LETTER TO EDITOR
Year : 2014 | Volume
: 1 | Issue : 3 | Page : 236--238
Steroid induced psychosis in dermatological practice
Pravesh Yadav1, Vibhu Mendiratta1, Taru Garg1, Kishore Kumar2,
1 Department of Dermatology and Sexually Transmitted Diseases, Lady Hardinge Medical College and Sucheta Kriplani Hospital, Shaheed Bhagat Singh Marg, New Delhi, India
2 Department of Psychiatry, Lady Hardinge Medical College and Sucheta Kriplani Hospital, Shaheed Bhagat Singh Marg, New Delhi, India
RZ-97, Phase-III, Prem Nagar, Najafgarh, New Delhi - 110 043
|How to cite this article:|
Yadav P, Mendiratta V, Garg T, Kumar K. Steroid induced psychosis in dermatological practice.Astrocyte 2014;1:236-238
|How to cite this URL:|
Yadav P, Mendiratta V, Garg T, Kumar K. Steroid induced psychosis in dermatological practice. Astrocyte [serial online] 2014 [cited 2021 Dec 1 ];1:236-238
Available from: http://www.astrocyte.in/text.asp?2014/1/3/236/157770
Steroids are commonly prescribed by dermatologists. Steroids have been implicated in a variety of neuropsychiatric side effects. The psychiatric signs, symptoms and syndromes associated with corticosteroid treatment include (DSM-IV substance-induced) mood disorders (hypomania, mania, mixed states, depression), anxiety and panic disorder, delirium, suicidal thinking and behavior in the context of affective syndromes or delirium, aggressive behavior, insomnia and agitation with clear consciousness, depersonalization, dementia; and isolated cognitive impairments (impaired attention, concentration, memory and word finding difficulties). We herein report two patients who developed psychosis as an adverse effect to different formulations, dose, duration and indication of systemic steroids.
A 30-year-old married female presented to the Emergency Department with multiple targetoid lesions over extremities including palms and soles along with extensive oro-genital, ocular erosions for a day, following intake of allopurinol for 2 weeks for rheumatoid arthritis. A diagnosis of allopurinol-induced erythema multiforme major was made after excluding herpes. Allopurinol was stopped and patient was started on oral antihistaminics along with intravenous fluids, however, the patient required injection dexamethasone 8 mg/intravenously/day in view of the sudden and severe progression of lesions all over her body in the next 24 h. Next day the patient developed unusual behavior in the form of agitation and confusion. She would point in air as if she was seeing something not visible to others in her vicinity. She would become fearful and apprehensive when someone, even her family members, approached her. Patient also complained of excessive salivation and severe headache. At times, she would tell her mother about seeing ants on her body and few men in black clothes around her. There were no similar complaints in the past or such history in her family members. Possibilities of infective etiology, seizure episode, head trauma, intracranial space occupying lesion (ICSOL) and recent use of any other drug or illicit substance like stimulant was ruled out. A psychiatric consultation was taken and mental status examination (MSE) of the patient confirmed disruptiveness and impulsivity; increased psychomotor activity; loss of contact to reality; increased speech volume and productivity; agitated affect; distorted and persecutory thoughts; auditory and visual hallucinatory experiences; impaired higher mental functions like attention, concentration and memory; intelligence adequate; judgment impaired and insight absent. Patient was diagnosed with the possibility of steroid-induced psychosis and she was put on tab risperidone 1 mg at bed time daily. Steroids were not stopped abruptly in view of life-threatening condition, instead it was planned to gradually taper it off over the next few days. Patient's symptoms showed improvement with treatment. The skin condition gradually improved over the next 2 weeks and steroids were tapered off. Risperidone was stopped gradually over next month without any relapse.
