LETTER TO THE EDITORS

Thyrotoxicosis after parathyroidectomy mimicking myocardialinfarction: a case report and review of the literature

A. Kauffels • I. O. Lee • M. K. Schilling •

J. E. Slotta

Received: 16 December 2011 / Accepted: 14 March 2012 / Published online: 22 March 2012

� Springer-Verlag 2012

Sirs:

A 55-year-old female patient was presented to our surgical

department for elective parathyroidectomy for sHPT fol-

lowing terminal kidney failure due to a minimal change

glomerulonephritis with Ig-M sedimentation.

An open operation through a Kocher’s cut was per-

formed, and two hypertrophic parathyroid glands were

removed. Intraoperative parathyroid hormone (PTH) test

revealed a significant decrease of serum PTH levels by

*760 pg/ml after parathyroidectomy. The following sta-

tionary course was uneventful and patient was discharged

3 days after surgery.

Three days after discharge, patient was admitted to the

local Emergency Centre suffering from angina pectoris and

dyspnoea. An instantly performed ECG showed tachycar-

dia (120/min) and ST elevations (Fig. 1a) associated with

elevated hs-cTnT concentrations (180.9 pg/ml; normal

range \14.0 pg/ml; Fig. 1b). Assuming a STEMI, an

urgent coronary angiography was performed, but no signs

of arteriosclerotic coronary artery changes could be

detected (Fig. 1c). Tako-Tsubo syndrome was ruled out via

echocardiography revealing normal left ventricular func-

tion. Additional serum analyses finally revealed an extreme

elevation of thyroid hormones fT3 (11.4 pg/ml; normal

range 2.3–4.2 pg/ml) and fT4 (5.15 ng/dl; normal range

0.89–1.76 ng/dl), and a simultaneous reduction of TSH

(0.04 lIU/ml; normal range 0.55–4.78 lIU/ml). Conse-

quently, thyrotoxicosis following parathyroidectomy was

diagnosed and a therapy with ivabradine was started.

Genesis of the cardiac symptoms was thought to be

induced most likely secondarily to the thyrotoxicosis.

Thyroid hormone levels regressed to normal range during

the next few days, ECG changes reversed and the patient

was discharged 7 days after admission.

Herein, we describe a case of thyrotoxicosis as a post-

operative complication after an—from surgical view-

point—uneventful parathyroidectomy. Thyrotoxicosis

manifested with clinical signs of a myocardial infarction

with corresponding changes in ECG. Symptomatic treat-

ment with limitation of heart rate was followed by spon-

taneous normalization of thyroid hormone levels.

Parathyroidectomy is a standard surgical procedure

mainly for pHPT, but also in cases of failure of conser-

vative treatment of secondary or tertiary hyperparathy-

roidism, parathyroidectomy might be a treatment option to

overcome musculoskeletal pain, pathological fractures and

pruritus.

Parathyroidectomy is classically performed via

Kocher’s cut. Nowadays, technical advances have lead to

novel concepts for minimally invasive parathyroid surgery,

such as endoscopic parathyroidectomy, minimally invasive

video-assisted parathyroidectomy (MIVAP) with median

access, or a lateral approach (VAPLA), and open mini-

mally invasive parathyroid surgery using a central or a

lateral approach. Besides these cervical approaches, there

are further surgical approaches to the parathyroid glands

(e.g., transoral, transaxillary). Besides formation of visible

cervical scars, which shall be reduced or be at least

invisible using alternative than cervical approaches, main

complications after parathyroidectomy are lesions of the

recurrent nerves [1], intraoperative hypokalemia, as well as

A. Kauffels � M. K. Schilling � J. E. Slotta (&)

Department of General, Visceral, Vascular, and Pediatric

Surgery, Saarland University Hospital,

66421 Homburg/Saar, Germany

e-mail: jan.e.slotta@uks.eu

I. O. Lee

Department for Internal Medicine III, Saarland University

Hospital, 66421 Homburg/Saar, Germany

123

Clin Res Cardiol (2012) 101:687–690

DOI 10.1007/s00392-012-0446-0

complications caused by CO2 insufflation for video-assis-

ted minimally invasive techniques.

