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2.
Am J Health Syst Pharm ; 73(4): 206-15, 2016 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-26843497

RESUMO

PURPOSE: The predictive performance of glomerular filtration rate (GFR) estimation equations based on cystatin C versus serum creatinine (SCr) values in critically ill patients was evaluated. METHODS: A retrospective observational study was performed in the medical intensive care unit (ICU) of a university hospital from October 2006 through September 2007. All consecutively admitted critically ill patients older than 18 years who stayed in the ICU for more than 48 hours with a urinary bladder catheter in place were included in the study. Data collected included SCr, cystatin C, serum albumin, blood urea nitrogen, and 24-hour urine creatinine clearance [Formula: see text] levels. The following equations were also used to determine the estimated GFR that was compared with the reference [Formula: see text] for all patients in the study: Arnal-Dade using cystatin C, Cockcroft-Gault using actual body weight, Cockcroft-Gault using ideal body weight, Jelliffe, Modification of Diet in Renal Disease (MDRD), and four-variable version MDRD (MDRD-4). RESULTS: This study included 241 measurements corresponding to 131 critically ill patients. The cystatin C-based equation underestimated [Formula: see text], whereas overestimation by every SCr-based formula was observed in the whole cohort and in the [Formula: see text] subgroup; MDRD-4 was the most biased equation in every analysis. There were no significant differences in precision, except for great variability in the subgroup with a [Formula: see text] of <60 mL/min/1.73 m(2), where the MDRD equation showed better results than the cystatin C-based equation (33.5% versus 38.9%). No equations fulfilled concordance requirements with [Formula: see text]. CONCLUSION: A retrospective observational study showed no evidence of superiority of a cystatin C-based equation over SCr-based equations to estimate the GFR in an ICU population.


Assuntos
Creatinina/sangue , Cistatina C/sangue , Taxa de Filtração Glomerular , Nefropatias/diagnóstico , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Creatinina/urina , Estado Terminal , Feminino , Humanos , Unidades de Terapia Intensiva , Testes de Função Renal , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Adulto Jovem
3.
Medicine (Baltimore) ; 93(24): 359-63, 2014 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-25500705

RESUMO

Pulmonary tumor thrombotic microangiopathy (PTTM) is a rare clinical entity where tumor cell embolisms in pulmonary circulation induce thrombotic microangiopathy (TMA), respiratory failure, and subacute cor pulmonale.We describe 3 cases of PTTM that presented as the initial manifestation of metastatic gastric adenocarcinoma with TMA and pulmonary infiltrates.All 3 cases had similar clinical and laboratory features, which included moderate thrombocytopenia without renal failure, hemolysis with extremely high serum lactate dehydrogenase levels, leukoerythroblastosis in peripheral blood smear, altered coagulation tests, lymphadenopathies, and interstitial pulmonary infiltrates. All patients died within 2 weeks of diagnosis. Two cases were initially misdiagnosed as idiopathic thrombotic thrombocytopenic purpura and treated with plasma exchange with no response. One patient had bone marrow infiltration by malignant cells. Autopsies revealed PTTM associated with gastric disseminated adenocarcinoma (signet-ring cell type in 2 patients and poorly differentiated type in 1).PTTM should be considered in the differential diagnosis of patients with fulminant microangiopathic hemolytic anemia, such as atypical thrombotic thrombocytopenic purpura, mainly those with pulmonary infiltrates, disseminated intravascular coagulation, or Trousseau syndrome.


Assuntos
Adenocarcinoma/complicações , Pneumopatias/etiologia , Neoplasias Gástricas/complicações , Microangiopatias Trombóticas/etiologia , Adenocarcinoma/patologia , Adulto , Diagnóstico Diferencial , Evolução Fatal , Feminino , Humanos , Pulmão/irrigação sanguínea , Pneumopatias/diagnóstico , Masculino , Metástase Neoplásica , Neoplasias Gástricas/patologia , Microangiopatias Trombóticas/diagnóstico , Adulto Jovem
5.
Respir Physiol Neurobiol ; 187(2): 157-63, 2013 Jun 15.
Artigo em Inglês | MEDLINE | ID: mdl-23537586

