Background Chronic spontaneous urticaria (CSU) may occasionally exhibit long‐lasting lesions with bruising, usually considered a hallmark of urticarial vasculitis (UV). Histopathology of these chronic urticarial lesions has not been extensively studied. Methods Skin biopsies from patients with anti‐H1 resistant CSU were evaluated for several parameters (edema, location, intensity, and cell composition of the inflammatory infiltrate, and abnormalities in the blood vessels). Results We studied 45 patients (37 female/8 male, mean age 49.3 years) with CSU, 60% of whom with occasional bruising lesions and 3 patients with hypocomplementemic UV. Histopathology in CSU showed mainly perivascular and interstitial inflammatory infiltrate (91.1%), including eosinophils (80%), neutrophils (77.8%), and lymphocytes (71.1%), vasodilatation (88.9%), intravascular neutrophils (95.6%), dermal edema (51.1%), swelling of endothelial cells (51.1%), and minor and rare fibrinoid necrosis and karyorrhexis (6.7%). Significant karyorrhexis and frank fibrinoid necrosis were observed, respectively, in two and three cases of UV. In patients with occasional bruising, mast cells occurred in fewer cases whereas eosinophils were more frequent, but no statistically significant difference was found for other parameters. Conclusions Histopathological findings were not significantly different between CSU with or without bruising lesions. Bruising may be associated with more severe forms of CSU with no histopathological signature, although UV cannot be completely excluded based on histopathology.
Pharyngitis with petechiae and exudative palatine tonsillitis are typical manifestations of infectious mononucleosis (IM). Lingual tonsillitis (LT) is an uncommon manifestation of IM. 1,2 We recently encountered a child with LT complicating IM.A 6-year-old boy presented to the emergency department in a hospital in regional New South Wales with a 12-day history of sore throat and fever. On presentation, he had severe odynophagia. His speech had a muffled quality described as being a 'hot potato voice'. He was treated with oral penicillin and a single dose of oral steroids by his general practitioner.He was miserable, febrile and dehydrated with mild tachycardia. Exudative palatine tonsillitis and upper cervical lymphadenitis were seen. No stridor, trismus or breathing difficulty were noted and the rest of the examination was unremarkable.Investigations revealed a leucocytosis with increased neutrophils and lymphocytes, elevated Alanine transaminase and Aspartate aminotransaminase and the Epstein-Barr virus IgM was positive.A lateral airway radiograph showed a rounded soft tissue mass at the base of the tongue markedly narrowing the pharyngeal airway suggestive of enlarged lingual tonsil (Fig. 1).He was treated with analgesia, intravenous fluids, parenteral penicillin and a short course of intravenous and oral steroids. The symptoms gradually resolved over the following 5 days.The clinical, laboratory and radiological features suggested a diagnosis of LT complicating IM.A literature search found only a few case reports of LT complicating IM, one an adolescent who had a palatine tonsillectomy at a younger age. 1,2 We hypothesise LT complicating IM is under-recognised and hence under-reported as it is overshadowed by more obvious palatine tonsillitis.Our case highlights the following: (i) In a child with severe odynophagia and a voice with a muffled quality sometimes described as being a hot potato voice, LT needs to be considered as a differential diagnosis; (ii) in the absence of onsite paediatric otolaryngology services, lateral airway radiograph is helpful in arriving at the diagnosis; and (iii) there is modest evidence that corticosteroids are beneficial in children with acute respiratory obstruction due to tonsillar enlargement in Epstein-Barr virus infection. 3
Impaired skin barrier is one of the hallmarks of atopic dermatitis (AD), with abnormalities in the cornified envelope, lipid lamellae, tight junctions and cutaneous microbiome. These findings are also present in nonlesional skin of AD individuals, suggesting that epidermal barrier defects may be the initial step towards the development of AD and eventually other atopic diseases (atopic march). It is currently known that pathophysiology of AD involves an interplay between this dysfunctional skin barrier and a predominantly type 2 skewed innate and adaptive immune responses, which further disrupt the skin barrier through type 2 cytokines. In this setting, there is enhanced penetration of environmental and food allergens through a deficient barrier, leading to an increased susceptibility to sensitization. During the sensitization process, thymic stromal lymphopoietin (TSLP) polarizes skin dendritic cells to a T-helper 2 response, and TSLP seems to be a key cytokine in the sensitization of food allergy, allergic asthma and rhinitis. In this review, the authors describe the current knowledge of the pathophysiology of the epidermal barrier, its disruption in AD and how it may be involved in the development of atopic comorbidities and the role of barrier repair therapy on the prevention of the atopic march progression.
A positive serum basophil histamine release assay is a marker for ciclosporin-responsiveness in patients with chronic spontaneous urticaria. Clin Transl Allergy 2012; 2: 19.
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