Bility of drug induced (DSF) hypertension was suspected. Subsequently, DSF was decreased to 250 mg/ day and BP reduced to 150/96 mm of Hg per week later. DSF was further lowered to 125 mg/day following this observation and antihypertensive agents like telmisartan 40 mg and hydrochlorothiazide 12.five mg/daywere also initiated on the physician’s advice. A month later (week8), patient reported with increased giddiness and physical fatigue with BP of 90/60 mm of Hg in spite of abstinent. Antihypertensive agents were withdrawn and DSF was discontinued totally. Fortnight later (week10), patient had reached his premorbid levels of BP to 110/70 mm of Hg. Psycho education about health-related illness, life style modifications like common workouts and dietary measures were advised. Six months later, patient had maintained total abstinence from alcohol also as tobacco, and his BP was 130/80 mm of Hg [Figure 1].DISCuSSIONDSF, an alcohol deterring agent that is certainly comparatively nontoxic substance when administered alone, markedly alters the intermediary metabolism of alcohol. It acts by inhibiting aldehyde dehydrogenase, alcohol dehydrogenase and dopamine betahydroxylase (DBH).[9] DSF together with its two metabolites, diethyldithiocarbamate, and carbon disulphide inhibit DBH activity, a norepinephrine (NE) biosynthetic enzyme, which ordinarily catalyzes the formation of NE from dopamine.[10] This increases urinary excretion from the most important dopamine metabolite homovanillic acid and decreases urinary excretion of NE and its significant metabolite vanillylmandelic acid.[6] Moreover, sideeffects of DSF which include fatigue, tremor, decreased sexual potency, headache, and dizziness is usually mediated by sympathetic nervous technique where NE may be the neurotransmitter.[11] Central nervous system alpha adrenergic receptors modulate peripheral autonomic activities both, which regulate BP.[6] Possibly, changes in central or peripheral NE activity are accountable for the increase200 180 Blood pressure in mm of Hg 160 140 120 100 80 60 ——————————- Abstinentfrom alcohol ————————— DSF-500 mg —————-250 mg ——-125 mg Telmisartan 40 mg + HTZ 12.5 mg Systolic BP Diastolic BPBaseline2 four 6 8 Potential study duration in weeksfigure 1: Systolic and diastolic blood pressure variations in an abstinent patient diagnosed with alcohol dependence on disulfiram (DSF) therapy (HTZ-hydrochlorothiazide) Indian Journal of Psychological Medicine | Apr – Jun 2013 | Vol 35 | IssueKulkarni and Bairy: Disulfiram induced reversible hypertensionin BP. Peripheral synthesis of NE is almost certainly not affected by the DSF as it is noted to have no impact around the pressor effect of tyramine and NE,[6] as also plasma levels of NE improve following longterm highdose (500 mg/day) DSF therapy.162405-09-6 Formula [4] Having said that, DSF increases the nitroglycerine induced postural hypotension whilst decreasing the accompanying tachycardia.199003-22-0 site [6] This implies that DSF impairs the BP regulation by means of central nervous system by inhibition with the central DBH activity resulting in decreased central NE synthesis, which may well interfere using the central alphaadrenergic activity at the bulbar sympathetic cardioaccelerator, and vasomotor centers, resulting in enhanced BP,[3] opposite of which can be noted with antihypertensive agents like central alpha agonists (clonidine, methyldopa, reserpine, and guanfacine).PMID:23800738 DSF has an inhibitory effect on certain cytochrome P450 (2E1, 2C9, 3A4, 3A5) enzymes.[9] Nicotine also has an inhi.