Rajiv Memorial Education Society’s College of Pharmacy, Kalburagi-585102.
Background: Iatrogenic Cushing’s syndrome is a disorder characterized by chronic exposure to high levels of exogenous corticosteroids, most commonly dexamethasone. While corticosteroids are widely prescribed for their anti-inflammatory and immunosuppressive effects, their inappropriate or prolonged use—particularly in settings where medications are accessible without proper medical oversight—can lead to severe endocrine and systemic complications. These include characteristic physical changes such as moon face, central obesity, skin thinning, and muscle weakness, along with more serious consequences like metabolic derangements, opportunistic infections, osteoporosis, and adrenal suppression. In India and other developing countries, steroid misuse is prevalent due to over-the-counter availability and prescriptions by non-specialist practitioners, making iatrogenic Cushing’s syndrome an important yet preventable public health concern. Case Presentation: We report a case of a 49-year-old female admitted with vomiting, abdominal pain, and diarrhea for two days. Further evaluation revealed classical features of Cushing’s syndrome, including moon face, central obesity, and pedal edema. Laboratory and imaging studies indicated enter colitis, sepsis, acute kidney injury, and elevated serum cortisol levels. The patient had been taking dexamethasone 0.5 mg daily and diclofenac sodium 50 mg twice daily for over three years, prescribed by a local RMP. She was treated with IV fluids, antibiotics, supportive medications, and electrolyte replacement. Conclusion: This case highlights the critical role of clinical pharmacists in identifying and preventing steroid misuse, educating patients and healthcare providers, ensuring rational drug therapy, and assisting in the safe tapering and monitoring of corticosteroid use. Their involvement is vital in reducing the burden of preventable drug-induced conditions, especially in resource-limited settings.
Glucocorticoids such as dexamethasone are widely utilized for their potent anti-inflammatory and immunosuppressive properties in the management of a variety of conditions including autoimmune diseases, allergies, and malignancies. However, prolonged or high-dose use of these agents can lead to significant adverse effects, one of the most concerning being iatrogenic Cushing’s syndrome (ICS) [1,2]. ICS is characterized by clinical manifestations such as moon face, central obesity, striae, muscle weakness, and metabolic disturbances due to chronic exposure to exogenous corticosteroids [3]. The indiscriminate or unsupervised use of dexamethasone, particularly in outpatient settings or over-the-counter availability, contributes significantly to the incidence of iatrogenic Cushing’s syndrome [4]. Despite being preventable, this condition continues to be reported across diverse patient populations, often with delayed diagnosis due to overlapping symptoms with other endocrine disorders [5]. Moreover, long-term glucocorticoid therapy not only predisposes patients to metabolic complications but also increases the risk of opportunistic infections, adding to the clinical burden and complexity of management. This case report aims to highlight a clinical presentation of dexamethasone-induced iatrogenic Cushing syndrome, drawing attention to the importance of cautious steroid use and early recognition of its complications.
Case Presentation
A 49-year-old female patient was admitted to the High Dependency Unit (HDU), with complaints of vomiting, abdominal pain, and loose stools for the past two days. The episodes were multiple, watery in consistency, foul-smelling, and non-blood-tinged. The patient was apparently healthy until four months ago, when she began gaining weight and developed facial puffiness and swelling in both upper and lower limbs. On general examination, she was found to have hypotension with a blood pressure of 90/60 mmHg, an elevated pulse rate of 90 bpm, respiratory rate of 20 breaths per minute, and SpO2 of 92%. Physical examination revealed characteristic signs such as moon face (facial edema), central obesity, and pedal edema.
Systemic examination findings included:
• Respiratory system (RS): Bilateral air entry present (B/L AE+).
• Cardiovascular system (CVS): S1 and S2 heart sounds heard; no murmurs.
• Central nervous system (CNS): Patient was conscious but disoriented.
• Per abdomen (P/A): Abdomen was soft with diffuse tenderness; no organomegaly noted.
Figure A: Facial puffiness with moon face appearance due to steroid therapy.
Figure B: Swelling of upper and lower limbs indicating generalized fluid retention.
Upon further inquiry, her attenders revealed that she had been suffering from bilateral knee pain and had been under treatment by a local RMP (Registered Medical Practitioner). She had been taking Tab. Dexamethasone 0.5 mg once daily and Tab. Diclofenac sodium 50 mg twice daily for the past three years. Routine laboratory investigations were advised, including CBC, HIV, CRP, HBsAg, LFT, RFT, serum electrolytes, stool culture, blood culture, procalcitonin test, and serum cortisol levels. Radiological investigations included a chest X-ray, abdominal and pelvic ultrasound (USG), and a CT scan of the brain.
