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1.
Eur Respir J ; 40(5): 1201-10, 2012 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-22408203

RESUMEN

The study compares the ability of the PSI (pneumonia severity index), CURB-65 (confusion, urea >7 mol·L(-1), respiratory rate ≥ 30 breaths·min(-1), blood pressure <90 mmHg systolic or ≤ 60 mmHg diastolic, and age ≥ 65 yrs), CURB and CRB-65 scales and the Severe Community-Acquired Pneumonia (SCAP) score to predict 30-day mortality in healthcare-associated pneumonia (HCAP) patients, and analyses differences in the demographics, aetiology and outcomes of community-acquired pneumonia (CAP), HCAP and pneumonia in immunocompromised patients. 629 consecutive patients admitted to a tertiary care university hospital were prospectively categorised as having CAP (n=322) or HCAP (n=307), and the HCAP patients were further sub-divided into those who were immunocompromised (n=219) or immunocompetent (n=88). The 30-day mortality rate was 9.0% in the CAP group and 24.1% in the HCAP group. In the HCAP group, the PSI and SCAP scores had similar prognostic power (area under the curve (AUC) of 0.68 and 0.67, respectively) and performed better than the CURB-65 score (AUC ≤0.62). Among the immunocompetent HCAP patients, the PSI and CURB-65 scores were more sensitive than the others at every threshold, whereas SCAP was more specific than both of these. In the immunocompromised group, the PSI was highly sensitive but poorly specific at all thresholds. Our results suggest that prognostic tools should be designed for subsets of HCAP patients.


Asunto(s)
Infección Hospitalaria/diagnóstico , Huésped Inmunocomprometido , Neumonía/diagnóstico , Índice de Severidad de la Enfermedad , Anciano , Anciano de 80 o más Años , Infecciones Comunitarias Adquiridas/diagnóstico , Femenino , Humanos , Terapia de Inmunosupresión , Masculino , Persona de Mediana Edad , Estudios Prospectivos
2.
Eur J Case Rep Intern Med ; 6(2): 001021, 2019.
Artículo en Inglés | MEDLINE | ID: mdl-30931265

RESUMEN

OBJECTIVE: We describe a rare case of group G streptococcus (GGS) sepsis complicated by bacterial toxin myopathy. CASE: A 65-year-old man, with a history of infection of his shoulder prosthesis, presented with multiorgan failure and notable myalgia likely caused by toxins. The patient was treated successfully with antibiotics and prosthesis removal. CONCLUSION: This case suggests infection by GGS should be considered in a patient presenting with myalgia associated with sepsis. LEARNING POINTS: Infection by GGS should be considered in a patient presenting with myalgia associated with sepsis.The differential diagnosis in this case included a neurological condition (meningitis or atypical Guillain-Barré syndrome) and sepsis with myopathy induced by bacterial toxins.Group G streptococcus (GGS) infection in a prosthetic shoulder was successfully treated with antibiotics and prosthesis removal.

3.
Tumori ; 102(Suppl. 2)2016 Nov 11.
Artículo en Inglés | MEDLINE | ID: mdl-27079907

RESUMEN

PURPOSE: In a substantial proportion of patients with thymoma, many different types of paraneoplastic syndromes are observed. The association between thymoma and autoimmune liver diseases, however, has been found in very few cases. METHODS: We report the case of a 31-year-old man affected by autoimmune hepatitis associated with myasthenia gravis and thymoma, successfully treated with extended thymectomy. RESULTS: The patient is free from neoplastic and hepatic disease 4 years after surgery. Eighteen months after thymectomy, an exacerbation of hepatitis was successfully treated with steroids. CONCLUSIONS: To the authors' knowledge, only 7 cases of myasthenia gravis associated with thymoma and autoimmune hepatitis have been reported in the English-language literature. The exact role of thymoma in immune-mediated hepatitis is unclear. It seems likely that thymoma-associated T-cell abnormalities, due to the presence of thymoma, may have a role in the development of this rare clinical triad of autoimmune hepatitis, thymoma and myasthenia gravis.


Asunto(s)
Hepatitis Autoinmune/complicaciones , Hepatitis Autoinmune/diagnóstico , Timoma/complicaciones , Timoma/diagnóstico , Corticoesteroides/uso terapéutico , Adulto , Biomarcadores , Hepatitis Autoinmune/tratamiento farmacológico , Humanos , Biopsia Guiada por Imagen , Masculino , Timoma/cirugía , Tomografía Computarizada por Rayos X , Resultado del Tratamiento , Ultrasonografía
4.
Intern Emerg Med ; 10(5): 581-6, 2015 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-25633233

