Influencia de la enfermedad periodontal sobre las células sanguíneas y los niveles de proteína c reactiva / Periodontal disease influence on the blood cells and the levels of c-reactive protein

Periodontitis is a chronic inflammatory disease that is related with some systemic alterations. The severity of the inflammation in the periodontal tissues has been associated with a low-grade measurable systemic inflammation, and some studies have suggested an increase in the C-reactive protein levels and in number of white blood cells in patients with periodontal diseases. The red blood cells also could be affected by periodontitis with trends toward anemia. There are still controversies in relation to the direct influence of periodontal diseases in the occurrence of systemic inflammations. Thus, the aim of this study was to accomplish a literature review in order to verify the possible influence of the periodontal disease on blood cells and C-reactive protein levels

La Periodontitis es una enfermedad inflamatoria crónica que está relacionada con algunas alteraciones sistémicas. La gravedad de la inflamación de los tejidos periodontales ha sido asociada a una inflamación sistémica considerada de bajo grado y, algunos estudios han sugerido que hay un aumento en los niveles de proteína C-reactiva y en el número de leucocitos de la sangre en pacientes periodontalmente comprometidos. Las células de la serie roja de la sangre también podrían verse afectadas por la presencia de periodontitis, influyendo asi en la aparición de anemias. A pesar de eso, aún hay controversias en hasta qué punto las enfermedades periodontales podrían influenciar de forma directa en la aparición de las inflamaciones sistémicas. De esa forma, el objetivo de este trabajo fue realizar una revisión de literatura para verificar la posible influencia de la enfermedad periodontal sobre las células sanguíneas y los niveles de proteína C-reactiva

Evaluation of the role of thrombophilia associated factors in pre-eclampsia

To evaluate the role of thrombophilia associated factors in pre-eclamptic pregnant women. A case control study was conducted on 30 severe pre-eclamptic pregnant women [group A], and 30 normotensive pregnant women [group B] from Shatby University Maternity Hospital. Routine laboratory tests, protein C, protein S, antithrombin III, factor V Leiden and anticardiolipin antibodies [IgM, IgG] were measured for both groups. Informed consent of the patients was taken. There was not any significant difference in the values of factor V Leiden, protein C, protein S, antithrombin III, and anticardiolipin IgG between pre-eclamptic and normotensive pregnant women. However, anticardiolipin IgM was shown to be significantly higher in the pre-eclamptic patients. Severe pre-eclamptic patients were 3.5 times more likely to develop elevated levels of anticardiolipin IgM. Routine screening for inherited thrombophilia disorders is not recommended in pre-eclamptic females

Factor XII deficiency and habitual abortion: the Haegman connection

To evaluate the role of factor XII deficiency in cases of habitual abortions. A case control study was conducted on 50 women with history of three or more consecutive first-trimester abortions [group A] of unexplained nature from outpatient clinic of Shatby Maternity University Hospital, and 25 healthy women with no history of recurrent miscarriage, thrombotic disease or adverse pregnancy outcomes [group B]. Blood sample was taken from each patient to assay the following parameters: protein S [PS], protein C [PC], antithrombin III [ATIII], and coagulation factor XII [FXII]. The subsequent miscarriage rate with abnormal FXII is significantly higher than that with normal FXII. However, there were no statistically significant differences in the subsequent miscarriage rates between normal and abnormal PC, PS and ATIII values. Factor XII deficiency might play a role in recurrent miscarriages

Quantificação dos niveis sericos de anticorpos anti-PGL-I, neopterina e proteina C reativa em pacientes com hanseniase durante a poliquimioterapia / ?

A hanseniase e doença infecciosa, causada pelo Mycobacterium leprae, um parasita intracelular obrigatorio nao cultivavel em meios artificiais. Esta doença pode se manifestar sob amplo espectro clinico, correspondendo a distintos padroes da resposta imunologica do hospedeiro ao M. leprae. Em um polo deste espectro, esta a forma de resistencia ao bacilo, a hanseniase tuberculoide (HT), na qual se desenvolve acentuada resposta imune celular especifica com efetivo controle da mutilaçao bacilar. O outro polo do espectro esta representado pela hanseniase virchoviana (HV), forma de baixa resistencia, em que a resposta imune celular seletivamente falha em eliminar o bacilo do organismo, resultando na disseminaçao da doença. O grupo dimorfo (HD) apresenta manifestaçoes intermediarias variaveis entre HT e HV, de acordo com o grau de resposta imune ao M. leprae. Considerando que na hanseniase existem poucos estudos avaliando os niveis sericos de anticorpos anti-PGL-I, neopterina e proteina C reativa (CRP) no momento do diagnostico e durante o tratamento poliquimioterapico, realizamos este estudo com os sguintes objetivos: A. Avaliar a resposta imune e inflamatoria de pacientes com hanseniase no momento do diagnostico e aos 2, 4, 6 e 12 meses de tratamento com poliquimioterapia (PQT) e nos estados reacionais, mediante a determinaçao dos niveis sericos de anti-PGL-I, de neopterina e de CRP....