The laboratory results showed:
• Haemoglobin (Hb): 9.7 g/dL (low)
• Neutrophils: 79% (elevated)
• Lymphocytes: 14% (decreased)
• C-Reactive Protein (CRP): 127 mg/L (elevated)
• Blood Urea: 100 mg/dL (elevated)
• Serum Creatinine: 2.5 mg/dL (elevated)
• Potassium (K+): 2.63 mmol/L (decreased)
• SGOT: 46 IU/L (elevated)
• SGPT: 42 IU/L (elevated)
• Total Protein: 5.9 g/dL (decreased)
• Alkaline Phosphatase (ALP): 161 U/L (elevated)
• Serum Cortisol: 33.19 mcg/dL (elevated)
• Procalcitonin: 11 mcg/L (elevated)
The USG abdomen revealed findings suggestive of enterocolitis. Blood culture showed growth of Escherichia coli species.
Based on the clinical history, examination, and investigations, the patient was diagnosed with enterocolitis with sepsis and septic shock, acute kidney injury (AKI), and Cushing’s syndrome secondary to chronic steroid abuse.
Treatment:
On Day 1, the patient was started on intravenous fluids (Normal Saline and Ringer Lactate) at 100 mL/hr to correct dehydration and electrolyte imbalance. Antibiotic therapy included Inj. Ciprofloxacin IV 100 mL twice daily and Inj. Piperacillin-Tazobactam (Piptaz) 2.25 g in 50 mL NS twice daily. Supportive medications included Inj. Pantoprazole 40 mg once daily and Inj. Ondansetron (Emset) 4 mg twice daily. On Day 2, oral medications were initiated: Tab. Doxycycline 100 mg twice daily, Tab. Sporolac, Tab. Racecadotril 100 mg twice daily, along with continued supportive care including oral rehydration salts (ORS), Inj. Dexamethasone 8 mg once daily, and intravenous potassium chloride (KCl) 2 ampoules in 500 mL NS for hypokalemia correction.
DISCUSSION
Cushing’s syndrome resulting from prolonged exogenous corticosteroid use, particularly dexamethasone, is a well-documented but often under-recognized condition. The clinical features commonly include moon face, central obesity, muscle weakness, hypertension, and metabolic abnormalities. In our case, the patient presented with classical signs of iatrogenic Cushing’s syndrome along with severe complications such as enterocolitis, sepsis, septic shock, and acute kidney injury — likely precipitated by immunosuppression secondary to chronic steroid abuse. This case closely mirrors the report by Zaveri et al. [2], where a patient with prolonged dexamethasone intake developed classical features of Cushing’s syndrome including moon facies, central obesity, and pedal edema. Similar to our patient, their case also involved long-term unsupervised use of dexamethasone prescribed by a non-specialist, emphasizing the need for better regulation of steroid prescriptions and public awareness about their adverse effects. Another similar case is documented by Gireesh KM et al. [4], who reported a patient with features of iatrogenic Cushing’s syndrome secondary to over-the-counter dexamethasone use. In that case, the individual developed metabolic disturbances and immunosuppression, predisposing them to infections. Our case showed more advanced complications, including septic shock and acute kidney injury, highlighting the potential severity of outcomes when early signs are missed or ignored. Both referenced cases reinforce the clinical trajectory observed in our patient and underscore the dangers of long-term glucocorticoid therapy without appropriate monitoring. Furthermore, they advocate for routine screening for adrenal suppression in patients on chronic steroid therapy and the importance of educating primary care practitioners and rural healthcare providers about the risks associated with unsupervised corticosteroid use.
CONCLUSION
This case highlights the serious consequences of long-term, unsupervised dexamethasone use, leading to iatrogenic Cushing’s syndrome complicated by enterocolitis, sepsis, and acute kidney injury. It underscores the importance of early recognition and appropriate management of steroid-induced complications. The clinical pharmacist plays a pivotal role in such cases by ensuring rational drug use, identifying potential adverse drug effects, educating patients and caregivers about the risks of prolonged corticosteroid use, and monitoring therapy through regular follow-ups. In rural and semi-urban settings, where patients often receive treatment from unqualified practitioners, the clinical pharmacist can serve as a crucial link in the healthcare team to promote medication safety and prevent steroid misuse. Furthermore, pharmacists can aid in dose tapering, managing drug interactions, and supporting the interdisciplinary team in infection control and electrolyte management, ultimately contributing to improved patient outcomes.
REFERENCES
Kailash Bhovi*, Shantveer Halcher, Cushing’s Syndrome Induced by Prolonged Dexamethasone Therapy: A Clinical Case Report, Int. J. of Pharm. Sci., 2025, Vol 3, Issue 10, 1248-1252 https://doi.org/10.5281/zenodo.17340557
10.5281/zenodo.17340557
