Intravenous Immunoglobulin Therapy-Induced Erythema Multiforme in a Patient with Chronic Lymphocytic Leukemia.

This case report discusses immunoglobulin-induced erythema multiforme (EM), a rare and understudied condition that requires further investigation. The report presents the case of a 69-year-old woman with a history of chronic lymphocytic leukemia who developed an acute hypersensitivity reaction to intravenous gamma globulin medication. The patient received intravenous immunoglobulin (IVIG) to normalize and stabilize her immunoglobulin levels and reduce the risk of recurrent infections due to her immunodeficiency with predominantly antibody defects. However, after the second administration of the medication, the patient experienced an acute skin rash and was admitted to the hospital for treatment. The treatment plan included systemic desensitizing therapy, systemic antihistamine therapy, corticosteroid therapy, and local therapy. After a course of therapy, the patient's skin condition improved, and her overall well-being improved. However, due to the acute hypersensitivity reaction, the IVIG therapy was discontinued. The multidisciplinary team of specialists concluded that the patient had developed EM. The discussion provides an overview of EM, including its causes, clinical presentation, diagnostic tools, and therapy principles. The discussion also describes the use of human IVIG preparations in treating various immunodeficient and inflammatory diseases, highlighting the importance of monitoring patients for adverse effects. The case of this patient underscores the potential risks associated with immunoglobulin therapy and emphasizes the need for healthcare providers to remain vigilant for adverse reactions. By promptly diagnosing and treating EM, healthcare providers can minimize its impact on patients' overall well-being.

Hidradenitis suppurativa in surgeons' practice: Prevalence and treatment approach according to the Hurley stage in Latvia.

Hidradenitis suppurativa (HS) is a chronic, recurrent, debilitating, and frequently misdiagnosed inflammatory skin disease that often requires surgical intervention. To assess the prevalence of HS patients in surgeons' practice and surgeons' approach to treating HS patients, we created a self-administered, Hurley stage-based questionnaire that was distributed during the Latvian Association of Surgeons meeting. Of the total 60 questionnaires distributed, 56 (93%) were collected and 53 (88%) of them were considered valid. Overall, 73.6% of the surgeons confirmed having seen patients with chronic inflamed suppurative lesions in the skin folds during their practice. Median reported number of HS patients in the surgeons' practice was 3, ranging from 0 to 30. Similarly, 73.6% of surgeons would undertake HS treatment. The proportion of surgeons undertaking treatment was higher if the surgeons had diagnosed HS by themselves but was not affected by personal knowledge of HS. Surgeons chose monotherapy for Hurley stages I, II, and III in 64.2%, 64.2%, and 62.3% of the cases, respectively. The most common therapeutic choice for monotherapy was topical antiseptics (26.4%) or topical antibiotics (20.8%) for Hurley stage I and surgery or systemic antibiotics for Hurley stage II (20.8% or 17.0%, respectively) and Hurley stage III (32.1% or 11.3%, respectively). A wide diversity of treatment approaches in specified clinical scenarios was observed, which indicates the need for local guidelines.

Eradication of damaged keratinocytes in cutaneous lichen planus forms demonstrated by evaluation of epidermal and follicular expression of CK15, indices of apoptosis and regulatory protein S100.

The study of cytoskeleton arrangement and its contribution to survival of cell-to-cell contacts appears to be essential for understanding of numerous cellular and tissue processes. Applying CK15, S100 labeling and TUNEL reaction to cutaneous lichen planus subtypes, we found CK15 expression in the outer and inner root sheath of hair follicles, the basal epidermal layer, and eccrine glands. Its follicular expression was decreased in nearby inflammatory infiltrates. The CK15 immunopositivity was mostly described as weak (92.3%) for lichen planus but equally subdivided into weak, moderate and strong in lichen planopilaris (2 = 32.514; df = 4; p < 0.001). The greatly varying apoptotic index was the highest in the lichen planopilaris involving the scalp: 81.2 ±10.7; 87.8 ±10.7 and 88.0 ±10.5 for the basal, spinous and upper epidermal layers, respectively. S100 positive epidermal and follicular cells did not differ in the lesions demonstrated in the study groups; still immunoreactivity was more pronounced in the scalp region of lichen planopilaris. Damage of cell-to-cell contacts was confirmed by electron microscopy. Apart from immunocyte-mediated keratinocyte death, cytoskeleton-based injury and loss of cell-to-cell and matrix contacts may be of great importance, leading to eradication of degrading cells and thus contributing to the pathogenesis of lichen planus.