Betamethasone is a glucocorticoid which is about eight to ten times as active as prednisolone
on a weight-for-weight basis.
Betamethasone is very soluble in water and is therefore less likely to cause local gastric
irritation than corticosteroids which are only slightly soluble. This is important when high doses
are required, as in immune-suppressive therapy.
Betamethasone does not normally cause retention of salt and water and the risk of inducing
oedema and hypertension is almost negligible.
A wide variety of diseases may sometimes require corticosteroid therapy. Some of the principal
indications are:
 Bronchial asthma, severe hypersensitivity reactions, anaphylaxis, rheumatoid arthritis,
systemic lupus erythematosus, dermatomyositis, mixed connective tissue disease
(excluding systemic sclerosis), polyarteritis nodosa;
 Inflammatory skin disorders, including pemphigus vulgaris, bullous pemphigoid and
pyoderma gangrenosum;
 Minimal change nephrotic syndrome, acute interstitial nephritis;
 Ulcerative colitis, Crohn's disease, sarcoidosis, rheumatic carditis;
 Haemolytic anaemia (autoimmune), acute and lymphatic leukaemia, malignant lymphoma,
multiple myeloma, idiopathic thrombocytopenic purpura;
 Immunosuppression in transplantation.

Posology:
Betamethasone Tablets are best taken dissolved in water, but they can be swallowed whole
without difficulty. The lowest dosage that will produce an acceptable result should be used;
when it is possible to reduce the dosage, this must be accomplished by stages. During
prolonged therapy, dosage may need to be increased temporarily during periods of stress or in
exacerbations of illness (see section 4.4).
Adults:
The dose used will depend on the disease, its severity and the clinical response obtained. The
following regimens are for guidance only. Divided dosage is usually employed.
Short term treatment:
 2-3mg daily for the first few days, then reducing the daily dose by 250 or 500mcg (0.25 or
0.5mg) every two to five days, depending upon the response.
Rheumatoid arthritis:
 500mcg (0.5mg) to 2mg daily. For maintenance therapy the lowest effective dosage is used.
Most other conditions:
 1.5 to 5mg daily for one to three weeks, then reducing to the minimum effective dosage.
Larger doses may be needed for mixed connective tissue diseases and ulcerative colitis.
Paediatric population:
A proportion of the adult dosage may be used (e.g. 75% at 12 years, 50% at 7 years and 25% at
1 year) but clinical factors must be given due weight (see section 4.4).
Method of Administration:
Oral
 

Undesirable effects may be minimised by using the lowest effective dose for the minimum
period and by administering the daily requirement as a single morning dose, or whenever
possible as a single morning dose on alternate days. Frequent patient review is required to
appropriately titrate the dose against disease activity (see “Posology and Method of
Administration”).
Caution is advised with the use of corticosteroids in patients who have suffered a recent
myocardial infarction because of the risk of myocardial rupture.
Caution is advised on the use of corticosteroids in patients with hypothyroidism or myasthenia
gravis.
Suppression of the inflammatory response and immune function increases the susceptibility to
infections and their severity. The clinical presentation may often be atypical and serious
infections such as septicaemia and tuberculosis may be masked and may reach an advanced
stage before being recognised.
Chickenpox is of particular concern since this normally minor illness may be fatal in
immunosuppressed patients. Patients (or parents of children) without a definite history of
chickenpox should be advised to avoid close personal contact with chickenpox or herpes zoster
and if exposed they should seek urgent medical attention. Passive immunisation with varicella
zoster immunoglobulin (VZIG) is needed by exposed non-immune patients who are receiving
systemic corticosteroids or who have used them within the previous 3 months; this should be
given within 10 days of exposure to chickenpox. If a diagnosis of chickenpox is confirmed, the
illness warrants specialist care and urgent treatment. Corticosteroids should not be stopped and

