Acamprosate, sold under the brand name Campral.

A medication used along with counselling to treat alcohol dependence.

Over 3-12 months it increases the number of people who do not drink at all and the number of days without alcohol.

Its primary effectiveness is for maintaining abstinence from alcohol.

Its target population includes patients who won continued sobriety after a period of abscess who do not have severe renal impairment.

It appears to work as well as naltrexone.

Pregnancy category C.

Routes of administration oral .

Bioavailability 11%.

Protein binding Negligible

Metabolis Nil.

Elimination half-life20 h to 33 h

Excretion Renal

It is thought to stabilize chemical signaling in the brain that would otherwise be disrupted by alcohol withdrawal.

By itself, it is not an effective therapy for alcoholism in most individuals.

It is a first line medication to consider for patients who desire a complete absence from alcohol, and it is especially effective after a period of sobriety.

It is most beneficial when used in combination with psychosocial support as it aids in reducing alcohol consumption as well as full abstinence.

Side effects include: allergic reactions, abnormal heart rhythms, diarrhea, and low or high blood pressure, while less serious side effects include headaches, insomnia, and impotence.

Diarrhea is its most common side-effect.

Should not be taken by people with kidney problems.

Un like naltrexone or disulfiram acamprosate is not affected by liver function.

The label contains warnings about increases of suicidal behavior, major depressive disorder, and kidney failure.

Adverse effects include: diarrhea, nausea, depression, and anxiety, headache, stomach pain, back pain, muscle pain, joint pain, chest pain, infections, flu-like symptoms, chills, heart palpitations, high blood pressure, fainting, vomiting, upset stomach, constipation, increased appetite, weight gain, edema, sleepiness, decreased sex drive, impotence, forgetfulness, abnormal thinking, abnormal vision, distorted sense of taste, tremors, runny nose, coughing, difficulty breathing, sore throat, bronchitis, and rashes.

A significant component of acamprosate  is a calcium molecule, so it should be avoided in patients with hypercalcemia.

It is believed to act as an NMDA receptor antagonist and positive allosteric modulator of GABAA receptors.

It has an agnostic effect on GABA receptors and the weak  antagonistic effect at N-methyl-D-aspartame receptors and metabotropic glutamate receptor 5.

Ethanol acts on the central nervous system by binding to the GABAA receptor, increasing the effects of the inhibitory neurotransmitter GABA.

In chronic alcohol abuse, one of the main mechanisms of tolerance is attributed to GABAA receptors becoming downregulated.

When alcohol is no longer consumed, down-regulated GABAA receptor complexes are so insensitive to GABA that the typical amount of GABA produced has little effect, leading to physical withdrawal symptoms.

GABA normally inhibits neural firing.

GABAA receptor desensitization results in unopposed excitatory neurotransmission leading to neuronal over-excitation

One of its mechanisms of action is the enhancement of GABA signaling at GABAA receptors via positive receptor modulation.

It may open the chloride ion channel in a way that does not require GABA as a cofactor.

It has been successfully used to control tinnitus, hyperacusis, ear pain and inner ear pressure during alcohol use due to spasms of the tensor tympani muscle.

Alcohol also inhibits the activity of N-methyl-D-aspartate receptors (NMDARs).

Chronic alcohol consumption leads to upregulation of N-methyl-D-aspartate receptors.

When, sudden alcohol abstinence causes the excessive numbers of NMDARs to be more active than normal it contributes to the symptoms of delirium tremens and excitotoxic neuronal death.

The withdrawal from alcohol induces a surge in release of excitatory neurotransmitters like glutamate, which activates NMDARs.

Acamprosate reduces this glutamate surge, and protects cultured cells from excitotoxicity induced by ethanol withdrawal and from glutamate exposure combined with ethanol withdrawal.

It is not metabolized by the human body.

Its bioavailability from oral administration is approximately 11%, and is decreased when taken with food.

It is excreted unchanged via the kidneys.

Evidence suggests it is neuroprotective to the effects of alcohol withdrawal, and possibly other causes of neurotoxicity).


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