Pemphigus vulgaris with drug-induced acute pancreatitis: A case report

Jefferey Joel*

Clinical Pharmacist, Kauvery Hospital, Alwarpet, Chennai, Tamil Nadu

*Correspondence

Abstract

Background: Pemphigus vulgaris is a potentially life-threatening autoimmune blistering disorder involving the skin and mucous membranes. Severe disease often requires intensive immunosuppressive therapy, wound care, infection control, and multidisciplinary management.

Case presentation: We report the case of a 24-year-old male admitted on 14-02-2026 with pemphigus vulgaris confirmed by direct immunofluorescence and strong anti-desmoglein positivity. He had widespread erosions and blisters involving the body and oral mucosa, with positive Nikolsky sign. He was treated with intravenous methylprednisolone followed by tapering oral prednisolone, daily wound care, and systemic antimicrobial therapy. During hospitalization, he developed polymicrobial bacterial infection and fungal infections, including Candida tropicalis in urine and later mucormycosis requiring antifungal escalation. Owing to extensive wound involvement, debridement of the forehead and scalp with dermal matrix application was performed on 09-03-2026. Subsequently, he developed acute pancreatitis, suspected to be drug induced secondary to corticosteroid therapy. On 13-03-2026, serum amylase was 1055.6 U/L and serum lipase was >1200 U/L. The patient remained under active treatment at the time of reporting.

Conclusion: This case highlights the complexity of managing severe pemphigus vulgaris complicated by polymicrobial infection, advanced wound care needs, invasive fungal disease, and probable corticosteroid-induced acute pancreatitis.

Keywords: Pemphigus vulgaris; Acute pancreatitis; Drug-induced pancreatitis; Methylprednisolone; Mucormycosis; Candida tropicalis; Polymicrobial infection

Introduction

Pemphigus vulgaris is a chronic autoimmune blistering disease characterized by autoantibody-mediated acantholysis, leading to intraepidermal blistering of the skin and mucous membranes. In severe disease, extensive epidermal loss predisposes to fluid loss, pain, malnutrition, and serious secondary infections. Systemic corticosteroids remain the cornerstone of treatment, but their use may be associated with adverse effects, including metabolic complications, opportunistic infections, and rarely, acute pancreatitis [1,2].

Drug-induced acute pancreatitis is an uncommon but clinically significant event. Corticosteroids have been implicated as one of the possible causes, especially when pancreatitis develops after exposure and other common etiologies are less likely [3,4]. We describe a case of severe pemphigus vulgaris with confirmed autoimmune serology, complicated by polymicrobial infection, invasive fungal involvement, extensive wound care requirements, and probable corticosteroid-induced acute pancreatitis.

Case Presentation

A 24-year-old male was admitted on 14-02-2026 with extensive blistering and erosive lesions involving the body and oral mucosa. Dermatology evaluation documented widespread erosions and blisters with positive Nikolsky sign, consistent with pemphigus vulgaris. The diagnosis was confirmed by direct immunofluorescence, and anti-desmoglein (anti-DSG) antibody level was 193, strongly positive.

Initial management included systemic corticosteroid therapy. The patient received intravenous methylprednisolone 500 mg once daily for 3 days, followed by intravenous methylprednisolone 250 mg once daily for 2 more days, and was later transitioned to oral prednisolone in a tapering regimen. Intravenous immunoglobulin (IVIG) was administered from 23-02-2026 to 27-02-2026.

Because of extensive skin barrier loss, he required intensive wound care. Dressing was performed once daily using octenisan mitts, followed by whole-body application of silver sulfadiazine (Silverex SSD) and sterilized vaseline gauze coverage. Plastic surgery consultation was obtained for wound management. On 09-03-2026, he underwent wound debridement of the forehead and scalp with dermal matrix application.

The hospital course was complicated by multiple secondary infections. Early BioFire findings documented Streptococcus species, Bacteroides fragilis, Proteus species, and Pseudomonas aeruginosa. Additional culture data showed the following:

15-02-2026 urine cultureProteus mirabilis
19-02-2026 blood culture from right IJVAerobic GNB identified as Pseudomonas aeruginosa, noted to be carbapenem resistant
24-02-2026 urine culture:Enterococcus faecium
24-02-2026 right femoral aerobic cultureKlebsiella species
28-02-2026 right femoral A-line cultureAcinetobacter baumannii
07-03-2026 blood cultureGram-positive cocci
Urine cultureCandida tropicalis

