Fasciitis-like primary breast pyoderma gangrenosum: A rare case report

29-Year-Old Woman With Fever and Bilateral Lower Extremity Lesions

Pyoderma gangrenosum (PG) is a chronic, ulcerative neutrophilic dermatosis. PG presents a diagnostic challenge, largely due to the many mimicking diseases, the lack of confirmatory laboratory or biological markers, and the absence of widely accepted diagnostic criteria. In particular, PG is often mistaken for necrotizing soft tissue infections (NSTI). We reviewed four major textbooks each in general surgery, plastic surgery, trauma surgery, vascular surgery, emergency medicine, and dermatology. We also performed a search of review articles addressing NSTI and necrotizing fasciitis (NF). Ten out of the 20 non-dermatology textbooks did not list PG anywhere, and only two listed a differential diagnosis for PG. None of the non-dermatology textbooks indicated PG in the NSTI differential diagnosis, while three of the dermatology textbooks included PG in the NSTI differential diagnosis. PG was listed in all of the dermatology textbooks. Only one of the NSTI and NF articles mentioned PG in the differential diagnosis. There is an underrepresentation in major textbooks of surgery and emergency medicine and in NSTI and NF review articles when it comes to diagnosing PG. This might be leading to trainees and advanced providers in these fields being uninstructed on PG, and likely contributes to PG misdiagnosis and mismanagement. We recommend PG be included in the differential diagnosis of chronic ulcers and NSTI in non-dermatology textbooks. We also suggest adding identification and diagnosis of inflammatory mimickers of NSTI (e.g. PG) in teaching modules in surgical and emergency specialties to address this knowledge gap.

Necrotising fasciitis (NF) is mostly a polymicrobial, severe soft tissue infection that progresses rapidly, penetrating through the subcutaneous tissue to the fascial planes and the muscles. The pyoderma gangrenosum (PG), on the other hand, is a rare, rapidly progressive (except for the post-surgical PG), autoinflammatory ulcerative skin and soft tissue condition. In this study, we tried to emphasise the importance of diagnosing the NF as well as the PG. Although these two clinical presentations have some standard features, awareness of different symptoms in detail affect the outcome. Any surgical discipline can face NF or PG and, therefore, should be aware of them to decrease the mortality rate. Forty-five patients with NF and PG who were treated between January 2008 and October 2018 were included in the study and evaluated retrospectively for age, sex, localisation, onset of symptoms and diagnosis, predisposing factors, characteristics of tissue defects, laboratory findings, Laboratory Risk Indicator for Necrotising Fasciitis (LRINEC) scores, isolated microbiological agents, surgical intervention, and mortality rate. Demographic, laboratory, and clinical data were analysed. Among these 45 patients, 14 patients had PG, and 31 patients had NF. The mean age and SD for the NF and PG groups were 50.80 ± 17.67 and 50.78 ± 12.72, respectively. Five patients had rheumatological disorders; four patients had diabetes mellitus (DM) in the PG group. Males had higher risk than females in NF (odds ratio [OR] = 0.077, 95% confidence interval [CI] 0.017-0.34), and females had higher risk in PG (relative risk [RR] = 5). We compared the LRINEC score of NF patients with PG patients. The mean value of this score was 4.53 for PG patients, and 6.06 for NF patients. Fifteen patients (33.3%) had a radiological evaluation. MRI, CT, and USI were used as imaging modalities. Necrotising fasciitis and PG are two distinct entities that are in general difficult to distinguish. Therefore, differential diagnosis and rapid treatment are crucial for lowering the mortality rate.

