Tinea incognito is an atypical form of dermatophytosis caused by previous use of topical or systemic immunosuppressive therapy, most often corticosteroids. Modification of the clinical presentation frequently leads to diagnostic delay and misdiagnosis, especially in patients with concomitant chronic inflammatory skin diseases such as psoriasis. We present a narrative review of the literature on tinea incognito in patients with psoriasis during immunosuppressive therapy. We screened 386 abstracts and included 16 comparable case reports focusing on tinea incognito occurring in patients with psoriasis or during antipsoriatic treatment. The review summarizes clinical presentations, diagnostic challenges, and therapeutic approaches reported in the literature. Additionally, we present a clinical case of a 27-year-old man with a long history of plaque psoriasis treated with methotrexate and cyclosporine. The patient developed rapidly progressive skin lesions with pustular features and further deterioration despite systemic antipsoriatic therapy. Initial mycological examinations were negative. Histopathological examination revealed a chronic purulent perifollicular inflammatory process with extension into the subcutaneous tissue. The correct diagnosis was confirmed after a repeat skin biopsy with periodic acid–Schiff and Grocott staining and fungal culture of the skin tissue, which revealed Trichophyton rubrum. The review highlights that clinical features are often nonspecific and may overlap with inflammatory dermatoses. This underscores the need for a high index of clinical suspicion for fungal infection in atypical or refractory psoriatic lesions. It also emphasizes the importance of repeated mycological and histopathological examinations to achieve an accurate diagnosis, avoid inappropriate escalation of immunosuppression, and enable timely antifungal treatment.

Background and Objectives: Pemphigus vulgaris (PV) is a rare autoimmune blistering disease caused by IgG au-toantibodies against desmoglein 1 and/or desmoglein 3, leading to flaccid blisters on the skin and mucous membranes. The course of PV during pregnancy represents a special clinical challenge due to immunological changes accompanying physiological immunosuppression and the need to protect the developing fetus. Materials and Methods: To analyze the current state of knowledge, a literature review was performed covering the years 2015–2025. Publications describing PV diagnosed during pregnancy or in neonates were screened, and nine case reports discussing ten patients meeting the inclusion criteria were selected for detailed analysis. In this study, we also present our own clinical case of PV in pregnancy to complement the literature review and provide practical insight into disease management. Results: In most cases, the disease was diagnosed in the first trimester of pregnancy, and the most common symptoms were flaccid blisters and erosions of the oral mucosa. The diagnosis was confirmed by direct immunofluorescence (DIF) and ELISA testing. The first-line treatment remained systemic glucocorticosteroids (GCS), mainly prednisolone, which is considered the safest. In resistant cases, intravenous immunoglobulins (IVIg) were used, which were considered effective and safe, though their use may limit the transplacental transfer of autoantibodies to the fetus. In newborns, the symptoms rarely occurred, were mild, and resolved spontaneously. Drugs with proven teratogenic effects, such as methotrexate, cyclophosphamide, and mycophenolate mofetil, are contraindicated during pregnancy. In the case of rituximab therapy, it is recommended to postpone pregnancy for at least 12 months after the completion of treatment to minimize the potential risk of immunosuppression in the newborn. Conclusions: The treatment of PV during pregnancy requires close interdisciplinary cooperation. Therapy should be carefully individualized, taking into account both therapeutic efficacy and fetal safety. Perhaps then, pregnancy-related pemphigus diseases, given their peculiarities, should be classified as a distinct variety within the desmosomal type of autoimmune blistering diseases.

