 |
 |

Thyroidectomy for Selected Patients With Thyrotoxicosis
Elizabeth A. Mittendorf, MD;
Christopher R. McHenry, MD
Arch Otolaryngol Head Neck Surg. 2001;127:61-65.
ABSTRACT
 |  |
Objective To examine the indications for operation and the frequency, efficacy,
and outcome of surgical therapy for thyrotoxicosis.
Methods The medical records of all patients who underwent thyroidectomy between
1990 and 1998 were reviewed. Operative indications, laboratory evaluations,
extent of thyroidectomy, pathologic findings, and morbidity and mortality
were determined for patients with thyrotoxicosis.
Results Of the 347 patients who underwent thyroidectomy, 54 (16%) had thyrotoxicosis,
secondary to Graves' disease (32 patients), toxic multinodular goiter (18
patients), thyroiditis (2 patients), or amiodarone (2 patients). The indications
for operation were compressive symptoms or substernal extension or both (35
patients), patient preference (12 patients), thyrotoxicosis (4 patients),
or a dominant nodule (3 patients). Most patients received pharmacological
preparation, followed by total (32 patients), near-total (13 patients), subtotal
(8 patients), or unilateral (1 patient) thyroidectomy. The initial 8 patients
with Graves' disease underwent subtotal thyroidectomy, and after a mean 28-month
follow-up, 1 was euthyroid; 2, hyperthyroid; and 5, hypothyroid. Associated
carcinoma was present in 4 (7%) of the 54 patients. Symptomatic hypocalcemia
occurred in 10 patients (19%), with a mean free thyroxine level of 60.49 ±
16.09 pmol/L vs 40.41 ± 19.56 pmol/L (4.70 ± 1.25 ng/dL vs 3.14
± 1.52 ng/dL) in 25 patients (46%) with asymptomatic hypocalcemia (P<.05). Vocal cord paresis and a hematoma requiring
operative evacuation occurred in 1 patient each. There was 1 mortality in
a patient with amiodarone-induced thyrotoxicosis.
Conclusions Massive thyroid enlargement with compressive symptoms, a dominant nodule,
and patient preference are indications for surgical treatment of thyrotoxicosis.
Near-total or total thyroidectomy is safe and more effective than subtotal
thyroidectomy in preventing recurrence and should be considered in most patients
referred for surgical treatment of thyrotoxicosis. Transient postoperative
hypocalcemia is common and is related to the severity of thyrotoxicosis.
INTRODUCTION
THYROTOXICOSIS is a syndrome characterized by signs and symptoms of
hypermetabolism and increased sympathetic nervous system activity that results
from excessive thyroid hormone. The most common cause of thyrotoxicosis is
Graves' disease, accounting for 60% to 90% of all cases of thyrotoxicosis.1 Toxic multinodular goiter and a solitary toxic nodule
are less common causes of thyrotoxicosis. The treatment alternatives for thyrotoxicosis
include antithyroid drugs, thyroid ablation with iodine 131 (131I),
and thyroidectomy. In the United States, 131I is the predominant
modality used for treatment of thyrotoxicosis.2, 3
Many clinicians have questioned the necessity of surgical therapy for thyrotoxicosis.
At one large tertiary care institution, only 3 patients with Graves' disease
were treated with thyroidectomy during a 25-year period.4
Factors that need to be considered when deciding on an appropriate treatment
plan for patients with thyrotoxicosis include patient age; associated ophthalmopathy;
the size of the thyroid gland; the presence of compressive symptoms, substernal
thyroid extension, or a concomitant dominant nodule; contraindications to
the use of radioiodine; intolerance to antithyroid drugs; response to previous
therapy; and patient preferences. The purpose of this study was to determine
how often thyroidectomy is performed for treatment of thyrotoxicosis, delineate
the reasons why patients with thyrotoxicosis are referred for thyroidectomy,
and assess the efficacy and outcome of surgical therapy for thyrotoxicosis.
PATIENTS AND METHODS
A retrospective review of all patients undergoing thyroidectomy between
1990 and 1998 was completed, and those who underwent thyroidectomy for thyrotoxicosis
were identified. Their medical records were reviewed for demographic data,
the cause of thyrotoxicosis, clinical manifestations, results of baseline
thyroid function tests, alkaline phosphatase levels, and the presence of a
dominant nodule or substernal extension. In patients with Graves' disease,
the presence of ophthalmopathy was noted. Whether patients underwent preoperative
pharmacological preparation was determined, and the agents used were characterized.