Pyoderma gangrenosum (PG) is a chronic ulcerative neutrophilic dermatosis. It presents a diagnostic challenge due to the absence of disease-specific markers or histopathology, lack of universally accepted diagnostic criteria, and many mimicking diseases including necrotizing soft tissue infections (NSTI). PG cases often present first to specialties other than dermatology. We reviewed major educational resources in internal medicine, family medicine, and infectious disease for their coverage of PG. For each specialty, we reviewed five major textbooks, five prominent journals, and any commonly used online resources. Twelve of 15 textbooks mentioned PG, only three of which included a differential, with none including NSTI in the differential. Only two of 13 journals included review articles about PG, and none of these including NSTI in their differential. Interestingly, online resources tended to be the most complete; six of nine contained PG articles, nearly all including a differential and three listing NSTI within it. We found an underrepresentation of PG among major textbooks and journals in clinical specialties, especially in differentiating PG from its mimickers. While online resources may help fill this gap in knowledge, texts and journals remain essential. Misdiagnosis and resultant mismanagement of PG can lead to disastrous outcomes. We recommend that PG be added to the differential diagnoses of chronic ulcers in educational resources. We also suggest the addition of identification and differentiation of PG to learning materials and lectures for providers in specialties who may encounter PG, NSTI, or similarly presenting diseases to address this gap.

Pyoderma gangrenosum (PG) is a rare, chronic neutrophilic dermatosis. It is associated with underlying diseases in up to 75% of cases, most frequently with inflammatory bowel disease, inflammatory arthritis, and hematological disorders.1 It typically affects the lower limbs, while the breast is an unusual localization. Approximately 80% of known cases occur after surgeries, such as mastectomy.2 Herein, we report a case of a patient without a history of preceding surgery or trauma diagnosed with bilateral breast PG associated with rheumatoid arthritis (RA). A 68-year-old woman, with a history of type 2 diabetes, and seropositive RA presented with painful, bilateral lesions of the breast evolving for 1 month. She denied diarrhea, abdominal pain, fever, or night sweats. Physical examination revealed a 4 × 4 cm ulceration with necrotic debris and raised, violaceous borders on her right breast (Figure 1A,B). Multiple cribriform scars and nodules were present bilaterally (Figure 1A,C). A skin biopsy specimen showed a neutrophilic inflammation in the dermis with dense diffuse neutrophilic infiltrate. Complete laboratory investigations and mammography revealed normal findings. We retained the diagnosis of PG based on the rapid onset, the nipple-areolar complex sparing (NAC), the bilateral involvement, and the histopathological findings. Treatment was initiated with topical steroid and colchicine with progressive healing. PG is an uncommon ulcerative cutaneous condition. It can have different clinical presentations with varying degrees of severity. Clinically, it can present as ulcerative subtype, bullous, pustular, vegetative, drug-induced, post-surgical, or peristomal types.3 Our patient had clinical manifestations compatible with ulcerative PG with 2 distinct phases. The ulcerative phase consisted of an initial pustule which rapidly progressed to a necrotic center with erythematous, irregular edges, and the healing stage with projections of epithelium extending into the center of the ulcer termed Gulliver's sign. PG is frequently preceded by inflammatory arthritis, most commonly RA,4 the association of which portends a poor prognosis.5 In fact, the ulcers seem more refractory to treatment. The arthritis associated with PG can be seropositive or seronegative. The details regarding the clinical pattern of joint inflammation are variable, but the most common presentation is large-joint seronegative monoarticular arthritis.5 The type of inflammatory arthritis associated with PG may not be a helpful treatment guide as it was not significantly associated with treatment outcomes or healing time. The breast is an uncommon site for PG. Surgical intervention is the main inducer of the lesions.2 Regarding our patient, there was no previous history of surgery or injury and the etiology of PG remains unclear. Unnoticed minor trauma may partially explain it. Misdiagnosis of PG is common, and differential diagnosis in the breast often includes inflammatory breast cancer, chronic granulomatous mastitis and acute bacterial infections.2 This common mistake often leads to antibiotic therapy and unnecessary debridement which may even be harmful and perpetuate the pathergic response. Hence, correlation of clinical features which include a rapid onset of ulceration with undermined edges and cribriform scars, NAC sparing, and bilateral involvement, negative microbiological cultures and histopathological findings that shows a neutrophilic inflammation in the dermis without granulomas unlike chronic granulomatous mastitis is important, to rule out these serious diagnoses. Su et al propose diagnostic criteria for PG and require 2 major and 2 out of 4 minor criteria to establish the diagnosis.6 Major criteria include rapid progression of painful, necrolytic, cutaneous ulcer with an irregular violaceous border and exclusion of other causes of cutaneous ulceration.6 Minor criteria include history suggestive of pathergy or clinical findings of cribriform scarring, systemic diseases associated with PG, compatible histopathological findings, and response to treatment.6 Our patient met both of the 2 major criteria and all 4 of the minor criteria. Therefore, although an unusual site, our case illustrates the importance of considering the diagnosis of PG in patients with RA in the differential diagnosis of rapidly progressing ulcerative lesions on the breast. Prompt recognition of PG and timely initiation of treatment are critical to avoid disease spread, unesthetic scarring, hospitalization, physical morbidity, and psychological consequences. None.