RESUMEN

Anemia is a common finding in elderly individuals. Several studies have shown a strong relationship between anemia, morbidity and mortality, suggesting anemia as a significant independent predictor of adverse outcome in elderly hospitalized patients. The pathophisiology of anemia in the elderly is not yet completely understood. Several mechanisms are involved. We investigated the prevalence of anemia in a cohort of 193 elderly patients admitted to the Internal Medicine Ward of Ca'Granda Policlinico Hospital along 6 months, and its relationship to comorbidities and to the length of hospitalization. Anemia was classified according to the WHO criteria. The majority of patients (48 %) had a mildmoderate, normocytic anemia; severe anemia was found in 8 out of 92 anemic patients. In a subgroup of patients erythropoietin was tested and resulted statistically higher if compared to non-anemic controls (p = 0.003). Considering the most common cause of anemia, nutritional deficiency, chronic renal disease and anemia of chronic disease were found respectively in 36, 15 and 25 % of cases. Unexplained anemia was diagnosed in 24 % of patients, according to the literature. Anemia was independently associated with increased length of hospital stay. Our study confirmed a high prevalence of anemia in elderly patients, and its association with a higher number of comorbidities and a longer stay. A correct clinical approach to anemia in elderly hospitalized patients is essential, considering its negative impact on patients' quality of life, and its social burden in term of healthcare needs and costs.


Asunto(s)
Anemia/epidemiología , Hospitalización , Factores de Edad , Anciano , Anciano de 80 o más Años , Anemia/complicaciones , Estudios de Casos y Controles , Estudios de Cohortes , Femenino , Humanos , Italia , Masculino , Prevalencia
5.
Eur J Intern Med ; 52: e12-e14, 2018 06.
Artículo en Inglés | MEDLINE | ID: mdl-29657108
9.
Blood ; 109(1): 362-4, 2007 Jan 01.
Artículo en Inglés | MEDLINE | ID: mdl-16960153

RESUMEN

Juvenile hemochromatosis (JH) is a rare autosomal recessive disorder of iron metabolism, genetically heterogeneous. In JH, symptomatic organ involvement occurs as early as the second decade of life. Heart failure and/or arrhythmias are the most frequent causes of death. Phlebotomy is the safest, most effective, and most economic therapeutic approach in hemochromatosis patients but is not indicated during the treatment of severe congestive heart failure with unstable hemodynamic status. The treatment of iron overload in these prohibitive clinical situations has to be carried out using iron chelators. We report a case of heart failure in the setting of unrecognized juvenile hemochromatosis successfully treated by the simultaneous administration of deferoxamine and deferiprone. To our knowledge, this is the first patient affected by JH treated with combined chelation regimen.


Asunto(s)
Terapia por Quelación/métodos , Deferoxamina/uso terapéutico , Insuficiencia Cardíaca/etiología , Hemocromatosis/tratamiento farmacológico , Quelantes del Hierro/uso terapéutico , Piridonas/uso terapéutico , Adulto , Sustitución de Aminoácidos , Péptidos Catiónicos Antimicrobianos/genética , Fibrilación Atrial/etiología , Análisis Mutacional de ADN , Deferiprona , Deferoxamina/administración & dosificación , Quimioterapia Combinada , Insuficiencia Cardíaca/tratamiento farmacológico , Hemocromatosis/complicaciones , Hepcidinas , Humanos , Infertilidad Masculina/etiología , Quelantes del Hierro/administración & dosificación , Masculino , Mutación Missense , Linaje , Mutación Puntual , Piridonas/administración & dosificación , Inducción de Remisión
10.
Arthritis Res Ther ; 7(2): R250-5, 2005.
Artículo en Inglés | MEDLINE | ID: mdl-15743471

RESUMEN

Neutrophils are known to be targets for the biological activity of tumour necrosis factor (TNF)-alpha in the pathogenesis of rheumatoid arthritis (RA). Therefore, these cells may be among the targets of anti-TNF-alpha therapy. In this study we evaluated the effect of therapy with adalimumab (a fully human anti-TNF-alpha mAb; dosage: 40 mg subcutaneously every other week) on certain phenotypic and functional aspects of neutrophils obtained from 10 selected patients with RA and 20 healthy control individuals. Peripheral blood neutrophils were obtained at baseline and during anti-TNF-alpha therapy (2, 6 and 12 weeks after the first administration of adalimumab). All patients had been receiving a stable regimen of hydroxychloroquine, methotrexate and prednisone for at least 3 months before and during the study. Baseline neutrophil chemotaxis was significantly decreased in RA patients when compared with control individuals (P < 0.001). Two weeks after the first administration of adalimumab, chemotactic activity was completely restored, with no differences noted between patients and control individuals; these normal values were confirmed 6 and 12 weeks after the start of anti-TNF-alpha therapy. Phagocytic activity and CD11b membrane expression on neutrophils were similar between RA patients and control individuals; no modifications were observed during TNF-alpha neutralization. The production of reactive oxygen species, both in resting and PMA (phorbol 12-myristate 13-acetate)-stimulated cells, was significantly higher in RA patients at baseline (P < 0.05) and was unmodified by anti-TNF-alpha mAb. Finally, we showed that the activation antigen CD69, which was absent on control neutrophils, was significantly expressed on neutrophils from RA patients at baseline (P < 0.001, versus control individuals); however, the molecule was barely detectable on cells obtained from RA patients during adalimumab therapy. Because CD69 potentially plays a role in the pathogenesis of arthritis, our findings suggest that neutrophils are among the targets of anti-TNF-alpha activity in RA and may provide an insight into a new and interesting mechanism of action of anti-TNF-alpha mAbs in the control of inflammatory arthritis.