The indications for operation, extent of thyroidectomy, management of the
parathyroid glands, weight of the resected thyroid gland, postoperative calcium
levels, final pathologic findings, and morbidity and mortality were also identified.
Operative reports were reviewed to determine success at identifying the recurrent
laryngeal nerves and the frequency of parathyroid gland autotransplantation.
A comparative analysis of free thyroxine (FT4) and alkaline
phosphatase levels was completed for patients with symptomatic vs asymptomatic
postoperative hypocalcemia. The severity of thyrotoxicosis in patients with
Graves' disease was compared with that in patients with other causes of thyrotoxicosis.
The reference ranges for the laboratory indices analyzed were: FT4,
9.40 to 25.87 pmol/L (0.73 to 2.01 ng/dL); thyrotropin, 0.46 to 3.59 mIU/L;
calcium, 2.1 to 2.5 mmol/L (8.4 to 10.0 mg/dL); and alkaline phosphatase,
25 to 136 U/L. The statistical significance of differences was determined
using a t test. P<.05
was considered significant.
RESULTS
Of the 347 patients undergoing thyroidectomy, 54 (16%) were referred
for treatment of thyrotoxicosis. Of these, 43 (80%) were women. Ages ranged
from 23 to 85 years (mean age, 42 years). The cause of thyrotoxicosis was
Graves' disease in 32 patients (59%), toxic multinodular goiter in 18 (33%),
relapsing thyroiditis in 2 (4%), and amiodarone-induced thyrotoxicosis in
2 (4%) patients. The mean ± SD FT4 level in patients with
Graves' disease was 54.18 ± 19.43 pmol/L vs 33.08 ± 17.63 pmol/L
(4.21 ± 1.51 ng/dL vs 2.57 ± 1.37 ng/dL) in patients with thyrotoxicosis
from other causes (P<.05).
Preoperative pharmacological preparation varied according to the cause
and severity of thyrotoxicosis. All patients with Graves' disease received
10 days of iodine treatment before surgery to reduce the vascularity of the
thyroid gland. Twenty-eight of 32 patients with Graves' disease received an
antithyroid drug, 17 of whom also received a ß-receptor antagonist. Two
patients with intolerance to antithyroid drugs received a ß-receptor
antagonist, and 2 patients with subclinical thyrotoxicosis received preoperative
iodine alone. Twelve of 18 patients with toxic multinodular goiter received
an antithyroid drug preoperatively, 4 of whom also received a ß-receptor
antagonist. No pharmacological preparation was necessary in 6 patients with
toxic multinodular goiter, all of whom had subclinical thyrotoxicosis. The
2 patients with relapsing thyroiditis were treated with a ß-receptor
antagonist alone. The 2 patients with amiodarone-induced thyrotoxicosis were
treated with an antithyroid drug, 1 of whom also received prednisone.
The indications for operation in the 32 patients with Graves' disease
were massive thyroid enlargement with compressive symptoms (17 patients),
a dominant nodule (3 patients), and patient preference (12 patients), including
2 who had failed radioiodine treatment and 6 patients with concerns about
radioiodine-induced aggravation of their ophthalmopathy. The extent of thyroidectomy
in patients with Graves' disease included 17 total, 7 near-total, and 8 subtotal
thyroidectomies. The average weight of the resected thyroid gland was 72 g
(range, 20-210 g). In our early experience, we performed subtotal thyroidectomy,
leaving bilateral 3-g remnants of thyroid tissue in 8 patients, 1 of whom
after a mean 28-month follow-up was euthyroid; 2, hyperthyroid; and 5, hypothyroid.
Pathologic evaluation of the dominant nodule in 3 patients with Graves' disease
revealed a 2-cm papillary carcinoma in 1 and a follicular adenoma in 2. One
patient without a dominant nodule had an incidental occult microscopic papillary
carcinoma.
Eighteen patients underwent thyroidectomy for toxic multinodular goiter,
with substernal extension in 11 and compressive symptoms in 13. A total thyroidectomy
was performed in 12 patients, near-total thyroidectomy in 5, and a unilateral
resection of a large substernal goiter in a single elderly patient with subclinical
thyrotoxicosis, minimal disease in the contralateral thyroid lobe, and a markedly
attenuated recurrent laryngeal nerve on the side of the substernal goiter.
