Clomipramine 175mg - FDA Homepage

Using the average of the above concentrations, a fully breastfed infant would receive about 2. The other woman was taking 75, and then mg daily. Using the average of the above fore- and hindmilk concentrations, a fully breastfed infant would receive about 1.

At 33 days postpartum, a breastmilk sample table 12 to 15 hours after the dose contained clomipramine in a concentration of Breastfeeding was instituted on day 7 postpartum during maternal use of clomipramine mg daily.

In the infant whose mother was taking 75, and then mg daily, the infant had a combined drug and metabolite plasma level of 3. The infant plasma level was 5. Follow-up for 1 to 3 years in a group of 20 breastfed infants whose mothers were taking various tricyclic antidepressants found no adverse effects on growth and development.

There is a risk of postural hypotension, which can lead to falls, and anticholinergic effects including constipation, dry mouth, and urinary retention. They can have serious cardiac effects and can be fatal in overdose. Costs of antidepressants are relatively low, although can be higher for some newer agents. Antipsychotics Antipsychotics are commonly used for treating behavioral and psychotic symptoms of dementia BPSD , although this indication is not licensed and the US Food and Drug Administration has issued two black box warnings about the use of respectively second-generation [ 62 ] and first-generation antipsychotics [ 63 ] in elderly demented people.

There are two case reports of the use of quetiapine for treating ISB. Two case reports describe the successful use of haloperidol. Side effects of antipsychotics can be very significant.

There is a small but definite increased risk of stroke or cardiac events in people with dementia, and this has led to national advice in many countries to avoid their use in dementia wherever possible. Sedation and impairment of cognitive function is common. Atypical antipsychotics can produce weight gain and a metabolic syndrome.

Older agents may have anticholinergic effects and more rarely cause dermatological, hematological, or endocrine problems. Older antipsychotic agents are mostly low in cost, but newer ones may be substantially more expensive. Anticonvulsants Anticonvulsants have been trialed for the treatment of ISB in dementia; however, the underlying mechanism by which they affect sexual function is still poorly understood [ 68 ].

Gabapentin is known to cause reduced libido, anorgasmia, and erectile dysfunction [ 42 ]. Three case reports describe reduced ISB in people with dementia treated with gabapentin [ 69 , 70 , 71 ]. Carbamazepine has been associated with lower testosterone levels in young women with epilepsy [ 72 ]. There are two case reports of its use in ISB.

A year-old man diagnosed with frontotemporal dementia failed to respond to paroxetine. Valproate salts have not proved useful in controlling agitation in dementia [ 75 ], and currently, there is no evidence that they might work in ISB. Anticonvulsants can have a wide range of side effects including sedation, gastro-intestinal problems, risk of falls, hypo- or hypertension, and endocrine changes. Gabapentin and its close relative pregabalin are relatively expensive, valproate salts intermediate in cost depending on formulation , and carbamazepine relatively inexpensive.

Cholinesterase inhibitors Cholinesterase inhibitors may affect sexual function in many ways, including altering testosterone levels, but the exact processes involved are still uncertain [ 76 ]. Studies evaluating the effects of cholinesterase inhibitors on ISB are conflicting.

The commonest side effects are gastro-intestinal, but there can be effects on sleep and arousal. Donepezil is available as a generic form which is less expensive than others. Antiandrogens and other drugs with antiandrogenic activity Antiandrogens may reduce androgen levels or inhibit binding at androgen receptors.

Medroxyprogesterone MPA does not bind to androgen receptors, but indirectly decreases the level of testosterone by inhibiting the secretion of pituitary luteinizing hormone LH and follicle-stimulating hormone FSH.

One subject relapsed, but symptoms were much milder than before [ 82 ]. However, in the light of the present data, these results can be interpreted as an overall decrease in the total number of GRs.

We suggest the following model for the in vitro effects of antidepressants on the GR. Treatment with antidepressants inhibits steroid transport, induces GR translocation, and reduces GR expression Pariante et al, , a ; present paper. These three effects could be mediated by the same mechanism. For example, blocking of steroid transport can increase the intracellular levels of steroids from the media—even steroid stripping of serum cannot be absolute Miller et al, —thus leading to translocation of the GR.

Antidepressants could also induce GR translocation through their effect on cAMP-dependent protein kinases Rangarajan et al, ; Chen and Rasenick, ; Miller et al, ; Blom et al, Translocation of GR, in turn, could lead to the reduction in GR expression.

In fact, GR translocation by both GR agonists and GR antagonists has been associated with a GR downregulation, which takes place over few hours and is because of a reduction in the protein half-life and an inhibition of GR mRNA synthesis; this reduction is temporary and can be followed by a subsequent upregulation Schmidt and Meyer, Therefore, it is possible that the inhibition of the transporters precedes the GR downregulation.

