Pneumocistose diagnosticada durante a gestação: relato de caso

A infecção pelo vírus da imunodeficiência humana (HIV) cursa com um amplo espectro de apresentações clínicas, desde a fase aguda até a fase avançada da doença. Em indivíduos não tratados o tempo médio entre o contágio com o vírus e o surgimento da doença ocorre em torno de dez anos. O aparecimento de infecções oportunistas e neoplasias é definidor da Síndrome da Imunodeficiência Adquirida, sendo que nessas situações a contagem de linfócitos TCD4+ está abaixo de 200 células/mm³. A pneumocistose, uma pneumonia fúngica, é causada pelo fungo Pneumocystis jirovecii. É considerada doença definidora da síndrome da imunodeficiência adquirida (SIDA), possui alta morbimortalidade, curso clínico grave; sendo uma causa comum de doença pulmonar oportunista em imunodeprimidos. Há poucos relatos de pneumocistose em pacientes gestantes infectadas pelo vírus da imunodeficiência humana (HIV), sendo que nesta parcela de pacientes, a pneumocistose é considerada uma doença rara. Descrevemos um caso em que a paciente não realizou Pré-Natal durante a gestação, apresentando como primeira manifestação clínica do HIV/SIDA, a pneumocistose.Human Immunodeficiency Virus (HIV) infection has a broad clinical presentation, from acute to advanced stages of the disease. The average time between infection and emergence of disease in untreated individuals is about ten years. Opportunistic infections and malignancies are AIDS-defining diseases and, in these situations, TCD4+ lymphocyte count is lower than 200 cells/mm³. Pneumocystosis, a fungal pneumonia, caused by Pneumocystis jirovecii, is considered an AIDS-defining disease with high morbidity, mortality and severe clinical course. It is the most common opportunistic infection affecting immunocompromised patients. There are few pneumocystosis reports in HIV pregnant patients as, in this group, pneumocystosis is considered rare. We report a case in which patient had no prenatal care and presented pneumocystosis as the first clinical manifestation of HIV/AIDS

Leishmaniose visceral infantil: relato de caso

leishmaniose visceral (LV) é uma infecção causada por protozoários tripanosomatídeos do gênero Leishmania, as espécies são: Leishmania donovani e Leishmania infantum (conhecido como Leishmania chagasi na América do Sul). A LV é uma doença parasitária grave, com elevada morbimortalidade em todo o mundo. É considerada a doença tropical mais negligenciada, em termos de desenvolvimento de novos medicamentos. Considerada um importante problema de saúde em todo o Brasil, principalmente na área endêmica de Paracatu-MG. Acomete principalmente crianças com menos de cinco anos de idade. A transmissão ocorre através da picada de fêmeas hematófagas dos vetores Lutzomyia longipalpis ou L. cruzi, infectados pela Leishmania (L.) chagasi. Os sinais clínicos da LV variam de acordo com a resposta imune do hospedeiro, podendo assumir formas assintomáticas, oligossintomáticas e a forma clássica; os principais sinais incluem febre, hepatoesplenomegalia, perda de peso e pancitopenia. Indivíduos não tratados, crianças desnutridas, indivíduos infectados pelo HIV ou em uso de drogas imunossupressoras são grupos de risco, sendo que nesses casos a LV apresenta alta letalidade. O diagnóstico é feito através da demonstração da Leishmania em aspirados de linfonodo, medula óssea e baço; por meio de sorologia, ou teste rápido como o rK39, são amplamente utilizados, e apresentam sensibilidade variável. O tratamento é realizado com antimoniais pentavalentes e anfotericina B lipossomal ou desoxicolato. Não há vacina humana; portanto o combate ao vetor é a melhor medida de prevenção. Relatamos um caso de LV em criança de 04 anos de idade, natural e procedente de Paracatu-MG.Visceral leishmaniasis (VL) is an infection caused by protozoa of the genus Leishmania tripanosomatídeos, the species are: Leishmania donovani and Leishmania infantum (known as Leishmania chagasi in South America). The VL is a severe parasitic disease with high morbidity and mortality worldwide. It is considered the most neglected tropical disease, in terms of the development of new medicines. Considered an important health problem throughout Brazil, mainly in the endemic area of Paracatu, MG. It affects mainly children under five years of age. Transmission occurs through the bite of female Lutzomyia longipalpis blood-feeding of vectors or L. cruzi infected by Leishmania (L.) chagasi. The clinical signs of VL vary according to the immune response of the host, and may take forms asymptomatic, oligosymptomatic metastases and the classical form; the main signs include fever, hepatosplenomegaly, weight loss and pancytopenia. Untreated individuals, malnourished children, individuals infected by HIV or in use of immunosuppressant drugs are risk groups, being that in these cases the VL presents high lethality. The diagnosis is made through demonstration of Leishmania in lymph node aspirates, bone marrow and spleen; through serology, or rapid test as the rK39, are widely used and present variable sensitivity. The treatment is performed with antimony pentavalents and liposomal amphotericin B or desoxycholate. There is no human vaccine; therefore the fight against vector is the best preventive measure. There is no human vaccine; therefore the fight against vector is the best preventive measure. We report one case of VL in children 04 years of age, natural and coming in Paracatu, MG

