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Monographs of essential oils that have caused contact allergy / allergic contact dermatitis
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
In one reference center for toxic bullous dermatoses in France, in the period 2009–2017, three female patients were seen who had developed severe acute contact dermatitis due to topically applied black cumin oil (13). They showed polymorphic lesions that mimicked erythema multiforme, bullous fixed drug eruption, Stevens-Johnson syndrome, or toxic epidermal necrolysis (TEN). All 3 patients had severe impairment with more than 15% of the body surface area involved, with Nikolsky sign and fever, and had a hospital length of stay of more than 10 days. Histologic examination of a skin biopsy was performed in all cases and revealed epidermal apoptosis characterized by confluent nests of apoptotic keratinocytes, with subepidermal detachment or epidermal regenerative changes, and a slight to moderate perivascular infiltrate of lymphocytes in the superficial dermis. Results from direct immunofluorescence were negative. All later had strongly positive patch tests to their own black cumin oils, diluted 1% in petrolatum. The severity of the cases suggests, according to the authors, a systemic effect of black cumin oil, inducing an extension of the lesions away from the area of application, even after topical use alone (13).
Benzydamine
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
An 81-year-old woman presented with pruritic, erythematous, scaly and enlarging plaques over the dorsum of her hands and forearms, on her chin and the centre of the forehead. Histopathology showed a dense lymphoid infiltrate in the superficial papillary dermis with focal interstitial and perivascular extension. The infiltrate was largely composed of lymphocytes. Immunophenotyping revealed a T-lymphocyte CD4/CD8 ratio of 5:6. The direct immunofluorescence study was negative. A T-cell receptor gamma gene rearrangement showed a polyclonal pattern. Patch and photopatch testing revealed a positive photopatch to benzydamine 1% pet. The patient now told that for several years she had used a gynecological solution containing 0.1% benzydamine HCl for vaginal hygiene. After ceasing its use, complete remission was achieved without recurrence in the following year. The patient was diagnosed with lymphomatoid photocontact dermatitis from benzydamine (12).
Linear IgA disease
Published in Lionel Fry, Atlas of Bullous Diseases, 2020
Direct immunofluorescence is the most reliable test for establishing the diagnosis. As with other bullous disorders, the biopsy should be taken from uninvolved perilesional skin as the immunoglobulin deposits are destroyed within the blister region.
A novel report of nivolumab-induced transient and persistent acantholytic dermatosis associated with multiple cutaneous toxicities in a patient with metastatic melanoma
Published in Acta Oncologica, 2022
Yana Kost, Daiva M. Mattis, Bijal Amin, Daniel E. Sammartino, Beth N. McLellan
On physical examination the rash was composed of discrete, pink, edematous, papules with a follicular appearance that was scattered diffusely on the trunk and proximal extremities (Figure 1). A punch biopsy of the lower back revealed spongiosis, suprabasilar acantholysis with dyskeratosis, and vesicles present in the epidermis (Figure 2). Eosinophils were present in the epidermal vesicles and dispersed among acantholytic keratinocytes. A superficial perivascular mixed inflammatory cell infiltrate was present composed predominantly of lymphocytes, with histiocytes and eosinophils. Direct immunofluorescence studies were performed and were negative for an immunobullous disorder. The histology and clinical findings supported a diagnosis of grade 2 GD. Given the patient’s significant discomfort, he was started on 100 mg doxycycline twice daily as well as a tapered course of 60 mg prednisone while continuing to hold immunotherapy treatment. After three weeks of treatment, the patient’s rash and symptoms improved. Two months later the rash remained stable on 5 mg of prednisone daily and nivolumab therapy was reinitiated. However, the rash worsened within 4 weeks of resuming immunotherapy and subsequent treatment with 300 mg of dupilumab (IL-4 receptor antagonist) every other week while continuing 5 mg of prednisone led to temporary partial symptom improvement.
IgA negative immunofluorescence in diagnoses of adult-onset Henoch-Schönlein purpura
Published in Baylor University Medical Center Proceedings, 2020
Pooja Poudel, Steven H. Adams, Kanish Mirchia, Hanish Jain, Ambika Eranki
The minority of cases in which IgA is absent may reflect variation in the duration of the lesion, as some of the instigating IgA deposition may have dissipated before the time of biopsy.4 This explanation is supported by observations that direct immunofluorescence IgA positivity is increased when the biopsy is taken closer to the onset of the lesions and declines with the progression of time. One study showed that in suspected HSP, the direct immunofluorescence positivity is around 85% when the biopsy is performed within 7 days of onset of skin lesions, but drops to around 15% if more time elapses before a biopsy is taken.4 Utilizing the timing explanation for negative IgA findings in a minority of HSP cases, we can explain why the direct immunofluorescence for case 1 yielded negative IgA results. The onset of lesions for this patient occurred at least 2 weeks before his skin biopsy. However, in case 2, the onset of lesions was noticed only 7 days before the date of skin biopsy, and yet direct immunofluorescence IgA was still negative.
Esophageal lichen planus: towards diagnosis of an underdiagnosed disease
Published in Scandinavian Journal of Gastroenterology, 2019
Franziska Schauer, Carmen Monasterio, Kristin Technau-Hafsi, Johannes Steffen Kern, Adhara Lazaro, Peter Deibert, Peter Hasselblatt, Henning Schwacha, Steffen Heeg, Volker Brass, Armin Küllmer, Arthur Robert Schmidt, Annette Schmitt-Graeff, Wolfgang Kreisel
We described clinical, endoscopic, histologic, and immunofluorescence criteria for a reliable diagnosis of esophageal involvement in lichen planus (ELP). Our data suggest that ELP is an underdiagnosed condition. Esophago-gastro-duodenoscopy should be performed in patients with known LP if dysphagia is present. Endoscopic screening in all LP patients is unrealistic due to the high prevalence of the disease. Endoscopists and pathologists must include ELP into the differential diagnosis of esophageal diseases. Direct immunofluorescence may increase diagnostic accuracy. Depending on the extent of lesions ELP may be classified into severe ELP, mild ELP, or no ELP. Severe ELP requires early start of effective therapy. Acitretin, a synthetic retinoid used for therapy of cutaneous LP seems not to prevent ELP. Topical budesonide is a prudent therapeutic option. In analogy to EoE [54,55] it is probable, that therapy of patients with severe ELP should not be completely discontinued. For patients with mild ELP we suggest a wait and see strategy and regular endoscopic controls. In patients with symptomatic stenosis endoscopic dilation should be the first measure followed by therapy with topical budesonide. Figure 3 shows a suggestion for a diagnostic and therapeutic approach to esophageal lichen planus.