Mild COVID-19 Illness as a Risk Factor for Venous Thromboembolism.

Introduction From the beginning of the current coronavirus disease 2019 (COVID-19) pandemic, there is cumulative evidence suggesting that patients hospitalized due to this disease are at a high risk for venous thromboembolism (VTE). The association between mild non-hospitalized illness and VTE is unclear. The purpose of this research is to assess the association between VTE and mild COVID-19 infection. Methods A case-control study was conducted. The cases were adult patients diagnosed with VTE from March 1, 2020 to March 31, 2021. The controls were randomly chosen adult patients who required healthcare services that were equivalent to those of the cases, for any cause, during the same time period, without a VTE diagnosis. To assess the association between mild COVID and VTE, a multivariate logistic regression analysis was conducted, considering other thromboembolic risk variables, such as age, gender and active cancer, among others. A p-value <0.05 was considered statistically significant. Results A total of 186 cases and 475 controls were analyzed. There were 21 (11.3%) and 31 (6.5%) patients infected with mild COVID-19 in the previous three months in the groups of cases and controls, respectively. Mild COVID-19 infection was statistically significant as a risk factor for VTE both in the univariate analysis and in the multivariate analysis, OR=1.82 (95% CI 1.02-3.26) and OR=2.62 (95% CI 1.34-5.13), respectively. Conclusion Mild COVID-19 infection might be an independent risk factor for VTE. We conclude that the results suggest some thromboprophylaxis strategy should be considered in certain patients with COVID-19 infection in an outpatient fashion.

[Secondary hemophagocytic syndrome due to recurrent infections in a severely burned patient]. / Síndrome hemofagocítico secundario a infecciones graves en un quemado.

The hemophagocytic syndrome represents an infrequent, occasionally misdiagnosed and usually fatal heterogeneous entity. Infections, drugs, autoimmune diseases and cancer are often triggers of the secondary hemophagocytic syndrome. Its physiopathogenic mechanism is explained by an impaired and inefficacious function of the NK and T cytotoxic cells that leads to an ineffective and uncontrolled immune response, inducing cellular damage, multiorganic failure with macrophage proliferation and hemophagocytosis. The main objective of the different therapeutic options, commonly combinations of steroids and chemotherapy, is the suppression of the uncontrolled immune response. Occasionally, the clinical condition of some patients represents a contraindication for intensive treatment. We report a case of a severely burned patient that fulfilled the revised criteria for the hemophagocytic syndrome and was successfully treated with the combination of intravenous immunoglobulins and steroids.

Síndrome hemofagocítico secundario a infecciones graves en un quemado / Secondary hemophagocytic syndrome due to recurrent infections in a severely burned patient

El síndrome hemofagocítico constituye una entidad infrecuente, heterogénea, subdiagnosticada, y muchas veces fatal. En los casos secundarios, los desencadenantes pueden ser numerosos, tales como infecciones, fármacos, enfermedades autoinmunes y neoplasias. El mecanismo fisiopatogénico se explica por la presencia de una función disminuida o defectuosa de células NK y linfocitos T citotóxicos, que resulta en una activación inmune inefectiva y descontrolada, conduciendo al daño celular, falla multiorgánica y proliferación macrofágica con hemofagocitosis. Existen diferentes opciones terapéuticas, mayormente combinaciones de citostáticos y esteroides, cuyo objetivo es la supresión de la respuesta inmune descontrolada. Ocasionalmente, la condición clínica de algunos pacientes con síndrome hemofagocítico impide la utilización de esquemas terapéuticos intensivos. Comunicamos el caso de un paciente quemado grave, que reúne los criterios diagnósticos de síndrome hemofagocítico, quien presentó una evolución favorable con el tratamiento combinado de esteroides e inmunoglobulinas endovenosas.(AU)

The hemophagocytic syndrome represents an infrequent, occasionally misdiagnosed and usually fatal heterogeneous entity. Infections, drugs, autoimmune diseases and cancer are often triggers of the secondary hemophagocytic syndrome. Its physiopathogenic mechanism is explained by an impaired and inefficacious function of the NK and T cytotoxic cells that leads to an ineffective and uncontrolled immune response, inducing cellular damage, multiorganic failure with macrophage proliferation and hemophagocytosis. The main objective of the different therapeutic options, commonly combinations of steroids and chemotherapy, is the suppression of the uncontrolled immune response. Occasionally, the clinical condition of some patients represents a contraindication for intensive treatment. We report a case of a severely burned patient that fulfilled the revised criteria for the hemophagocytic syndrome and was successfully treated with the combination of intravenous immunoglobulins and steroids.(AU)