the dose may need to be increased.
Live vaccines should not be given to individuals with impaired immune responsiveness. The
antibody response to other vaccines may be diminished.
Patients should be advised to take particular care to avoid exposure to measles and to seek
immediate medical advice if exposure occurs. Prophylaxis with intramuscular normal
immunoglobulin may be needed.
Adrenal suppression:
Adrenal cortical atrophy develops during prolonged therapy and may persist for years after
stopping treatment.
In patients who have received more than physiological doses of systemic corticosteroids
(approximately 1mg betamethasone or equivalent) for greater than 3 weeks, withdrawal should
not be abrupt. How dose reduction should be carried out depends largely on whether the disease
is likely to relapse as a dose of systemic corticosteroids is reduced. Clinical assessment of
disease activity may be needed during withdrawal. If the disease is unlikely to relapse on
withdrawal of systemic corticosteroids but there is uncertainty about hypothalamic-pituitaryadrenal
(HPA) suppression, the dose of systemic corticosteroid may be reduced rapidly to
physiological doses. Once a daily dose equivalent to 1mg betamethasone is reached, dose
reduction should be slower to allow the HPA-axis to recover.
Abrupt withdrawal of systemic corticosteroid treatment, which has continued up to 3 weeks is
appropriate if it is considered that the disease is unlikely to relapse. Abrupt withdrawal of doses
of up to 6mg daily of betamethasone, or equivalent for 3 weeks is unlikely to lead to clinically
relevant HPA-axis suppression, in the majority of patients. In the following patient groups,
gradual withdrawal of systemic corticosteroid therapy should be considered even after courses
lasting 3 weeks or less:
 Patients who have had repeated courses of systemic corticosteroids, particularly if taken for
greater than 3 weeks,
 When a short course has been prescribed within one year of cessation of long-term therapy
(months or years),
 Patients who have reasons for adrenocortical insufficiency other than exogenous
corticosteroids therapy,
 Patients receiving doses of systemic corticosteroid greater than 6mg daily of betamethasone
(or equivalent),
 Patients repeatedly taking doses in the evening.
During prolonged therapy any intercurrent illness, trauma or surgical procedure will require a
temporary increase in dosage; if corticosteroids have been stopped following prolonged therapy
they may need to be temporarily re-introduced.
Special precautions
Particular care is required when considering the use of systemic corticosteroids in patients with
the following conditions and frequent patient monitoring is necessary.
A. Osteoporosis (post-menopausal females are particularly at risk).
B. Hypertension or congestive heart failure.
C. Existing or previous history of severe affective disorders (especially previous steroid
psychosis).
D. Diabetes mellitus (or a family history of diabetes).
E. History of tuberculosis.
F. Glaucoma (or a family history of glaucoma).
G. Previous corticosteroid-induced myopathy.
H. Liver failure - blood levels of corticosteroid may be increased, (as with other drugs which
are metabolised in the liver).
I. Renal insufficiency.
J. Epilepsy.
K. Peptic ulceration.

Patients should carry 'steroid treatment' cards which give clear guidance on the precautions to
be taken to minimise risk and which provide details of prescriber, drug, dosage and the duration
of treatment.
Patients/and or carers should be warned that potentially severe psychiatric adverse reactions
may occur with systemic steroids (see section 4.8). Symptoms typically emerge within a few
days or weeks of starting treatment. Risks may be higher with high doses/systemic exposure
(see also section 4.5 pharmacokinetic interactions that can increase the risk of side effects),
although dose levels do not allow prediction of the onset, type, severity or duration of reactions.
Most reactions recover after either dose reduction or withdrawal, although specific treatment
may be necessary. Patients/carers should be encouraged to seek medical advice if worrying
psychological symptoms develop, especially if depressed mood or suicidal ideation is
suspected. Patients/carers should also be alert to possible psychiatric disturbances that may
occur either during or immediately after dose tapering/withdrawal of systemic steroids,
although such reactions have been reported infrequently.
Particular care is required when considering the use of systemic corticosteroids in patients with
existing or previous history of severe affective disorders in themselves or in their first degree
relatives. These would include depressive or manic-depressive illness and previous steroid
psychosis.
Paediatric population
Corticosteroids cause dose-related growth retardation in infancy, childhood and adolescence,
which may be irreversible. Treatment should be limited to the minimum dosage for the shortest
possible time. In order to minimise suppression of the HPA axis and growth retardation,
consideration should be given to administration of a single dose on alternate days.
Elderly
The common adverse effects of systemic corticosteroids may be associated with more serious
consequences in old age, especially osteoporosis, hypertension, hypokalaemia, diabetes,
susceptibility to infection and thinning of the skin. Close clinical supervision is required to
avoid life-threatening reactions.
 

Steroids may reduce the effects of anticholinesterases in myasthenia gravis, cholecystographic
X-ray media and non-steroidal anti-inflammatory agents.
Rifampicin, rifabutin, carbamazepine, phenobarbitone, phenytoin, primidone,
aminoglutethimide and ephedrine enhance the metabolism of corticosteroids; thus the
corticosteroid therapeutic effect may be reduced.
The desired effects of hypoglycaemic agents (including insulin), anti-hypertensives and
diuretics are antagonised by corticosteroids, and the hypokalaemic effects of acetazolamide,
loop diuretics, thiazide diuretics and carbenoxolone are enhanced.
The efficacy of coumarin anticoagulants may be enhanced by concurrent corticosteroid therapy
and close monitoring of the INR or prothrombin time is required to avoid spontaneous
bleeding.
The renal clearance of salicylates is increased by corticosteroids and steroid withdrawal may
result in salicylate intoxication.
The risk of hypokalaemia is increased with theophylline, ulcer healing drugs such as
carbenoxolone and antifungals such as amphotericin B.
Increased toxicity may result if hypokalaemia occurs in patients on cardiac glycosides.
Ritonavir and oral contraceptives may result in increased plasma concentrations or
corticosteroids.
The effect of corticosteroids may be reduced for 3-4 days after mifepristone.
The growth promoting effect of somatropin may be inhibited by corticosteroids.
An increase in the incidence of gastrointestinal bleeding may occur if NSAIDS are taken
concomitantly with corticosteroids.