RESUMO

Inhaled nitric oxide (NO) causes selective pulmonary vasodilatation and may improve gas exchange. The study was aimed to evaluate the acute effects of inhaled NO on pulmonary gas exchange in severe unilateral pneumonia, where hypoxemia results from increased intrapulmonary shunt. We studied 8 patients without preexisting lung disease (59±18 yr; 4M/4F) with early unilateral severe pneumonia and respiratory failure. Pulmonary and systemic hemodynamics and gas exchange, including ventilation-perfusion (V;A/Q;) distributions, were measured at baseline and while breathing 5 and 40 parts per million (ppm) of NO. Inhaled NO caused a dose-dependent fall in pulmonary vascular resistance (by 12% and 21%, with 5 and 40ppm, respectively; p<0.01, each) and improvement of PaO2 (by 25% and 23%; p<0.05, each), owing to the reduction of intrapulmonary shunt (by 23% and 27%; p<0.05, each), without changes in the amount of perfusion to low V;A/Q; ratio alveolar units. Patients with greater baseline intrapulmonary shunt exhibited greater improvement in arterial oxygenation (r(2)=0.55, p<0.05). We conclude that low doses of inhaled NO improve pulmonary gas exchange in acute severe pneumonia.


Assuntos
Broncodilatadores/administração & dosagem , Óxido Nítrico/administração & dosagem , Pneumonia/terapia , Administração por Inalação , Idoso , Análise de Variância , Pressão Sanguínea/efeitos dos fármacos , Depsipeptídeos/efeitos dos fármacos , Feminino , Lateralidade Funcional , Hemodinâmica/efeitos dos fármacos , Humanos , Hiperemia/complicações , Hiperemia/terapia , Masculino , Pessoa de Meia-Idade , Pneumonia/complicações , Pneumonia/microbiologia , Troca Gasosa Pulmonar , Adulto Jovem
6.
Am J Trop Med Hyg ; 81(4): 595-9, 2009 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-19815872

RESUMO

Severe imported malaria is an important problem in many countries in which this disease is not endemic. This retrospective study describes the characteristics of 20 adults with severe imported malaria admitted to our intensive care unit from 1991 through 2007. All episodes were caused by Plasmodium falciparum and all patients had returned from sub-Saharan Africa, except for one transfusion recipient. All persons were considered non-immune, and none had taken appropriate chemoprophylaxis. The median time between the initiation of symptoms and the diagnosis was seven days. Five patients died (mortality rate = 25%). A higher frequency of unrousable coma and acidosis and a higher median Apache II score at admission was noted in the persons who died. Mortality by severe malaria remains high despite high quality management, which highlights the importance of chemoprophylaxis and early diagnosis and treatment.


Assuntos
Malária Falciparum/diagnóstico , Adolescente , Adulto , Idoso , Antimaláricos/administração & dosagem , Antimaláricos/uso terapêutico , Feminino , Humanos , Malária Falciparum/mortalidade , Malária Falciparum/prevenção & controle , Malária Falciparum/terapia , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Viagem , Adulto Jovem
8.
J Hepatol ; 43(2): 272-82, 2005 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-15964095

RESUMO

BACKGROUND/AIMS: Hepatic stellate cells (HSCs) are believed to participate in liver fibrogenesis and portal hypertension. Knowledge on human HSCs is based on studies using HSCs isolated from normal livers. We investigated the phenotypic, genomic and functional characteristics of HSCs from human cirrhotic livers. METHODS: HSC were obtained from normal and cirrhotic human livers. Cells were characterized by immunocytochemistry and gene microarray analysis. Cell proliferation, Ca(2+) changes and cell contraction were assessed by 3H-thymidine incorporation and by using an epifluorescence microscope. RESULTS: HSCs freshly isolated from human cirrhotic livers showed phenotypical features of myofibroblasts. These features were absent in HSCs freshly isolated from normal human livers and become prominent after prolonged culture. HSCs from cirrhotic human livers markedly express genes involved in fibrogensis, inflammation and apoptosis. HSCs from normal livers after prolonged culture preferntially expressed genes related to fibrogenesis and contractility. Agonists induced proliferation, Ca(2+) increase and cell contraction in HSCs isolated from human cirrhotic livers. Response to agonists was more marked in culture-activated HSCs and was not observed in HSCs freshly isolated from normal livers. CONCLUSIONS: HSCs from human cirrhotic livers show fibrogenic and contractile features. However, the current model of HSCs activated in culture does not exactly reproduce the activated phenotype found in cirrhotic human livers.