The average weight of the resected gland in patients with toxic multinodular
goiter was 184 g (range, 34-1025 g). One patient had an incidental 2.5-cm
medullary carcinoma diagnosed on final pathologic examination.
Two patients with relapsing thyroiditis experienced alternating episodes
of symptomatic hyper- and hypothyroidism for 5 and 10 years' duration. Their
FT4 levels were 30.37 pmol/L (2.36 ng/dL) and 55.34 pmol/L (4.3
ng/dL), and both had a low radioiodine uptake. Near-total and total thyroidectomies
were performed, with excision of a 10-g and 24-g thyroid gland. The final
pathologic finding was chronic lymphocytic thyroiditis in both patients, 1
of whom also had an incidental 0.4-cm papillary carcinoma.
Two patients underwent total thyroidectomy for amiodarone-induced thyrotoxicosis
that was resistant to antithyroid medications. One patient, previously described,5 was a 72-year-old man with significant cardiopulmonary
disease and refractory ventricular arrhythmias, who had a 30.7-g thyroid resected.
The second patient was an 85-year-old paraplegic man with significant cardiopulmonary
disease, refractory supraventricular arrhythmias, and a massive multinodular
goiter, causing shortness of breath, dysphagia, and swelling of his face and
neck. He had a computed tomographic scan that showed a large substernal goiter
displacing the trachea and esophagus (Figure
1). At operation, the patient was noted to have a massive substernal
goiter (Figure 2). The weight of
the resected thyroid gland was 292 g. On the fifth postoperative day, the
patient developed acute respiratory distress, secondary to an aspiration pneumonia.
Because of his comorbid diseases and in accordance with his living will, the
family allowed him to die, with comfort measures only. This was the only mortality
in our series.
|
|
|
|
Figure 1. Computed tomographic scan of a
patient with amiodarone-induced thyrotoxicosis and multinodular goiter showing
(A) a large substernal goiter displacing the trachea and esophagus and (B)
extension of the thyroid to the level of the arch of the aorta.
|
|
|
|
|
|
|
Figure 2. Intraoperative photograph of a
large substernal thyroid gland in a patient with amiodarone-induced thyrotoxicosis
and multinodular goiter (the patient's head is to the right).
|
|
|
Intraoperatively, the recurrent laryngeal nerves were identified in
all patients. There was no incidence of nerve transection. Two or more parathyroid
glands were preserved in situ in all patients. Thirteen patients (24%) had
1 or 2 parathyroid glands autotransplanted into the sternocleidomastoid muscle.
Postoperative complications included vocal cord paresis in 1 patient
that resolved 1 month after a near-total thyroidectomy for Graves' disease.
One patient developed a hematoma that required operative evacuation following
subtotal thyroidectomy for Graves' disease. Two patients, both with Graves'
disease treated by subtotal thyroidectomy, developed recurrent thyrotoxicosis.
Postoperative hypocalcemia occurred in 35 patients (65%), 10 (29%) of whom
were symptomatic. The mean pretreatment FT4 level in patients with
symptomatic hypocalcemia was 60.49 ± 16.09 pmol/L vs 40.41 ±
19.56 pmol/L (4.70 ± 1.25 ng/dL vs 3.14 ± 1.52 ng/dL) in patients
with asymptomatic hypocalcemia (P<.05). The mean
pretreatment alkaline phosphatase level in patients with symptomatic hypocalcemia
was 147 ± 55 U/L vs 145 ± 80 U/L in patients with asymptomatic
hypocalcemia (P>.05). No patient developed permanent
recurrent laryngeal nerve injury, permanent hypoparathyroidism, or thyroid
storm. The average follow-up for the entire group was 22 months.
COMMENT
Graves' disease, an autoimmune disorder of uncertain origin, accounted
for 59% (32 patients), and toxic multinodular goiter, a disease characterized
by multiple autonomously functioning thyroid nodules, accounted for 18 (33%)
of the patients with surgically-treated thyrotoxicosis in our series. Patients
with toxic multinodular goiter were noted to have larger thyroid glands and
more frequent substernal extension and compressive symptoms. Although patients
with toxic multinodular goiter were more likely to have local symptoms related
to marked thyroid enlargement, patients with Graves' disease had more severe
thyrotoxicosis, as evidenced by significantly higher pretreatment FT4 levels. Thyrotoxicosis from thyroiditis or amiodarone-induced thyrotoxicosis
was uncommon. No patient with a solitary toxic nodule was referred for surgery
in our series.