Hemofilia adquirida A e B principais apresentações clínicas da doença de Pott em crianças: Hemofilia adquirida A e B main clinical presentations of Pott disease in children

A hemofilia é uma doença sanguínea caracterizada por distúrbios nos mecanismos de coagulação do sangue, podendo ser de origem hereditária ou adquirida. A hemofilia adquirida ocorre devido à produção de autoanticorpos contra a atividade pró-coagulante dos fatores VIII (Hemofilia A) e IX (Hemofilia B). O objetivo desse trabalho é a realização de um estudo observacional e exploratório sobre os artigos publicados nos últimos 5 anos sobre a hemofilia adquirida A e B, uma vez que é uma enfermidade considerada rara. Dos 68 resultados obtidos na pesquisa, apenas 7 abordaram de forma objetiva sobre o tema, sendo utilizados na confecção do estudo. Segundo a literatura, as manifestações clínicas envolvem sangramento mucocutâneo, urogenital e gastrointestinal, e são mais prevalentes em idosos. Em crianças, o sangramento pode ser menos expressivo, provocando dúvidas quanto ao diagnóstico. O tratamento da hemofilia envolve a reposição dos fatores de coagulação deficientes e o uso de imunossupressores, ainda que nas obras analisadas apenas o tratamento hemostático tenha sido descrito, revelando uma carência de estudos sobre o uso de imunossupressores nos casos de hemofilia adquirida

Incidência da síndrome pré-menstrual na prática de esportes: aspectos atuais: Incidence of pre-menstrual syndrome in sports: current aspects

A síndrome pré-menstrual (SPM) é uma constelação complexa de alterações de humor, comportamentais e físicas que se limitam à fase pré-menstrual. Esses sintomas se recuperam dentro de alguns dias após o início da menstruação.  Assim, o objetivo desse estudo é demonstrar a incidência da síndrome pré-menstrual na prática de esportes a partir de uma revisão integrativa sobre o tema. Para isso, foi realizado uma revisão integrativa sobre o tema, onde foi considerado textos publicados desde 2010, em inglês e português e que estejam disponíveis para leitura, no PUBMED, LILACs e Scielo. Esta revisão sistemática fornece algum suporte adicional para diretrizes clínicas que recomendam o exercício como um tratamento eficaz para a TPM. As análises secundárias realizadas também fornecem novas evidências de que o exercício pode ser útil no alívio de sintomas psicológicos, físicos e comportamentais específicos associados à TPM, além de auxiliar no gerenciamento do perfil global de sintomas

In situ evaluation of podocytes in patients with focal segmental glomerulosclerosis and minimal change disease.

