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CASE REPORT
Ahead of print publication  

A case of steroid induced psychosis


 Department of Pyschiatry, Centre of Excellence in Mental Health, ABVIMS and Dr. Ram Manohar Lohia Hospital, New Delhi, India

Date of Submission10-Sep-2021
Date of Decision26-Sep-2021
Date of Acceptance29-Oct-2021
Date of Web Publication15-Mar-2022

Correspondence Address:
Ashish Narvariya,
168, 2nd Floor, Site-1, M-Block, New Rajinder Nager, New Delhi - 110 060
India
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aip.aip_116_21

  Abstract 


Corticosteroids are one of the widely used drugs in medicine; however, the use of steroids is associated with undesirable side effects. We present here a case of 18-year-old girl with nephrotic syndrome who developed auditory hallucinations, muttering to self, social withdrawal, and fearfulness after she was given steroids for her treatment. Steroids were tapered and stopped, and she was started on olanzapine after which she improved completely. Although a relationship between hypothalmic–pitutary axis and psychosis has been clearly established, still there is a dearth of literature in the area of steroid-induced psychosis and its management.

Keywords: Hypothalamic pituitary axis, psychosis, steroids



How to cite this URL:
Batra S, Narvariya A, Kandpal M. A case of steroid induced psychosis. Ann Indian Psychiatry [Epub ahead of print] [cited 2022 Dec 2]. Available from: https://www.anip.co.in/preprintarticle.asp?id=339659




  Introduction Top


Corticosteroids are one of the widely used drugs in medicine for immunologic and inflammatory disorders, systemic lupus erythematous and systemic vasculitis, nephrotic syndrome, asthma, cancer, etc., However, the use of steroids is associated with undesirable side effects including among others metabolic, endocrine, digestive, immunological, ophthalmological, dermatological, and neuropsychiatric disorders.[1] Corticosteroids are associated with changes in the temporal lobe, detected by structural, functional, and spectroscopic imaging.[1],[2]

In DSM-V, steroid-induced psychosis is classified under substance or medication-induced psychosis.[3] It is an uncommon dose-dependent disorder more prevalent in persons having predisposition for psychosis or are on medications that will augment the effect of the steroids.[3] The disease is possibly underreported in the general population as not all of the psychoses are severe, nor necessarily long lasting, and mostly they resolve without intervention.[3]

Corticosteroid-induced symptoms mostly occur during the first few weeks of therapy and usually resolve with discontinuation or dosage reduction of corticosteroids.[1]


  Case Report Top


We present here a case of a 18-year-old single Christian female with symptoms of generalized anasarca with serum albumin as 1.6 g/dl, 24-h urinary protein 216.8 mg/day in 300 ml of urine, serum creatinine 1.5 mg/dl, lipid profile showing 399 mg/dl of cholesterol, triglycerides 275 mg/dl, high-density lipoprotein = 55 mg/dl, very-low-density lipoprotein = 55 mg/dl, Calculated Low Density Cholesterol (CLDL) = 289.0 mg/dl diagnosed as nephrotic syndrome, following which renal biopsy was done with features suggestive of minimal change disease. She was started on oral dexamethasone which was gradually built up to 20 mg over a week. Within 2 days of administering dexamethasone, the patient was quieter than usual and would remain lost for hours while muttering to herself with disturbed sleep. She also complained of hearing male voices which would tell her that she and her family members would be killed in an encounter.

On mental status examination, the patient was noted to be fearful but cooperative and attentive. She was muttering to herself during the interview. In addition, she was withdrawn with poor eye contact and would smile inappropriately. His speech was not spontaneous and decreased in productivity but was coherent with normal rate and volume. She was alert and oriented to person, place, and situation. She had no aggressive or self-harm behavior. Her mood was reported as “paranoid” and her affect was rather silly. She denied suicidal or homicidal thinking, intentions, or plans or thoughts of wanting to hurt self or others. However, she reported to have auditory hallucinations, in which she heard male voices threatening her and her family members.

Patient had no prior psychiatric or drug history and after a clean brain scan, normal routine investigations such as complete blood count, liver function test, kidney function test, Serum Electrolytes (SE), random blood sugar, thyroid profile, Vitamin B12, folic acid, drug screen, and Anti-Nuclear Antibodies (ANA); the patient was diagnosed as steroid-induced psychosis. Gradually, steroids were tapered and eventually stopped. As per informant, the patient achieved premorbid level within a week after stopping steroids.

After a month, steroids were reintroduced in view of Minimal Change Disease, but this time more slowly with more gradual increments in dose. When Dexamethasone reached up to 10 mg within a week, then patient again started having muttering to self, social withdrawal, fearfulness, and auditory hallucinations as before. The patient was observed for a week, and the patient had similar symptoms throughout which confirmed our diagnosis. Steroids were tapered and stopped, and the patient was started on olanzapine 7.5 mg.

After 3 weeks, the patient had complete resolution of symptoms and was started on cyclophosphamide for minimal change disease.