These microbiological findings guided sequential antibacterial and antifungal escalation. In view of resistant Gram-negative bacterial infection, including carbapenem-resistant Pseudomonas aeruginosa and Acinetobacter baumannii, the patient received polymyxin B and sulbactam. In response to Gram-positive cocci in blood culture, vancomycin was added. Tigecycline was also introduced as part of antibacterial management. The antibacterial agents administered during hospitalization included piperacillin–tazobactam 4.5 g intravenously three times daily for 5 days, vancomycin 1 g twice daily from 26-02-2026 to 02-03-2026, polymyxin B 7.5 lakh units twice daily from 02-03-2026 onward, sulbactam 3 g three times daily from 02-03-2026 to 03-03-2026, ampicillin 2 g every 6 hours from 02-03-2026 to 04-03-2026, and tigecycline 100 mg twice daily from 03-03-2026 onward.

The patient also developed fungal complications. Candida tropicalis was isolated in urine culture. Fluconazole had been used previously. Subsequently, amphotericin B was administered for fungal management. At the current stage, fungal growth was identified as mucormycosis, for which amphotericin B was stopped and the patient was started on loading doses of injectable isavuconazole 200 mg three times daily for 6 doses, followed by 200 mg once daily, which was ongoing at the time of reporting.

During continued treatment, the patient developed acute pancreatitis, considered drug induced, with corticosteroid therapy suspected as the most likely offending agent based on the temporal association with high-dose intravenous methylprednisolone followed by oral prednisolone taper. ICU doctors reviewed the patient. On 13-03-2026, serum amylase was 1055.6 U/L and serum lipase was >1200 U/L, supporting the diagnosis of acute pancreatitis. At the time of reporting, the patient was still under treatment.

Discussion

This case demonstrates the severe and multifaceted complications that may occur in pemphigus vulgaris requiring prolonged hospitalization. The diagnosis was supported by classical clinical features, direct immunofluorescence, and strongly positive anti-DSG antibodies. Severe pemphigus vulgaris behaves clinically like a high-risk erosive dermatosis, with major compromise of the skin barrier and high susceptibility to infection [1,2].

A striking feature of this case is the broad infectious burden. The patient developed polymicrobial bacterial infection involving Gram-negative bacilli, Gram-positive cocci, and fungal pathogens. Resistant organisms included carbapenem-resistant Pseudomonas aeruginosa and Acinetobacter baumannii, which justified escalation to polymyxin B and sulbactam. The later emergence of Gram-positive cocci in blood culture prompted vancomycin, while tigecycline was also added as part of broad antibacterial management. Such stepwise escalation reflects real-world management in critically ill patients with extensive wounds, invasive lines, and prolonged antimicrobial exposure.

The fungal burden in this patient also evolved over time. Initial fungal isolation of Candida tropicalis from urine indicated opportunistic fungal involvement in the setting of immunosuppression and prolonged hospitalization. Later progression to mucormycosis markedly increased the seriousness of the clinical picture. Mucormycosis is a life-threatening invasive fungal infection that typically affects immunocompromised patients and requires rapid antifungal therapy and source control. In this patient, antifungal treatment was escalated from amphotericin B to isavuconazole, which is an accepted therapeutic option in mucormycosis [5,6].

Another important complication was acute pancreatitis, which developed after corticosteroid exposure. Drug-induced acute pancreatitis is rare but recognized, and corticosteroids are among the reported causative agents [3,4]. In this patient, markedly elevated pancreatic enzymes, ICU review, and the temporal relationship with high-dose methylprednisolone followed by oral steroid therapy supported the diagnosis of probable corticosteroid-induced pancreatitis. Although full exclusion of other causes should ideally be documented in the final submission, the suspected adverse drug reaction remains clinically important.

The patient’s requirement for forehead and scalp debridement with dermal matrix application further emphasizes the severity of skin and soft tissue involvement. Successful management required coordination across dermatology, intensive care, plastic surgery, microbiology, and clinical pharmacology. This case therefore highlights the importance of multidisciplinary monitoring in patients with severe autoimmune blistering disease, especially when exposed to high-dose corticosteroids and prolonged antimicrobial therapy.

Conclusions

This case describes a 24-year-old male with pemphigus vulgaris confirmed by direct immunofluorescence and strong anti-desmoglein positivity, whose prolonged hospital course was complicated by polymicrobial bacterial infection, Candida tropicalis infection, mucormycosis, extensive wound burden requiring debridement with dermal matrix application, and probable corticosteroid-induced acute pancreatitis. The case underscores the need for close microbiological surveillance, timely antimicrobial escalation, meticulous wound care, and vigilance for serious adverse drug reactions in severe pemphigus vulgaris.

Conflicts of Interest

The authors declare no conflict of interest.

References

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