An unexpected allergic skin reaction to peppermint oil capsules.

Peppermint oil capsules are prescribed to manage abdominal colic and distension, a common complaint in postcaesarean section patients. Arachis (peanut) oil is contained within one frequently prescribed peppermint formulation: Colpermin. This ingredient is contraindicated in patients with peanut and soya allergy; however, this is not stated in the side effects or contraindications section of the British National Formulary, or present on the medication packaging. A postpartum woman in her early 30s had an unexpected allergic reaction to the capsules, in the form of a generalised body rash, fortunately with no anaphylactic features. The patient reported the same reaction to soya in the past. After review of the patient's clinical and medication history, Colpermin capsules were thought to be responsible for the patient's symptoms. This case highlights the necessity for clearer documentation in prescribing formularies and on medication packaging to ensure patient safety.

VEXAS syndrome as a cause of debilitating fatigue and intermittent fever.

VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is a newly discovered complicated autoinflammatory syndrome associated with haematological and rheumatological manifestations, recognized for the first time in 2020. In this case report, we describe the first case of VEXAS syndrome in the North Denmark Region. A 76-year-old male was briefly admitted with COVID-19 and a myriad of symptoms including jaw pain, arthralgia, skin rash, malaise, intermittent fever and weight loss. After a prolonged diagnostic evaluation, VEXAS syndrome was suspected and confirmed with the presence of a mutated ubiquitin-like modifier activating enzyme 1 (UBA1) gene.

Factors related to the mortality risk of severe hand, foot, and mouth diseases (HFMD): a 5-year hospital-based survey in Guangxi, Southern China.

BACKGROUND: To understand the factors influencing clinical outcomes of severe hand, foot, and mouth diseases (HFMD), and to provide scientific evidence for reducing the mortality risk of severe HFMD. METHODS: From 2014 to 2018, children diagnosed with severe HFMD cases in Guangxi, China, were enrolled in this hospital-based study. The epidemiological data obtained through face-to-face interviews with the parents and guardians. Univariate and multivariate logistics regression models were used to analyze the factors influencing the clinical outcomes of severe HFMD. The impact of the EV-A71 vaccination on inpatient mortality was analyzed by a comparison approach. RESULTS: A total of 1565 severe HFMD cases were enrolled in this survey, including 1474 (94.19%) survival cases and 91 (5.81%) death cases. The multivariate logistic analysis demonstrated that HFMD history of playmates in the last three months, first visit to the village hospital, time from the first visit to admission less than two days, no correct diagnosis for HFMD at the first visit, and having no rash symptoms were the independent risk factors for severe HFMD cases (all p < 0.05). While EV-A71 vaccination was a protective factor (p < 0.05). The EV-A71 vaccination group versus the non-vaccination group showed 2.23% of death in the vaccination group and 7.24% of death in the non-vaccination group. The EV-A71 vaccination protected 70.80% of the death of severe HFMD cases, with an effective index of 4.79. CONCLUSIONS: The mortality risk of severe HFMD in Guangxi was related to playmates had HFMD history in last 3 months, hospital grade, EV-A71 vaccination, patients visit hospital previously, and rash symptom. EV-A71 vaccination can significantly reduce mortality among severe HFMD. The findings are of great significance for the effective prevention and control of HFMD in Guangxi, southern China.

Diisocyanates influence models of atopic dermatitis through direct activation of TRPA1.

We recently used EPA databases to identify that isocyanates, most notably toluene diisocyanate (TDI), were the pollutant class with the strongest spatiotemporal and epidemiologic association with atopic dermatitis (AD). Our findings demonstrated that isocyanates like TDI disrupted lipid homeostasis and modeled benefit in commensal bacteria like Roseomonas mucosa through disrupting nitrogen fixation. However, TDI has also been established to activate transient receptor potential ankyrin 1 (TRPA1) in mice and thus could directly contribute to AD through induction of itch, rash, and psychological stress. Using cell culture and mouse models, we now demonstrate that TDI induced skin inflammation in mice as well as calcium influx in human neurons; each of these findings were dependent on TRPA1. Furthermore, TRPA1 blockade synergized with R. mucosa treatment in mice to improve TDI-independent models of AD. Finally, we show that the cellular effects of TRPA1 are related to shifting the balance of the tyrosine metabolites epinephrine and dopamine. This work provides added insight into the potential role, and therapeutic potential, or TRPA1 in the pathogenesis of AD.

Probable enterotoxin-associated toxic shock syndrome caused by Staphylococcus epidermidis.

BACKGROUND: We describe a case of a toxic shock-like syndrome in a child, which was associated with Staphylococcus epidermidis instead of Staphylococcus aureus or Streptococcus pyogenes, the usual causes of toxic shock syndrome. CASE PRESENTATION: The patient was an 8-year-old boy who developed a toxic shock syndrome-like illness, including fever, hypotension, and rash. The Staphylococcus epidermidis isolate was cultured from urine, but this organism was unavailable for toxin testing. Multiple blood cultures were negative. Instead, a highly novel assay was used on acute plasma from the patient which demonstrated the presence of the genes for superantigens, staphylococcal enterotoxins A, C, D, and E. Superantigens are the known causes of toxic shock syndrome. CONCLUSIONS: Our study suggests strongly that Staphylococcus epidermidis was causing the TSS symptoms through the known Staphylococcus aureus superantigens. It is unknown how many other such patients exist; this should be explored. Of great importance is that PCR performed directly on blood plasma in the absence of microbial isolation could be used to demonstrate superantigen genes.