Síndrome hemofagocítico secundario a infecciones graves en un quemado / Secondary hemophagocytic syndrome due to recurrent infections in a severely burned patient

El síndrome hemofagocítico constituye una entidad infrecuente, heterogénea, subdiagnosticada, y muchas veces fatal. En los casos secundarios, los desencadenantes pueden ser numerosos, tales como infecciones, fármacos, enfermedades autoinmunes y neoplasias. El mecanismo fisiopatogénico se explica por la presencia de una función disminuida o defectuosa de células NK y linfocitos T citotóxicos, que resulta en una activación inmune inefectiva y descontrolada, conduciendo al daño celular, falla multiorgánica y proliferación macrofágica con hemofagocitosis. Existen diferentes opciones terapéuticas, mayormente combinaciones de citostáticos y esteroides, cuyo objetivo es la supresión de la respuesta inmune descontrolada. Ocasionalmente, la condición clínica de algunos pacientes con síndrome hemofagocítico impide la utilización de esquemas terapéuticos intensivos. Comunicamos el caso de un paciente quemado grave, que reúne los criterios diagnósticos de síndrome hemofagocítico, quien presentó una evolución favorable con el tratamiento combinado de esteroides e inmunoglobulinas endovenosas.

The hemophagocytic syndrome represents an infrequent, occasionally misdiagnosed and usually fatal heterogeneous entity. Infections, drugs, autoimmune diseases and cancer are often triggers of the secondary hemophagocytic syndrome. Its physiopathogenic mechanism is explained by an impaired and inefficacious function of the NK and T cytotoxic cells that leads to an ineffective and uncontrolled immune response, inducing cellular damage, multiorganic failure with macrophage proliferation and hemophagocytosis. The main objective of the different therapeutic options, commonly combinations of steroids and chemotherapy, is the suppression of the uncontrolled immune response. Occasionally, the clinical condition of some patients represents a contraindication for intensive treatment. We report a case of a severely burned patient that fulfilled the revised criteria for the hemophagocytic syndrome and was successfully treated with the combination of intravenous immunoglobulins and steroids.

Síndrome hemofagocítico secundario a infecciones graves en un quemado. / [Secondary hemophagocytic syndrome due to recurrent infections in a severely burned patient].

The hemophagocytic syndrome represents an infrequent, occasionally misdiagnosed and usually fatal heterogeneous entity. Infections, drugs, autoimmune diseases and cancer are often triggers of the secondary hemophagocytic syndrome. Its physiopathogenic mechanism is explained by an impaired and inefficacious function of the NK and T cytotoxic cells that leads to an ineffective and uncontrolled immune response, inducing cellular damage, multiorganic failure with macrophage proliferation and hemophagocytosis. The main objective of the different therapeutic options, commonly combinations of steroids and chemotherapy, is the suppression of the uncontrolled immune response. Occasionally, the clinical condition of some patients represents a contraindication for intensive treatment. We report a case of a severely burned patient that fulfilled the revised criteria for the hemophagocytic syndrome and was successfully treated with the combination of intravenous immunoglobulins and steroids.

Endocrine and cytokine responses in humans with pulmonary tuberculosis.

Endocrine responses during chronic infections such as lung tuberculosis are poorly characterized. Hormonal changes are likely to occur since some of the cytokines produced during this disease could affect endocrine mechanisms that, in turn, influence the course of infectious/inflammatory processes. A main purpose of this work was to study endocrine responses involving pituitary, adrenal, gonadal, and thyroid hormones in parallel to IFN-gamma, IL-10, and IL-6 levels in tuberculosis patients with different degree of pulmonary involvement. We have also studied whether products derived from peripheral immune cells obtained from the patients can affect the in vitro production of adrenal steroids. The population studied comprised HIV-negative newly diagnosed, untreated male patients with mild, moderate, and advanced lung tuberculosis, and matched, healthy controls. IFN-gamma, IL-10, and IL-6 levels were elevated in patients with tuberculosis. Dehydroepiandrosterone and testosterone levels were profoundly decreased and growth hormone levels were markedly elevated in patients, in parallel to modest increases in cortisol, estradiol, prolactin, and thyroid hormone concentrations. Supernatants of peripheral blood mononuclear cells obtained from the patients and stimulated in vitro with Mycobacterium tuberculosis antigens significantly inhibited dehydroepiandrosterone secretion by the human adrenal cell line NCI-H295-R. These results support the hypothesis that at least some of the endocrine changes observed in the patients may be mediated by endogenous cytokines. The endocrine profile of tuberculosis patients would favor a reduction of protective cell-mediated immunity and an exacerbation of inflammation leading to perpetuation of the lung injury and to the hypercatabolic condition that characterizes this disease.