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Allergic and Immunologic Reactions
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Saira N. Agarwala, Aspen R. Trautz, Sylvia Hsu
Laboratory studies: A skin biopsy can be performed in atypical cases. The histology classically depicts a septal panniculitis. Laboratory abnormalities can assist in the diagnosis of an underlying cause. A complete blood count can help to assess for infection or malignancy. Erythrocyte sedimentation rate and/or C-reactive protein can indicate widespread inflammation and possible systemic disease. Antistreptolysin O titers and rapid streptococcal tests can evaluate for possible strep infection as the precipitating factor. A chest x-ray can assess for sarcoidosis and tuberculosis.
The skin
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
In established lesions of EN, there is thickening of the fibrous septae between fat lobules. The septal thickening results from a combination of collagen deposition and infiltrate of chronic inflammatory cells, predominantly lymphocytes and histiocytes (septal panniculitis). Multinucleated histiocytes are often present in loosely arranged granulomas (Figure 19.30B). Early lesions tend to show an abundance of neutrophils in the subcutis.
Medium vessel vasculitis
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
Erythema nodosum is not associated with livedo, retiform purpura, or ulceration, and the presence of such lesions should raise suspicion of a vasculitic process. Histopathology helps rule out this condition, as septal panniculitis without vasculitis is observed in EN [6]. Erythema induratum (nodular vasculitis) may or may not ulcerate and can mimic PAN. Histopathology shows evidence of granulomatous lobular panniculitis with vasculitis [39].
Acute generalized pustular bacterid concomitant with erythema nodosum, polyarthritis, and Achilles tendinitis
Published in Modern Rheumatology, 2019
Yuki Arita, Hiroaki Taguchi, Ryota Hanada, Toshihiro Tono, Yasuo Ohsone, Utako Okata, Rie Irie, Yutaka Okano
There have been no reports to definitely show the onset mechanism of AGPB. Considerations about the mechanism were carried out in some reports. Tumor necrosis factor alpha and interferon gamma produced by an infection focus act on epidermis cornification cells and promote production of complement C3 and activate complements [8]. Activated complements lead complement C5a to move under the corner layer. The complement C5a causes the accumulation of neutrophils to move under the corner layer and forms a pustule. According to another report, epidermis cornification cells secrete cytokine, such as interleukin beta, providing a neutrophilic migration and form a pustule. Septal panniculitis caused by the infiltration of lymphocytes and neutrophils is the histopathological definition of EN [9]. In terms of neutrophil infiltration, EN is similar to bacterid. In our case, we thought the possibility of a common trigger contributing to both EN and bacterid.
Large-vessel giant cell arteritis eleven months after a diagnosis of erythema nodosum
Published in Modern Rheumatology Case Reports, 2020
Takahiro Tsuji, Kotaro Kunitomo
A 77-year-old woman was referred to our department for evaluation following a six-month history of fever and night sweats. She had a history of endometrial cancer (corpus cancer Ia, pT1aN0M0, endometrioid adenocarcinoma) that was successfully treated with surgery. A laboratory examination on her first visit revealed the following findings: white blood cell count, 10.0 × 109/L; haemoglobin, 11.1 g/dL; platelet count, 379.0 × 109/L; C-reactive protein (CRP), 7.46 mg/dL; ferritin, 216 ng/mL; procalcitonin, 0.17 ng/mL; IgG, 1,262 mg/dL; IgA, 311 mg/dL; IgM, 45 mg/dL; C3, 131 mg/dL; C4, 39 mg/dL. The results of liver and renal function tests were within normal limits. Urinalysis showed no abnormalities. Rheumatoid factor (RF), anti-nuclear antibodies (ANA), myeloperoxidase anti-neutrophil cytoplasmic antibodies (MPO-ANCA) and proteinase 3 anti-neutrophil cytoplasmic antibodies (PR3-ANCA) were not detected. An interferon γ release assay (IGRA) and two blood cultures were negative. Tumour markers (CEA, CA19-9 and CA125) were within normal limits. Computed tomography (CT) revealed mild enlargement of the mesenteric lymph nodes and there were no other abnormal findings. Positron emission tomography with 18F-fluorodeoxyglucose (FDG) combined with computed tomography (FDG-PET/CT) showed no abnormal uptake in the enlarged lymph nodes. A bone marrow examination also showed no abnormalities. As we were unable to identify the cause of fever, the patient was carefully monitored. Two months after her first visit, a rash developed on her leg. There were painful nodular skin lesions on the bilateral anterior surfaces of the lower extremities. There were no other symptoms other than fever and skin lesions. Her CRP level was elevated from 7.46 to 10.91 mg/dL. Biopsies from skin lesions showed septal panniculitis with perivascular inflammatory lymphocytic infiltration suggestive of EN (Figure 1(a–c)). No diseases associated with EN were identified. She was treated with colchicine because she failed to respond to non-steroidal anti-inflammatory drugs (NSAIDs) and potassium iodide. The skin lesions improved and her CRP level decreased from 10.91 to 2.82 mg/dL after colchicine therapy. Although colchicine was effective for EN, its oral administration was discontinued because of diarrhoea. Her CRP level and skin lesions varied due to the intermittent nature of the treatment with colchicine. Fever, fatigue, neck pain, chest pain, backache, headache and myalgia developed 11 months after the diagnosis of EN and her CRP level increased to 23.22 mg/dL. She was admitted to our department for evaluation of fever and systemic inflammation. Her clinical course from the first visit to admission is shown in Figure 2.