Pyoderma gangrenosum (PG) can represent a diagnostic challenge, leading to missed or delayed diagnosis. With prolonged immunosuppressive therapy, the risk of infections is elevated, predisposing patients to receive anti-infective treatments and, in serious cases, amputations. Limb amputations have been reported as complication of PG misdiagnosis but can also occur as a complication of long-standing PG ulcers. We aimed to describe the clinical characteristics of patients with PG leading to limb amputation through a multicenter retrospective case series between 2010 and 2020 including patients with PG who underwent limb amputation. We report a descriptive analysis of these patients' clinical course and outcome. Ten patients with PG who underwent at least one limb amputation were identified. Six were male (60%). Mean age was 65years. All patients had ulcerative PG on the lower extremities, with a mean PG ulcer duration of 30.6months. Six patients had PG-related comorbidities such as ulcerative colitis, myelodysplasia, and inflammatory arthritis. Other significant comorbidities included diabetes mellitus (DM) (five patients), coronary artery disease (five patients), and chronic kidney disease (two patients). The majority of patients (8/10) were correctly diagnosed with PG prior to amputation, whereas two patients were misdiagnosed with necrotizing soft tissue infections (NSTIs). All patients received intravenous antibiotics without substantial improvement. Eight patients developed sepsis and shock-like symptoms and the diagnosis of NSTIs was considered. Below-knee amputation was performed in six patients and above-knee amputation in four. Four patients had amputation performed twice because of recurrent NSTIs. Conclusion This multicenter case series sheds light on practice gaps for physician assessing patients with PG, in that limb amputation may result from PG misdiagnosis or complications thereof. Elderly patients (above 65years) with coexisting lower extremity PG, DM, and/or chronic cardiac or renal disease should be managed with particular care toward preventing infection/NSTIs to prevent further complications such as limb amputations.