Patients with thyrotoxicosis constituted 16% (54/347) of all patients
referred for thyroidectomy at our institution during the 9-year study. The
most common reason for recommending surgical therapy was marked thyroid enlargement,
with associated substernal extension or compressive symptoms or both. In patients
with massive thyroid enlargement, multiple radioiodine treatments are often
required to treat thyrotoxicosis, with little effect on the size of the thyroid
gland. This was true for 2 of our patients with Graves' disease, who opted
for surgical treatment after 1 and 2 treatments with 131I failed
to ameliorate their thyrotoxicosis.
An associated dominant nodule with abnormal findings on fine-needle
aspiration biopsy was the principal indication for surgery in 3 (9%) of our
patients with Graves' disease, 1 diagnosed as having a papillary carcinoma
and 2 as having a follicular adenoma. This underscores the importance of obtaining
an 123I thyroid scintiscan in patients with a dominant thyroid
nodule and a fine-needle aspiration biopsy that is consistent with a follicular
neoplasm when a serum thyrotropin level is low.6
This is necessary to differentiate a hypofunctioning nodule in a patient with
Graves' disease, where the risk of malignancy varies from 10% to 50%, from
a hyperfunctioning nodule, where the incidence of malignancy is less than
1%.6, 7
Patient preference was the primary reason for operation in 12 (38%)
of the 32 patients with Graves' disease. Two patients had failed either 1
or 2 radioiodine treatments, and 6 patients were concerned about the potential
for radioiodine-induced aggravation of their ophthalmopathy. Tallstedt and
colleagues8 have previously reported the potential
for worsening of Graves' eye disease in patients treated with 131I.
Total thyroidectomy has been recommended for patients with severe or progressive
ophthalmopathy and high levels of thyrotropin receptor antibodies.9 Total removal of the abnormal thyroid antigens is
advocated to decrease thyrotropin receptor antibodies and other antibodies
that are directed against the extraocular muscles and optic nerve.9 One of the major advantages of surgical treatment
that appeals to many patients is the rapid reversal of symptomatic thyrotoxicosis,
whereas a 6- to 12-week delay in symptom resolution is not unusual for patients
receiving radioiodine therapy. These reasons underscore the clinician's responsibility
to discuss all therapeutic alternatives for thyrotoxicosis with the patient.
Another generally accepted indication for surgical management of Graves'
disease is for pregnant women who are intolerant to antithyroid drugs. This
is an uncommon scenario. Optimally, the surgery should be performed during
the second trimester, with the use of an intravenous ß-receptor antagonist,
if necessary. No pregnant patients with thyrotoxicosis and intolerance to
antithyroid drugs were referred for surgical therapy in our series.
The overall incidence of carcinoma in our surgically-treated patients
with thyrotoxicosis was 7% (4 patients). This included an incidentally discovered
2-cm medullary carcinoma in 1 (6%) of our 18 patients with toxic multinodular
goiter; a papillary carcinoma in 2 (6%) of 32 patients with Graves' disease,
1 of whom had an occult microscopic lesion; and a 0.4-cm occult papillary
carcinoma in 1 of our 2 patients with lymphocytic thyroiditis. Pellegriti
and colleagues10 have previously reported a
4.7% incidence of clinically relevant and 3.3% incidence of occult differentiated
thyroid carcinoma in a series of 450 patients with Graves' disease.
Bilateral subtotal thyroidectomy has been advocated for patients with
Graves' disease to establish a euthyroid state and to reduce the risk of recurrent
laryngeal nerve injury and hypoparathyroidism. How much thyroid tissue to
leave to achieve a euthyroid state remains controversial. Bradley and Liechly11 described their technique of leaving two 5-g remnants,
each attached to an intact inferior thyroid artery, and reported that a euthyroid
state was achieved in 92% of 107 patients followed up for more than 2 years.
Others have not been able to demonstrate a clear-cut relationship between
the size of the remnant and achievement of a euthyroid state.12
Even if such a determination could be made, standardizing the remnant size
is inherently difficult.
