Corticosteroids are the steroid hormones, which are mainly used in the treatment of rheumatoid arthritis, osteoarthritis, rheumatic fever, gout, allergic reactions, renal disease, haematological disorders and shock. The use of glucocorticoids in supra physiological doses for more than 2-3 weeks causes a number of undesirable effects. Most of the adverse effects are extension of pharmacological actions such as hyperglycaemia, Cushing syndrome, oedema, hypertension, CCF, steroid myopathy, glaucoma, various fungal infections etc. Diclofenac is a Non-Steroidal Anti Inflammatory Drug; it is high potent anti-inflammatory and analgesic drug. The mechanism of acute bronchitis due to the diclofenac still not known but increased production of leukotrienes may cause bronchitis. Here we report a 45 years old female patient was experienced moon face, pedal oedema, increased RBS, LDL, total cholesterol, abdominal striae, acute bronchitis and increased blood presser due to the prolonged using of corticosteroids and NSAIDs since 2 years regularly.

1. www.iajpr.com
Page1404
Indo American Journal of Pharmaceutical Research, 2015 ISSN NO: 2231-6876
A CASE REPORT ON CORTICOSTEROIDS INDUCED CUSHING'S SYNDROME AND
NSAIDS INDUCED ACUTE BRONCHITIS
R. Siddarama*
, Y. Hrushikesh Reddy, Gangula Amareswara Reddy, P Gowtham, H Shree Hari, R
Phanindra Nayak, M. Javeed Baig
P Rami Reddy Memorial College of Pharmacy, Kadapa, Andhra Pradesh, India – 516003.
Corresponding author
R Siddarama
Department of Clinical Pharmacy,
P Rami Reddy Memorial College of Pharmacy,
Kadapa, Andhra Pradesh, India - 516003
siddaramapharmd22@gmail.com
+917306209795
Copy right © 2015 This is an Open Access article distributed under the terms of the Indo American journal of Pharmaceutical
Research, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
ARTICLE INFO ABSTRACT
Article history
Received 15/04/2015
Available online
30/04/2015
Keywords
Corticosteroids,
NSAIDs,
Cushing’s Syndrome,
Acute Bronchitis,
ADR Analysis,
Re-Challenge
And De-Challenge.
Corticosteroids are the steroid hormones, which are mainly used in the treatment of
rheumatoid arthritis, osteoarthritis, rheumatic fever, gout, allergic reactions, renal disease,
haematological disorders and shock. The use of glucocorticoids in supra physiological doses
for more than 2-3 weeks causes a number of undesirable effects. Most of the adverse effects
are extension of pharmacological actions such as hyperglycaemia, Cushing syndrome,
oedema, hypertension, CCF, steroid myopathy, glaucoma, various fungal infections etc.
Diclofenac is a Non-Steroidal Anti Inflammatory Drug; it is high potent anti-inflammatory
and analgesic drug. The mechanism of acute bronchitis due to the diclofenac still not known
but increased production of leukotrienes may cause bronchitis. Here we report a 45 years old
female patient was experienced moon face, pedal oedema, increased RBS, LDL, total
cholesterol, abdominal striae, acute bronchitis and increased blood presser due to the
prolonged using of corticosteroids and NSAIDs since 2 years regularly.
Please cite this article in press as R Siddarama et al. A Case Report on Corticosteroids Induced Cushing's Syndrome And Nsaids
Induced Acute Bronchitis. Indo American Journal of Pharm Research.2015:5(04).

2. www.iajpr.com
Page1405
Vol 5, Issue 04, 2015. R Siddarama et al. ISSN NO: 2231-6876
INTRODUCTION
Cushing syndrome is defined as abnormality in high blood levels of cortisol or other exogenous compounds of
glucocorticoids. This can be iatrogenic or endogenous cortisol secretion, due to the either an adrenal tumour or hyper secretion of
adrenocorticotropic hormone by the pituitary gland [1]. The pathophysiological mechanism differs depending upon the cause of
Cushing syndrome [2]. The commonly occurring cause for Cushing syndrome is administration of exogenous glucocorticoid
hormones on prolonged use and especially used in the treatment of lymph proliferative disorders at levels of higher doses [3]. the most
common systemic side effects of administration of glucocorticoids for prolonged use which includes Cushing’s syndrome,
hypertension, cataract, skin atrophy, dyslipidaemia, hypo-thalamo-pituitary-adrenal axis suppression, failure to thrive, glaucoma,
striae and a predisposition to life-threatening infections [4].