Subcutaneous thrombotic vasculopathy (STV) is a rare, non-inflammatory occlusive disorder of the cutaneous microvasculature that predominantly involves the subcutaneous tissue and may closely mimic inflammatory vasculitis. We describe a case of STV with overlapping features of leukocytoclastic vasculitis (LCV) in a 23-year-old woman presenting with rapidly progressive, painful purpuric skin lesions. The patient had a history of polysubstance use disorder and reported intravenous injection of crushed oral oxycodone and methylphenidate tablets. Histopathological examination of a deep skin biopsy revealed fibrin-rich thrombi occluding small vessels of the dermis and subcutaneous tissue. Fine granular IgA deposits in the walls of numerous superficial dermal blood vessels shown using direct immunofluorescence suggested LCV. Overall, the findings supported a mixed thrombotic-inflammatory vasculopathy with predominant features of STV. This case highlights the diagnostic complexity of STV and may suggest intravenous injection of crushed oral medications as a potential trigger through particle-induced microvascular obstruction and secondary thrombosis. In addition, we conducted a literature review indicating that STV remains a rare and likely underrecognized entity, with only a limited number of reported cases.

Background: Pemphigus diseases are rare autoimmune blistering disorders mediated by pathogenic autoantibodies directed mainly against desmoglein 1 and desmoglein 3. Although most cases are considered idiopathic, external triggers that can disrupt immune tolerance have been described. Vaccination has been discussed as a potential precipitating factor in autoimmune skin diseases. However, the relationship between vaccination and the induction of pemphigus-related autoantibodies has not been comprehensively summarized. Methods: We conducted a narrative review of all available studies published in the last 25 years identified through medical databases, excluding studies on COVID-19 vaccinations. Reports describing either new-onset pemphigus or exacerbation of preexisting pemphigus with a temporal association to vaccination were included. Clinical characteristics, vaccine type, latency period, direct immunofluorescence findings, and ELISA results for desmoglein autoantibodies were analyzed. In addition, we present our own clinical-laboratory experience illustrating this issue. Results: The current evidence consists predominantly of case reports and small case series. Published cases describe pemphigus vulgaris and pemphigus foliaceus occurring after vaccinations against influenza, hepatitis B, tetanus, diphtheria, pertussis, rabies, and other routinely administered immunizations. The latency period most often ranged from several days to a few weeks. Immunopathological findings were consistent with classical pemphigus diseases, including intercellular IgG deposits in the epidermis and circulating autoantibodies against desmoglein 1 and/or desmoglein 3. Our patient was a 78-year-old woman who developed cutaneous form of pemphigus vulgaris, diagnosed with direct immunofluorescence (DIF) and multiplex ELISA, 10 days after diphtheria–tetanus–pertussis vaccination. The patient had a positive family history of autoimmune blistering disease, namely mucous membrane pemphigoid. Conclusions: Based on the currently available evidence, a direct causal relationship between vaccination and pemphigus diseases cannot be established. Nevertheless, accumulated clinical and serological observations suggest that vaccination may act as a triggering factor in genetically or immunologically predisposed individuals, possibly by amplifying pre-existing subclinical autoreactive immune responses. Further population-based and mechanistic studies are required to clarify this association, while the overall benefits of vaccination remain substantial.

General pustular psoriasis (GPP) is a rare, potentially life-threatening neutrophilic dermatosis. Pediatric cases are uncommon and often misdiagnosed due to overlapping clinical and histopathological features with other pustular dermatoses. We present a case of an 11-year-old boy, initially diagnosed with Sneddon–Wilkinson syndrome, who presented with disseminated pustular eruptions, with no response to antibiotics, dapsone, and glucocorticosteroids. In histopathology, we observed subcorneal neutrophilic pustules. Due to atypical features and poor treatment response, the patient underwent genetic testing, which revealed a homozygous IL36RN gene c.338C>T (p.Ser113Leu) pathogenic variant, which enabled a definitive diagnosis of GPP. Treatment with acitretin led to clinical improvement. Pediatric GPP poses diagnostic and treatment challenges. Genetic testing for IL36RN pathogenic variants may aid in the diagnosis, especially in atypical cases. The presence of the biallelic IL36RN pathogenic variant supports the diagnosis of DITRA (Deficiency of the IL-36 Receptor Antagonist, ORPHA:404546)—a monogenic autoinflammatory form of GPP.