Podocyte injury in focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD) results from the imbalance between adaptive responses that maintain homeostasis and cellular dysfunction that can culminate in cell death. Therefore, an in situ analysis was performed to detect morphological changes related to cell death and autophagy in renal biopsies from adult patients with podocytopathies. Forty-nine renal biopsies from patients with FSGS (n = 22) and MCD (n = 27) were selected. In situ expression of Wilms Tumor 1 protein (WT1), light chain microtubule 1-associated protein (LC3) and caspase-3 protein were evaluated by immunohistochemistry. The foot process effacement and morphological alterations related to podocyte cell death and autophagy were analyzed with transmission electronic microscopy. Reduction in the density of WT1-labeled podocytes was observed for FSGS and MCD cases as compared to controls. Foot process width (FPW) in control group was lower than in cases of podocytopathies. In FSGS group, FPW was significantly higher than in MCD group and correlated with proteinuria. A density of LC3-labeled podocytes and the number of autophagosomes in podocytes/ pedicels were higher in the MCD group than in the FSGS group. The number of autophagosomes correlated positively with the estimated glomerular filtration rate in cases of MCD. The density of caspase-3-labeled podocytes in FSGS and MCD was higher than control group, and a higher number of podocytes with an evidence of necrosis was detected in FSGS cases than in MCD and control cases. Podocytes from patients diagnosed with FSGS showed more morphological and functional alterations resulting from a larger number of lesions and reduced cell adaptation

Ultrastructural deposits appearing as “zebra bodies” in renal biopsy: Fabry disease?– comparative case reports

Abstract Background Fabry Disease (FD) is a genetic disorder caused by alpha-galactosidase A deficiency. Certain drugs, such as hydroxychloroquine, can produce renal deposits that mimic morphological findings seen in FD, characterizing a type of drug-induced renal phospholipidosis. Case presentation Case 1: A 28-year-old female patient with systemic lupus erythematosus who had been using hydroxychloroquine for 14 months presented subnephrotic proteinuria. Renal biopsy showed deposits compatible with FD. Neither activity analysis of alpha-galactosidase A nor genetic analysis were available and were not performed. These deposits were not detected in a subsequent renal biopsy three years after withdrawal of the medication, characterizing a possible hydroxychloroquine-induced renal phospholipidosis. Case 2: A 29-year-old male patient presented with acroparesthesia, angiokeratomas, cornea verticillata and subnephrotic proteinuria. Deposits compatible with FD were detected upon renal biopsy. The evaluation of alpha-galactosidase A showed no activity in both blood and leukocytes. Genetic analysis identified an M284 T mutation in exon 6, and such mutation was also found in other family members. Conclusion Clinical investigation is necessary in suspected cases of Fabry Disease upon renal biopsy in order to confirm diagnosis. Drug-induced renal phospholipidosis should be considered in differential diagnosis in cases with intracellular osmiophilic, lamellar inclusions in electron microscopy

Evaluation of the Diagnostic Potential of uPAR as a Biomarker in Renal Biopsies of Patients with FSGS

Minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) are primary glomerulopathies leading to proteinuria, known as podocytopathies, which share syndromic and morphological similarities. Morphological similarity occurs in cases of FSGS in which the sclerotic lesion was not sampled in renal biopsy, due to the focal nature of the disease. Differentiating these entities is very important, especially in cases of suspected FSGS but with sclerotic lesion not sampled, as they are diseases that apparently have different pathogenic mechanisms and prognosis. The difference in uPAR expression in situ among these two entities may be related to a distinct molecular mechanism involved in pathogenesis. Thus, finding biomarkers involved in the pathogenesis and that can also help in differential diagnosis is very relevant. The aim of this work was to evaluate the potential of urokinase-type plasminogen activator receptor (uPAR) as a biomarker in renal biopsies of patients with podocytopathies (n=38). Immunohistochemistry showed that FSGS (n=22) had increased uPAR expression in podocytes compared with both the MCD group (n=16; p=0.0368) and control group (n=21; p=0.0076). ROC curve (p=0.008) showed that this biomarker has 80.95% of specificity in biopsies of patients with FSGS. Therefore, uPAR presented a high specificity in cases of podocytopathies associated with sclerosis and it can be considered a potential biomarker for FSGS

Podocin and uPAR are good biomarkers in cases of Focal and segmental glomerulosclerosis in pediatric renal biopsies.

