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t.me/Dr_Mouayyad_AlbtousH
Surgery ofParathyroid Glands
TomR.Kurzawinski
15
15.1 Introduction
Parathyroid glands were the last major organ to
be discovered (1850), perhaps a testimony to
their small size, varied location, and puzzling
physiology. Their role in calcium metabolism
and parathyroid hormone (PTH) excess and deciency was dened in the rst half of XX century.
Recent recognition of PTH structure, cloning of
receptors, and discovery of genes responsible for
familial syndromes, complemented our current
understanding of their role in health and disease.
Hyperparathyroidism (HPT) was initially
thought to be rare and always presenting with
advanced renal and skeletal pathology. Nowadays,
it is considered a common endocrine disorder,
four times more common in women than men,
with rising incidence of 25–30 new cases per
100,000 per year and prevalence of 1–7in 1000.
It is the third commonest endocrine condition
after thyroid disease and diabetes (prevalence
1in 13 and 1in 17, respectively) and frequently
diagnosed in asymptomatic patients.
Series of successful parathyroidectomies performed from 1925 onward, established surgery as
foremost treatment of HPT, the position it still
holds today. Number of patients with HPT
referred for surgery is increasing at the time when
T. R. Kurzawinski (*)
GI Surgery, University College Hospitals NHS Trust,
London, UK
e-mail: tom.kurzawinski@nhs.net
global healthcare funding is under severe pressure. Parathyroid surgeons must adopt pragmatic
approach when choosing diagnostic tests (not to
over investigate), selecting right operations (simpler, better), aiming for excellent outcomes (to
meet high expectations of our patients), and to
achieve all of these in most cost-effective way
(government priority).
15.2 Anatomy
Normal parathyroid glands are bean-shaped
structures measuring 2×4×6mm, orange brown
in color with an average weight of 30mg each.
Majority of patients (90%) have 4 parathyroids,
but it is possible to have more (5%) or less (5%)
than 4 glands. Parathyroid glands develop in tandem with thyroid from pharyngeal pouches, 2
inferior glands arising from third and 2 superior
from fourth pharyngeal pouches. Embryologic
development explains their varied locations in
the neck and mediastinum. Superior glands are
most frequently found within 1cm of RLN crossing inferior thyroid artery. Inferior glands are
more variable but most are found at inferior pole
of thyroid. Ectopic glands could be found behind
the esophagus, in the mediastinum, thyro-thymic
ligament, and carotid sheath. Parathyroids are
frequently enmeshed within brous thyroid capsule, but location deep within thyroid is rare
(0.1%). Inferior thyroid artery supplies majority
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
M. Sakr (ed.), Head and Neck and Endocrine Surgery,
https://doi.org/10.1007/978-3-031-64102-2_15
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442
T. R. Kurzawinski
of them (80%). Parathyroids are composed
mainly of chief cells secreting PTH and oxyphil
cells supporting them metabolically [1].
15.3 Physiology
Parathyroid glands regulate calcium homeostasis
by modulating bone metabolism and absorption
of calcium in kidney and intestine. Changes in
calcium concentration are sensed by calcium
sensing receptor (CaSR) on chief cells and lead
to rapid alterations in parathyroid hormone synthesis and secretion. Human PTH is a linear polypeptide synthesized by chief cells as a part of
large molecule and trimmed intracellularly to
active hormone containing 84 amino acids. In
response to hypocalcaemia, PTH is released from
secretory granules and acts directly on bone
(osteoclasts) and kidney (distal nephron) increasing calcium reabsorption. It also regulates formation of D3 (proximal tubules) and by this action
increase calcium absorption from intestine.
Circulating PTH is metabolized in liver and kidneys, and its biological ½ life is 5min [2].
15.4 Pathology
Hyperparathyroidism is an abnormal state of calcium homeostasis where one or many parathyroid glands secrete inappropriately large amount
of PTH.Classication of HPT into primary, sec-
ondary, and tertiary reects different mechanisms
by which excess of parathyroid hormone develops. Primary HPT (PHPT) is commonest of the
three and indicates that abnormal changes
occurred rst within parathyroid gland itself.