  Discussion Top


The pathophysiology of steroid-induced psychosis is poorly understood but basically follows that of other diseases such as Cushing's or Addison's in that abnormalities of the hypothalamo–pituitary adrenal axis have the potential to result in mood disorders by activating the glucocorticoid receptors preferentially, as the synthetic steroids suppress the secretion of cortisol by the adrenal glands. There is thus an imbalance created between glucocorticoid stimulation and mineralocorticoid receptor stimulation due to the preferential selection. Thus, the cortisol pathway is disturbed leading to cognitive impairment and emotional disturbances.[3] A relationship between HPA axis dysfunction and psychosis, mood, or anxiety disorders has been clearly established.[4] In patients with increased levels of glucocorticoids such as in Cushing's syndrome or in exogenous treatment with synthetic glucocorticoids, an impairment in glucocorticoid receptors function could be responsible for their “depressogenic” effect.[1]

Lewis and Smith reviewed 79 cases of steroid-induced psychosis and found that disturbances in reality testing were reported in 71% of the 79 cases, but only 14% had a psychotic disorder without evidence of significant mood changes or features of a delirium.[5] They found that depression was present in 40.5%, mania in 28%, a mixed state in 7.5%, and delirium in 10% of these cases.[5] Another study found that mania and hypomania were reported most commonly (in 35% of cases), followed by depressive symptoms in 28% and psychotic reactions in 24%.[6] In most cases, any associated delirium commonly resolves within days and psychosis within a week, though depression or manic symptoms may last up to 6 weeks after discontinuation of steroids.[3]

This is a rare case presentation where even at low dose of steroids without any family history of psychiatric illness, at such a young age patient had steroid-induced psychosis. Previously, she never suffered from psychiatric symptoms requiring psychiatric consultation, hospitalization, or specific drugs.

There are no FDA-approved medications to manage steroid-induced neuropsychiatric symptoms. Therefore, treatment is based on anecdotal evidence and a few case series and case reports. However, the first step in managing any steroid-induced psychiatric syndrome is to reduce the dosage of the medication to that of <40 mg/day of prednisone or its equivalent, and ideally to stop the drug, if possible. About three-fourths of psychiatric symptoms will resolve on cessation alone.[7],[8] Lewis and Smith found that approximately 90% of patients treated with a taper only achieved recovery.[5] Eighty-four percent of those treated with neuroleptics recovered.[9]

As previously reported in the literature and the present case indicate that most patients with a steroid-induced psychiatric syndrome experience a complete recovery, although a small percentage of patients have persistent symptoms. The literature also indicates that suicide potential must be assessed carefully in these patients. Depending on the clinical picture, treatment with steroid taper, neuroleptics, or electroconvulsive therapy, is generally effective in these patients.[9]

Minimizing the dose of corticosteroids is the primary preventive strategy with the goal of maintaining a 40 mg daily dose of prednisone or its equivalent since dosing plays a significant role in the development of neuropsychiatric symptoms. Patients who are at higher risk for psychiatric complications, especially those with a damaged blood–brain barrier and those with hypoalbuminemia, which increases the risk by a factor of two,[10] should be carefully considered for steroid therapy. Drugs that may increase the circulating levels of corticosteroids should also be avoided.[9]

Hence, it is important to detect early steroid psychosis and to decide whether treatment with steroids should be stopped or not or a strategy of dose reduction combined with a mood stabilizer or antipsychotic treatment such as haloperidol or chlorpromazine needs to be introduced.[2]

Medication cessation or dosage reduction should always be the first line of treatment and then antipsychotics could be added.[9] However, further research is needed to determine whether such medication hastens or causes symptom resolution, it would appear to contain symptoms, as it had an impressive effect in the patient described above.[9]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initial will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Airagnes G, Rouge-Maillart C, Garre JB, Gohier B. Homicide and associated steroid acute psychosis: A case report. Case Rep Med 2011;2011:564521.  Back to cited text no. 1
    
2.
Brown ES. Effects of glucocorticoids on mood, memory, and the hippocampus. Treatment and preventive therapy. Ann N Y Acad Sci 2009;1179:41-55.  Back to cited text no. 2
    
3.
Janes M, Kuster S, Goldson TM, Forjuoh SN. Steroid-induced psychosis. Proc (Bayl Univ Med Cent) 2019;32:614-5.  Back to cited text no. 3
    
4.
Bradley AJ, Dinan TG. A systematic review of hypothalamic-pituitary-adrenal axis function in schizophrenia: Implications for mortality. J Psychopharmacol 2010;24:91-118.  Back to cited text no. 4
    
5.
Lewis DA, Smith RE. Steroid-induced psychiatric syndromes. J Affect Disord 1983;5:319-32. Available from: https://linkinghub.elsevier.com/retrieve/pii/0165032783900228. [Last accessedon 2020 Nov 21].  Back to cited text no. 5
    
6.
Sirois F. Steroid psychosis: A review. Gen Hosp Psychiatry 2003;25:27-33.  Back to cited text no. 6
    
7.
The Boston Collaborative Drug Surveillance Program. Acute adverse reactions to prednisone in relation to dosage. Clin Pharmacol Ther 1972;13:694-8.  Back to cited text no. 7
    
8.
West S, Kenedi C. Strategies to prevent the neuropsychiatric side-effects of corticosteroids: A case report and review of the literature. Curr Opin Organ Transplant 2014;19:201-8.  Back to cited text no. 8
    
9.
Gable M, Depry D. Sustained corticosteroid- induced mania and psychosis despite cessation: A case study and brief literature review. Int J Psychiatry Med 2015;50:398-404. doi:10.1177/0091217415612735.  Back to cited text no. 9
    
10.
Chau SY, Mok CC. Factors predictive of corticosteroid psychosis in patients with systemic lupus erythematosus. Neurology 2003;61:104-7.  Back to cited text no. 10
    




 

 
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