TOPICAL STEROID INDUCED CUSHING SYNDROME
Hello everyone, I am a final year medical student. Recently I came across an interesting case in my clinical rotations.Here we discuss our individual patient's problems through series of inputs from available global online community of experts with an aim to solve those patient's clinical problems with collective current best evidence based inputs.
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This is a seemingly interesting case of a 22year old male who came with complaints of distension of abdomen and facial puffiness since 8 months. If my memory served me right I could only think of Cushing’s syndrome but I found it cryptic as to what might have been the cause with no known history of oral steroids. So, here goes my pursuit of finding the genesis of the disease.
HISTORY OF PRESENTING ILLNESS:
The patient was asymptomatic 1.5 years back then he developed red itchy ring like lesions over his thighs for which he heedlessly though intermittently applied over the counter clobeta GM for 7 months. He also took an ayurvedic syrup but all his efforts went in vain when he again started to notice a significant increase in his lesions and this time with an unusual increase in his weight from 50 to 70kgs in October 2019. He then went to hospital where he was diagnosed with tinea incognito and was prescribed antifungals.
Xyzal tablets
Ebernet cream
Sebafin cream
At his 1 month review in December he was prescribed itraconazole and ketoconazole.
The patient denied any kind of oral steriod usage which was a key point. He had no history of constipation or loose stools, fever, cough, abdominal pain, no history of hair loss or thining.
No h/o of hypertension, DM, thyroid, coronary artery disease, epilepsy and no h/o of body pains and delayed wound healing and no h/o of pedal edema emotional lability anorexia, easy fatiguability, no h/o of decreased vision , no h/o weakness, no h/o acne.
PERSONAL HISTORY
The patient is having a good appetite and mixed diet adequate sleep and bladder movements regular and he does not smoke or drink alcohol.
GENERAL EXAMINATION:
The patient is conscious coherent cooperative, has an obese build and moderately nourished.
He has no pallor, icterus, cyanosis, clubbing, lymphadenopathy and pedal edema.
He had a distended abdomen with purple striae
Facial puffiness was present
BP 120/80
Pulse 82bpm and regular
Temp- afebrile
RR- 20/min
SYSTEMIC EXAMINATION:
CVS:
S1 S2 heard , no murmurs.
RESPIRATORY SYSTEM:
Bilateral air entry present , normal vesicular breath sounds heard.
PER ABDOMEN:
soft non tender distenstion of abdomen present.
CNS: no abnormality detected.
The patient was then asked to stop the clobeta GM that he was using.He suffered severe supression of his HPA axis due to the abrupt cessation of his steroid cream causing adrenal insufficiency and had to be started on Hydrocortisone. It was followed by gradual tapering of the dose
INVESTIGATIONS:
Diagnosis: Exogenous topical steroid induced Cushings syndrome with suppressed HPA axis
Treatment:
Injection ACTH 0.4 ml IM at 7:00 a.m.
Serum cortisol level check at 8 a.m. and serum cortisol turned out to be 0.35 so patient was started on tab.hydrocortisone 5mg 2tablets in the morning 7am 1tablet at 12pm 1tablet at 5pm for 20days followed by gradual tapering off the dose
Tab.pantop 40mg OD PO
Tab.MVT OD
Monitor BP pr RR
Inform SOS
Advice at discharge.
Tab.hydrocortisone 5mg for 20days PO(2tabs 7am-1tab 12pm-1tab 5pm)
Tab.MVT PO OD
Tab.pantop 40mg OD PO
Follow up after 20days and dermatologist opinion for tinea incognito
FOLLOW UP: MY patient is presently alright with his busy SCHEDULE
His abdominal striae has been faded along the course of time
After starting medication his weight reduced around 10 kgs
Some facts about itraconazole worth knowing which could have also enhanced the effect causing his adrenal insufficiency:
Itraconazole increased methylprednisolone concentrations markedly with enhanced suppression of endogenous cortisol secretion, but had no effect on prednisolone pharmacokinetics. The pharmacokinetic interaction between methylprednisolone and itraconazole is probably related to inhibition of hepatic CYP3A4 activity by itraconazole
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014476/
Reversible adrenal insufficiency occurred in one among eight patients receiving high-dose itraconazole (600 mg day−1) for a mean duration of 5.5 months [39]. In our study, the baseline profile of cortisol during the itraconazole phase was not determined. However, the cortisol concentrations at 08.00 h t0 did not differ during the itraconazole phase compared with drug free values. Thus we postulate that the secretion of cortisol was maintained after 4 days of itraconazole administration. It seems reasonable to consider that suppression of endogenous cortisol is related only to the effect of the corticosteroid.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014476/
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