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https://doi.org/10.1530/EJE-21-0063
European Journal of Endocrinology
184:5 L17–L19 N Patel and R Mihai Phaeochromocytomas at high
altitudes
Relative hypoxia at high altitudes increases
the incidence of phaeochromocytomas
Neil Patel and Radu Mihai
Department of Endocrine Surgery, Churchill Cancer Centre, Oxford University Hospitals NHS Foundation Trust,
Oxford, Oxfordshire, UK
We read with great interest the recent paper reporting
a high incidence of phaeochromocytomas and
paragangliomas in an unselected population from the
western region of Canada (1). All cases were identifed
based on clinical data available over a 7 years period.
Interestingly, Alberta has a higher altitude (3678 ft,
https ://en -gb.t opogr aphic -map. com/m aps/l rg4/A lbert
a/) compared with other geographical areas from where
a lower incidence was reported in previous papers (Table
1). Similarly, detailed epidemiological data from multiple
geographical area are not easily available. Previous
reports involving the entire USA population cannot be
scrutinised as they lack ‘granular details’ regarding states
with different altitudes. There is, however, a convincing
trend that suggests that high altitude (as in Alberta)
and its associated relative hypoxia modulate the risk of
development of phaeochromocytomas.
In support of this hypothesis, in an analysis of 58
subjects from 23 families with SDHD mutations, subjects
with phaeochromocytomas lived at higher altitudes
and were exposed to higher altitude-years than those
without them. Furthermore, those who were diagnosed
with single tumours at their frst clinical evaluation lived
at lower average altitudes and were exposed to lower
altitude-years than those with multiple tumours (7).
Population-weighted elevations were approximately 260
m for the United States and 2 m for the central-Western
Netherlands (P~0), suggesting that low altitudes in The
Netherlands reduce penetrance and relax the natural
selection on SDHD mutations (7).
Previous basic research data provide a mechanism that
could explain this relation through the pseudohypoxia
model. Hypoxia-induced factor (HIF2α) is more intensely
expressed in both noradrenergic sporadic and hereditary
von–Hippel Lindau (VHL)-related tumours than in
sporadic and familial adrenergic tumours . HIF-2α is also
expressed in developing sympathetic neurones, where it
regulates the expression of tyrosine hydroxylase (TH), the
rate-limiting enzyme in catecholamine synthesis (8). Such
expression might confer onto these cells a susceptibility
to VHL-associated tumorigenesis, thereby explaining both
the development of such tumours and their associated
noradrenergic phenotype (9).
Robust data is available on the ability of hypoxia to
modulate enzymatic activity needed for catecholamine
production. Long-term hypoxia in ewes maintained at
high altitude (3820 m) results in a selective reduction in
plasma adrenaline following acute stress, due to a reduction
in tyrosine hydroxylase (TH), dopamine beta-hydroxylase
(DBH) and phenylethanolamine N-methyltransferase
(PNMT) expression (10). In animals conceived, born and
raised at high altitude (3800 m, 13% PO
2
), the activities
of the synthesizing enzymes, TH, DDC and PNMT, were
variably affected at some time during the perinatal period.
The activities of the catabolizing enzymes, MAO and
COMT, at high altitude were increased on the last days of
gestation but depressed after birth (11).
In laboratory settings, mouse pheochromocytoma
cells (MP712 cells) showed a two-fold increase in PNMT
mRNA after incubation in 5%O
2
, with an inverse
relationship between PNMT gene reporter gene expression
and O
2
concentration between 10 and 1%. Anoxia evokes
the most pronounced response, detectable within 15 min,
becoming maximal at 45 min then subsiding to normoxic
levels by 120 min (12).
Traditionally it is considered that noradrenaline
(NA) and adrenaline (Adr) are stored in different types
of intracellular granules. In a previous study using
Correspondence
should be addressed
to R Mihai
Email
radumihai@doctors.org.uk
Letter
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