This is because the increase in the intracellular levels of the glucocorticoid overcomes the GR downregulation, and possibly precedes the GR downregulation. However, if cells are treated in experimental conditions that do not elicit the effects on the transporter, the GR downregulation leads to a reduced GR-mediated gene transcription. For example, antidepressants give a reduction in GR-mediated gene transcription when cells are coincubated with corticosterone Pariante et al, a.

Moreover, Miller et al have recently found that incubation of LMCAT cells with desipramine alone induces a small decrease in the unstimulated GR-mediated gene transcription. In this case, even if the inhibition of the transporter increases the intracellular levels of dexamethasone as suggested by our experiments with 3H-cortisol , these are unable to compensate for the GR downregulation, possibly because of the short incubation, or possibly because the GR downregulation is present before the glucocorticoid is added differently than in the coincubation experiments.

Rodents have two isoforms of PGP: The mdr1a PGP is predominantly expressed at the BBB Regina et al, and expels cortisol from the brain of rodents, but not corticosterone, which is the endogenous glucocorticoid in these animals de Kloet et al, ; Karssen et al, This isoform is predominantly expressed in the adrenal and the ovaries Lee et al, , but is also expressed in the brain Regina et al, , particularly in the hippocampus Kwan et al, Although mdr1b PGP has not been detected in brain capillaries Regina et al, , it is expressed in rat brain endothelial cells in vitro Felix and Barrand, Consistent with this, mice that are knockout for mdr1a and mdr1b PGP show increased access of corticosterone to the brain although this effect is smaller than that on cortisol and increased negative feedback on the HPA axis by corticosterone Uhr et al, Therefore, there are intriguing—but still preliminary—lines of evidence suggesting that membrane transport of corticosterone regulates HPA axis function in rodents.

By inhibiting membrane steroid transport, antidepressants could directly increase the access of corticosterone to the brain, or the access of other steroids that are transported by PGP, like aldosterone Ueda et al, , and enhance GR and MR activation. Although in the brain the highest expression of PGP has been found at the BBB Lee et al, , our data show that this effect could also occur directly at the neuronal level.

In turn, the increased access of glucocorticoids to the brain could lead to the decrease in HPA axis activity and the GR and MR downregulation described in rats after 3—9 days of treatment with antidepressants Reul et al, ; Yau et al, This receptor downregulation is consistent with our data in vitro and, theoretically, could explain part of the lag time seen with antidepressants for the onset of their therapeutic action.

Chronically, that is, after 14 days or more of treatment, antidepressants induce GR and MR upregulation in the brain Pariante and Miller, Although catecholamines upregulate GR and MR expression Lai et al, , inhibition of catecholamines' uptake seems not to be relevant for the antidepressant-induced GR upregulation.

In fact, desipramine increases GR expression in the rat brain even following neurotoxic lesioning of noradrenergic neurones with DSP4 Rossby et al, Moreover, antidepressant-induced changes in GR expression in vitro are not blocked by antagonists of alpha- or beta-adrenergic receptors or of 5HT1a or 5HT2 serotonergic receptors Okugawa et al, ; Lai et al, The inhibition of steroid transporters—and the increased access of glucocorticoids to the brain—could explain this GR and MR upregulation, as a compensatory mechanism following the initial downregulation or as a consequence of the reduced HPA axis activity.

Inhibition of PGP and other membrane steroid transporters is not receptor mediated and is related to the drugs' physiochemical properties, that is, lipophilicity, electric charge, and ability to accept hydrogen bonds Ford, ; Castaing et al, ; Ekins et al, In conclusion, we have demonstrated that the antidepressant clomipramine regulates the intracellular levels of cortisol by inhibiting membrane steroid transporters, in LMCAT cells and neurones, that are similar to PGP in their substrates and modulators.

We propose that antidepressants in humans could inhibit the steroid transporters localized on the BBB and in neurones, and thus increase the access of cortisol to the brain and the negative feedback on the HPA axis. This is consistent with studies showing that treatment with GR and MR agonists Dinan et al, ; Bouwer et al, , including cortisol DeBattista et al, , has antidepressant effects in humans.

Hypothetically, the increased access of cortisol to the brain could balance the reduction of GR function described in patients with major depression Pariante and Miller, Or, perhaps, this effect could compensate for a 'reduction' of cortisol levels in the brain of depressed patients that was first and last described exactly 30 years ago: All six suicides had a clear history of depressive illness' Brooksbank et al, The steroid antagonist RU exerts different effects on the glucocorticoid and progesterone receptors.

