Yurilú Andreina González-Moret

Emerging evidence suggests a significant association between monocytes and the pathophysiology and prognosis of idiopathic pulmonary fibrosis (IPF). This review aims to systematically evaluate current knowledge regarding blood monocyte counts and their relationship with the etiology, progression, and prognosis of IPF. We conducted a systematic search in the PubMed database for articles published through 17 February 2025, using the MeSH terms “lung diseases, interstitial” and “monocytes,” which yielded 314 results. After filtering for full-text articles in English (n = 242), we included only studies focusing on blood monocyte counts with clinical implications in IPF. Articles relating to other cell types or non-IPF lung diseases were excluded. Our systematic search identified 12 relevant articles. Monocytes play an essential role in regulating inflammatory responses and resolution across multiple diseases, with established but incompletely understood contributions to lung fibrosis development in IPF. Correlations have been demonstrated between elevated blood monocyte counts and the following: (1) the presence and progression of interstitial lung abnormalities, (2) the progression from an indeterminate usual interstitial pneumonia (UIP) pattern on CT scans to definitive IPF, and (3) worse lung function parameters, an increased risk of acute exacerbations, and reduced overall survival in IPF patients. Monocytes serve as critical orchestrators throughout IPF’s natural history—from early interstitial changes to disease progression and acute exacerbations. Targeting monocyte recruitment pathways and reprogramming their differentiation represents a promising therapeutic approach, while circulating monocyte counts offer potential as accessible biomarkers for disease progression and treatment response. Future research should characterize stage-specific monocyte phenotypes to enable precision-targeted interventions.

Objective: The aim of this study was to investigate the impact of estrogen and progesterone analog supplementation on the development of autoimmune conditions.Methods: This retrospective observational study used data from the TriNetX network, which comprised over 100 million patients from 89 health care organizations. We compared patients exposed to estrogen and progesterone analogs to those exposed to progesterone‐only therapy, using 1:1 propensity score matching based on age, ethnicity, and additional criteria. The primary outcomes were incidences of various autoimmune conditions.Results: We included 3,338,925 patients in the group who received estrogen and progesterone and 2,090,758 patients in the group who received progesterone only. Prematching, the group who received combined therapy showed increased risks for Sjögren disease (risk ratio [RR] 1.46), rheumatoid arthritis (RR 1.1), and other autoimmune conditions. Postmatching, significant associations persisted for most conditions, with increased risks for systemic sclerosis, systemic lupus erythematosus, giant cell arteritis, Behcet disease, psoriatic arthritis, reactive arthritis, and ankylosing spondylitis. The group who received combination therapy appeared to have lower risks of developing antiphospholipid syndrome (RR 0.7).Conclusion: Combined estrogen and progesterone therapy is associated with an increased risk of several autoimmune conditions. The role of estrogen, despite its protective effects against some conditions, underscores the complex interplay of sex hormones in autoimmunity. Further prospective studies are needed to elucidate underlying mechanisms and evaluate causality.

Objective: Systemic lupus erythematosus (SLE) is characterized by widespread organ inflammation. Metformin, commonly used for diabetes mellitus type 2, has been explored for its anti‐inflammatory potential in SLE. This study investigates the association of metformin use on renal and cardiovascular outcomes in patients with SLE.Methods: This is a retrospective study. We used the multicenter research network (TriNetX) database from 88 health care organizations globally. Patients with SLE aged 18 and above, admitted between January 1, 2014, and April 21, 2024, were included. Propensity score matching compared patients with SLE on metformin with those not on metformin, considering demographics, laboratory results, comorbidities, and baseline medication use. The study assessed outcomes, including lupus nephritis (LN), chronic kidney disease (CKD), and major adverse cardiovascular events (MACEs) at one and five years after SLE diagnosis.Results: We identified 9,178 patients with SLE on metformin and 78,983 patients with SLE not on metformin. After propensity score matching, patients with SLE on metformin had higher levels of hemoglobin A1C, whereas patients not on metformin had higher levels of urea nitrogen. When comparing both groups, the risk of developing LN (risk ratio [RR] = 1.70 [1.17–2.41]; P = 0.004), CKD (RR = 1.27 [1.07–1.52]; P = 0.007), and MACEs (RR = 1.21 [1.00–1.46]; P = 0.04) was significantly higher among patients not on metformin at one year after SLE diagnosis. After five years, the risk of LN and CKD was also higher in patients with SLE not on metformin. MACE risk was no longer significant after five years of diagnosis between both groups.Conclusion: Patients with SLE not on metformin have a higher risk of developing LN, CKD, and MACEs compared with patients treated with metformin. Metformin's anti‐inflammatory potential offers promise as a complementary therapy for SLE. Nonetheless, further research and clinical trials are needed to clarify its mechanisms, optimal dosage, and long‐term effects.

