Simultaneous Occurrence of Sweet Syndrome and Necrobiosis Lipoidica in Patient with Several Cancers

Simultaneous Occurrence of Sweet Syndrome and Necrobiosis Lipoidica in Patient with Several Cancers Dr Simona Kordeva Department of Dermatology and Venereology, Medical Institute of Ministry of Interior, General Skobelev 79, 1606, Sofia, Bulgaria Assoc Prof Valentina Broshtilova Department of Internal Diseases, Pharmacology and Clinical Pharmacology, Pediatrics, Epidemiology, Infectious Diseases, and Skin Diseases. Faculty of Medicine, Sofia University "St Kliment Ohridski", Sofia, Bulgaria Konstantin Georgiev Tchernev Jr Onkoderma - Clinic for Dermatology, Venereology and Dermatologic Surgery, General Skobelev 26, 1606 Sofia, Bulgaria Prof Dr Georgi Tchernev  Onkoderma - Clinic for Dermatology, Venereology and Dermatologic Surgery, General Skobelev 26, 1606 Sofia, Bulgaria; Department of Dermatology and Venereology, Medical Institute of Ministry of Interior, General Skobelev 79, 1606, Sofia, Bulgaria Abstract Acute neutrophilic dermatosis, also known as Sweet syndrome, is a rare disorder that can arise from various etiologies, and in some cases, remains idiopathic. Malignancy-associated Sweet syndrome is uncommon and is often misdiagnosed for years before the correct diagnosis is established. Necrobiosis lipoidica is an inflammatory granulomatous skin disorder often associated with diabetes mellitus, but it may also occur in patients with hypertension, thyroid disease, other inflammatory conditions, or even in otherwise healthy individuals. Rare associations with malignancy have also been described. We report the case of a 64-year-old male presenting with the simultaneous occurrence of Sweet syndrome and Necrobiosis lipoidica on the background of pulmonal and bladder cancer. Infectious, drug-induced, and inflammatory etiologies of the disease were excluded as possible inductors. Routine investigations revealed a pulmonary tumor, alongside a past medical history of low-grade urothelial papillary carcinoma. The presence of multiple neoplasias was considered as the most likely causative factor for the exacerbation of Sweet syndrome. Introduction Acute febrile neutrophilic dermatosis, commonly referred to as Sweet syndrome, is a rare condition characterized by the sudden appearance of welldemarcated, tender, erythematous plaques or nodules, typically accompanied by systemic symptoms such as fever, arthralgia, and headaches [1]. Neutrophilic dermatoses represent a group of noninfectious disorders defined by neutrophilic infiltration of the skin, with or without vasculitis [1]. These conditions may occur idiopathically or as a secondary manifestation of an underlying localized or systemic disease [1]. Von den Diesch categorized Sweet syndrome into idiopathic, paraneoplastic, pregnancy-associated, and parainflammatory subgroups, reflecting its association with various systemic disorders [2]. In such cases, the syndrome may serve as an initial clinical manifestation of the underlying disease [3]. Sweet syndrome, in particular, has a strong association with malignancies, including myelodysplasia, various More Information How to cite this article: Kordeva S, Broshtilova V, Tchernev KG Jr, Tchernev G. Simultaneous Occurrence of Sweet Syndrome and Necrobiosis Lipoidica in Patient with Several Cancers. Eur J Med Health Res, 2025;3(6):18-24. DOI: 10.59324/ejmhr.2025.3(6).03 Keywords: Sweet syndrome, Necrobiosis lipoidica, pulmonary tumor, dual occurrence, cancer. This work is licensed under a Creative Commons Attribution 4.0 International License. The license permits unrestricted use, distribution, and reproduction in any medium, on the condition that users give exact credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if they made any changes. EUR J MED HEALTH RES Volume 3 | Number 6 | 2025 19 leukemias, lymphoma, multiple myeloma, and solid tumors [1]. The syndrome may develop prior to, simultaneously with, or following the diagnosis of an underlying malignancy [1]. Necrobiosis lipoidica is an inflammatory granulomatous skin disorder that typically presents as indolent, atrophic plaques, most commonly located on the lower extremities [4]. While often regarded as a dermatologic