Corticosteroids anticonvulsants

Uremia Antihistamines Antiparkinsonian agents Antispasmodics Ophthalmic preparations OTC sleep/allergy medications Tricyclic antidepressants Other medications Analgesics/NS AIDs Anticonvulsants Corticosteroids (high dose) Digoxin H2 blockers Insulin Muscle relaxants Narcotics Psychotropics (anxiolytic, antidepressant, antipsychotic) Sedative/hypnotic Sulfonylurea... 

Anticonvulsants Corticosteroids, gold, NSAIDs Phenytoin, carbamazepine, barbiturates Antiinflammatories... 

Drugs that may affect cyclosporine include allopurinol, amiodarone, androgens (eg, danazol, methyltestosterone), anticonvulsants (eg, carbamazepine, phenobarbital, phenytoin), azole antifungals (eg, fluconazole, ketoconazole), beta-blockers, bosentan, bromocriptine, calcium channel blockers, colchicine, oral contraceptives, corticosteroids, fluoroquinolones (eg, ciprofloxacin), foscarnet, HMG-CoA reductase inhibitors, imipenem-cilastatin, macrolide antibiotics, methotrexate, metoclopramide, nafcillin, nefazodone, orlistat, potassium-sparing diuretics, probucol, rifamycins (rifampin, rifabutin), serotonin reuptake inhibitors (SSRIs eg, fluoxetine, sertraline),... 

Spontaneous reports of osteoporosis, osteopenia, bone fractures, and delayed healing of bone fractures have been seen in the isotretinoin population. While causality to isotretinoin has not been established, an effect cannot be ruled out. Physicians should use caution when prescribing isotretinoin to patients with a genetic predisposition for age-related osteoporosis, a history of childhood osteoporosis conditions, osteomalacia, or other disorders of bone metabolism. This would include patients diagnosed with anorexia nervosa and those who are on chronic drug therapy that causes drug-induced osteoporosis/osteomalacia and/or affects vitamin D metabolism, such as systemic corticosteroids and any anticonvulsants. 

There are two major classes of pain medications, nonopioids and opioids. The nonopioids used to treat mild pain include agents such as acetaminophen, both steroid and nonsteroidal antiinflammatory drugs (NSAIDs), and acetylsalicylic acid. Anticonvulsants suppress neuronal firing and are also helpful in neuropathic pain. Antiinflammatory agents (e.g., NSAIDs or corticosteroids) may be particularly helpful when bony involvement occurs and are often used for low-intensity pain. Steroids decrease inflammatory edema and are useful in cases of nerve and spinal cord compression, lymphedema, visceral pain caused by organ enlargement, and bone pain. Finally, short-term corticosteroid therapy may also produce euphoria (thus ameliorating less severe depressions) as well as reverse anorexia. 

Corticosteroids, heparin treatment, particularly if used during pregnancy, and anticonvulsants have all been implicated in the development of osteoporosis. 

Stevens-Johnson syndrome and toxic epidermal necrolysis e.g. anticonvulsants, sulphonamides, aminopenicillins, oxicam NSAIDs, allopurinol, chlormezanone, corticosteroids. 

Pharmacokinetics. Carbamazepine is extensively metabolised one of the main products, an epoxide (a chemically reactive form), has anticonvulsant activity similar to that of the parent drug but may also cause some of its adverse effects. The t) of carbamazepine falls from 35 h to 20 h over the first few weeks of therapy due to induction of hepatic enzymes that metabolise it as well as other drugs, including corticosteroids (adrenal and contraceptive), theophylline and warfarin. Cimetidine and valproate inhibit its metabolism. There are complex interactions with other antiepilepsy drugs, which constitute a reason for monodrug therapy. 

Epilepsy and osteoporosis are very common and frequently overlap. Nevertheless, the prevalence of low bone density appears to be disproportionately higher in patients with epilepsy, and patients with epilepsy have an excessive risk of fractures. A meta-analysis of 94 cohort studies and 72 case-control studies has shown that anticonvulsant treatment is highly associated with fractures (relative risk over 2) (117). Other risk factors were low body weight, weight loss, physical inactivity, consumption of corticosteroids, primary hjrperparathjroidism, type 1 diabetes melhtus, anorexia nervosa, gastrectomy, pernicious anemia, and age over 70 years. 

Facial edema also has been observed. Reactions are often accompanied by fever, lymphadenopathy, elevated transaminases, leukocytosis, and eosinophilia. These rashes can progress to more severe, potentially fatal reactions, such as erythema multiforme, exfoliative dermatitis, or toxic epidermal necrolysis. Thus, if phenytoin is suspected as the etiology of the reaction, it should be discontinued immediately and an alternative anticonvulsant started if necessary. Corticosteroid therapy may mask some of the signs and symptoms of a hypersensitivity reaction, and patients on concomitant corticosteroids should be evaluated carefully for any symptoms resembling a hypersensitivity reaction. 

Paramax metoclopramide. paramethadione [ban, inn] (Paradione ) is an oxazolidinedione. It has anticonvulsant activity but only has restricted use as an antiepileptic (for absence seizures, petit mal) due to potential toxicity, paramethasone [ban, inn] (paramethasone acetate [usan]) is a CORTICOSTEROID, a GLUCOCORTICOID with ANTIINFLAMMATORY and ANTIAUERGIC properties. It has beeen used sytemically for a variety of inflammatory disorders, paramethasone acetate parametbasone. paramorphine tbebaine. 

The most common drugs responsible for acneform eruptions are ACTH, androgenic hormones, anticonvulsants (hydantoin derivatives, phenobarbital, trimethadione), corticosteroids, danazol, disulfiram, halogens (bromides, chlorides, iodides), lithium, oral contraceptives, tuberculostatics (ethionamide, isoniazid, rifampin), vitamins B2, B6, and B12. 

Drugs corticosteroids isotretmoin (Accutane), thiazides, anticonvulsants, j5 blockers, anabolic steroids, certain oral contraceptives Alcohol Obesity... 

Some drugs, for example anticonvulsants phenytoin, phenobarbital and corticosteroids can lead to osteomalacia and rickets by depressing vitamin D dependent calcium uptake in the intestine. 

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