Mutations at the activated protein C cleavage sites Arg336 and Arg562 of factor VIII in Thai patients with venous thrombosis.

Venous thrombosis is a multicausal disease, more than one genetic risk factor may cooperate to effect thrombotic risk. Factor V Leiden is found to be an important hereditary risk factor for venous thromboembolism. Analogous to factor V Leiden, a point mutation at amino acid positions Arg336 and Arg562 in factor VIII may predispose patients to thrombosis. Eighty-one Thai patients with venous thrombosis and 100 Thai healthy volunteers have been studied. Neither heterozygous nor homozygous mutations were detected both thrombosis patients or normal volunteers. However, further studies with larger samples of venous thrombosis patients are recommended.

A molecular model of a point mutation (Val297Met) in the serine protease domain of protein C

A heterozygous GTG to ATG (Val297Met) mutation was detected in a patient with inherited protein C deficiency and deep vein thrombosis. Cosegregation of the mutation with protein C deficiency was observed through a family pedigree study. Molecular models of the serine protease domains of wild type and mutant protein C were constructed by standard comparative method. Val 297 was found to be located in the hydrophobic core of the protein. Although the substitution of Met for Val does not greatly alter the hydrophobicity of the protein, it introduces a bulkier side chain, which yields steric hindrance between this residue and adjacent residues, such as Met364, Tyr393, Ile321, Ile323, and Val378. It seems that the Met can not fit into the tight packing into which it is trapped, thereby probably inducing misfolding and/or greater instability of the protein. Such misfolding and/or instability thereby eventually disturbs the catalytic triad, in consistent with the observed type I deficiency state.

Proteina C reactiva en recién nacidos sanos Hospital Simón Bolívar / Reactive C protein in newborn

La concentración sérica de proteína fué medida por aglutinación en 71 recién nacidos sanos a las 24 horas de edad, atendidos en el Hospital Regional Simón Bolívar, durante los meses de Mayo a Julio de 1992. Se utilizó una muestra que confiere un 95 por ciento de confiabilidad estadística; encontrando en 67 pacientes niveles de proteína C reactiva menores de 6 miligramos por litro, en un paciente entre 6 y 12 miligramos por litro, en dos pacientes entre 13 y 18 y en un paciente entre 42 y 48 miligramos por litro. Ninguno de los pacientes tenía riesgo de infección y tampoco la adquirió durante el período nenonatal temprano, Con los resultados obtenidos concluímos que el 98 por ciento de los pacientes recién nacidos sanos de dicho hospital presentan niveles entre 0 y 18 miligramos por litro; concentraciones que se pueden tomar como referencia para estudios de sensibilidad y especificidad frente al diagnóstico y exclusión de sepsis neonatal temprana y para el seguimiento de pacientes infectados durante el tratamiento

Protein C and protein S deficiency in thalassemic patients.

To investigate the status of the protein C-protein S anticoagulant pathway in thalassemic patients, we measured protein C and protein S levels of plasma of 30 adults and 18 children with beta-thalassemia/HbE disease, beta-thalassemia major and HbE disease. Mean +/- 1 SD values of protein C, protein S and other coagulant proteins produced by the liver were as follows: protein C 50.4 +/- 17.2%; protein S 58.8 +/- 25.5%; antithrombin III 78.1 +/- 12.8%; PLG 86.4 +/- 18.4%; prothrombin 71.0 +/- 13.1%; factor VII 72.7 +/- 21.5%; and factor X 79.2 +/- 15.6%. Protein C and protein S levels of thalassemic patients were significantly lower than those of other coagulant proteins produced by the liver. Decrease in protein C level was stronger than that of proteins S. gamma-Carboxylated protein C levels of splenectomized patients were significantly lower than those of nonsplenectomized patients. Severe decrease of protein C and protein S may be responsible for occurrence of thrombosis in thalassemic patients.