The reported incidence of recurrent hyperthyroidism in patients undergoing
subtotal thyroidectomy varies between 1.2% and 16.2% (Table 1).2, 11, 13, 14, 15, 16, 17, 18, 19
This can be explained in part by the differences in remnant size and may also
be related to differences in length of follow-up. It is our belief that recurrent
Graves' disease is an unacceptable outcome as it may subject patients to 131I therapy, which they may have chosen not to receive initially or
to reoperative surgery, which has an increased risk of injury to the recurrent
laryngeal nerves and the parathyroid glands. Early in our experience, subtotal
thyroidectomy with 3-g remnants was routinely performed for Graves' disease.
However, only 1 patient remained euthyroid, 2 developed recurrent hyperthyroidism,
and 5 developed hypothyroidism after a mean 28-month follow-up.
|
|
|
|
Rates of Recurrent Hyperthyroidism in Patients Undergoing Subtotal
Thyroidectomy*
|
|
|
Near-total or total thyroidectomy is our operation of choice for most
patients with thyrotoxicosis. Patients with a solitary toxic nodule are the
exception, and they are treated with thyroid lobectomy. Near-total or total
thyroidectomy eliminates the possibility of recurrent thyrotoxicosis, which
is always a concern when any sizable remnant of thyroid tissue is left behind.
It also simplifies the long-term assessment of patients' thyroid function
postoperatively. Since more than 30% of patients with thyrotoxicosis treated
by bilateral subtotal thyroidectomy become hypothyroid within 20 years of
surgery, close follow-up is required to prevent delay in recognition and treatment
of hypothyroidism.2, 13 Following
near-total or total thyroidectomy, all patients are immediately started on
a replacement dose of thyroid hormone.
Our results demonstrate that near-total and total thyroidectomy in patients
with thyrotoxicosis can be performed with a low morbidity. We attribute this
to several factors. The first is the use of preoperative pharmacological preparation
that has effectively eliminated thyroid storm. Iodine administration in patients
with Graves' disease has been helpful in reducing intraoperative bleeding,
which can affect the identification and preservation of the recurrent laryngeal
nerves and the parathyroid glands. Operative visualization of the recurrent
laryngeal nerves throughout their entire course has been important in eliminating
permanent vocal cord paralysis. Meticulous technique in maintaining parathyroid
gland blood supply and autotransplantation of parathyroid glands that cannot
be preserved in situ have been important in reducing the incidence of permanent
hypoparathyroidism. Other authors20, 21, 22
have documented that total thyroidectomy can be performed safely in patients
with Graves' disease or multinodular goiter.
Patients with chronic, remitting thyrotoxicosis secondary to thyroiditis
or amiodarone-induced thyrotoxicosis also benefit from near-total or total
thyroidectomy. Amiodarone-induced thyrotoxicosis is a rare disorder, reported
in fewer than 3% of patients taking this antiarrhythmic agent.23
Amiodarone is taken up by the thyroid gland, and its high iodine content produces
an increase in iodine stores available for hormone synthesis. It has also
been shown to damage thyroid cell membranes, resulting in increased release
of large stores of thyroid hormone.5 Amiodarone-induced
thyrotoxicosis has also been reported to occur in patients with preexisting
thyroid disease, most commonly multinodular goiter.5, 24
It is often resistant to amiodarone withdrawal and conventional pharmacological
therapy. Mulligan et al5 demonstrated that
near-total thyroidectomy is safe and effective in producing rapid resolution
of symptoms in patients with amiodarone-induced thyrotoxicosis. The only mortality
in our series occurred in a patient with amiodarone-induced thyrotoxicosis,
emphasizing that these patients may be at higher risk for surgery related
to their underlying comorbid diseases.
Transient postoperative hypocalcemia is common following thyroidectomy
for thyrotoxicosis, occurring in 35 (65%) of our patients. The causative mechanism
is not completely understood. Postoperative hypocalcemia has been attributed
to parathyroid insufficiency due to injury, devascularization, or inadvertent
excision of parathyroid glands.25 In patients
with thyrotoxicosis, other causes of temporary hypocalcemia include calcium
uptake by bone in patients with thyrotoxic osteodystrophy or parathyroid suppression
from increased calcium resorbed from the bone of patients with hyperthyroidism.26, 27 Transient postoperative hypocalcemia
was symptomatic in only 10 (19%) of our patients, with a mean pretreatment
FT4 level that was significantly higher than that in patients with
asymptomatic hypocalcemia (P<.05). This supports
earlier findings from our institution that the development of symptomatic
postoperative hypocalcemia is related to the severity of thyrotoxicosis.28 In most patients, symptomatic postoperative hypocalcemia
resolved within 2 weeks of surgery.
