Acute-on-Chronic Liver Failure Triggered by Cutaneous Loxoscelism.

Acute-on-chronic liver failure is a syndrome associated with a high short-term mortality rate. Severe systemic inflammation and single- and multiple-organ failure are a hallmark of this syndrome, with pro-inflammatory precipitating events occurring in the liver or extrahepatic regions. We report a case of a 69-year-old man with a previous diagnosis of alcohol-induced liver cirrhosis who presented with a poorly defined, erythematous-purplish, and edematous plaque with multiple hemorrhagic blisters over the left leg, one day after receiving a spider bite. During the following hours, the skin lesion progressed, and the patient developed hepatic encephalopathy, respiratory failure, and arterial hypotension, requiring the administration of vasopressors; blood analysis revealed hypercreatininemia, an elevated international normalized ratio (INR) value, and hyperbilirubinemia. The patient was diagnosed with acute-on-chronic liver failure caused by cutaneous loxoscelism. There was no hemolytic anemia, rhabdomyolysis, or disseminated intravascular coagulation in the patient, thus excluding the possibility of visceral loxoscelism.

Disseminated mucocutaneous trichosporonosis in a patient with histiocytic sarcoma

Abstract Trichosporon asahii is the causal agent of trichosporonosis. Patients with immunosuppression or hematological malignancies are at higher risk of infection. Skin and mucosal involvement appear as fast-growing papulonodular lesions and necrotic ulcers. Internal organ dissemination is lethal. Therapeutic success depends on the underlying disease. Here, the authors present the first case of disseminated mucocutaneous trichosporonosis in a patient with a post-mortem diagnosis of histiocytic sarcoma, a rare and aggressive haematolymphoid neoplasm. Regretfully, death occurred despite treatment with liposomal amphotericin B and supportive measures, showcasing the fatality of both diseases.

Disseminated mucocutaneous trichosporonosis in a patient with histiocytic sarcoma.

Trichosporon asahii is the causal agent of trichosporonosis. Patients with immunosuppression or hematological malignancies are at higher risk of infection. Skin and mucosal involvement appear as fast-growing papulonodular lesions and necrotic ulcers. Internal organ dissemination is lethal. Therapeutic success depends on the underlying disease. Here, the authors present the first case of disseminated mucocutaneous trichosporonosis in a patient with a post-mortem diagnosis of histiocytic sarcoma, a rare and aggressive haematolymphoid neoplasm. Regretfully, death occurred despite treatment with liposomal amphotericin B and supportive measures, showcasing the fatality of both diseases.

Isolation methodology is essential to the evaluation of the extracellular vesicle component of the senescence-associated secretory phenotype.

A hallmark of senescence is the acquisition of an enhanced secretome comprising inflammatory mediators and tissue remodelling agents - the senescence-associated secretory phenotype (SASP). Through the SASP, senescent cells are hypothesised to contribute to both ageing and pathologies associated with age. Whilst soluble factors have been the most widely investigated components of the SASP, there is growing evidence that small extracellular vesicles (EVs) comprise functionally important constituents. Thus, dissecting the contribution of the soluble SASP from the vesicular component is crucial to elucidating the functional significance of senescent cell derived EVs. Here, we take advantage of a systematic proteomics based approach to determine that soluble SASP factors co-isolate with EVs following differential ultracentrifugation (dUC). We present size-exclusion chromatography (SEC) as a method for separation of the soluble and vesicular components of the senescent secretome and thus EV purification. Furthermore, we demonstrate that SEC EVs isolated from senescent cells contribute to non-cell autonomous paracrine senescence. Therefore, this work emphasises the requirement for methodological rigor due to the propensity of SASP components to co-isolate during dUC and provides a framework for future investigations of the vesicular component of the SASP.

Nodular fasciitis: a benign mimicker of soft tissue malignancies / Fascitis nodular: un imitador benigno de las neoplasias malignas de tejidos blandos

La fascitis nodular es una masa subcutánea, benigna, autolimitada, que puede simular un sarcoma de tejidos blandos en su presentación clínica e histopatológica. Debido a que la mayoría de las descripciones de esta condición provienen de pacientes caucásicos, es necesario enfatizar su existencia en poblaciones poco representadas en la literatura. Se presenta el caso de un paciente mexicano, masculino, de 49 años, quien fue inicialmente mal diagnosticado y tratado como quiste epidérmico. Tras la recurrencia de la lesión, se realizó una adecuada técnica de biopsia y estudios de imagen, confirmando el diagnóstico de fascitis nodular. El presente reporte resalta la importancia de abordar con cautela las masas subcutáneas que puedan simular tanto tumores benignos como malignos para mejorar el pronóstico de los pacientes.

Nodular fasciitis is a benign, self-limited, subcutaneous tumor that may resemble a soft tissue sarcoma both clinically and histopathologically. Since most descriptions derive from Caucasian patients, further awareness is necessary in underrepresented populations. Here, we present a case of nodular fasciitis in a 49-year-old Mexican male who had been misdiagnosed and mistreated as an epidermal cyst. After recurrence, an adequate biopsy and imaging studies confirmed the diagnosis of nodular fasciitis. This case illustrates the importance of properly studying subcutaneous masses that can mimic a wide array of benign and malignant tumors to improve overall patient prognosis.

Aquagenic urticaria: Water, friend, or foe?