marker of diabetes mellitus, it is not pathognomonic indicator for the disease [5]. It may also occur in otherwise healthy individuals or in association with thyroid disorders, inflammatory diseases [6], and certain malignancies [7]. Although Sweet syndrome and Necrobiosis lipoidica are distinct entities, Necrobiosis lipoidica may coexist with underlying inflammatory conditions [6] that are capable of triggering Sweet syndrome [1]. Understanding the possible connection between Sweet syndrome, Necrobiosis lipoidica and malignancy may help clinicians in several ways: 1) to consider a diagnosis of Sweet syndrome when evaluating necrobiosis lipoidica lesions, 2) to investigate potential underlying systemic causes and address them, 3) to explore whether necrobiosis lipoidica might serve as a diagnostic marker for Sweet syndrome, and 4) examining the potential connection of both conditions not only to each other but also to distinct malignancies, such as low-grade urothelial papillary carcinoma and a solitary pulmonary tumour While this remains a hypothesis, in medicine the correct answer is often hidden in plain sight. We present a 64-year-old male with new-onset erythematous-livid plaques and nodules, histologically confirmed as Sweet syndrome and Necrobiosis lipoidica. An infectious trigger was excluded. A possible drug-induced etiology was also considered unlikely, as the patient’s initial hospitalization occurred before the medication (bisoprolol) was administered. Instead, the identified multiple neoplasias were regarded as the most probable causative factor for the exacerbation of Sweet syndrome. Case Report A 64-year-old male presented to the dermatology department in September 2025 with a primary complaint of newly developed erythematous-livid plaques and nodules on the lower extremities, persisting for 3-4 days. He also noted an upper respiratory tract infection 5-6 days prior, treated with unknown antibiotics. Past medical history included resected low-grade urothelial papillary carcinoma (2024), diverticula and polyps of the sigmoid colon, surgery for sigmo-vesical fistula (2024), arterial hypertension, and prostate hyperplasia. Current systemic therapy included candesartan 16 mg once daily (initiated one month prior), bisoprolol 5 mg once daily (used for three years, discontinued during the first hospitalization but restarted shortly before current hospitalization), and tamsulosin 0,4 mg daily taken from 2 years. The patient reports allergy to cephalosporins. Laboratory tests revealed slightly elevated WBC 11.9 x 10^9/l (normal range 4.0-11.0 x 10^9/L), slightly decreased PDW 9.2% (8.3%-17%), slightly elevated granulocytes 8.7 x 10^9/L (1.5-8.5 x 10^9/L), elevated erythrocyte sedimentation rate 44 mm/hr (men over 50: 0-20 mm/hr), borderline high LDL levels 3.5 mmol/l (below 2.6 mmol/l), elevated uric acid 460.0 micromol/l (200-430 micromol/l), elevated GGT levels 162.0 IU/L (5-40 IU/L), and elevated CRP 20.9 mg/L (below 10 mg/l). Dermatological examinations revealed plaques of various sizes with fibrotic changes and postinflammatory pigmentation in the abdominal area (Fig.1a,b) and upper extremities (Fig.2a,b). On the left lower leg (Fig.3a) and right lateral malleolus (Fig.3b), erythematous plaques and nodules were present, some covered with hemorrhagic crusts (Fig.3a-c). Enlarged lymph nodes were not palpable. Figure 1a,b: Plaques of Various Sizes with Fibrotic Changes and Post-Inflammatory Pigmentation in the Abdominal Area EUR J MED HEALTH RES Volume 3 | Number 6 | 2025 20 Figure 2a,b: Plaques of Various Sizes with Fibrotic Changes and Post-Inflammatory Pigmentation in the Upper Extremities Figure 3a,b,c: On the Left lower Leg (Fig.3a) and Right Lateral Malleolus (Fig.3b), Erythematous Plaques and Nodules are Present, some Covered with Hemorrhagic Crusts (Fig.3a-c) Regarding the edema of the lower extremities, a consultation was made with a vascular surgeon. The Doppler ultrasonography showed preserved pulsations of ATP bilaterally, but weakened ATA, preserved circulation of the lower extremities, preserved superficial and deep vein circulation, and bilateral sapheno-popliteal-femoral reflux, more pronounced on the left. Phlebitic changes were observed in the right