Assuntos
Divisão Celular/genética , Expressão Gênica/fisiologia , Genoma , Cirrose Hepática , RNA/genética , Cálcio/metabolismo , Células Cultivadas , DNA/biossíntese , DNA/genética , Humanos , Imuno-Histoquímica , Técnicas In Vitro , Cirrose Hepática/genética , Cirrose Hepática/metabolismo , Cirrose Hepática/patologia , Potenciais da Membrana , Microscopia de Fluorescência , Reação em Cadeia da Polimerase
11.
Hepatology ; 38(4): 919-29, 2003 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-14512879

RESUMO

Following cell activation, hepatic stellate cells (HSCs) acquire proinflammatory and profibrogenic properties. We investigated whether activated HSCs also display immune properties. Here we show that cultured human HSCs express membrane proteins involved in antigen presentation, including members of the HLA family (HLA-I and HLA-II), lipid-presenting molecules (CD1b and CD1c), and factors involved in T-cell activation (CD40 and CD80). Exposure of HSCs to proinflammatory cytokines markedly up-regulates these molecules. Importantly, cells freshly isolated from human cirrhotic livers (in vivo activated HSCs) highly express HLA-II and CD40, suggesting that HSCs can act as antigen-presenting cells (APCs) in human fibrogenesis. We also explored whether human HSCs can efficiently process exogenous antigens. Activated HSCs internalize low- and high-molecular-weight dextran and transferrin, indicating that they can perform fluid-phase and receptor-mediated endocytosis. Moreover, HSCs can perform phagocytosis of macromolecules because they internalize latex particles as well as bacteria. Interestingly, both culture-activated and in vivo activated HSCs express high levels of CD68, a protein involved in antigen trafficking. Finally, we studied whether HSCs modulate T-lymphocyte proliferation. In basal conditions, coculture of irradiated HSCs barely induces allogeneic T-lymphocyte proliferation. However, cytokine-stimulated HSCs stimulate the allogeneic T-lymphocyte response in an HLA-II-dependent manner. In conclusion, human activated HSCs express molecules for antigen presentation, internalize macromolecules, and modulate T-lymphocyte proliferation. These results suggest that HSCs may play a role in the immune function of the liver.


Assuntos
Células Apresentadoras de Antígenos/fisiologia , Fígado/citologia , Ativação Linfocitária , Apresentação do Antígeno , Antígenos CD/análise , Antígenos de Diferenciação Mielomonocítica/análise , Antígenos CD40/análise , Endocitose , Antígenos de Histocompatibilidade Classe II/análise , Humanos , Fígado/imunologia
12.
Gastroenterology ; 125(1): 117-25, 2003 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-12851877

RESUMO

BACKGROUND & AIMS: The renin-angiotensin system plays an important role in hepatic fibrogenesis. In other organs, myofibroblasts accumulated in damaged tissues generate angiotensin II, which promotes inflammation and extracellular matrix synthesis. It is unknown whether myofibroblastic hepatic stellate cells, the main hepatic fibrogenic cell type, express the renin-angiotensin system and synthesize angiotensin II. The aim of this study was to investigate whether quiescent and activated human hepatic stellate cells contain the components of the renin-angiotensin system and synthesize angiotensin II. METHODS: Hepatic stellate cells were freshly isolated from normal human livers (quiescent hepatic stellate cells) and from human cirrhotic livers (in vivo activated hepatic stellate cells). Culture-activated hepatic stellate cells were used after a second passage of quiescent hepatic stellate cells. Angiotensinogen, renin, and angiotensin-converting enzyme were assessed by quantitative polymerase chain reaction. Angiotensin II production was assessed by enzyme-linked immunosorbent assay and immunohistochemistry. RESULTS: Quiescent hepatic stellate cells barely express the renin-angiotensin system components--angiotensinogen, renin, and angiotensin-converting enzyme--and do not secrete angiotensin II. In contrast, both in vivo activated hepatic stellate cells and culture-activated hepatic stellate cells highly express active renin and angiotensin-converting enzyme and secrete angiotensin II to the culture media. Mature angiotensin II protein is also detected in the cytoplasm of in vivo activated and culture-activated hepatic stellate cells. Growth factors (platelet-derived growth factor and epidermal growth factor) and vasoconstrictor substances (endothelin-1 and thrombin) stimulate angiotensin II synthesis, whereas transforming growth factor-beta and proinflammatory cytokines have no effect. Vasodilator substances markedly attenuate the effect of endothelin-1. CONCLUSIONS: After activation, human hepatic stellate cells express the components of the renin-angiotensin system and synthesize angiotensin II. These results suggest that locally generated angiotensin II could participate in tissue remodeling in the human liver.


Assuntos
Angiotensina II/biossíntese , Hepatócitos/enzimologia , Sistema Renina-Angiotensina/fisiologia , Angiotensina II/metabolismo , Angiotensinogênio/metabolismo , Células Cultivadas , Fibroblastos/citologia , Fibroblastos/enzimologia , Fibroblastos/metabolismo , Hepatócitos/citologia , Hepatócitos/metabolismo , Humanos , Peptidil Dipeptidase A/genética , RNA Mensageiro/análise , Cicatrização
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