A NOVEL GENE MUTATION ASSOCIATED WITH COMMON VARIABLE IMMUNODEFICIENCY AND PYODERMA

Dear Editors, Pyoderma gangrenosum (PG) is an ulcerative neutrophilic dermatosis often associated with systemic diseases, such as rheumatoid arthritis, inflammatory bowel diseases, and hematological neoplasms. PG can occur in postoperative patients due to the pathergy phenomenon, which is the development of PG lesions at sites of trauma. The term "postoperative PG" (or "postsurgical PG") is used for the pathergic development of PG at surgical sites [1]. Cancer immunotherapy with immune checkpoint inhibitors (ICIs) may induce various immune-related adverse events, including neutrophilic dermatoses. We report a case of postoperative PG in a patient undergoing long-term therapy with nivolumab, an anti-PD-1 ICI.An 84-year-old man presented with a purulent lesion at a recent surgical site. Ten years prior, he underwent resection of gastric cancer, which recurred as peritoneal dissemination 3 years after the resection and was resistant to multiple lines of chemotherapy. Remission was achieved with nivolumab therapy and maintained for 5 years and 8 months with administration of nivolumab every 2 to 3 weeks without immune-related adverse events. Left inguinal hernia repair surgery was performed 19 days after the last infusion of nivolumab. The remission of gastric cancer was confirmed by imaging studies 4 weeks before the surgery. The diagnosis of inguinal hernia was also confirmed by the preoperative imaging studies and intraoperative findings. The surgery was completed successfully without any complications in the perioperative period. On postoperative day 14, he developed a fever of 39.7°C and a painful necrotic ulcer with violaceous borders, surrounding erythema, and subcutaneous abscess at the incision site (Figure 1A). His neutrophil count was elevated to 23.2 × 10 9 /L, and the C-reactive protein was elevated to 16.2 mg/dL. Although antibiotic drug therapy was initiated, bacterial cultures of the purulent exudates, necrotic tissues, and blood were negative. A skin biopsy specimen taken from a non-ulcerated margin demonstrated edema, dense diffuse infiltrate of neutrophils with nuclear dust, lymphocytes, and histiocytes throughout the dermis to the subcutaneous tissue, and hemorrhage without fibrin deposition (Figure 1B,C). Bacteria, mycobacteria, or fungi were not detected in serial sections. He did not have arthritis or bowel symptoms, and no hematological abnormality other than the increased neutrophil count was present. The diagnosis of postoperative PG was made, and intravenous prednisolone 60 mg (1 mg/kg) daily was started 3 days after presentation. As the ulcer continued to expand despite the prednisolone (and antibiotic drug) therapy for one week, we administered adalimumab twice at an interval of 2 weeks (160 mg and 80 mg). The PG lesion gradually improved, and prednisolone was tapered to 20 mg daily. Nivolumab was not restarted, as imaging studies 1 week after PG onset (6 weeks after the last infusion of nivolumab) showed no recurrence of gastric cancer, and nivolumab therapy might have a potential risk of PG exacerbation. However, he developed disseminated intravascular coagulation caused by the recurrence of peritoneal dissemination and lung metastasis 2 months after the cessation of nivolumab and died 2 months later.To our knowledge, four cases of ICI-associated PG have been reported previously, none of which were triggered by surgery (Supplementary Table S1) [2][3][4][5]. Alterations in T-cell immune tolerance induced by ICIs have been proposed to lead to T-cell dysregulation, such as abnormal IL-17 production, which may contribute to the development of PG [4,5]. ICI was discontinued in all cases. One case was associated with myelodysplastic neoplasm [3], but like in our case, the other reported cases did not have systemic diseases traditionally associated with PG [2,4,5]. In these cases, however, paraneoplastic association of PG with the primary underlying solid organ malignancies cannot be excluded. In our case, PG may also have developed in association with an occult recurrence of gastric cancer, although postoperative PG has less association with systemic disease [1]. Compared with the reported cases of ICI-associated PG, which typically developed within 6 months after the initiation of ICIs [2][3][4][5], our patient developed PG following surgery after prolonged nivolumab therapy. Therefore, it is possible that PG in our case developed independently of nivolumab. However, the unusual features of this case, namely, pyrexia and initial resistance to high-dose systemic corticosteroid therapy, both uncommon in postoperative PG [1], suggest a potential role for nivolumab-induced dysregulated inflammation following surgery in the development or exacerbation of postoperative PG.While a direct causal link between PG and nivolumab remains uncertain in this case, our findings suggest a potential risk of postoperative PG in patients undergoing ICI therapy.

