include, but are not limited to: Uncontrolled infections Known hypersensitivity to dexamethasone Cerebral malaria Systemic fungal infection Concurrent treatment with live virus vaccines (including smallpox vaccine) Adverse effects The exact incidence of the adverse effects of dexamethasone are not available, hence estimates have been made as to the incidence of the adverse effects below based on the adverse effects of related corticosteroids and on available documentation on dexamethasone. Common Acne Amnesia Birth defect Cataract (in cases of long-term treatment, it occurs in about 10% of patients) Confusion Depression Dyspepsia Euphoria Headaches Hiccups (in cases of long-term treatment, it occurs in about 11% of patients) Hyperglycemia Hypertension Impaired skin healing and wound repair Increased appetite Increased risk of viral, bacterial, fungal, and parasitic infections Insomnia Irritability Malaise Muscle atrophy and myopathy Nausea Ocular hypertension Osteoporosis Vertigo Vomiting Weight gain Unknown frequency Abdominal distension Adrenal suppression Allergic reactions (including anaphylaxis) Arterial thrombosis Aspergillosis Bruising Candidiasis Cardiomyopathy Cleft palate Corneal or scleral thinning Cushing's syndrome Edema Esophageal ulcer Facial plethora Glaucoma Growth stunting (in children) Herpes zoster Hypernatremia Hypertriglyceridemia Hypocalcemia Hypokalemia Intracranial hypertension (long-term treatment) Leukocytosis Mania Mucormycosis Pancreatitis (inflammation of the pancreas) Papilledema Peptic ulcer Protein catabolism (causing nitrogen depletion) Psychological dependence Psychosis Seizures Skin atrophy Striae Telangiectasia Thromboembolism Venous thrombosis Vertebral collapse Withdrawal Sudden withdrawal after long-term treatment with corticosteroids can lead to: Adrenal insufficiency Arthralgia Conjunctivitis Death Fever Hypotension Myalgia Nodule (medicine) (painful, itchy skin condition) Rhinitis Weight loss Interactions Known drug interactions include: Inducers of hepatic microsomal enzymes such as barbiturates, phenytoin, and rifampicin can reduce the half-life of dexamethasone. Cotreatment with oral contraceptives can increase its volume of distribution. Pharmacology Pharmacodynamics As a glucocorticoid, dexamethasone is an agonist of the glucocorticoid receptor (GR). It is highly selective for the GR over the mineralocorticoid receptor (MR), and in relation to this, has minimal mineralocorticoid activity. This is in contrast to endogenous corticosteroids like cortisol, which bind to and activate both the GR and the MR. Dexamethasone is 25 times more potent than hydrocortisone (cortisol) as a glucocorticoid. Its affinity (Ki) for the GR was about 1.2nM in one study. The activation of the GR by dexamethasone results in dose-dependent suppression of the hypothalamic–pituitary–adrenal axis (HPA axis) and of production of endogenous corticosteroids by the adrenal glands, thereby reducing circulating endogenous concentrations of corticosteroids like cortisol and corticosterone. Dexamethasone poorly penetrates the blood–brain barrier into the central nervous system due