Corticosteroids may antagonise the effects of neuromuscular blocking drugs such as
vecuronium.
Concurrent use of corticosteroids and fluoroquinolones may result in increased risk of tendon
rupture.
Concomitant use of betamethasone with quetiapine may result in the increased metabolism of
quetiapine and, depending on the clinical response, a higher dose of quetiapine may need to be
considered.
Co-treatment with CYP3A inhibitors, including cobicistat-containing products, is expected to
increase the risk of systemic side-effects. The combination should be avoided unless the benefit
outweighs the increased risk of systemic corticosteroid side-effects, in which case patients
should be monitored for systemic corticosteroid side-effects.
Corticosteroids may enhance the metabolism of tretinoin resulting in decreased levels of
tretinoin.

Pregnancy
Pregnancy category (C)
The ability of corticosteroids to cross the placenta varies between individual drugs, however,
betamethasone readily crosses the placenta. Administration of corticosteroids to pregnant
animals can cause abnormalities of foetal development including cleft palate, intra-uterine
growth retardation and effects on brain growth and development. There is no evidence that
corticosteroids result in an increased incidence of congenital abnormalities, such as cleft
palate/lip in man. However, when administered for prolonged periods or repeatedly during
pregnancy, corticosteroids may increase the risk of intra-uterine growth retardation.
Hypoadrenalism may, in theory, occur in the neonate following prenatal exposure to
corticosteroids but usually resolves spontaneously following birth and is rarely clinically
important. Myocardial hypertrophy and gastroesophageal reflux have been reported in
association with in-utero exposure to betamethasone.
As with all drugs, corticosteroids should only be prescribed when the benefits to the mother and
child outweigh the risks. When corticosteroids are essential however, patients with normal
pregnancies may be treated as though they were in the non-gravid state. Patients with preeclampsia
or fluid retention require close monitoring.
Betamethasone, systemically administered to a woman during pregnancy may result in a
transient suppression of the foetal heart rate parameters and biophysical activities that are
widely used for the assessment of foetal well – being. These characteristics can include a
reduction in foetal breathing movements, body movements and heart rate.
Breast-feeding
Corticosteroids may pass into breast milk, although no data are available for betamethasone.
Infants of mothers taking high doses of systemic corticosteroids for prolonged periods may
have a degree of adrenal suppression.
 

None known.

The incidence of predictable undesirable effects, including hypothalamic-pituitary-adrenal
(HPA) axis suppression correlates with the relative potency of the drug, dosage, timing of
administration and the duration of treatment. (See section 4.4)
Not known: frequency cannot be estimated from the available data

* Negative protein, nitrogen and calcium balance. Increased appetite. Hyperhidrosis. Increased high - density lipoprotein and low – density lipoprotein concentrations in the blood. Fluid and electrolyte disturbance (Sodium and water retention, hypertension, potassium loss, hypokalaemic alkalosis)

** Including affective disorder (such as irritable, euphoric, depressed and labile mood and suicidal thoughts), psychotic reactions (including mania, delusions, hallucinations and aggravation of schizophrenia), behavioural disturbances, irritability, anxiety, sleep disturbances and cognitive dysfunction including confusion and amnesia have been reported. Reactions are common and may occur in both adults and children. In adults, the frequency of severe reactions has been estimated to the 5-6%. Psychological effects have been reported on withdrawal of corticosteroids; the frequency is unknown. Psychological dependence. Increased intra-cranial pressure with papilloedema in children (pseudotumour cerebri), usually after treatment withdrawal. Aggravation of epilepsy.

Withdrawal symptoms and signs

Too rapid reduction of corticosteroid dosage following prolonged treatment can lead to acute adrenal insufficiency, hypotension and death (see “Special Warnings and Precautions for Use”).

A 'withdrawal syndrome' may also occur including; fever, myalgia, arthralgia, rhinitis, conjunctivitis, painful itchy skin nodules and loss of weight.

To report any side effect(s):

The National Pharmacovigilance and Drug Safety Centre (NPC)

Fax: +966-11-205-7662

Call NPC at +966-11-2038222, Exts: 2317-2356-2353-2354-2334-2340.

Toll free phone: 8002490000

E-mail: npc.drug@sfda.gov.sa

Website: www.sfda.gov.sa/npc

Management:

Treatment is unlikely to be needed in cases of acute over dosage.

Pharmacotherapeutic group: Corticosteroids for systemic use, plain, Glucocorticoids

ATC: H02A B01

Betamethasone sodium phosphate is an active corticosteroid with topical anti-inflammatory activity.

Absorption:

The vast majority of corticosteroids, including betamethasone, are absorbed from the gastrointestinal tract.

Biotransformation:

Corticosteroids are metabolised mainly in the liver but also in the kidney, and are excreted in the urine.

Synthetic corticosteroids, such as prednisolone, have increased potency when compared to the natural corticosteroids, due to their slower metabolism and lower protein-binding affinity.

None stated.

Not applicable.

Store below 30˚C, in a dry place.

§ Pack of 20 tablets in Alu-PVC (PVDC) blister, packed in a printed carton along with a leaflet.

§ Pack of 1000 tablets in Alu-PVC (PVDC) blister, packed in a printed carton along with a leaflet.

Any unused product or waste material should be disposed of in accordance with local requirements.