Betahistine Dihydrochloride 8mg Tablets
Each tablet contains 8mg betahistine dihydrochloride.
Excipient(s) with known effect: lactose monohydrate.
For the full list of excipients, see section 6.1.
Betahistine Dihydrochloride 8mg Tablets are white, circular, flat, bevelled edged tablets marked B8 on one side
Vertigo, tinnitus and hearing loss associated with Ménière's syndrome.
Adults, including the elderly: Initially 16 mg three times daily, taken preferably with meals. Maintenance doses are generally in the range 24 to 48 mg daily. Dosage should be altered according to clinical response.
Children: No dosage recommendations are made for children.
Use in patients with hypersensitivity to betahistine dihydrochloride or any component of the tablet. Use in patients with phaeochromocytoma.
Betahistine dihydrochloride is considered to be unsafe in patients with porphyria
Betahistine dihydrochloride should be administered with caution to patients with bronchial asthma or a history of peptic ulcer.
Betahistine dihydrochloride is not recommended for use in children.
Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicine.
interaction studies have been performed. Based on in-vitro
data no in-vivo
inhibition on Cytochrome P450 enzymes is expected. In vitro
data indicate an inhibition of betahistine metabolism by drugs that inhibit monoamino-oxidase (MAO) including MAO subtype B (e.g. selegiline). Caution is recommended when using betahistine and MAO inhibitors (including MAO-B selective) concomitantly.
Betahistine dihydrochloride should not be used concurrently with antihistamines.
There are no adequate data from the use of betahistine in pregnant women.
Animal studies are insufficient with respect to effects on pregnancy, embryonal/foetal development, parturition and postnatal development. The potential risk for humans is unknown. Betahistine should not be used during pregnancy unless clearly necessary.
It is not known whether betahistine is excreted in human milk. There are no animal studies on the excretion of betahistine in milk. The importance of the drug to the mother should be weighed against the benefits of nursing and the potential risks for the child.
No adverse effects known.
The following undesirable effects have been experienced with the below indicated frequencies in betahistine dihydrochloride-treated patients in placebo-controlled clinical trials (very common (≥ /100 to < 1/10); uncommon (≥ /1,000 to < 1/100); rare (≥ /10,000 to < 1/1,000); very rare (<1/10,000))
Common: nausea and dyspepsia
In addition to those events reported during clinical trials, the following undesirable effects have been reported spontaneously during post-marketing use and in scientific literature. A frequency cannot be estimated from the available data and is therefore classified as not known.
Immune systems disorders
Hypersensitivity reactions, e.g. anaphylaxis have been reported
Mild gastric complaints (e.g. vomiting, gastrointestinal pain, abdominal distension and bloating) have been observed. These can normally be dealt with by taking the dose during meals or by lowering the dose.
Nervous systems disorders
Skin and subcutaneous tissue disorders
Cutaneous and subcutaneous hypersensitivity reactions have been reported in particular angioneurotic oedema, urticaria, rash and pruritus
A few overdose cases have been reported. Some patients experienced mild to moderate symptoms with doses up to 640 mg (e.g. nausea, somnolence, abdominal pain). More serious complications (e.g. convulsion, pulmonary or cardiac complications) were observed in cases of intentional overdose of betahistine especially in combination with other overdosed drugs.
There is no specific antidote to betahistine dihydrochloride. Gastric lavage and symptomatic treatment is recommended.
Betahistine dihydrochloride is a histamine-like drug in which pharmacological activity can be attributed to a specific effects and/or more direct influences on recovery mechanisms the vestibular nuclei. It has weak agonist activity at histamine H1
receptors and moderate antagonist activity at H3
; receptors. The antagonist action of betahistine dihydrochloride at the H3
: receptor can be expected to potentiate the release of presynaptic histamine in vivo by blocking the auto-inhibitory feedback at histaminergic terminals, its action on medial vestibular nucleus cells is to significantly reduce their responsiveness to histamine. This action of betahistine dihydrochloride occurs at post-synaptic H1
receptors, since betahistine dihydrochloride lacks any effect at H2
receptors. The effects of betahistine dihydrochloride are thus consistent with a partial agonist action at these receptors, with betahistine dihydrochloride having little excitatory action on its own but reducing the excitatory responses to histamine by occupying H1
The reduced response of the medial vestibular nucleus cells to histamine in the presence of betahistine dihydrochloride may be the result of the activation of H2
receptor-coupled second-messenger pathways alone rather than the normal activation of both H1
second-messenger systems together. Thus, simultaneous stimulation of the H1
receptor pathways is know to cause a large amplification of the cellular cAMP response, above that caused by stimulation of the H2
receptor pathway alone. The reduction in the amplitude and total duration of the histamine-induced excitation in medial vestibular nucleus cells in the presence of betahistine dihydrochloride is suggestive of such a mechanism. This partial agonist action of betahistine dihydrochloride at H1
receptor may be an important part of its mechanism of action.
Betahistine dihydrochloride is completely absorbed after oral administration, and peak plasma concentrations of 14
C-labelled betahistine dihydrochloride are attained one hour after oral administration to fasting subjects.
Betahistine dihydrochloride is eliminated by the kidney with 85 - 90% of the radioactivity of an 8 mg dose appearing in the urine over 56 hours. Maximum excretion rates are reached within 2 hours of administration. Plasma levels of the parent drug are below the limits of detection of the assay.
Bioavailability has therefore been assessed from urinary excretion of its main metabolite, 2- pyridylacetic acid.
There is no evidence for presystemic metabolism. Biliary excretion is not important as a route of elimination of either the drug or its metabolites in the rat and is unlikely to be so in man.
No pre-clinical data exists which gives additional information to the prescriber which is not included in other sections of the SPC.
Colloidal anhydrous silica
Do not store above 25° C. Store in the original package. Keep container in the outer carton.
Blister strips consisting of 250 µm transparent PVC, a 60 g/m2
PVDC layer and 20µm hard temper aluminium foil, contained in a carton.
Pack sizes: 60, 84, 90, 100 and 120 tablets.
Athlone Pharmaceuticals Limited