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The Twentieth Century and Beyond
Published in Scott M. Jackson, Skin Disease and the History of Dermatology, 2023
Walter B. Shelley (1917–2009) was a long-time professor of dermatology at the University of Pennsylvania and, later in his career, at the Medical College of Ohio. Like a reincarnation of Unna, Shelley had for his whole career devoted equal parts of his energies to both the clinical and the scientific. He researched virtually every aspect of cutaneous biology (sweat glands, nerves, itch, hair, nails, etc.) and wrote hundreds of papers on his research. He was the first to describe a dozen or more dermatologic entities, including aquagenic urticaria, larva currens, autoimmune progesterone dermatitis, piezogenic pedal papules, and mid-dermal elastolysis. In his books, his greatest attribute—intellectual curiosity—is on full display, and the anecdotal evidence recorded by Shelley in such works as Advanced Dermatologic Therapy II (1987) for a time carried as much weight as the peer-reviewed, evidence-based medical articles written by his contemporaries. Such was the mastery this man had over his craft.
The menstrual cycle and the skin
Published in Miranda A. Farage, Howard I. Maibach, The Vulva, 2017
Birgit Drexler, Michael Landthaler, Silvia Hohenleutner
Although a report describing a premenstrual exacerbation of dermatitis herpetiformis was published in 1906 (45), the medical literature contains few reports that refer to the influence of the menstrual cycle on the activity of this disease. Clinically, it is difficult to distinguish the perimenstrual exacerbation of dermatitis herpetiformis from an autoimmune progesterone dermatitis (APD). The diagnosis must be based on histopathology, direct immunofluorescence, and a lack of evidence for an autosensitization to progesterone (46).
Urticaria and Angioedema
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Jenny M Stitt, Stephen C Dreskin
Only about 5% of chronic spontaneous urticaria/angioedema may have an identifiable cause. In rare cases, chronic urticaria/angioedema is associated with comorbid infection, environmental exposures or hormonal changes or systemic illness (Dreskin 2012). Appropriate management of these issues can result in resolution of the urticaria. In endemic areas, infections with multicellular parasites such as strongyloides or filaria elicit a significant IgE response and may result in chronic urticaria. Similarly, exposure to food, dietary supplements and medications may lead to chronic urticaria symptoms, however the exposure must be frequent, and would be considered a recurrent acute urticaria. Contact allergens such as detergents and soaps, latex, hair or nail products or other cosmetics may also cause contact hives, but exposure must be frequent and may also be better defined as contact urticaria. Food and environmental allergy are uncommon causes of chronic urticaria, and there is poor correlation with ingestion of suspected food triggers and provocation of urticaria in placebo controlled challenges. Some patients experience urticaria during menses or experience symptom flares during the menstrual cycle. These patients may have hypersensitivity to progesterone or autoimmune progesterone dermatitis. They may also have pseudoallergic reactions to analgesics such as NSAIDs taken for menstrual symptoms. Urticaria can rarely be due to systemic autoimmune illness. Cold-induced urticaria due to cryoglobulins has been rarely reported. There is no known association of urticaria with neoplasms, though acquired angioedema is associated with neoplastic disease, as discussed below.
A focused report on progestogen hypersensitivity
Published in Expert Review of Clinical Immunology, 2023
Diti H. Patel, Lauren M. Fine, Jonathan A. Bernstein
Progestogen hypersensitivity (PH), previously known as autoimmune progesterone dermatitis (APD), is an increasingly recognized syndrome, which presents as a hypersensitivity reaction to progestogens [1]. Progestogen hypersensitivity was first described by Shelley et al. in 1964 as a dermatologic presentation of pruritic vesiculobullous eruptions [2]. It has since been reported as a heterogenous mix of clinical presentations that are characteristically cyclical in nature and include urticaria, angioedema, asthma, and anaphylaxis in addition to the initially reported dermatitis [1,2]. Although many reports have appeared in the literature since the initial description, the epidemiology of PH remains unclear as there are no published estimates on its global incidence and prevalence. The average age of onset is in the late 20s, although the clinical presentation ranges broadly within the reproductive window, from menarche to menopause. The majority of cases occur as a result of normal fluctuations of endogenous progesterone during the menstrual cycle and pregnancy. However, exogenous progestin triggers including oral contraceptives, emergency contraceptives, hormonal intrauterine devices, and in vitro fertilization (IVF) are also commonly reported causes of PH [1,3]. The heterogeneous clinical presentation of PH in conjunction with frequently reported irregular menstrual cycles makes recognition of the cyclical nature of symptoms more difficult, and likely contributes to poor recognition of disease in clinical settings. With the increased use of exogenous progestins in contraception and fertility treatments, more emerging cases of hypersensitivity to exogenous progestins have been described and are likely to continue to emerge. In this short review, a brief summary of PH biology, pathophysiology, clinical presentation, and management will be presented with the objective of increasing awareness and recognition of this condition across clinical settings and specialties.