Systemic inflammation has been recognized as the cause and consequence of metabolic dysregulation in diabetes mellitus (DM). Presepsin has recently emerged as a promising biomarker for the detection of bacterial infections and sepsis. There is evidence that gut dysbiosis results in the increased circulating concentrations of Gram-negative bacteria lipopolysaccharide, the linkage of presepsin, which in turn promotes insulin resistance and correlates with the risk of diabetic complications. Thus, we hypothesized that presepsin could reflect the magnitude of systemic inflammation and metabolic decompensation in patients with DM even in the absence of infection. In this cross-sectional pilot study, we included 75 infection-free individuals with well-controlled (n = 19) and uncontrolled (n = 23) type 2 diabetes (T2D), well-controlled (n = 10) and uncontrolled (n = 10) type 1 diabetes (T1D), and normoglycemic controls (n = 13). Presepsin levels were compared between the groups and potential associations with demographic, clinical, and laboratory parameters were explored. We observed that the duration of DM was associated with presepsin values (p = 0.008). When the participants were classified into the type of DM groups, the presepsin levels were found to be lower in the patients with T2D compared to those with T1D (p = 0.008). However, significance in that case was driven by the difference between the well-controlled groups. After adjusting for the effects of DM duration, presepsin was significantly lower in the well-controlled T2D group compared to the well-controlled T1D group [1.34 (2.02) vs. 2.22 (4.20) ng/mL, p = 0.01]. Furthermore, we adjusted our findings for various confounders, including age, body mass index, and waist circumference, and found that the difference in the presepsin values between the adequately controlled groups remained significant (p = 0.048). In conclusion, our findings suggest that presepsin could potentially serve as a surrogate marker of inflammation and metabolic control in people with DM.

Pleomorphic dermal sarcoma (PDS) is a rare mesenchymal tissue tumor. Its differential diagnosis from similar tumors, such as low differentiated squamous cell carcinoma, fibrosarcoma, desmoplastic melanoma, atypical fibroxanthoma (AFX), may be difficult, as they have similar clinical and histological presentation. We present a case of an 83-year-old man exhibiting an exophytic scalp lesion. Excision of the lesion was performed, ensuring clear surgical margins and pathologic examination revealed an invasive pleomorphic dermal sarcoma. This case highlights a rare case of a large pleomorphic dermal sarcoma, and it discusses the histological, molecular features, its differential diagnosis and management of PDS.

Background and Clinical Significance: Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening hyperinflammatory syndrome characterized by uncontrolled activation of macrophages and cytotoxic lymphocytes. Secondary HLH is most commonly associated with infections, malignancies, and autoimmune disorders. Visceral leishmaniasis (VL) is an uncommon infectious trigger of HLH, and the considerable overlap in clinical manifestations frequently delays diagnosis. Early recognition of the infectious trigger is essential, because prompt targeted therapy may prevent the need for prolonged immunosuppressive treatment and substantially improve outcomes. Case Presentation: A 68-year-old livestock farmer from northern Greece presented with a one-month history of persistent fever, fatigue, and night sweats. Laboratory evaluation demonstrated pancytopenia, severe hyperferritinemia, hypertriglyceridemia, and elevated soluble interleukin-2 receptor (sCD25) levels. After extensive, relevant screening for other underlying etiologies, which proved to be negative, bone marrow examination revealed hemophagocytosis, while anti-Leishmania serology and polymerase chain reaction (PCR) analysis of bone marrow aspirate confirmed infection with Leishmania infantum. Treatment with liposomal amphotericin B along with intravenous dexamethasone resulted in rapid clinical and laboratory improvement. Serial ferritin and sCD25 measurements closely paralleled clinical recovery, supporting their potential usefulness as biomarkers of treatment response. The patient remained asymptomatic at one-month follow-up. Conclusions: Secondary HLH associated with VL is rare, but potentially fatal. Clinicians should maintain a high index of suspicion in patients presenting with prolonged fever, splenomegaly, cytopenia, and marked hyperferritinemia, particularly in endemic regions. Early diagnosis and prompt initiation of targeted therapy are associated with favorable outcomes.