Pathological changes causing enlargement and
increased inappropriate secretion of PTH include
formation of adenoma (single 80%, double 4%),
hyperplasia (15%), and rarely cancer (1%).
Distinction between hyperplasia and adenoma is
difcult and is based on nding a rim on normal
parathyroid tissue at the periphery of the adenoma. Secondary HPT is caused by prolonged
hypocalcaemia due to chronic renal disease, low
vitamin D (rickets), or malabsorption. Low calcium stimulates parathyroid glands leading to
compensatory hypertrophy and increased output
of PTH.Despite high PTH levels calcium remains
low and in early stages secondary HPT can be
reversed (e.g. renal transplant).
Long lasting secondary HPT can lead to
development of parathyroid nodules autonomously secreting PTH resulting in rising calcium level, a condition known as tertiary HPT.
Hyperparathyroidism could be sporadic or
familial. Familial HPT accounts for 1–2% of
cases of HPT in adults but 24–46% in children.
Familial HPT is caused by inherited or de novo
mutations of genes responsible for multiple
endocrine neoplasia type 1 and 2a (MEN1 and
MEN2a), hyperparathyroidism jaw tumour syndrome (HPT-JT), and familial isolated HPT
(FIHPT) (Table15.1).
t.me/Dr_Mouayyad_AlbtousH
15 Surgery ofParathyroid Glands
Table 15.1 Familial causes of primary hyperparathyroidism (PHPT)
Inheritance and
Condition
MEN 1 Autosomal
MEN 2A Autosomal
JTHPT Autosomal
FIHPT Different
FHH/
NSHPT
mutation Organs affected
Parathyroid (90%), neuroendocrine tumors (NET) of the pancreas and
dominant
MEN1 gene on
chromosome 11
dominant
MEN2A gene on
chromosome 10
dominant
HRPT2 gene on
chromosome 1
mutations: MEN1,
CaSR, HRPT2
Autosomal
dominant
CaSR gene
gastrointestinal tract (60%), pituitary adenomas (30%), NET of thymus and
bronchus, adrenal hyperplasia and adenomas, lipomas, leiomyomas, and skin
disorders such as angiobiromas and collagenomas
Parathyroid (20–30%), medullary thyroid carcinoma and adrenal
phaeochromocytomas
Mainly HPT and bro-osseous lesions of mandible and maxilla. Risk of
parathyroid carcinoma in 10–15%. Associated with renal lesions–renal cell
carcinoma, Wilm’s tumor, hamartomas, and cysts
Parathyroid gland
with high calcium. Nowadays, diagnosis of
15.5 Clinical Presentation
PHPT is made earlier. Approximately, 80–85%
of patients are diagnosed with biochemical
A range of clinical symptoms caused by prolonged oversecretion of PTH and hypercalcemia
abnormalities before they develop any
symptoms.
vary from inconspicuous (fatigue) to painful
(renal colic) and dangerous (hypercalcemic crisis). Hypercalcuria can lead to kidney stones,
15.6 Investigations
nephrocalcinosis, renal impairment, and nephrogenic diabetes insipidus. Prolonged reabsorption
of calcium from the bones causes osteopenia,
osteoporosis, and in severe cases bone deformity
known as osteitis brosa cystica. Weakened
bones can cause bone pain and increase risks of
fractures of long bones and collapse of vertebrae.
Persistently elevated calcium levels can cause
abdominal pain, frequently nonspecic but sometimes associated with peptic ulcer or pancreatitis.
Other presentations include neuropsychiatric disorders, muscle weakness and pain, depression,
and fatigue. Very high, untreated calcium levels
can cause hypercalcemic crisis and present as
thirst, nausea, vomiting, and lead to dehydration,
confusion, coma, ventricular arrhythmias, and
death [3–5].
In the past, most patients presented with
severe complications but introduction of automated multichannel analyzers in 1970s dramatically increased number of patients diagnosed
Biochemical tests: The diagnosis of PHPT is
established by measuring serum calcium and
PTH, which shows hypercalcemia and inappropriately high PTH levels. Routine biochemical
assessment of patients with PHPT should include
renal function tests and vitamin D3 levels. In
asymptomatic patients presenting with a mild
hypercalcemia, marginally elevated PTH, and
hypocalcuria, the diagnosis of FHH should be
excluded by measuring the calcium to creatinine
ratio (low in FHH). Genetic testing for mutations
of the CaSR could be used in ambiguous cases.