There are <100 reported cases of aquagenic urticaria. Although most are sporadic, several diseases have been associated. Diagnosis is based on provocation tests. Second-generation antihistamines are the first-line treatment.

Mitral valve infective endocarditis associated with bacterial meningitis: case report / Endocarditis infecciosa de la válvula mitral asociada a meningitis bacteriana: reporte de caso

Abstract: Infective endocarditis affects multiple systems, and is usually from a bacterial infection of the endocardial surface of the heart. Neurologic complications occur in 20 to 40 percent of patients and are associated with a higher mortality rate. This case is from a 37-year-old man with a history of chronic lower back pain and chronic use of intravenous opioids (tramadol), who suddenly experienced disorientation, drowsiness, and aphasia. At admission, he presented fever of 38 oC, heart rate of 115 bpm, blood pressure 100/60 mmHg and breathing rate of 24 rpm. The physical examination revealed a IV/VI holosystolic murmur over the apex, radiating to the axilla, as well as Osler nodes and Janeway lesions at cutaneous level. The rest of the physical and neurological examination did not present any abnormalities. Fluid infusion and empirical antibiotic therapy were started (vancomycin and ceftriaxone). Cranial tomography did not show alterations and the echocardiogram revealed severe mitral regurgitation and a 1 × 0.9 cm-sized vegetation on the anterior leaflet of the mitral valve. Laboratory tests reported: leukocytosis of 23,000/mm3, platelets of 108,000/mm3. The cerebrospinal fluid analysis showed: turbid appearance, glucose of 32 mg/dL, proteins of 165 mg/dL, lymphocytes of 0, leukocytes of 1,760/mm3, data compatible with bacterial meningitis, as well as culture at 72 hours with Staphylococcus aureus isolation. After 72 hours of admission, he presented deterioration of mental status and respiratory failure, so mechanical ventilation support was initiated. Because of the risk of embolism, mitral valve replacement was performed and after improvement, he was extubated without complications or sequelae. This case highlights the importance of associating risk factors with a thorough physical examination, essential to establish the diagnosis approach and timely treatment of infective endocarditis with systemic involvement.

Resumen: La endocarditis infecciosa afecta múltiples sistemas, y generalmente se debe a una infección bacteriana de la superficie endocárdica del corazón. Las complicaciones neurológicas continúan ocurriendo en aproximadamente 20 a 40% de todos los pacientes con endocarditis infecciosa y representan un factor asociado con una mayor tasa de mortalidad. Este caso trata de un paciente masculino de 37 años con antecedente de lumbalgia crónica y uso de fármacos intravenosos (Tramadol). Inició con alteración del estado de alerta manifestada por desorientación, somnolencia y afasia. Al ingreso presentó fiebre de 38 oC, frecuencia cardiaca de 115 lpm, presión arterial 100/60 mmHg y frecuencia respiratoria de 24 rpm. En la exploración física se auscultó soplo holosistólico grado IV/VI en el apex, irradiado a la axila; además, en región plantar y palmar presencia de nódulos de Osler y lesiones de Janeway. El resto del examen físico y neurológico no presentó alteración. Se inició la infusión de líquidos y la terapia antibiótica empírica (Vancomicina y Ceftriaxona). La tomografía craneal no mostró alteraciones y el ecocardiograma reveló una grave regurgitación mitral y una vegetación en la valva anterior de la válvula mitral de 1 x 0.9 cm. Los laboratorios reportaron: leucocitosis de 23,000/mm3,­ plaquetas de 108,000/mm3. El líquido cefalorraquídeo con un aspecto turbio, glucosa de 32 mg/dL, proteínas de 165 mg/dL, linfocitos de 0, leucocitos de 1,760/mm3, datos compatibles con meningitis bacteriana, así como cultivo a las 72 horas con aislamiento de Staphylococcus aureus. Después de 72 horas del ingreso, presentó deterioro del estado neurológico e insuficiencia respiratoria, por lo que se dio soporte con ventilación mecánica. Debido al riesgo de embolia, se realizó reemplazo de válvula mitral. Posteriormente fue extubado sin complicaciones ni secuelas. El caso destaca la importancia de asociar los factores de riesgo con un examen físico completo, minucioso, para establecer un diagnóstico y tratamiento oportuno en endocarditis infecciosa con afectación sistémica.

Mechanisms of epithelial thickening due to IL-1 signalling blockade and TNF-α administration differ during wound repair and regeneration.

IL-1 and TNF-α are always present during wound repair, but their pleiotropic and synergistic effects are incompletely understood. In this work, we evaluated the role of IL-1 in wound repair, and examined whether TNF-α administration impaired scarless wound repair. First, we characterised wound repair in outbred CD-1 mice according to age and sex in an ear punch wound model. Then, we examined the effects of Interleukin 1 receptor antagonist (IL-1ra) and TNF-α placement inside ear wounds by means of loaded Heparin beads in young and middle-aged male and female mice. Wounds in middle-aged females repaired with scarless characteristics, whereas those in young males showed fibrotic scarring. Rather than improving wound repair in young males, IL-1 signalling blockade increased epithelial thickness and IL-1ß and TNF-α expression, and diminished epidermal apoptosis. TNF-α impaired wound repair in middle-aged females, which exhibited acanthosis and overexpression of IL-1, but no change in apoptosis. These findings suggest that this mechanism of epidermal thickening differs from that observed in IL1-ra-treated animals.