antiemetic dexamethasone
administration on days 2 and 3 can
be spared when combined with an
NK 1 RA and palonosetron in HEC. 54
Glucocorticosteroids alone are
insufficient as first-line therapy
for patients receiving moderate or
highly emetogenic chemotherapy.
The increased efficacy and booster
effect of 5-HT 3 RAs combined
with dexamethasone makes this
combination the standard of care
for prevention of acute CINV
induced by moderately to highly
emetogenic chemotherapy in
both adults and children 1,3,55 unless
contraindicated.
However, glucocorticosteroids
should be prescribed with
caution because there is some
evidence that they interfere
with the antineoplastic effect
of chemotherapy (for example,
in osteosarcoma and brain
tumours). 3,4 They may also reduce
the delivery of chemotherapy
to brain tumours by repairing
damage in the blood–brain barrier. 4
Glucocorticosteroids should not be
added to chemotherapy regimens
in which glucocorticosteroids are
already included. 7
Patients might experience
short-term hyperglycaemia and
immunosuppression and adrenal
suppression when used for
a prolonged period.
Use of glucocorticosteroids as
antiemetic premedication should
be avoided for 3–5 days prior to
and 90 days after chimeric antigen
62 | 2019 | hospitalpharmacyeurope.com
receptor (CAR)-T therapies. During
lymphodepleting chemotherapy
regimens, a glucocorticosteroid-
sparing approach to antiemetic
prophylaxis should be maintained. 7
Their use should also be
avoided with immune checkpoint
inhibitors when administered
without cytotoxic chemotherapy.
As there are still inconclusive
data for the concurrent use of
glucocorticosteroids with immune
checkpoint inhibitors combined
with emetogenic chemotherapy,
a corticosteroid-sparing approach
to antiemetic prophylaxis on
a case-by-case and regimen basis
is recommended. 7
Agents with a low
therapeutic index
Dopamine RAs, benzodiazepines,
cannabinoids and others are
classified as agents with a low
therapeutic index. They are
characterised by a lower efficacy
and a greater potential for adverse
effects compared with agents
having a high therapeutic index.
Their use should be restricted to
patients intolerant of or refractory
to first-line agents and they may
have some place as salvage agents
for patients with breakthrough
emesis.
Metoclopramide, is a substituted
benzamide dopamine antagonist,
causing central and peripheral
dopamine D 2 antagonism at low
doses. Before the introduction
of 5-HT 3 RAs, metoclopramide