Asunto(s)
Anticuerpos Monoclonales/farmacología , Antirreumáticos/farmacología , Artritis Reumatoide/tratamiento farmacológico , Enfermedades Autoinmunes/tratamiento farmacológico , Neutrófilos/efectos de los fármacos , Factor de Necrosis Tumoral alfa/antagonistas & inhibidores , Adalimumab , Adulto , Anciano , Anciano de 80 o más Años , Anticuerpos Monoclonales/uso terapéutico , Anticuerpos Monoclonales Humanizados , Antígenos CD/biosíntesis , Antígenos CD/genética , Antígenos de Diferenciación de Linfocitos T/biosíntesis , Antígenos de Diferenciación de Linfocitos T/genética , Antirreumáticos/uso terapéutico , Artritis Reumatoide/sangre , Enfermedades Autoinmunes/sangre , Biomarcadores , Antígeno CD11b/biosíntesis , Antígeno CD11b/genética , Células Cultivadas/efectos de los fármacos , Células Cultivadas/inmunología , Células Cultivadas/metabolismo , Factores Quimiotácticos/farmacología , Quimiotaxis de Leucocito/efectos de los fármacos , Femenino , Regulación de la Expresión Génica , Humanos , Inmunofenotipificación , Lectinas Tipo C , Mediciones Luminiscentes , Masculino , Persona de Mediana Edad , N-Formilmetionina Leucil-Fenilalanina/farmacología , Neutrófilos/inmunología , Neutrófilos/metabolismo , Fagocitosis/efectos de los fármacos , Especies Reactivas de Oxígeno/metabolismo , Acetato de Tetradecanoilforbol/farmacología , Zimosan/farmacología
11.
Cell Immunol ; 220(1): 20-9, 2002 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-12718936

RESUMEN

The CD69 glycoprotein is an early activation antigen of T and B lymphocytes but it expression is induced in vitro on cells of most hematopoietic lineages, including neutrophils after stimulation with PMA or fMLP. In this study, we investigated whether CD69 expression on human neutrophils could be modulated by inflammatory or anti-inflammatory cytokines (IL-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-18, G-CSF, GM-CSF, TNF-alpha, TGF-beta, IFN-alpha, IFN-gamma). Resting neutrophils from healthy subjects did not express CD69 on the cell surface; moreover, a preformed intracellular pool of CD69 was not evident in these cells. CD69 was barely detectable on these cells after overnight incubation in medium while overnight incubation with GM-CSF, IFN-gamma or IFN-alpha significantly induced CD69 expression on neutrophils with GM-CSF appearing to be the most potent inducer. This induction was dependent on a new protein synthesis as it was significantly inhibited by cycloheximide (about 50% inhibition). CD69 cross-linking on GM-CSF-primed neutrophils sinergized with LPS and increased TNF-alpha production and secretion suggesting a role for CD69-positive neutrophils in the pathogenesis and maintenance of different inflammatory diseases.


Asunto(s)
Antígenos CD/biosíntesis , Antígenos de Diferenciación de Linfocitos T/biosíntesis , Regulación de la Expresión Génica/efectos de los fármacos , Factor Estimulante de Colonias de Granulocitos y Macrófagos/farmacología , Interferón-alfa/farmacología , Interferón gamma/farmacología , Neutrófilos/efectos de los fármacos , Factor de Necrosis Tumoral alfa/biosíntesis , Adulto , Antígenos CD/genética , Antígenos CD/fisiología , Antígenos de Diferenciación de Linfocitos T/genética , Antígenos de Diferenciación de Linfocitos T/fisiología , Antígeno CD11b/biosíntesis , Antígeno CD11b/genética , Cicloheximida/farmacología , Factor Estimulante de Colonias de Granulocitos/farmacología , Humanos , Inflamación/inmunología , Inflamación/metabolismo , Interleucinas/farmacología , Lectinas Tipo C , Neutrófilos/inmunología , Neutrófilos/metabolismo , Fagocitosis/efectos de los fármacos , Inhibidores de la Síntesis de la Proteína/farmacología , ARN Mensajero/biosíntesis , ARN Mensajero/genética , Estallido Respiratorio/efectos de los fármacos , Factor de Crecimiento Transformador beta/farmacología , Factor de Necrosis Tumoral alfa/genética , Factor de Necrosis Tumoral alfa/metabolismo , Factor de Necrosis Tumoral alfa/farmacología
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