This is important, as FHH is a benign disease
with no end-organ damage and does not need
treatment. Bone density scan and ultrasound of
the kidneys should be considered.
Genetic mutations causing HPT are rare in
adults but frequent in children. Positive genetic
test is helpful in establishing diagnosis of familial
HPT, planning treatment, and initiating biochemi-
443
t.me/Dr_Mouayyad_AlbtousH
444
cal and genetic screening of other members of
family. In patients with positive family history,
testing for mutations should start with the MENIN
gene [6] followed by parabrinomin (HRPT2)
gene [7–9] if the gland is an atypical adenoma or
carcinoma. RET mutation analysis is recommended for patients with features consistent with
MEN2a [10]. Alternative to sequential genetic
screening described above is to perform an analysis of all genetic mutations associated with hyperparathyroidism at once. Currently available panel
of genetic tests include MEN1 and 2, CaSR,
CDC73, CDKN 1A, 1B, 2B, 2C and is cheaper
than performing these tests separately.
Imaging of abnormal parathyroid glands is
a critical part of the preoperative workup especially in patients with sporadic PHPT.Its role is
to identify the position of enlarged gland in the
neck or mediastinum and differentiate between
single and multiple glands disease. Identication
of a single enlarged gland by using two different
imaging techniques (concordant ndings) enables
surgeon to plan minimally invasive approach.
Imaging is less helpful in familial and renal HPT
when neck exploration and removal of multiple
glands is usually required. In these situations,
embarking on surgery without localization studies is acceptable [11].
Ultrasound (US) scanning of the neck is usually performed using a high-frequency
(12–15 MHz) transducer, which enables the
detection of enlarged parathyroid glands, description of their size and position in relation to thyroid and other anatomical structures (Fig.15.1).
Adenomas typically appear as homogenously
echoic nodules on gray scale and are highly vascular on color Doppler imaging. Limitations of
US include difculty in identifying adenomas,
which are either deep-seated (retro-sternal/mediastinal) or related to air-lled structures such as
the trachea and esophagus. In addition, US is an
operator-dependent investigation, and therefore
outcomes will tend to relate to the level of experience of the centre and individual radiologist.
Nuclear imaging is usually performed with
99m
([
Tc] methoxyisobutylnitrile (MIBI)), which
avidly localizes in mitochondria present in large
numbers in the oxyphil cells of parathyroid tis-
T. R. Kurzawinski
Fig. 15.1 Ultrasound image clearly demonstrating an
enlarged parathyroid gland
sue. Parathyroid adenomas and to lesser degree
hyperplastic glands demonstrate higher tracer
uptake in the early stage and delayed washout in
the late image as compared to the surrounding
thyroid tissue. The use of SPECT, which produces 3D images from two cameras, has been
shown to improve its sensitivity [12] (Fig.15.2).
Nuclear imaging is better than ultrasound at
detecting ectopic adenomas. However, in the
presence of thyroid nodules, differentiation of the
abnormal parathyroid and thyroid tissue can be
difcult. A systematic review of 54 studies identied the sensitivity of ultrasound to be 78% in
detecting solitary adenomas, 35% in hyperplasia,
and 16% in double adenomas. The sensitivity of
MIBI was 88% in detecting solitary adenomas,
44% in detecting hyperplastic glands, and 30% in
detecting double adenomas [13].
Computed tomography (CT), magnetic reso-
nance imaging (MRI), and venous sampling are
rarely required in modern practice and should be
reserved for cases where standard investigations
are negative or in recurrent HPT requiring reoperation. Axial, thin cuts, contrast-enhanced CT
images from the base of the skull through the
mediastinum can help to identify abnormal parathyroids in the neck not seen on other scans and
ectopic glands in the mediastinum. MRI is limited by similar appearances of cervical lymph
nodes and parathyroid adenomas and venous
sampling is an invasive test, which is now almost
completely obsolete [14].
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