A 68-year-old woman with no past history had been suffering from loose stools seven times a day with a small amount of blood for a year. She was admitted to our hospital because of impaired adduction and orbital pain on the right side. A head MRI revealed a contrast enhanced lesion through the right orbital apex and cavernous sinus (Fig. 1a). She was diagnosed to have Tolosa-Hunt syndrome (THS) based on the characteristic image. The ocular symptoms resolved with prednisolone 50 mg, and an MRI 2 months later showed that the lesion had disappeared (Fig. 1b). When prednisolone was reduced to 10 mg, a deep, fist-sized ulcer developed on her right leg, with red-purple edematous erythema (Fig. 2a). A skin biopsy revealed abscess formation in the deep dermis with neutrophil infiltration, leading to the diagnosis of pyoderma gangrenosum (PG). What could be the underlying cause in this case? A whole body CT revealed the increased wall thickness of the entire colon. Although the frequency of diarrhea with no blood had decreased significantly, colonoscopy revealed diffusely rough and edematous mucosa with shallow ulcers from the sigmoid colon to the cecum (Fig. 2b,c), consistent with ulcerative colitis (UC). Considering the severity of PG, 5-aminosalicylic acid and increased prednisolone to 30 mg were administered, which resulted in remission of both the UC and PG. Inflammatory bowel disease (IBD) causes various extraintestinal complications.1 PG is histopathologically characterized by a proliferative, gangrenous ulcer with neutrophil infiltration, and a well-known complication of IBD, accounting for 1.8% of cases.2 THS is considered to be an inflammatory granulomatous disease of unknown cause,3 and to our knowledge, only one case of THS associated with IBD has been described in Crohn's disease.3 We report for the first time a case of UC complicated by THS and PG.

Dear Editor, Pyoderma gangrenosum (PG) is a rare neutrophilic inflammatory skin condition characterized by painful purulent pustules or enlarging ulcers with raised, undermined and violaceous borders. PG has been associated with various systemic diseases, such as inflammatory bowel disease, monoclonal gammopathy, hematologic disease, inflammatory arthritis, malignancy and hidradenitis suppurativa.1 There have been several reported cases of occurrences and recurrences of PG after COVID-19 infection and vaccination. In this case report, we describe a patient with a history of PG, which had been in remission for several years prior to vaccination that experienced a recurrence of PG at the same sites as the previous involvement. A 57-year-old man with a 20-year history of idiopathic PG underwent multiple treatments, including systemic corticosteroids, cyclosporine and dapsone, without any improvement in his condition. However, after receiving intravenous infliximab at a dosage of 5 mg/kg, the lesions completely resolved. After 2 years of remission, the patient presented to our clinic with a new onset of recurrence of the previous PG involvement after receiving an mRNA-based SARS-CoV-2 vaccine (Biontech) (Figure 1a,c and d). The patient received the first dose of the RNA COVID-19 vaccine and developed isolated pustules. As symptoms were limited, only topical therapy was recommended, which improved the condition. The patient then decided to proceed with the second dose of the RNA COVID vaccine, given the presence of vulnerable family members, which resulted in the appearance of multiple diffuse erosive lesions all over the body. A new biopsy confirmed the diagnosis of pyoderma gangrenosum (Figure 1b). No systemic symptoms were reported, and laboratory examinations ruled out hematologic, autoimmune and gastroenterological diseases. Given the absence of any other significant medical history, the patient's relapse was believed to be triggered by the COVID-19 vaccination, and the patient chose not to receive the scheduled third dose. Adalimumab was prescribed at a dosage of 160 mg at Week 0, 80 mg at Week 2, and 40 mg every week from Week 4, resulting in initial gradual improvement of the lesion but subsequent recurrence. Adalimumab was discontinued, and Infliximab 5 mg/kg was administered, leading to the clearance of the lesions within 2 months (Figure 1a,c and d). Although rare, there have been reports of COVID-19 vaccine-induced exacerbation of autoimmune and autoinflammatory diseases. Several cases of PG have been reported as a potential side-effect following SARS-CoV-2 vaccination.2-7 In this case, the Naranjo Adverse Drug Reaction Probability Scale score was 9 out of 13, indicating a definite relationship between the vaccination and the recurrence of PG (Table 1). This association is further strengthened by the recurrence of PG after both doses of the vaccine. The exact mechanism by which the vaccines trigger PG is not clear. We know that cases of PG have been reported even after natural infection and PG and COVID-19 share an hyperactivation of innate immune cells. After the transcription of mRNA for the Spike protein, the latter acts as PAMPs to activate the inflammasome.8 In genetically predisposed individuals, this can lead to the onset or reactivation of autoinflammatory diseases such as PG. This hypothesis is supported by data that highlight an increase in IL-1b in COVID-19 patients, a fundamental cytokine in PG, as well as the ability of the spike protein to activate NLRP3, which is involved in the pathogenesis of PG. This case report supports the hypothesis that COVID-19 vaccines may cause unintended immune-stimulatory effects that trigger PG, highlighting the necessity of ongoing surveillance of individuals with pre-existing autoimmune disorders after COVID-19 vaccination. Additionally, it emphasizes the significance of timely identification and management of any adverse events linked to vaccination. COVID-19 may have led to under-reporting of PG cases despite the pandemic's scale,9 emphasizing the importance of reporting such cases and promoting awareness. None declared. L. Bettolini, S. Bighetti, S. Mezzana, A. Gelmetti, P. Calzavara-Pinton and V. Maione: None declared. The data that support the findings of this study are available from the corresponding author upon reasonable request.