Thyrotoxicosis following parathyroidectomy is a very

rare complication (Table 1), which has been first described

in 1992 in three patients after parathyroidectomy, among

those two patients had a clinically manifest thyrotoxicosis,

appearing within 2 weeks after surgery and declining

during 3 months [2, 3]. Nearly all reports present bio-

chemical data on increased fT3/fT4 levels and depression

of TSH. Further, biochemical signs of postoperative

hyperthyroidism are negative serum levels of anti-thyroid

antibodies, as well as reduced radio-iodine or Tc99m

uptake rates (Table 1). Obviously, underlying disease for

parathyroidectomy has no influence on the appearance of

thyrotoxicosis, since this complication has been observed

after parathyroidectomy for pHPT [4], as well as sHPT [5]

and tHPT [6]. It is speculated that besides surgical trauma

to thyroid gland, also humoral factors might trigger

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tro

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nin

e T

[p

g/m

l]

0

20

40

60

80

100

120

140

160

180

200

par

ath

yro

idec

tom

y

C

A

B

Fig. 1 a 12-lead ECG at the

day of admission, before

coronary angiography, showing

relevant ST-segment elevation

in leads II, III, aVF, as well as

V1–V3. b Time course of serum

troponin T levels. Arrowindicates time point of

parathyroidectomy. c Coronary

angiogram at the day of

admission showing no stenoses

or occlusion of the smooth-

walled coronary arteries.

Angulation of the coronary

arteries consistent with arterial

hypertension

688 Clin Res Cardiol (2012) 101:687–690

123

development of thyrotoxicosis [7]. However, there are no

reliable predictive biochemical markers for the develop-

ment of thyrotoxicosis after parathyroidectomy [4].

Symptoms of postoperative thyrotoxicosis have been

reported to be mild and self-limiting [3, 4, 8] and to be

dependent on an increased release of thyroid hormones and

not on increased production [2]. Thus, in most cases

thyrostatic therapy is unessential and only symptomatic

treatment is required [9]. Risk for the development of

postoperative thyrotoxicosis seems to be dependent on the

extent of parathyroid surgery [6, 10].

However, there are reported cases with even severe

symptoms of thyrotoxicosis including angina pectoris fol-

lowing coronary artery spasm [4] or atrial fibrillation

Table 1 Overview on reports on postparathyroidectomy thyrotoxicosis

Author Year Patient/s Age Underlyingdisease

Onset ofthyrotoxicosis

Duration Biochemicalmarkers

Clinical symptoms

Espiritu RP 2010 2 females 55, 84 pHPT 7 days 1–2 months : fT3/4, ; TSH, :TG, ; RIU

Parker G 2010 1 male 59 pHPT 10 days 2 months : fT4, ; TSH,antibodiesnonreactive, ;RIU (after2 months)

Progressive dyspnoea, acuteorthopnoea, peripheraland pulmonary edema,mildly abnormalechocardiogram, transientatrial fibrillation

RudofskyG

2009 1 female 33 tHPT 3 days 4 weeks : fT3/4, ; TSH, :TG, anti-thyroidantibodiesnegative, ;Tc99m uptake(after 2 months)

Palpitations, warm sweatyhands, fine tremor, brisktendon reflexes

Sato H 2008 1 female 59 sHPT 3 days 12 days : fT3/4, ; TSH,anti-thyroidantibodiesnegative, ;Tc99m uptake(12 days)

Palpitation, chest pain,atrial fibrillation,hypertension

Lederer SR 2008 2 males 27, 49 tHPT 2–3 months : fT3/4, ; TSH

Stang MT 2005 n = 412(199)