A case report of a blueberry muffin baby caused by congenital self-healing indeterminate cell histiocytosis.

BACKGROUND: Blueberry muffin is a descriptive term for a neonate with multiple purpuric skin lesions. Many causes are known, amongst them life-threatening diseases like congenital infections or leukemia. Indeterminate cell histiocytosis (ICH) is an exceptionally rare cause of blueberry muffin rash. ICH is a histiocytic disorder which can be limited to the skin or can present with systemic involvement. A mutation that has been described in histiocytic disorders is a MAP2K1 mutation. In ICH, this mutation has previously been described in merely one case. CASE PRESENTATION: A term male neonate was admitted to the neonatology ward directly after birth because of a blueberry muffin rash. ICH was diagnosed on skin biopsy. The lesions resolved spontaneously. The patient is currently 3 years old and has had no cutaneous lesions or systemic involvement so far. This disease course is similar to that of the Hashimoto-Pritzker variant of LCH. CONCLUSIONS: ICH can manifest in neonates as resolving skin lesions. It is limited to the skin in most cases, but systemic development is possible. Therefore, it is essential to confirm the diagnosis with a biopsy before the lesions resolve and to monitor these patients closely with routine follow-up.

Photo-Induced Sweet Syndrome: A Case Report.

Sweet syndrome is a rare dermatologic condition frequently accompanied by fever and neutrophilia. Underlying triggers and etiology of the sweet syndrome remain elusive, although infection, malignancy, medications, and more rarely, sun exposure have been associated with its development. We present a case of a 50-year-old female who developed a painful, mildly pruritic rash on sun-exposed areas of the neck, arms, and legs. She also reported chills, malaise, and nausea upon presentation. Before developing the rash, she had preceding upper respiratory infection symptoms, used ibuprofen for joint pain, and had extensive sunlight exposure on the beach. Laboratory findings were significant for leukocytosis with absolute neutrophilia, elevated C-reactive protein, and elevated erythrocyte sedimentation rate. Skin punch biopsy demonstrated papillary dermal edema with dense neutrophilic infiltration. Further evaluation for hematologic or solid organ malignancy was negative. Following the administration of steroids, the patient demonstrated significant clinical improvement. While rare, ultraviolet A and B sunlight has been shown in rare situations to be associated with the development of the Sweet syndrome. The underlying mechanism for the development of photo-induced Sweet syndrome remains unknown. However, excessive sunlight exposure should be considered a potential cause when evaluating the underlying triggers for the development of the Sweet syndrome.

Botanical Briefs: Daffodils (Narcissus Species).

Daffodils (Narcissus species) are the most common cause of irritant contact dermatitis among florists. Calcium oxalate crystals contained in the sap of the daffodil plants lead to irritant contact dermatitis on the skin. Daffodil rash commonly presents with fissuring, scaling, and erythema of the fingertips, hands, and forearms. The best preventative measure is to wear appropriate protective gloves and clothing.

Epidermal Growth Factor Receptor Inhibitor-Induced Symmetrical Drug-Related Intertriginous and Flexural Exanthema: Should You Discontinue the Offending Agent?

Epidermal growth factor receptor (EGFR) inhibitors cause numerous cutaneous adverse events (AEs), including papulopustular eruptions, paronychia, acral fissures, xerosis, alopecia, and trichomegaly. Symmetrical drug-related intertriginous and flexural exanthema (SDRIFE) is a cutaneous reaction that has been uncommonly reported in association with EGFR inhibitors, though the optimal management strategy for this condition is unknown. We present 2 cases of SDRIFE secondary to EGFR inhibitor therapy in which the EGFR inhibitor was successfully continued while topical therapy was administered for effective control of symptoms. We also review the literature on EGFR inhibitor-related SDRIFE to assess the range of approaches to treating this condition. Our analysis suggests that the dermatologist is critical in diagnosing and treating this cutaneous AE, which may be supported with skin-directed therapy and may not require discontinuation of cancer treatment.

[Adult-onset Still's disease : Diagnosis and treatment according to the new S2e guidelines of the German Society of Rheumatology (DGRh)]. / Adultes Still-Syndrom : Diagnostik und Therapie unter Berücksichtigung der neuen DGRh(Deutsche Gesellschaft für Rheumatologie)-S2e-Leitlinie.

Adult-onset Still's disease (AOSD) is a rare autoinflammatory disease characterized by intermittent fever and a combination of symptoms, such as an evanescent rash synchronous with fever, arthralgia/arthritis, lymphadenopathy and hepatosplenomegaly. The diagnosis is based on a characteristic constellation of symptoms and the exclusion of infections, hemato-oncological diseases, infectious diseases and alternative rheumatological causes. The systemic inflammatory reaction is reflected by high levels of ferritin and C­reactive protein (CRP). The pharmacological treatment concept includes glucocorticoids often in combination with methotrexate (MTX) and ciclosporine (CSA) for reduction of steroids. The interleukin 1 (IL-1) receptor antagonist anakinra, the IL-1beta antibody canakinumab or an IL­6 receptor blockage with tocilizumab (off label for AOSD) are used where there is no response to MTX or CSA. Anakinra or canakinumab can be used as a primary option in AOSD in cases of moderate and severe disease activity.