IntroductionEruptive keratoacanthoma (EKA) development at a split-thickness skin graft donor site is rare and medically challenging. We present a case of a 47-year-old man with 8% TBSA burns to the left lower extremity. He received split-thickness skin grafts from his right thigh and had an uneventful postoperative recovery. However, seven weeks later, a non-painful nodular lesion appeared at the donor site, followed by an eruption of multiple similar lesions. A biopsy confirmed EKA. Though rare, EKA and other dermatologic complications can arise at graft donor sites. Given the widespread use of split-thickness skin grafts in burn care, providers must be aware of potential skin complications at these sites. This study aimed to review the existing literature to identify trauma-induced dermatologic conditions occurring within split-thickness skin graft donor sites.MethodsFirst, a search was conducted to explore dermatologic complications associated with trauma. A literature review was then performed using PubMed, Google Scholar, and Medline, specifically examining dermatologic issues at donor sites following split-thickness skin grafts.ResultsThe review identified four rare dermatologic conditions that developed in split-thickness graft donor sites across 22 articles: herpes zoster, SCC, keratoacanthoma, and bullae. Of the articles, 1 (4.5%) studied herpes zoster, 12 (54.5%) focused on SCC, 4 (18.1%) examined keratoacanthoma, and 5 (22.7%) reviewed bullae. Our findings indicate that herpes zoster eruption in a donor site, although rare, can lead to fatal results for patients. This highlights the need for awareness of burn-related immunosuppression and its potential consequences, including disseminated herpes zoster infection. SCC and keratoacanthoma also demand rapid and accurate diagnosis due to their differing management yet similar presentation. While SCC often requires excision to prevent progression of disease, keratoacanthoma calls for different management which vary from surgery to surveillance. Lastly, bullae, although rare, has increased in incidence in the past two decades, requiring distinct treatments ranging from steroids to immunosuppressive therapies. Each of these conditions can significantly impact patient outcomes and necessitate vigilant surveillance of graft donor sites.ConclusionsSplit thickness skin grafts can lead to trauma-induced dermatologic conditions, including squamous cell carcinoma, keratoacanthoma, herpes zoster, and bullae. Given the immunocompromised status of burn patients, routine surveillance of both graft donor and recipient sites is crucial. Accurate diagnosis of these conditions are crucial for burn providers to ensure timely and appropriate management.Applicability of Research to PracticeThis case underscores the importance for burn care providers to recognize, diagnose, and manage postoperative trauma induced dermatologic complications in graft donor sites.Funding for the StudyN/A

no malignant transformation at all, nor any local or distant metastasis. This case is the largest in size ever reported in the literature, measuring 21 cm 17 cm 12 cm. Although the radiological findings sug gested the involvement of the pericranium, surgical exploration and the management plan favored simple excision with a free margin and skin graft coverage. During extended followup , no signs or symptoms of recurrence were noted. This case illustrates the im portance of the knowledge of the patterns of recur rence and the malignant potential of such lesions together with their application to various presen tations.