In conclusion, our results demonstrate that surgical therapy has an
important role in patients with thyrotoxicosis, accounting for 54 (16%) of
the 347 thyroidectomies performed at our institution during a 9-year period.
Our series emphasizes that massive thyroid enlargement with compressive symptoms,
a dominant nodule with abnormal fine-needle aspiration biopsy findings, failed
radioiodine therapy, or patient preference, especially when there are concerns
about radioiodine-induced aggravation of ophthalmopathy, are established indications
for surgical treatment of thyrotoxicosis. Near-total or total thyroidectomy,
when it can be performed safely, should be considered for definitive management
of Graves' disease, toxic multinodular goiter, chronically remitting thyrotoxicosis
secondary to thyroiditis, and amiodarone-induced thyrotoxicosis. Transient
symptomatic postoperative hypocalcemia is common in patients with surgically-treated
thyrotoxicosis and is related to the severity of thyrotoxicosis.
AUTHOR INFORMATION
Accepted for publication June 28, 2000.
From the Department of Surgery, MetroHealth Medical Center, Case Western
Reserve University School of Medicine, Cleveland, Ohio.
Corresponding author and reprints: Christopher R. McHenry, MD, Department
of Surgery, MetroHealth Medical Center, Case Western Reserve University School
of Medicine, 2500 MetroHealth Dr, Cleveland, OH 44109-1998.
REFERENCES
 |  |
1. Braverman LE, Utiger RD. Introduction to thyrotoxicosis. In: Braverman LE, Utiger RD, eds. Werner and Ingbar's
The Thyroid. 7th ed. Philadelphia, Pa: Lippincott-Raven; 1996:522-524.
2. Franklyn JA, Daykin J, Drolc Z, Farmer M, Sheppard MC. Long-term follow-up of treatment of thyrotoxicosis by three different
methods. Clin Endocrinol (Oxf). 1991;34:71-76.
PUBMED
3. Wartofsky L, Glinoer D, Solomon B, Lagasse R. Differences and similarities in treatment of diffuse goiter in Europe
and the United States. Exp Clin Endocrinol. 1991;97:243-251.
ISI
| PUBMED
4. Esselstyn CB Jr. Discussion: surgery still has a role in Graves' hyperthyroidism. Surgery. 1993;114:1112.
5. Mulligan DC, McHenry CR, Kinney W, Esselstyn CB. Amiodarone-induced thyrotoxicosis: clinical presentation and expanded
indications for thyroidectomy. Surgery. 1993;114:1114-1119.
ISI
| PUBMED
6. McHenry CR, Slusarczyk SJ, Askari AT, et al. Refined use of scintigraphy in the evaluation of nodular thyroid disease. Surgery. 1998;124:656-662.
FULL TEXT
|
ISI
| PUBMED
7. Belfiore A, Garofalo MR, Giuffrida D, et al. Increased aggressiveness of thyroid cancer in patients with Graves'
disease. J Clin Endocrinol Metab. 1990;70:830-835.
FREE FULL TEXT
8. Tallstedt L, Lundell G, Torring O. Occurrence of ophthalmopathy after treatment for Graves' hyperthyroidism: the Thyroid Study Group. N Engl J Med. 1992;326:1733-1738.
ABSTRACT
9. Rastad J, Karlsson FA. Surgical management of Graves' disease: preoperative preparation and
extent of surgery. Problems Gen Surg. 1997;14:132-154.
10. Pellegriti G, Belfiore A, Giuffrida D, Lupo L, Vigneri R. Outcome of differentiated thyroid cancer in Graves' patients. J Clin Endocrinol Metab. 1998;83:2805-2809.
FREE FULL TEXT
11. Bradley III EL, Liechly RD. Modified subtotal thyroidectomy for Graves' disease: a two-institution
study. Surgery. 1983;94:955-958.
