Leishmaniasis is a systemic parasitic disease that can affect unusual sites such as the lungs.

We report a case of a 45-year-old male with human immunodeficiency virus infection who presented with abdominal pain and vomiting. Imaging studies revealed minimal bilateral ground-glass opacities in the lungs, hepatosplenomegaly, and diffuse lymphadenopathy. A bronchoscopy with bronchoalveolar lavage cytology evaluation showed abundant macrophages containing numerous intracellular organisms with characteristic dot-like kinetoplasts, confirming the diagnosis of Leishmaniasis. Special stains for other infections were negative.

This case highlights the value of bronchoalveolar lavage cytology in diagnosing non-neoplastic lung pathologies, including parasitic infections like Leishmaniasis, thereby enabling prompt and targeted treatment.

The diagnostic value of primary biliary cholangitis (PBC)-specific antibodies in patients with elevated alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT) levels, and other identifiable causes, was unclear. Our study aimed to determine whether etiological treatments in PBC-specific antibody-positive patients could improve liver biochemical tests, thereby distinguishing them from individuals with PBC.

We enrolled patients who were positive for PBC-specific antibodies and elevated ALP and/or GGT levels but with other identifiable etiologies. Changes in liver biochemistry following non-ursodeoxycholic acid etiological treatments were monitored.

A total of 155 patients with positive PBC-specific antibodies and elevated ALP and/or GGT levels due to non-PBC diseases were enrolled. Among them, 100 patients were diagnosed with non-PBC liver diseases, mainly metabolic-associated fatty liver disease, drug-induced liver injury, and autoimmune hepatitis. Additionally, 55 patients had non-liver diseases, predominantly connective tissue diseases. The median follow-up duration was 15.9 (4.7–25.6) months. Among 141 patients who completed follow-up after receiving etiological treatments, 85.1% (120/141) showed improvement in ALP and/or GGT levels, with 51.8% (73/141) achieving normalization of both ALP and GGT. However, 68 patients continued to exhibit elevated ALP and/or GGT, with 55 patients displaying isolated GGT elevation and 11 patients showing liver histological changes not consistent with PBC.

PBC-specific antibodies, along with elevated ALP and GGT levels, may occur in various non-PBC diseases. Etiological treatments may improve or even resolve cholestatic biochemistry. For these patients, initiating etiological treatment rather than immediately starting ursodeoxycholic acid therapy would be justified.

Liver injury in Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) is a multifaceted disorder, lacking cohort homogeneity due to a variety of potential causes, including drugs, arsenic and other heavy metals, glyphosate, infections, and ultraviolet radiation. The goals of this review were (1) to analyze the role of diagnostic algorithms in assessing causality for potential culprits involved in the development of liver injury associated with immune-mediated SJS and TEN, which represent immune-based variant disorders within a continuous spectrum. Milder forms are classified as SJS or SJS/TEN overlap, while TEN is known as the most serious form; and (2) to interpret the findings that allow for the characterization of the different types of these disorders. The manuscript is based on an extensive literature search for single case reports, case cohorts, and review articles. Search terms included: Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis, and specific diagnostic algorithms such as the Roussel Uclaf Causality Assessment Method (RUCAM) and the Algorithm of Drug Causality for Epidermal Necrolysis (ALDEN). For the purpose of basic feature description, the uniform term SJS/TEN is used in the current analysis. SJS/TEN presents with five different cohort types: SJS/TEN type (1), which refers to a cohort of SJS/TEN caused by drugs, as assessed by both ALDEN and RUCAM; type (2), representing SJS/TEN due to drugs and assessed by ALDEN only, but not by RUCAM; type (3), which includes a cohort of SJS/TEN caused by drugs, assessed by non-ALDEN and non-RUCAM tools; type (4), which focuses on a cohort of SJS/TEN caused by non-drug culprits, assessed by various tools; and type (5), which considers a cohort of SJS/TEN caused by unknown culprits. Using this new SJS/TEN typology will help better characterize individual features, personalize treatment, and clarify pathogenetic specifics for each of the five disease types. This new SJS/TEN typology provides clarity by replacing issues of inhomogeneity with cohort homogeneity.

Type 2 diabetes mellitus (T2DM) is a prevalent yet complex metabolic disorder that has shown a rising incidence over the past few decades. Recent research has identified flavonoids as compounds capable of both preventing and managing T2DM through various mechanisms. These mechanisms include enhancing insulin sensitivity, stimulating insulin secretion, modulating intestinal microbiota, inhibiting glucose absorption, and reducing gluconeogenesis. Moreover, numerous studies have suggested that flavonoids may influence gut hormones. Therefore, we propose that flavonoids could serve as effective therapeutic agents for T2DM by modulating intestinal hormone levels. This review aimed to elucidate the potential pathways through which flavonoids may impact T2DM, with a particular emphasis on their role in regulating the enteroendocrine system.

Hepatocellular carcinoma (HCC) is one of the deadliest malignant tumors in the world, and its incidence and mortality have increased year by year. HCC research has increasingly focused on understanding its pathogenesis and developing treatments.The Wnt signaling pathway, a complex and evolutionarily conserved signal transduction system, has been extensively studied in the genesis and treatment of several malignant tumors. Recent investigations suggest that the pathogenesis of HCC may be significantly influenced by dysregulated Wnt/β-catenin signaling. This article aimed to examine the pathway that controls Wnt signaling in HCC and its mechanisms. In addition, we highlighted the role of this pathway in HCC etiology and targeted treatment.

Patients with obstructive sleep apnea (OSA) and metabolic syndrome (MetS) have a higher prevalence and mortality rate of cardiovascular diseases, posing a significant burden on both individuals and society. Although the precise pathophysiological relationship between OSA and MetS remains unclear, their bidirectional interaction may create a harmful cycle of mutual reinforcement. This review explored the current treatment progress for OSA and MetS, including continuous positive airway pressure therapy, weight management, and metabolic surgeries. Studies indicate that while continuous positive airway pressure therapy effectively alleviates OSA symptoms, its impact on metabolic markers is limited, emphasizing the importance of long-term weight control. Metabolic surgeries, such as gastric bypass and sleeve gastrectomy, significantly reduce weight and directly improve metabolic abnormalities associated with MetS, such as insulin resistance and dyslipidemia, thereby lowering the risk of cardiovascular diseases. In contrast, mandibular advancement devices primarily improve symptoms of OSA and indirectly enhance metabolic function by improving sleep quality and reducing intermittent hypoxemia. Although mandibular advancement devices have a limited direct impact on metabolic parameters, they may offer potential benefits in lowering blood pressure and managing MetS. Understanding and breaking the cycle between OSA and MetS can significantly reduce the associated cardiovascular risks.