great saphenous vein. Fraxiparin 0.8 ml s.c. once a day was prescribed. Regarding the newly appeared erythemo-livid plaques and nodules on the lower limbs and in the abdominal area, two biopsies were taken from the abdominal area and the left lower leg. The biopsy taken from the abdominal area showed abundant parakeratosis, irregular acantholysis, pronounced neutrophil extravasation, moderate interstitial mixed inflammatory infiltrate with many nuclear neutrophils throughout the dermis, fibrinoid necrosis (Fig.4a) of small-caliber vessels with foci of neutrophilic abscesses in the middle dermal compartment. Histology was compatible with acute neutrophilic febrile dermatosis / Sweet syndrome (Fig.4a,b). Histology from the left lower leg was compatible with Necrobiosis lipoidica (Fig.5a-c). Systemic therapy with methylprednisolone i.v. was initiated according to a tapering regimen (60 mg i.v. x 2 days, then reduced to 40 mg i.v. x 2 days, 30 mg i.v. x 2 days, and 20 mg i.v. x 2 days), alongside famotidine 40 mg twice daily, pentoxifylline 400 mg three times daily, and topical methylprednisolone aceponate applied twice daily for 7 days (for the lower legs). Due to the association between bisoprolol and possible exacerbation of Sweet syndrome, cardiology consultation was requested. As bisoprolol had not been administrated during the first hospitalization but was reintroduced before recurrence, it was replaced with nebivolol 5 m. Recommendations were given for outpatient follow-up by a cardiologist and possible optimization of therapy. Due to anamnestic data of a past upper respiratory tract infection and suspicion of a post/parainfectious EUR J MED HEALTH RES Volume 3 | Number 6 | 2025 21 genesis of the disease, nasal and throat secretions were taken (the cultures remained sterile) and a chest X-ray of the lungs and heart was performed, which revealed a rounded inhomogeneous lesion (37 mm) in the right perihilar region extending to the lower pole. A consultation with a pulmonologist was made due to suspicion of paraneoplastic genesis of Sweet syndrome, in view of which a CT scan of the lungs with contrast was recommended, which showed a tumor formation in the right lung base. A subsequent consultation with a thoracic surgeon was recommended for assessment regarding histological verification of the tumor process through fine-needle biopsy and subsequent surgical removal of the tumor formation. Outpatient regimen included oral corticosteroid therapy (methylprednisolon 16 mg daily for 7 days, followed by 12 mg for 7 days, 8 mg for 7 days, 4 mg for 7 days, and 2 mg for another 7 days), esomeprazole 40 mg twice daily for 35 days, pentoxifylline 400 mg three times a day for an indefinite period, and topical pimecrolimus cream once daily. Figure 4a,b: Acute Neutrophilic Febrile Dermatosis / Sweet Syndrome: Abundant Parakeratosis, Irregular Acantholysis, Pronounced Neutrophil Extravasation, Moderate Interstitial Mixed Inflammatory Infiltrate with Many Segmentonuclear Neutrophils throughout the Dermis, Fibrinoid Necrosis (a) of Small-Caliber Vessels with Foci of Neutrophilic Abscesses in the Middle Dermal Compartment (a,b); 4a: Fibrinoid Necrosis x SS x 100 x HE; 4b: Sweet Syndrome x 100 x HE Figure 5a-c: Necrobiosis Lipoidica; 5a: Necrobiosis Lipoidica x HE x 40; 5b: Necrobiosis Lipoidica - Septal Panniculitis x HE x 100; 5c: Necrobiosis Lipoidica x 100 x HE Discussion Acute febrile neutrophilic dermatosis, also known as Sweet syndrome, was first described by Dr. Robert Douglas Sweet in 1964 [8]. The exact pathogenesis remains unclear; however, the condition has been associated with infections, autoimmune diseases, certain medications, and neoplasms [9]. These associations suggest an abnormal hypersensitivity reaction, likely mediated by cytokines, with subsequent neutrophilic infiltration triggered by interleukin (IL)-1 [9]. Several factors have been linked to its pathogenesis, including autoantibodies, dermal dendrocytes, HLA serotypes, immune complexes and leukotactic mechanisms [9]. Moreover, lesional skin in affected patients demonstrates higher levels of inflammatory cell markers compared to other neutrophilic dermatoses [9,10]. Malignancy-associated Sweet syndrome, is a recognized