There are controversies whether Minimal Change Disease (MCD) and Focal and Segmental Glomerulosclerosis (FSGS) are distinct glomerular lesions or different manifestations within the same spectrum of diseases. The uPAR (urokinase-type plasminogen activator receptor) and some slit diaphragm proteins may be altered in FSGS glomeruli and may function as biomarkers of the disease in renal biopsies. Thus, this study aims to evaluate the diagnostic potential of uPAR and glomerular proteins for differentiation between MCD and FSGS in renal pediatric biopsy. Renal biopsies from 50 children between 2 and 18 years old were selected, with diagnosis of MCD (n = 29) and FSGS (n = 21). Control group consisted of pediatric autopsies (n = 15) from patients younger than 18 years old, with no evidences of renal dysfunction. In situ expressions of WT1, nephrin, podocin and uPAR were evaluated by immunoperoxidase technique. Renal biopsy of patients with MCD and FSGS expressed fewer WT1 (p≤0.0001, F = 19.35) and nephrin (p<0.0001; H = 21.54) than patients in the control group. FSGS patients expressed fewer podocin than control (p<0.0359, H = 6.655). FSGS cases expressed more uPAR than each of control and MCD (p = 0.0019; H = 12.57) and there was a positive and significant correlation between nephrin and podocin (p = 0.0026, rS = 0.6502) in these cases. Podocin had sensitivity of 73.3% and specificity of 86.7% (p = 0.0068) and uPAR had sensitivity of 78.9% and specificity of 73.3% (p = 0.0040) for diagnosis of FSGS patients. The main limitation of the study is the limited number of cases due to the difficulty in performing biopsy in pediatric patients. Podocin and uPAR are good markers for FSGS and differentiate these cases from MCD, reinforcing the theory of distinct glomerular diseases. These findings suggest that podocin and uPAR can be used as biomarkers in the routine analysis of renal biopsies in cases of podocytopathies when the lesion (sclerosis) is not sampled

Upregulation of Cardiac IL-10 and Downregulation of IFN-γ in Balb/c IL-4−/− in Acute Chagasic Myocarditis due to Colombian Strain of Trypanosoma cruzi

Inflammatory response in Chagas disease is related to parasite and host factors. However, immune system regulation has not been fully elucidated. Thus, this study is aimed at evaluating IL-4 influence on acute phase of Trypanosoma cruzi experimental infection through dosage of cytokine levels in cardiac homogenate of infected Balb/c WT and Balb/c IL-4−/− as well as its histopathological repercussions. For such purpose, mice were divided into two groups: an infected group with 100 forms of the Colombian strain and an uninfected group. After 21 days of infection, animals were euthanized and the blood, spleen, and heart were collected. The spleen was used to culture splenic cells in 48 h. Subsequently, cytokines TNF-α, IL-12p70, IL-10, IFN-γ, and IL-17 were measured in the blood, culture supernatant, and heart apex by ELISA. The base of the heart was used for histopathological analysis. From these analysis, infected Balb/c IL-4−/− mice showed milder inflammatory infiltrate compared to Balb/c WT, but without changes in nest density and collagen deposition. IL-4 absence culminated in lower cardiac tissue IFN-γ production, although it did not affect TNF-α expression in situ. It also decreased TNF-α systemic production and increased IL-10, both systemically and in situ. In addition, IL-4 absence did not influence IL-17 expression. Splenocytes of IL-4-deficient mice produced higher amounts of IFN-γ, TNF-α, and IL-17 and lower amounts of IL-10. Thus, IL-4 absence in acute phase of experimental infection with T. cruzi Colombian strain reduces myocarditis due to lower IFN-γ production and greater IL-10 production in situ and this pattern is not influenced by splenocyte general repertoire