ISI
| PUBMED
12. Jortso E, Lennquist S, Lindstrom B, Norby K, Smeds S. The influence of remnant size, antithyroid antibodies, thyroid morphology,
and lymphocytic infiltration on thyroid function after subtotal resection
for hyperthyroidism. World J Surg. 1987;11:365-371.
FULL TEXT
|
ISI
| PUBMED
13. Davenport M, Talbot CH. Thyroidectomy for Graves' disease: is hypothyroidism inevitable? Ann R Coll Surg Engl. 1989;71:87-91.
ISI
14. Kasuga Y, Sugenoya A, Kobayashi S, et al. Clinical evaluation of the response to surgical treatment of Graves'
disease. Surg Gynecol Obstet. 1990;170:327-330.
ISI
| PUBMED
15. Okamoto T, Fujimoto Y, Obara T, Ito V, Aiba M. Retrospective analysis of prognostic factors affecting the thyroid
function status after subtotal thyroidectomy for Graves' disease. World J Surg. 1992;16:690-696.
FULL TEXT
|
ISI
| PUBMED
16. Patwardhan NA, Moront M, Rao S, Rossi S, Braverman LE. Surgery still has a role in Graves' hyperthyroidism. Surgery. 1993;114:1108-1113.
ISI
| PUBMED
17. Sugino K, Mimura T, Ozaki O, et al. Early recurrence of hyperthyroidism in patients with Graves' disease
treated by subtotal thyroidectomy. World J Surg. 1995;19:648-652.
FULL TEXT
|
ISI
| PUBMED
18. Miccoli P, Vitti P, Rago T, et al. Surgical treatment of Graves' disease: subtotal or total thyroidectomy? Surgery. 1996;120:1020-1025.
FULL TEXT
|
ISI
| PUBMED
19. Torring O, Tallstedt L, Wallin G, et al. Graves' hyperthyroidism: treatment with antithyroid drugs, surgery,
or radioiodine: a prospective, randomized study. J Clin Endocrinol Metab. 1996;81:2986-2993.
FREE FULL TEXT
20. Liu Q, Djuricin G, Prinz RA. Total thyroidectomy for benign disease. Surgery. 1998;123:2-7.
ISI
| PUBMED
21. Perzik SL. The place of total thyroidectomy in the management of 909 patients
with thyroid disease. Am J Surg. 1976;132:480-483.
FULL TEXT
|
ISI
| PUBMED
22. Reeve TS, Delbridge L, Cohen A, Crummer P. Total thyroidectomy: the preferred option for multinodular goiter. Ann Surg. 1987;206:782-786.
ISI
| PUBMED
23. Nademanee K, Piwonka RW, Singh BN, Hershman JM. Amiodarone and thyroid function. Prog Cardiovasc Dis. 1989;31:427-437.
FULL TEXT
|
ISI
| PUBMED
24. Martino E, Aghini-Lombardi R, Mariotti S, et al. Amiodarone: a common source of iodine-induced thyrotoxicosis. Horm Res. 1987;26:158-171.
FULL TEXT
|
ISI
| PUBMED
25. Hans SS, Lee OT. Post-thyroidectomy hypoparathyroidism. Am Surg. 1976;42:930-933.
ISI
| PUBMED
26. Michie W, Duncan T, Hamer-Hodges DW, et al. Mechanisms of hypocalcemia after thyroidectomy for thyrotoxicosis. Lancet. 1971;1:508-514.
ISI
| PUBMED
27. MoseKilde L, Christensen MS. Decreased parathyroid function in hyperthyroidism: interrelationships
between serum parathyroid hormone, calcium, phosphorus metabolism and thyroid
function. Acta Endocrinol. 1977;84:566-575.
28. McHenry CR, Speroff T, Wentworth D, Murphy T. Risk factors for postthyroidectomy hypocalcemia. Surgery. 1994;116:641-648.
ISI
| PUBMED
CiteULike Connotea Del.icio.us Digg Reddit Technorati Twitter
What's this?
RELATED ARTICLE
Archives of OtolaryngologyHead & Neck Surgery Reader's Choice: Continuing Medical Education
Arch Otolaryngol Head Neck Surg. 2001;127(1):94.
FULL TEXT
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
The Optimal Treatment for Pediatric Graves' Disease Is Surgery
Lee et al.
J. Clin. Endocrinol. Metab. 2007;92:801-803.
FULL TEXT
|