CASE REPORT
A 45 Years old female patient was admitted in general medicine department RIMS, Kadapa with the chief complaints of
facial puffiness, swelling of limbs, abdominal distension and striaes, shortness of breath and with gradually progressing fever since 1
month. and Present history of the patient shows that the decreased urine output and constipation since 1 month. As she was a known
patient with rheumatoid arthritis, she was prescribed with corticosteroids (prednisolone) and Non-Steroidal Anti-inflammatory drugs
(diclofenac) and was on regular treatment for past 2 years. on general examination the patient was conscious and coherent but on
physical appearance was looking weak, pale and her vitals were as follows BP-150/90 mm of Hg, PR-84bpm, CVS-S1,S2+ ,RS-
Wheezing’s+, CNS- no abnormality present, P/A- distension+, striated.
Investigations:
On laboratory examination of the patient, results were found to be as follows, Blood profile: Hb-10 gm%, TC-9000cells/mm3
, Differential count- polymorphs-55% , Lymphocytes- 43%, Esinophills-2%.Random Blood Sugar-143mgs/dl, Blood urea-20mgs/dl,
Total Cholesterol-254mgs/dl, HDL-50mgs/dl, LDL-182 mgs/dl, VLDL-24mgs/dl, TG-118mgs/dl. Liver Function test: serum
creatinine-0.8mgs/dl, Total Bilirubin-1.5mgs/dl, Direct Bilirubin-0.8mgs/dl, alkaline phosphatase-80IU/L, SGOT-41U/L, SGPT-
35U/L, Total Protiens-7.2g/dl. TSH-1.5micro IU/ml. USG Abdomen- Hepatomegaly with fatty changes and chest x-ray- acute
bronchitis. So based on subjective and objective evaluation patient have experienced Cushing’s syndrome and acute bronchitis due to
the prolonged usage of corticosteroids(prednisolone) and NSIDS(diclofenac). Clinical evaluation was done and patient was treated
symptomatically with parenteral diuretics(lasix 40mg iv bid), parenteral anti-ulcer drug (pantaprazole 40mg iv bid), parenteral
bronchodilator(deriphylline 110mg iv bid)oral vitamin supplements (calcium 100mg od) and syrup purgative (lactulose 10ml bid).
ADR Analysis
Causality assessment:
After collecting the past and current history from the patient, ADR Analysis was done by using naranjos scale, WHO-UMC,
karch and lasagna scales shown in Table: 1. the most suspected drug to produce Cushing’s syndrome and acute bronchitis were due to
the Corticosteroids and NSAID'S. Here we also performed severity, predictability and preventability scales shown in Table 2.
Re-challenge:
Patient had similar complaints in the past, so for confirmatory purpose we reintroduced the same amount of the drugs
(prednisolone-60mg bd and diclofenac-50mg bd) 1 month back. Then she was experienced with facial puffiness, swelling of both
limbs(shown in figure; 1), abdominal distension, abdominal striae, increased RBS(143mg/dl), LDL(182mg/dl), total
cholesterol(254mg/dl), blood pressure(150/90mmof hg) and acute bronchitis (shown in figure: 2).
De-challenge:
After complete evaluation of the re-challenge information the suspected drugs were stopped administrating.
Figure-1: Facial puffiness, swelling of both limbs.

3. www.iajpr.com
Page1406
Vol 5, Issue 04, 2015. R Siddarama et al. ISSN NO: 2231-6876
Figure - 2: Acute bronchitis.
Table1: Causality assessment of suspected drugs.
S.NO
ADR SCALES
(CAUSALITY ASSESSMENT)
SUSPECTED DRUGS CAUSING ADR
PREDNISOLONE DICLOFENAC
1. Naranjo's scale Definite ADR (score - 9) Definite ADR (score - 9)
2. WHO-UMC Scale Certain Certain
3 Karch and lasagna Definite ADR Definite ADR
Table2: Severity, Predictability and Preventability scales.