Pyoderma gangrenosum (PG) is a rare neutrophilic dermatosis that can mimic other severe conditions, complicating diagnosis. We report a case of PG of the knee initially mistaken for necrotizing fasciitis (NF) in a 68-year-old woman who presented with knee swelling, erythema, papules, and pustules following a fall. Despite antibiotic therapy and surgical debridement for suspected NF, the patient's fever persisted, and laboratory markers (elevated WBC and C-reactive protein) did not improve. Histopathology revealed a dense neutrophilic infiltrate, and negative cultures ruled out infection, leading to a PG diagnosis. Treatment with oral prednisolone (60 mg/day) rapidly resolved symptoms, followed by negative pressure wound therapy, skin grafting, and adalimumab initiation. The patient stabilized without relapse. Key diagnostic clues included abundant pustules, characteristic of pustular PG, and the absence of fat tissue necrosis during surgery. This case highlights the diagnostic challenge of distinguishing PG from NF, as both may involve deep tissue inflammation. While histopathology and cultures are critical, results are delayed, necessitating reliance on clinical observations. Careful assessment of skin lesions and evaluation of fat necrosis (finger test)can prevent unnecessary surgical interventions, emphasizing the importance of considering PG in atypical presentations of suspected NF.

Patient: Female, 67-year-old Final Diagnosis: Pyoderma gangrenosum Symptoms: Purpura Medication:— Clinical Procedure: — Specialty: Hematology Objective: Unknown etiology Background:Pyoderma gangrenosum (PG) is a sterile neutrophilic dermatosis that can be associated with systemic diseases, such as ulcerative colitis, polyarthritis, diabetes mellitus, myelodysplastic syndrome, and/or myeloid leukemia, and is often misdiagnosed as a necrotizing infection. Few reports have described imaging studies of PG; however, necrotizing fasciitis (NF) exhibits distinct imaging characteristics. If deep fascial involvement is not demonstrated on magnetic resonance imaging (MRI), NF is excluded.Case Report:We present a case of PG mimicking NF on MRI in a 67-year-old woman with acute myeloblastic leukemia. After undergoing a second cycle of decitabine therapy, she was admitted for pain in her lower left leg. The condition was initially misdiagnosed as NF because MRI findings demonstrated signal intensity in the fascia. MRI revealed fasciitis that exhibited linear fluid signal intensity in the fascia of lower left leg. Despite broad-spectrum antibiotics, the lesion rapidly progressed to a swollen hemorrhagic patch with bullae and an ulcer. Skin biopsy results ultimately led to the diagnosis of PG, based on histopathological findings. The patient was treated with intravenous steroids and regular wound dressing. The skin lesion on the lower left leg exhibited a good response.Conclusions:Despite the presence of a lesion that invaded the fascia on MRI, our patient was diagnosed with PG following a skin biopsy and completely recovered with steroid treatment. To distinguish PG from NF, it is more important to identify the characteristic clinical features than to rely solely on imaging findings.

Necrotizing soft tissue infections (NSTIs) are rare but life-threatening conditions characterized by rapidly progressive tissue destruction. Although methicillin-resistant Staphylococcus aureus (MRSA) is a well-known pathogen, community-acquired MRSA (CA-MRSA) is an uncommon cause of NSTI, especially in otherwise healthy pediatric patients.We report the case of a previously healthy 13-year-old boy who developed NSTI of the lower extremity after sustaining a trivial insect bite. On admission, he presented with rapidly progressive swelling, erythema, and severe pain out of proportion to physical findings. Computed tomography revealed fat stranding and thickening of the superficial fascia, and the finger test was positive. Emergency debridement revealed a necrotic area of subcutaneous fat and fascia measuring approximately 15 × 8 cm, and MRSA was identified in swab cultures. The patient required re-debridement, followed by negative pressure wound therapy (NPWT). A split-thickness skin graft was performed on day 21, after confirming negative wound cultures, with no graft-related complications. The patient was discharged in good condition after 62 days of hospitalization.This case illustrates that CA-MRSA, though rarely causing NSTI, can lead to severe, rapidly progressive infections even in healthy children. Clinicians should maintain vigilance, as even minor injuries may serve as portals of entry. Early recognition, timely surgical debridement, and empiric MRSA coverage are critical to optimizing outcomes, and this case contributes to the limited literature on pediatric CA-MRSA NSTI in Japan.