57.5 ± 13.5 pHPT ‘‘Immediatepostoperativeperiod’’

\254 days : fT3/4, ; TSH Alterations in energy level,insomnia, tremor,palpitations, diarrhea,weight loss

Lim W 2003 1 female 26 sHPT Day 2 : fT3/4, ; TSH,anti-thyroidantibodiesnegative, ;Tc99m thyroidscan

Fever, sweating,restlessness, agitation,nausea, hypertension,tachycardia, diarrhea,dyspnoea, left ventriculardysfunction

Musi N 2000 1 female 48 sHPT Day 3 20 days : fT3/4, ; TSH,anti-thyroidantibodiesnegative, RIU ;day 8

Tachycardia, hypertension,agitation, stupor

LindblomP

1999 15 males,11 females

Median 65(21–84)

pHPT 1–3 days : fT3/4, ; TSH Palpitation, tremor, fatigue,transpiration, anginapectoris

BergenfelzA

1994 n = 20 pHPT Day 4 : fT4

Walfish PG 1992 n = 3 pHPT 2 weeks 2 months ; RIU

Currentcase

2011 n = 1 55 sHPT 6 days 13 days : fT3/4, ; TSH Dyspnoea, angina pectoris,tachycardia, ECG: signsof myocardial infarction

pHPT primary hyperparathyroidism, sHPT secondary hyperparathyroidism, tHPT tertiary hyperparathyroidism, fT3 free triiodothyronine, fT4 freethyroxine, TSH thyrotropin, TG thyroglobulin, RIU radioiodine uptake

Clin Res Cardiol (2012) 101:687–690 689

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requiring cardioversion for reversion to normal sinus

rhythm [8]. In our case, conservative therapy with ivabra-

dine for heart rate limitation was performed. Beta blockers

were avoided due to a known allergy of the patient. Taking

into account that neither coronary artery stenosis nor other

morphologic cardiac pathology were found, ECG changes

at admission are best explained by thyrotoxicosis-induced

coronary vasospasm with subsequent reduced myocardial

perfusion, ST-segment elevations and hs-cTnT-release.

These thyrotoxicosis-induced changes have been reported

in the literature, whereas underlying pathomechanisms

proposed by the authors vary from direct myocardial tissue

damage to coronary vasospasm induced by elevated thy-

roid hormone levels. Elevation of hs-cTnT might even be

due to reduced myocardial perfusion during tachycardia.

Regardless of the thyrotoxic state of our patient, another

possible explanation could be a thrombolytic myocardial

infarction, but taking into account that the patient had no

risk factors for embolic disease and no atherosclerotic

changes, this mechanism is rather unlike in our case. In

conclusion, after echocardiographic exclusion of a Tako-

Tsubo syndrome, we assume that a temporary coronary

vasospasm (Prinzmetal’s angina) lead to clinical symp-

toms, ECG changes and increased hs-cTnT levels. As our

patient was highly suspicious for having had a STEMI,

indication for coronary angiography was given. With

regard to thyrotoxicosis and terminal kidney failure, addi-

tional laevoangiography was renounced to reduce contrast

dosage to a minimum. However, sodium perchlorate is a

suitable agent to prevent further damage to the thyroid

gland arising from the application of iodine contrast.

Concluding, this is the second report on transient thy-

rotoxicosis after parathyroidectomy for sHPT. We present

the case of a Caucasian female patient presenting with

clinical, biochemical and ECG changes of an acute STEMI.

Thyrotoxicosis as a postoperative complication following

parathyroidectomy is underestimated both in frequency of

occurrence and its severity. Since onset of thyrotoxicosis

usually occurs at a time when patients are already dis-

charged, a corresponding education of patients is advisable

prior to discharge. Whether routine monitoring of serum

thyroid hormones is reasonable cannot be answered based

on the data actually available in the literature.

Conflict of interest All authors declare that they have no conflicts

of interest.

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