A 20-year-old unmarried male, diagnosed case of borderline tuberculoid leprosy with ulnar neuritis presented to emergency department with complaints of decreased sleep for 11 days, irrelevant and excessive talk including abusive language for 3 days. Since the morning of presentation, patient also developed aggressive behavior and violent anger outbursts. At night had difficulty in sleeping and was gradually getting unmanageable. There was no history of head trauma, loss of consciousness, seizure like episode or abuse of substance such as alcohol, stimulant, cannabis preceding the onset of behavioral symptoms. He did not have fever, vomiting or headache. There was no history of any pervasive deviation in mood (sadness or happiness) or auditory/visual hallucinatory experiences. Family history for any psychiatric illness was insignificant. Systemic evaluation was normal. MSE corroborated above clinical findings and in addition, showed increased psychomotor activity, loss of contact to reality, poor rapport; excessive and irrelevant speech; irritable affect; persecutory thoughts; illusionary experiences; impaired attention and concentration; adequate memory and intelligence; impaired judgment and absent insight. Computed tomography (CT) scan of head did not reveal any abnormality. On inquiry, it was found that he was receiving multibacillary antileprosy treatment for 4 months and was currently on 20 mg of prednisolone. Patient had been on 40 mg prednisolone, which had been tapered off presently to 20 mg. Patient was diagnosed as a case of steroid-induced psychosis and administered injection haloperidol and promethazine. Prednisolone was tapered to 10 mg and stopped after 2 weeks. Patient was continued on haloperidol and promethazine. Later, the patient developed rigidity and tremulousness in all four limbs, suggestive of extrapyramidal side effect due to haloperidol. Creatine phosphokinase (CPK) level was found raised to 1279 units/l (normal: Up to 171 units/l). Hence, the patient was shifted to oral olanzapine, trihexyphenidyl (THP) and lorazepam. He showed recovery in his deviant behavior and other symptoms with the treatment. After 2-3 weeks, THP was also tapered off but olanzapine was continued for next few months and then stopped. He did not develop any episodes in the follow up.
Glucocorticoids are widely prescribed for a variety of skin diseases and are known to cause a variety of neuropsychiatric as well as somatic side effects. The incidence of neuropsychiatric effects of steroids range from 2% to 60%, ,, reflecting the variability in definitions, the variability in dose, and the heterogeneous and unpredictable nature of steroid-induced neuropsychiatric reactions.
One of the common indications for steroids in dermatology is systemic lupus erythematosus (SLE). Central nervous system (CNS) lupus may by itself cause neuropsychiatric symptoms and, moreover, no single laboratory test is available to establish a definitive diagnosis of lupus cerebritis and to differentiate the same from steroid-induced manifestations. Corticosteroid-induced psychosis has been reported in 5% patients with SLE on prednisone on doses varying from 0.75 to 1 mg/kg/day, which may resolve after tapering down prednisone. , Hypoalbuminemia has been reported to be a predictive factor for steroid-induced psychosis. ,
However, there are no studies available evaluating and comparing the incidence of neuropsychiatric symptoms in dermatology patients receiving steroids vis-à-vis other diseases. This is of special interest because various dermatological diseases for which steroids are prescribed already have a significant psychological impact on the quality of life, which may predispose to neuropsychiatric effects of steroids. So, the incidence may be higher and clinical profile of manifestations may be varied when steroids are prescribed for dermatological disorders. Larger cohort studies are required to confirm this hypothesis.
The mechanisms underlying psychiatric symptoms largely remain unclear and include corticosteroid effects on dopaminergic and cholinergic systems, , decrease in serotonin release,  and toxic effects on hippocampal neurons. 
A strong dose-response relationship has been shown in patients receiving prednisone therapy.  However, since neuropsychiatric effects have been attributed to doses as low as 2.5 mg of prednisolone per day,  whether some difference in metabolism of steroids causes this variation is yet to be evaluated. We also observed steroid-induced psychosis triggered with two different dose regimens.
The onset of corticosteroid-induced neuropsychiatric symptoms may occur within hours of treatment initiation, as well as after the cessation of therapy. However, majority of reactions occur early in the course of corticosteroid treatment (i.e., within days). A prospective study reported that 86% patients developed symptoms within the first week of starting steroids; two-thirds of patients developed symptoms within 5 days.  The duration of neuropsychiatric effects is also highly variable; however, more than 90% of patients may recover from steroid-related neuropsychiatric manifestations within 6 weeks. 
Patients who did not experience psychiatric side effects with corticosteroids in the past may develop symptoms on subsequent exposure.  There is no clear evidence that a history of psychiatric disorders  or a family history of psychiatric illness  is a risk factor for glucocorticoid-associated neuropsychiatric effects. Female gender may be a risk factor for developing neuropsychiatric complications of steroids even after exclusion of cases of SLE and rheumatoid arthritis (diseases that occur more often in women) from the analysis.  However, the explanation for this finding is still elusive.
