal and thyroglobulin autoantibody titers were present in 3 of 31 (9.7%) subjects receiving I, and I-induced hypo- and hyperthyroidism developed in 2 and 1, respectively. Fine needle biopsy revealed marked lymphocytic infiltration in all 3 cases. After withdrawal of I, thyroid dysfunctions spontaneously remitted, and antibody titers as well as lymphocytic infiltration decreased markedly. Follow-up of these 3 subjects for an additional 2 yr showed normalization of antibody titers in 2. Thus, among subjects with endemic goiter, low dose I successfully normalized thyroid volume and body I supplementation; nevertheless, reversible I-induced thyroid dysfunctions and autoimmunity were observed in nearly 10% of the subjects.

Adult↗
PubMed1998

Metastatic thyroid carcinoma arising from congenital goiter due to mutation in the thyroperoxidase gene.

A very large cervical tumor that extended to the upper mediastinum was seen in a newborn after an uneventful pregnancy. The computed axial tomography scan confirmed the presence of a solid mass with precise limits and scattered foci of calcifications situated in the anterolateral region of the neck. The infant underwent thyroidectomy on the seventh day after birth. Pathological examination revealed a follicular carcinoma of the thyroid and probable dyshormonogenetic hyperplastic goiter. At 5 months of age, whole body scans indicated the presence of lung and bone metastases, which were treated with therapeutic doses of radioiodine. Genomic DNA was obtained from the newborn, her parents, her paternal aunt, and her paternal grandparents. Denaturing gradient gel electrophoresis analysis of PCR fragments corresponding to exon 14 of the thyroid peroxidase (TPO) gene indicated the presence of a mutant TPO allele present in the propositus, her father, and her paternal grandmother. Sequencing of the TPO gene demonstrated a mutation resulting from an insertion of a single extra cytosine in a stretch of seven cytosines at positions 2505-2511. The insertion caused a frame shift and a stop signal in exon 16. This sequence would translate into a structurally modified and probably inactive TPO protein. We conclude that the aggressive thyroid metastatic carcinoma arose from a dyshormonogenetic goiter caused by a defective TPO protein.

Bone Neoplasms↗
PubMed1999

Chloracne, goiter, arthritis, and anemia after polychlorinated biphenyl poisoning: 14-year follow-Up of the Taiwan Yucheng cohort.

In 1979, a mass poisoning involving 2,000 people occurred in central Taiwan from ingestion of cooking oil contaminated by polychlorinated biphenyls (PCBs) and polychlorinated dibenzofurans (PCDFs). We studied the prevalence of medical conditions in the exposed individuals and in a neighborhood control group. Starting with a registry of the exposed individuals from 1983, we updated the addresses of exposed individuals and identified a control group matched for age, sex, and neighborhood in 1979. In 1993, individuals 30 years of age or older were interviewed by telephone. We obtained usable information from 795 exposed subjects and 693 control subjects. Lifetime prevalence of chloracne, abnormal nails, hyperkeratosis, skin allergy, goiter, headache, gum pigmentation, and broken teeth were observed more frequently in the PCB/PCDF-exposed men and women. The exposed women reported anemia 2. 3 times more frequently than controls. The exposed men reported arthritis and herniated intervertebral disks 4.1 and 2.9 times, respectively, more frequently than controls. There was no difference in reported prevalences of other medical conditions. We conclude that Taiwanese people exposed to high levels of PCBs and PCDFs reported more frequent medical problems, including skin diseases, goiter, anemia, and joint and spine diseases.

Acne Vulgaris↗
PubMed1996

Effect of posture on the flow-volume loop in two patients with euthyroid goiter.

In two patients with a goiter and respiratory symptoms occurring only in the recumbent posture, flow-volume loops (FVLs) were performed in various body postures: while sitting upright, supine, and left and right lateral decubitus. In both patients, flow rates, upper airway obstruction indices, and FVL morphologic features with patients in recumbent postures indicated the appearance of upper airway flow limitation with patients in the recumbent posture as compared with the upright posture. In the one patient who underwent thyroid surgery, these posture-related changes disappeared. We conclude that in patients with a goiter (or any extrinsic mass near to the upper airway), the comparison of FVLs performed in various body positions may help to clarify the origin of posture-related respiratory symptoms.

Adult↗
PubMed1985

Spectrum of advanced upper airway obstruction due to goiters.

Five patients with advanced upper airway obstruction due to goiter were identified in our institution. All had symptoms of respiratory insufficiency to such a degree that surgery was clearly indicated. Functional characteristics of this group were compared with prior series of goiter patients who had less severe respiratory symptoms. A peak inspiratory flow less than 1.5 L/sec characterized this group who required surgery.

Aged↗