subtype, in which clinical manifestations may occur before, after, or at the same time as the cancer diagnosis [9]. Approximately 21% of patients with Sweet syndrome have an associated malignancy, EUR J MED HEALTH RES Volume 3 | Number 6 | 2025 22 of which about 85% are hematological disorders and 15% are solid tumors, most commonly adenocarcinomas of the breast, gastrointestinal tract, and genitourinary system [9,11]. In cases of paraneoplastic genesis, the cutaneous manifestations may represent the first sign of malignancy and are often associated with poorer prognosis [12]. Del Pozo et al [12] reported concurrent Sweet syndrome and leukemia cutis in patients with myeloid disorders, all of whom had fatal outcomes [12]. Almost all organs may be involved in malignancyassociated Sweet syndrome, with extracutaneous sites most commonly affected including the eyes, neuromuscular system, joints, heart, liver, kidneys and lungs [13]. According to the literature, Sweet syndrome is considered a hypersensitivity reaction to infections, autoimmune or inflammatory conditions, and malignancies [13]. In our case, several arguments support the malignancy-associated subtype: 1) the lack of response to antibiotics administered for the reported upper respiratory infection, which rules out an infectious etiology; 2) bisoprolol was not used during the initial diagnosis in May 2025 and was only introduced months later, with no exacerbations until September 2025, making a drug-induced cause less likely; 3) the simultaneous occurrence of Necrobiosis lipoidica, which may indicate a potential link through shared inflammatory pathways; although no evidence of autoimmune or inflammatory comorbidities were identified; and 4) the incidental discovery of a pulmonary tumor. Lung cancer associated with Sweet syndrome is rare, with only a few cases reported in the literature [14]. Xie et al [15] reported a rare case of lung adenocarcinoma associated with Sweet syndrome and decline in peripheral blood cells count. In certain cases, Sweet syndrome has been reported as the initial presenting symptom leading to the diagnosis of gastric cancer [16]. Baloglu et al [17] reported a case of Sweet syndrome in a patient with high grade non-muscle invasive bladder tumor, in which the skin lesions regressed following treatment of the malignancy. In our patient, the incidentally discovered solid tumor formation in the right perihilar region alongside the resected low-grade urothelial papillary carcinoma, further highlights the rarety of this report. The simultaneous occurrence of Necrobiosis lipoidica in a patient Sweet syndrome is remarkable, as such was previously considered unlikely given the distinct nature of the two conditions. In the literature, the simultaneous occurrence of Sweet syndrome with other conditions, such as relapsing polychondritis (an autoimmune disease), has been reported rarely [18], which can suggest a common underlying pathway. Dual presentations are more commonly observed in patients with hematological malignancies [18]. Another paper reported a rare observation of two reactive dermatoses occurring together in two unrelated patients - one of whom had an associated malignancy [19]. In that case, the simultaneous occurrence of Sweet syndrome and erythema nodosum was described in a patient with acute myelogenous leukemia [19]. Although clinically distinct, this coexistence could suggest a shared pathogenic mechanism [19]. In our case, no hematologic malignancy was identified, and given that the two entities are entirely different (unlike the previously reported reactive dermatoses), this dual occurrence represents an extremely rare observation. It raises the possibility that our current understanding of the etiology and pathogenic mechanisms may be incomplete, suggesting the existence of a yet unknown shared underlying mechanism. An interesting observation by Cohen et al [20] postulated that the causative agent of erythema nodosum or Sweet syndrome may stimulate the release of various cytokines, particularly interleukin-1 [20]. Depending on the depth of involvement, this could result in the development of Sweet syndrome lesions when localized in the dermis, or erythema nodosum lesions when