Objective: Unusual clinical course Background: Idiopathic giant cell myocarditis (IGCM) is an uncommon and frequently fatal type of myocarditis. It primarily affects young individuals and has the potential to result in heart failure and life-threatening arrhythmias. IGCM seems to be dependent on activation of CD4-positive T lymphocytes and can show improvement with treatment aimed at reducing T-cell function. We present a case of a 65-year-old patient who presented with features of acute heart failure refractory to guideline-directed medical therapy (GDMT), due to IGCM. A review of the natural history and treatment of IGCM is also presented. Case Report: A 65-year-old woman with multiple comorbidities was admitted to our hospital for ventricular tachycardia in the setting of progressive non-ischemic heart failure, unresponsive to GDMT. This led to further investigation, including an endomyocardial biopsy, which revealed inflammatory infiltration, with multinucleated giant cells and lymphocytes in the absence of granuloma formation, prompting a diagnosis of IGCM. An implantable cardioverter-defibrillator (ICD) was placed for secondary prevention of sudden cardiac death and the patient was initiated on combined immunosuppressive therapy. Owing to numerous comorbidities, she was determined to be unsuitable for a heart transplant. Unfortunately, she eventually died from complications secondary to the disease. Conclusions: IGCM remains a challenging clinical diagnosis with a poor long-term outcome without heart transplantation. This case highlights the importance of considering atypical causes of heart failure in patients who do not respond to conventional therapies. Early recognition and appropriate management, involving medical and interventional approaches, are crucial in improving outcomes for patients with IGCM.

Introducción. Las lesiones radiolúcidas del complejo maxilar mandíbula tienen su origen en estructuras odontogénicas y no odontogénicas. El objetivo de este trabajo es describir las características de lesiones radiolúcidas del complejo maxilar-mandíbula de pacientes en un centro radiológico. Metodología. Se realizó un estudio descriptivo de corte transversal. La población está representada por 1,000 radiografías panorámicas. La muestra quedó conformada por 105 casos seleccionados por un muestreo de conveniencia no probabilístico. Las radiografías fueron tomadas con un equipo panorámico Gendex 9,000, por un mismo operador, y fueron analizadas por un investigador calificado. Resultados. La mayoría de las lesiones radiolúcidas se ubicaron en el rango etario de 50 a 59 años (30=28.6%), fueron del género masculino (54=51.4%), y estuvieron ubicadas en mandíbula (83=79.0%). Respecto a la estructura dentaria, en su mayoría las lesiones estuvieron ubicadas en la porción periapical (65=61.9%), en relación con la forma, ésta fue predominantemente irregular (68=64.8%), con bordes difusos (51=48.6%) y estructura interna unilocular (74=70.5%). En ninguno de los casos se evidenció asociación estadísticamente significativa (p>0.05). Discusión. La gran diversidad de diagnósticos hallados se puede explicar por las condiciones geográficas, sociales, culturales, proceso biológico de envejecimiento, y condiciones inherentes al sitio de recolección de datos. Conclusiones. La mayoría de las lesiones se localizan en mandíbula, en relación con la estructura dentaria son periapicales, presentan bordes difusos y están presentes en el grupo etario de 50 a 59 años. Las lesiones fueron en su mayoría de forma irregular bordes difusos y con estructura interna unilocular.

Introducción. El Síndrome de Burnout afecta mundialmente a más de 100,000,000 personas, con prevalencia entre 47 y 76% en médicos residentes. El objetivo de este trabajo fue determinar la relación entre el Síndrome de Burnout y los niveles de proteína C-reactiva ultrasensible en médicos residentes de un hospital universitario en Caracas, Venezuela. Metodología. Estudio transversal y descriptivo. El instrumento de recolección de datos, así como el test Maslach Burnout Inventory, fueron enviados en formato electrónico. Posteriormente, se seleccionó dos submuestras, a quienes se les determinó la concentración de proteína C-reactiva ultrasensible. Resultados. La muestra inicial fue de 174 residentes, de los cuales 57 (32.8%) presentaban Burnout. Los residentes positivos para la presencia del síndrome tenían niveles más elevados de proteína C-reactiva ultrasensible (>0.50mg/dl) (р=0.001) con respecto al grupo sin Burnout. Igualmente, los residentes de género femenino (р=0.046), aquellos que dormían menos de 8 horas al día (р=0.032) y que estaban sometidos a estrés familiar (р=0.036) presentaron una asociación estadísticamente significativa para desarrollar el síndrome de Burnout. Finalmente, se evidenció cómo los residentes de menor edad tenían mayores puntajes en la subescala despersonalización (p=0.036). Discusión. El estrés crónico (entre ellos el Síndrome de Burnout) puede activar de manera continua ejes fisiológicos estresores (hipotálamo-hipófisis- suprarrenal y simpático- adrenal); conllevando a la producción de citosinas y proteínas de fase aguda (como proteína C-reactiva ultrasensible), promoviendo un estado proinflamatorio en el individuo y el desarrollo de patologías crónicas. Conclusiones. El Síndrome de Burnout y las variables sociodemográficas/ laborales representan una condición de estrés crónico que pueden asociarse entre sí y conducir al desarrollo de distintas enfermedades a largo plazo.