Hypertensive iridocyclitis associated with delayed onset biopsy proven Cytomegalovirus retinitis.

We describe a case of primary hypertensive iridocyclitis with biopsy-proven Cytomegaloviral retinitis. It is an observational case report of a 69-year-old diabetic gentleman on azathioprine for Crohn’s disease who presented with recurrent episodes of hypertensive iridocyclitis. On the 4th a􀄴 endance in 5 months, a granular white lesion was noted in the temporal periphery of the mid-peripheral fundus and a chorioretinal and vitreous biopsy performed. Vitreous PCR was positive for Cytomegalovirus (CMV). Hematoxylin and eosin staining revealed cytomegaliclike inclusions within necrotic neural retina. Transmission electron microscopy revealed herpes family virus particles and immunohistochemistry demonstrated CMV protein. This case provides further evidence implicating CMV infection in the etiology of hypertensive iridocyclitis. With hindsight, the cumulative eff ect of diabetes and azathioprine on the immune surveillance system proved sufficient to render the patient susceptible to CMV retinitis.

El aumento de la expresión del ARNm de la enzima convertidora de angiotensina I homóloga (ECA-2) inducido por atorvastatina se asocia a menor fibrosis e hipertrofia ventricular izquierda en un modelo de cardiomiopatía diabética / Atorvastatin induced increase in homologous angiotensin i converting enzyme (ACE2) mRNA is associated to decreased fibrosis and decreased left ventricular hypertrophy in a rat model of diabetic cardiomyopathy

Objetivos. Evaluar el efecto de atorvastatina sobre la progresión del remodelado cardiaco y la expresión de ECA-2 en el miocardio de ratas diabéticas. Materiales y métodos. La diabetes fue inducida en ratas Holtzman con una inyección intraperitoneal de estreptozotocina. Los animales fueron divididos en tres grupos: (1) ratas control, (2) ratas diabéticas y (3) ratas diabéticas tratadas con atorvastatina (50 mg/kg/día). Después de ocho semanas de tratamiento, los corazones fueron extraídos para el análisis morfométrico, la cuantificación de colágeno y la determinación de los niveles de ARNm de ECA y ECA-2. Resultados. El índice de hipertrofia ventricular y el depósito de colágeno se incrementaron significativamente en las ratas diabéticas. La administración de atorvastatina previno estos cambios sin modificar los niveles de colesterol. La hiperglicemia produjo un incremento significativo en los niveles del ARNm de ECA y una marcada disminución en la expresión de ECA-2 en el miocardio de ratas diabéticas. La administración de atorvastatina indujo la expresión del ARNm de ECA-2 e inhibió la sobreexpresión del ARNm de ECA en el miocardio de las ratas diabéticas. Conclusiones. Nuestros resultados indican que la atorvastatina, independientemente de su capacidad para disminuir el colesterol, normaliza la relación de la expresión de ECA/ECA-2 y atenúa el desarrollo del remodelado adverso en el corazón diabético.

Objectives. This study has investigated the effect of atorvastatin on the progression of cardiac remodelling and ACE- 2 expression in diabetic myocardium in rats. Materials and Methods. Diabetes was induced in Holtzman rats with an intraperitoneal injection of streptozotocin. The animals were divided into 3 groups: (1) normal control rats, (2) diabetic rats and (3) diabetic rats treated orally with atorvastatin (50 mg/kg/day). After eight weeks of treatment, the hearts were removed for morphometric studies, collagen content assay and genetic expressions of ACE and ACE2 mRNA. Results. Myocardial hypertrophy index and collagen deposition were increased in diabetic rats, but not in the treated-diabetic rats, without producing changes in cholesterol levels. Myocardial ACE mRNA levels were increased while ACE2 mRNA levels were decreased in diabetic rats. Atorvastatin administration attenuated overexpression of ACE mRNA and overexpression of ACE-2 mRNA in diabetic rats. Conclusions. Our results indicate that atorvastatin, independently of its cholesterol-lowering capacity, lowers the ACE/ACE2 ratio to normal values and attenuates the development of adverse remodeling in the diabetic heart.

Macrolide-Resistance of Mycoplasma Pnuemoniae in Respiratory Tract Infection in Children / 实用儿科临床杂志

Objective To investigate the mycoplasma pneumoniae(MP) infection of the respiratory tract infection in children,the macrolide-resistant situation and resistance mechanism of MP. Methods The cultured throat swab specimens were obtained from 80 pediatric outpatients with respiratory tract infection from Dec.2008 to Mar.2009 in Beijing friendship hospital.The 23S rRNA gene of throat swab specimens and positive-cultured specimens were amplified using nested-PCR,and the products were further verified by electrophoresis and DNA sepuencing,which were collected from the outpatients.The specimens were divided into 2 groups depending on the findings of the gene sequencing whether they had gene mutation:sensitive and resistance group.The DNA sequence of samples were compared to the sequence of MP reference strain in genbank in order to findout MP drug resistant gene.The differences in macrolids therapy were investigated between 2 groups before the throat swab obtained.The drug resistance rates were compared between outpatients and inpatients. Results Thirty-two throat swab specimens were proved to be MP by direct nested-PCR,and 8 throat speeimens were proved to be MP by isolation and culrures.Total 33 cases(including 1 was positive-culture but nagative-direct PCR) were proved to be MP positive.Sixteen were identical to the M129 standard sequence,and 17 had point mutation in gene of 23S rRNA V region.Ten had A to G mutation at position 2063,3 had A to G mutation at position 2064,2 had A to G mutation at position 2067,1 had G to A mutation at position 2062,1 had A to T mutation at position 2063.There was no significant difference between the sensitive and resistance group in whether had macrolids before the throat swab obtained(P =0.909).And there was no significant difference in MP drug resistance rate between outpatients and inpatients(P =0.459). Conclusions The major mutation were A2063G and A2064G,and A2063T,A2067G,G2062A were newly found mutation points which were possibly related to macrolids resistance.

Detection of Chlamydia trachomatis by PCR with reactive arthritis

Chlamydia trachomatis has been shown to induce reactive arthritis in people, especially after sexually acquired genitourinary infection. To determine the connection between Chlamydia trachomatis with reactive arthritis, in this study we examined antigen Chlamydia trachomatis lipopolysarcaride. Antibody IgG, and DNA of chlamydia trachomatis were investigated in samples (urine, serum, and synovial fluid) from 52 patients were diagnosed and treated in Rheumatology Department, Bach Mai Hospital from August 2001 to August 2003. As results we found that 38.5% urine samples positve with antigen LPS. Antibody IgG positive in 44.2% of serum samples and in 34.6% of synovial fluid samples. Special DNA of Chlamydia trachomatis was detected in 53.2% of synovial fluid samples and in 42.2% of urine samples positive. This results will contribute to determine the role of DNA-Chlamydia trachomatis in reactive arthritis diagnosis.