Steroid psychosis mechanism

Sacks et al. (2005) reported the case of a 72-year-old man, described as professionally successful, intelligent, and cultivated, with polymyalgia rheumatica, who after being treated with prednisone developed a psychosis and dementia , which several behavioral neurology and neuropsychiatry consultants initially diagnosed as early dementia or Alzheimer's disease . [12] Large dosage variations in the patient's medication (including a self-increased dosage from 10 mg/day to as much as 100 mg/day for at least 3 months) produced extreme behavioral changes, from missed appointments to physical altercations, and eventually admission to a psychiatric ward and later to a locked Alzheimer facility. During this time, neuropsychological testing showed a decline in the patient's previously superior IQ as well as deficits in memory, language, fluency, and visuospatial function, which given the patient's age was considered to be compatible with early dementia. When the steroid treatment ended after a year, the patent's confusion and disorganized appearance stopped immediately. Within several weeks, testing showed strong improvement in almost all cognitive functions. His doctors were surprised at the improvement, since the results were inconsistent with a diagnosis of dementia or Alzheimer's. Testing after 14 months showed a large jump in Full Scale IQ from 87 to 124, but mild dysfunction in executive function, memory, attentional control, and verbal/nonverbal memory remained. [12]

The most commonly used AAS in medicine are testosterone and its various esters (but most commonly testosterone undecanoate , testosterone enanthate , testosterone cypionate , and testosterone propionate ), [53] nandrolone esters (most commonly nandrolone decanoate and nandrolone phenylpropionate ), stanozolol , and metandienone (methandrostenolone). [1] Others also available and used commonly but to a lesser extent include methyltestosterone , oxandrolone , mesterolone , and oxymetholone , as well as drostanolone propionate , metenolone (methylandrostenolone), and fluoxymesterone . [1] Dihydrotestosterone (DHT; androstanolone, stanolone) and its esters are also notable, although they are not widely used in medicine. [54] Boldenone undecylenate and trenbolone acetate are used in veterinary medicine . [1]

Systemic lupus erythematosus can cause inflammation of virtually any tissue of the body. Depending on the tissue affected and the intensity of the inflammation, the function of the organs can be disturbed. Brain inflammation in lupus is referred to as cerebritis.

When lupus affects the brain, it can lead to headache , seizure, stroke , or psychosis. Psychosis is a serious mental disorder featuring defective thought processes, frequently with delusions or hallucinations. Psychosis is not common in patients with lupus and occurs when the disease is first diagnosed in under 3% of patients. It occurs at sometime during the course of the disease in 5% of patients. Moreover, though infrequent, psychosis is now used by doctors as a classical criteria for the diagnosis of systemic lupus.

The psychosis of lupus is typically treated with antipsychotic medications, high doses of cortisone-related (steroid) medications, such as prednisone or prednisolone , and powerful immune suppression drugs, such as cyclophosphamide (Cytoxan).

It should be noted that steroid medications, such as prednisone and prednisolone, can cause psychosis! (This is not common, but can occur.) Therefore, a patient with lupus could develop psychosis as a toxic side effect of the prednisone. For example, a lupus patient taking prednisone for pleurisy could develop psychosis as a side effect of the drug.

Psychosis, when it is a result of the lupus disease itself, is referred to as one of the neuropsychiatric manifestations of lupus.

Corticosteroid myopathy presents as weakness and wasting of the proximal limb and girdle muscles and is generally reversible following cessation of therapy.

Corticosteroids inhibit intestinal calcium absorption and increase urinary calcium excretion leading to bone resorption and bone loss. Bone loss of 3% over one year has been demonstrated with prednisolone 10 mg per day. Postmenopausal females are particularly at risk for loss of bone density. Sixteen percent of elderly patients treated with corticosteroids for 5 years may experience vertebral compression fractures. One author reported measurable bone loss over two years in women on concomitant therapy with prednisolone mg per day and tamoxifen. [ Ref ]

Steroid psychosis mechanism

steroid psychosis mechanism

Corticosteroid myopathy presents as weakness and wasting of the proximal limb and girdle muscles and is generally reversible following cessation of therapy.

Corticosteroids inhibit intestinal calcium absorption and increase urinary calcium excretion leading to bone resorption and bone loss. Bone loss of 3% over one year has been demonstrated with prednisolone 10 mg per day. Postmenopausal females are particularly at risk for loss of bone density. Sixteen percent of elderly patients treated with corticosteroids for 5 years may experience vertebral compression fractures. One author reported measurable bone loss over two years in women on concomitant therapy with prednisolone mg per day and tamoxifen. [ Ref ]

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