Steroids affect collateral sensitivity to gemcitabine of multidrug-resistant human lung cancer cells. Eur J Pharmacol Altered regulation of CREB by chronic antidepressant administration in the brain of transgenic mice with impaired glucocorticoid receptor function.

Expression of an mdr gene is associated with a new form of resistance to dexamethasone-induced apoptosis. Prednisone augmentation in treatment-resistant depression with fatigue and hypocortisolaemia: Cimetidine Co-administration with the histamine2 H2 -receptor antagonist, cimetidine an inhibitor of several P enzymes, including CYP2D6 and CYP3A4 , may increase plasma concentrations of tricyclic antidepressants, whose dosage should therefore be reduced.

Oral contraceptives No interaction between chronic oral contraceptive use 15 or 30 micrograms ethinylestradiol daily and clomipramine 25 mg daily has been documented.

Oestrogens are not known to be inhibitors of CYP2D6, the major enzyme involved in clomipramine clearance and, therefore, no interaction is expected. Although, in a few cases with high dose oestrogen 50 micrograms daily and the tricyclic antidepressant imipramine, increased side effects and therapeutic response were noted, it is unclear as to the relevance of these cases to clomipramine and lower dose oestrogen regimens.

Monitoring therapeutic response of tricyclic antidepressants at high dose oestrogen regimens 50 micrograms daily is recommended and dose adjustments may be necessary. Antipsychotics Co-medication of antipsychotic e.

Combination with thioridazine may produce severe cardiac arrhythmias. Methylphenidate This drug may also increase plasma concentrations of tricyclic antidepressants, whose dosage should therefore be reduced.

Grapefruit, grapefruit juice, or cranberry juice Concomitant administration of Clomipramine with grapefruit, grapefruit juice, or cranberry juice may increase the plasma concentrations of clomipramine. In cigarette smokers, clomipramine steady-state plasma concentrations were decreased 2-fold compared to non-smokers no change in N- desmethylclomipramine. Colestipol and cholestyramine Concomitant administration of ion exchange resins such as cholestyramine or colestipol may reduce the plasma levels of clomipramine.

Staggering the dosage of clomipramine and resins, such that the drug is administered at least 2 h before or h after the administration of resins, is recommended. John's wort Concomitant administration of clomipramine with St. John's wort during the treatment may decrease the plasma concentrations of clomipramine.

Interactions affecting other drugs Anticholinergic agents Tricyclic antidepressants may potentiate the effects of these drugs e. Antiadrenergic agents Clomipramine may diminish or abolish the antihypertensive effects of guanethidine, betanidine, reserpine, clonidine and alpha-methyldopa.

Patients requiring co-medication for hypertension should therefore be given antihypertensives of a different type e. It would be advisable to review all antihypertensive therapy during treatment with tricyclic antidepressants. CNS depressants Tricyclic antidepressants may potentiate the effects of alcohol and other central depressant substances e.

Sympathomimetic drugs Clomipramine may potentiate the cardiovascular effects of adrenaline, ephedrine, isoprenaline, noradrenaline, phenylephrine, and phenylpropanolamine e. Anticoagulants Tricyclic antidepressants may potentiate the anticoagulant effect of coumarin drugs by inhibiting their metabolism by the liver.

Careful monitoring of plasma prothrombin is therefore advised. Drugs that can cause increase plasma clomipramine levels or which in themselves prolong the QTc interval The risk of QTc prolongation and torsades de pointes is likely to be increased if clomipramine is co-administered with other drugs that can cause QTc prolongation.

Therefore concomitant use of such agents with clomipramine is not recommended see section 4. Examples include certain antiarrhythmics, such as those of Class 1A such as quinidine, disopyramide and procainamide and Class III such as amiodarone and sotalol , tricyclic antidepressants such as amitriptyline , certain tetracyclic antidepressants such as maprotiline , certain antipsychotic medications such as phenothiazines and pimozide , certain antihistamines such as terfenadine ; lithium, quinine and pentamidine.

This list is not exhaustive. Clomipramine hydrochloride should be administered with caution in patients with urinary retention, prostatic hypertrophy or constipation or in patients with increased intraocular pressure due to its anticholinergic properties. Tricyclic antidepressants are known to lower the convulsive threshold and clomipramine should, therefore, be used with extreme caution in patients with a history of convulsive disorders and other predisposing factors, e.

Caution should be observed in prescribing Clomipramine in hyperthyroid patients or in patients receiving thyroid medication cojointly.

Depressed patients with suicidal tendencies should be carefully supervised during treatment. Elderly patients and young children can be particularly sensitive to the side-effects and a reduced dose, especially initially, should be employed. Blood sugar concentrations may be altered in diabetics.

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