localized in the subcutaneous tissue [19], [20]. Necrobiosis lipoidica is a rare granulomatous condition characterized by well-defined plaques, usually affecting the shins [21]. The conditions is often associated with diabetes mellitus (58.5%) or may even precede its onset, although lesions can also occur in patients without diabetes (40.7%) [21]. While the lower legs are the most typical site, other locations may also be involved [21]. Beyond diabetes, common comorbidities include hypertension (45.2%), dyslipidemia (43,6%) and thyroid disease (24.5%) [21]. Malignancy in patients with Necrobiosis lipoidica has been reported only rarely, with limited articles describing such cases. One report described a 58-year-old male with indurative erythematous lesions, later confirmed as necrobiosis lipoidica, on the lower leg, who was later diagnosed with lymphomatoid granulomatosis by lung biopsy [22]. The skin lesions were interpreted as a cutaneous manifestation and possible early indicator of lymphomatoid granulomatosis [22]. To date, no reported cases have described a possible dual association of Sweet syndrome and Necrobiosis lipoidica with malignancy in the literature. A theory proposed for the co-existence of Sweet syndrome and Behcet’s disease suggests the possibility of a shared pathogenic pathway, whereby neutrophil activation leads to tissue infiltration, resulting in organand skinspecific lesions [23]. However, Necrobiosis lipoidica and Behcet’s disease are two distinctive conditions - one being a localized chronic granulomatous cutaneous disorder and the other a systemic inflammatory EUR J MED HEALTH RES Volume 3 | Number 6 | 2025 23 vasculitis. This raises several questions: 1) could a common pathogenic pathway exist for both Sweet syndrome and Necrobiosis lipoidica, or 2) does the malignant component act as the key trigger initiating overlapping pathological pathways? These considerations, in our opinion, deserve further investigation. The simultaneous occurrence of Necrobiosis lipoidica raises the possibility of an association between the two conditions. To our knowledge, this may represent the first reported case of their concurrent presentation in the context of multiple neoplasias. Furthermore, this raises an interesting observation and question as to whether Necrobiosis lipoidica might serve as a potential diagnostic clue for Sweet syndrome. The primary approach to treating Sweet syndrome is addressing the underlying cause; in our case, surgical removal of the pulmonary tumor is recommended. First-line therapy typically involves corticosteroids [24]. However, following imaging and clinical assessment, discontinuation of the corticosteroid therapy was advised due to their possible immunosuppressive effects. Second-line treatment should be tailored to the patient’s comorbidities and may include acitretin, biologic agents such as adalimumab, anakinra, infliximab, rilonacept, or tocilizumab, as well as colchicine, dapsone, indomethracin, potassium iodine or thalidomide [24]. Conclusions Rare occurrences may be overlooked if clinicians do not consider all possible differential diagnoses in certain cases. What appears straightforward at first glance is not always the correct diagnosis, and a thorough exploration of the underlying etiology is essential. Modern medicine increasingly emphasizes understanding 1) why certain diseases develops, 2) why some conditions have well-defined pathological mechanisms while others do not, and 3) how distinct diseases might share common pathological pathways. It also raises the question of whether a specific trigger could be the key factor in the development of multiple distinctive conditions. These questions remain largely unanswered, highlighting the need for further research. Conflict of Interest The authors declare no conflict of interest. Ethics Approval Statement Ethics approval statement is not required. Written informed consent for publication of their details was obtained from the patient. References [1] Vashisht P, Goyal A, Hearth-Holmes MP. Sweet syndrome. [Updated 2022 Sep 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK431050/ [2] O’Regan GM, Ho WL, Limaye S, et al. 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