There is no clear evidence that any specific mode of corticosteroid administration either divided daily dose, alternate day dosage or high dose pulse therapy can reduce the incidence of psychiatric complications. ,
Currently, there are no Food and Drug Administration (FDA)-approved medications for the management of steroid-induced neuropsychiatric side effects. The first step in the treatment of corticosteroid-induced psychiatric symptoms is to discontinue the steroids, if possible, or to attempt to decrease the dose to less than the equivalent of 40 mg/day of prednisone. , A vast majority of patients treated only with a steroid taper may achieve clinical recovery. 
Use of low-dose antipsychotics generally produces fairly rapid resolution of corticosteroid-induced psychosis. Low-dose neuroleptic treatment has led to resolution of psychotic symptoms in 83% of patients.  Olanzapine has been proven to be effective in patients with corticosteroid-induced manic or mixed symptoms. 
Steroid-induced psychosis is a common condition, though seldom reported by the dermatologists. An active vigil must be exercised for steroid-induced psychiatric manifestations as oral steroids are frequently prescribed by the dermatologists. The baseline workup before starting steroids should essentially include a psychiatric evaluation in addition to hematological and biochemical investigations. Family members should be counseled about the common symptomatology of neuropsychiatric illness to prevent more severe manifestations.
We would like to conclude by saying that knowledge of early and subtle neuropsychiatric manifestations of steroid-induced psychiatric illness is essential and an active watch for the same must be maintained by the physician and the family members throughout the course of treatment or maybe even after the stoppage irrespective of the dose/duration/indication/mode for systemic steroid therapy.
|1||Lewis DA, Smith RE. Steroid-induced psychiatric syndromes. A report of 14 cases and a review of the literature. J Affect Disord 1983;5:319-32.|
|2||Bolanos SH, Khan DA, Hanczyc M, Bauer MS, Dhanani N, Brown ES. Assessment of mood states in patients receiving long-term corticosteroid therapy and in controls with patient-rated and clinician-rated scales. Ann Allergy Asthma Immunol 2004;92:500-5.|
|3||Boston Collaborative Drug Surveillance Program. Acute adverse reactions to prednisone in relation to dosage. Clin Pharmacol Ther 1972;13:694-8.|
|4||Chau SY, Mok CC. Factors predictive of corticosteroid psychosis in patients with systemic lupus erythematosus. Neurology 2003;61:104-7.|
|5||Appenzeller S, Cendes F, Costallat LT. Acute psychosis in systemic lupus erythematosus. Rheumatol Int 2008;28:237-43.|
|6||Black AC. Biochemical mechanisms of steroid-induced psychosis. N Y State J Med 1982;82:1024.|
|7||Gilad GM, Rabey JM, Gilad VH. Presynaptic effects of glucocorticoids on dopaminergic and cholinergic synaptosomes. Implications for rapid endocrine-neural interactions in stress. Life Sci 1987;40:2401-8.|
|8||Beshay H, Pumariega AJ. Sertraline treatment of mood disorder associated with prednisone: A case report. J Child Adolesc Psychopharmacol 1998;8:187-93.|
|9||Wolkowitz OM, Reus VI, Weingartner H, Thompson K, Breier A, Doran A, et al. Cognitive effects of corticosteroids. Am J Psychiatry 1990;147:1297-303.|
|10||Hong SI, Cho DH, Kang HC, Chung DJ, Chung MY. Acute onset of steroid psychosis with very low dose of prednisolone in Sheehan's syndrome. Endocr J 2006;53:255-8.|
|11||Hall RC, Popkin MK, Stickney SK, Gardner ER. Presentation of the steroid psychoses. J Nerv Ment Dis 1979;167:229-36.|
|12||Wollheim FA. Acute and long-term complications of corticosteroid pulse therapy. Scand J Rheumatol Suppl 1984;54:27-32.|
|13||Wysenbeek AJ, Leibovici L, Zoldan J. Acute central nervous system complications after pulse steroid therapy in patients with systemic lupus erythematosus. J Rheumatol 1990;17:1695-6.|
|14||Davis JM, Leach A, Merk BS, Janicak PG. Treatment of steroid psychoses. Psychiatr Ann 1992;22:487-91.|
|15||Goldman LS, Goveas J. Olanzapine treatment of corticosteroid-induced mood disorders. Psychosomatics 2002;43:495-7.|