CAUSALITY ASSESSMENT
SUSPECTED DRUGS CAUSING ADR
PREDNISOLONE DICLOFENAC
Severity Moderate level 4(b) Severe, level 5
Predictability Predictable type-A Predictable type- B
Preventability Not Preventable Not Preventable
DISCUSSION
Cushing syndrome results from a set of clinical presentation caused by hyper-cortisolism [5]. Cushing syndrome may be due
to the endogenous causes such as ectopic ACTH production, pituitary tumour, and exogenous causes like exogenously administration
of corticosteroids. The most common cause of Cushing syndrome is exogenous administration of glucocorticoids than the Endogenous
Cushing syndrome [6]. Cushing syndrome can be broadly divided into two types depending upon the plasma level of ACTH: ACTH
dependent Cushing syndrome and ACTH–independent Cushing syndrome. Cushing’s syndrome due to exogenous corticosteroids
administration is variably described as steroid- induced Cushing’s syndrome, exogenous Cushing’s, or iatrogenic Cushing syndrome
[7]. The common clinical presentations of Cushing’s syndrome are obesity, which implies in the face, neck, spinal canal, trunk, and
abdomen [8]. Fat deposition, in the temporal fossae, cheeks result in "moon" face and in the back of neck results in "buffalo hump".
The enlarging trunk, breasts, and abdomen due to stretching of the fragile skin it may leads to development of broad, reddish-purple
striae. The red-purple livid striae are most commonly found over the abdomen, but are also present on the arms, upper thighs and
breasts. This striaes are greater than 1 cm in width which is typical, and almost pathognomonic [9]. In the patients with Cushing
syndrome, 50% of them may develop Psychiatric abnormalities in such patients. Common psychiatric abnormalities which comprise:
lethargy, paranoia, agitated depression, overt psychosis, insomnia, irritability, anxiety, emotional liability, and panic attacks [10].
CONCLUSION
Corticosteroids are having more ADRs (adverse drug reaction) profile. So, proper information about side effects should be
provided to the patients and precautions should be taken and regularly monitor the patients’ blood cortisol levels who are receiving the
oral corticosteroids.
CONFLICT OF INTERESTS
The authors have declared that they have no conflict of interest.

4. www.iajpr.com
Page1407
Vol 5, Issue 04, 2015. R Siddarama et al. ISSN NO: 2231-6876
REFERENCES
1. Miller WL. The adrenal cortex and its disorders. In: Brook CG, Hind marsh PC, editors. Clinical pediatric endocrinology. 4th ed.
Oxford: Blackwell Science; 2001. p. 321-76.
2. Soffer LJ, Iannaccone A, Gabrilove JL. Cushing's syndrome: A study of fifty patients. Am J Med 1961; 30:129.
3. Siklar Z, Bostancı I, Atli Ö, Dallar Y. An infantile Cushing syndrome due to misuse of topical steroid. Pediatr Dermatol 2004;
21:561-3.
4. West DP, Micali G. Principles of paediatric dermatological therapy. In: Harper J, Oranje A, Prose N, editors. Textbook of
Pediatric Dermatology. 1st ed. London, Blackwell Science Ltd; 2000. p. 1731-42.
5. Newell-Price J, Bertagna X, Grossman AB, et al. Cushing’s syndrome. Lancet 2006; 367(9522): 1605-17.
6. Steffensen C, Bak IS, Rubeck KZ, Jorgensen JO. Epidemiology of Cushing's syndrome. Neuroendocrinology 2010; 92(Suppl 1):
1-5.
7. Hopkins RL, Leinung MC. Exogenous Cushing’s syndrome and glucocorticoid withdrawal. Endocrinol Metab Clin North Am
2005; 34: 371-84, ix.
8. Wajchenberg BL, Bosco A, Marone MM, et al. Estimation of body fat and lean tissue distribution by dual energy X-ray
absorptiometry and abdominal body fat evaluation by computed tomography in Cushing’s disease. J Clin Endocrinol Metab 1995;
80: 2791-4.
9. Mountjoy KG. The human melanocyte stimulating hormone receptor has evolved to become super-sensitive to melanocortin
peptides. Mol Cell Endocrinol 1994; 102: R7-11.
10. Kelly WF. Psychiatric aspects of Cushing's syndrome. QJM 1996; 89: 543-51.
54878478451150426