This gentle man was well 4 months back. In July 2021 he developed multiple flaccid blisters located initially on the trunk and extremities and gradually became generalized. Blisters used to rupture spontaneously and gave rise to erosions. Erosions were studed with crusts, had no tendency to heal rather gradually increased in size by peripheral extension and coalescing with each other. He complained of severe burning of the lesional skin. He was non-diabetic and non-hypertensive. He was diagnosed as a case of Pemphigus vulgaris on the basis of clinical findings, skin histopathology and DIF findings. He was put on treatment with injectable Triamcinolone acetonide and P.O Azathioprine 100 mg/day by his 1st physician. A few months after beginning the treatment he stopped developing blisters but had no improvement of his burning and erosions and was referred to us. We started P.O Prednisolone 60 mg/day and continued Azathioprine 100 mg/day. A few days after starting the treatment he developed fever and deteriorated clinically. He was evaluated for fever and clinical deterioration. Swab from the erosions was tested by gram stain and C/S and revealed growth of staphylococcus aurius, S. electrolytes revealed hyperkalemia and hyponatraemia. Based on C/S reports oral ciprofloxacin was added. Hyperkalemia and hyponatraemia was corrected accordingly. Though more than 2 weeks have elapsed since the initiation of treatment, he has no improvement rather he deteriorated clinically. What might be the cause of this clinical deterioration?
I would believe you have evaluated for all of the most common reasons (autoimmune to metabolic) but if looking for not so common presentation have they completed evaluation for cryoglobulinemia?
Since publication of the case we have had four additional cases - and clinical presentation is a challenge. The "blisters" that develop into erosions could be related to a vasculitis - as they improved by secondary intention, perhaps they were full thickness insults to the skin. Treatment (?) can often alter course and test results, but interpretation of the patient story will allow you to surmise and there will be other aspects flagged in the lab work (viscosity, other immunoglobulin, RF, as examples) or in the data (biopsy of nerve/vascular/skin).
https://scholars.direct/Articles/neurodegenerative-disorders/jnd-3-014.php?jid=neurodegenerative-disorders
Allen Orehek, thanks for your valuable pieces of information. It is highly appreciable.
Approach to such type of case would be systematic. We have to rule out underlying autoimmune disease and Should be taken swab sample from blister and send to HPE . Rule out underlying metabolic etiology.
Alok Kumar Bharti, thanks for your suggestions. I appreciate your response.
Despite a 14 (Fourteen) days twice daily course of oral ciprofloxacin his fever didn't subsided. We continued oral prednisolone 60 mg daily, started oral linezolid 600 mg bid and regular wound dressing with vaseline gauge and stopped oral azathioprine. Ten days after starting oral linezolid pt's fever subsided but he developed hyperglycemia (possibly steroid induced.). A endocrinologist was consulted and Inj. insulin (Actrapid) was initiated. Due to recurrent episodes of hypoglycemia Insulin was replaced by oral hypoglycemic agent (Vildagliptin). We started tapering of prednisolone after 4 weeks of it's initiation and we added 10 mg methotrexate per week as an adjuvant. Patient improved clinically and was discharged.
In such type of cases , Judicious use of steroids for 2-3 week then taper it slowly plus gram positive coverage in the view of MRSA ,use Tab linezolid plus Control the Blood sugar by OHA if risk of Hypoglycemia with Inj insulin and treatment of other comorbid condition will be very useful
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