Short-term atorvastatin therapy improves arterial stiffness of middle-aged systemic lupus erythematosus patients with pathological pulse wave velocity.

Objectives Statins have been proposed as a potential treatment for systemic lupus erythematosus (SLE) due to their immunomodulatory properties, their role restoring endothelial function and preventing atherosclerosis. We evaluate the effect of a short period treatment with a low dose of atorvastatin and its withdrawal on early stage subclinical atherosclerosis. Methods Thirty-seven SLE females received 20 mg/day atorvastatin during eight weeks. At baseline, at the end of treatment and six months after atorvastatin withdrawal, disease activity, subclinical atherosclerosis -assessed by measuring carotid-femoral pulse wave velocity (PWV) - and quantification of circulating endothelial progenitor cells (EPC) - as a surrogate biological marker of subclinical atherosclerosis - were carried out. Results The group of SLE patients with baseline pathological arterial stiffness showed a significant decrease of PWV after atorvastatin therapy (8.43 ± 1.45 m/s vs 7.42 ± 1.06 m/s; p = 0.002) that is maintained six months after treatment finished. Only patients of the middle-aged group showed a nearly significant decrease in the PWV measured along the study (7.16 ± 1.23 m/s vs 6.76 ± 0.82 m/s; p = 0.05). Atorvastatin induced a significant decrease in the circulating EPC percentage (0.65 ± 0.67 vs 0.40 ± 0.31; p = 0.023) as well as a downward trend of disease activity that it is observed by a decrease in SLE disease activity index simultaneously with an increase in C3 complement and significant decrease in serum concentration of vascular endothelial grow factor (VEGF) and sVCAM-1. Conclusions Short-term atorvastatin therapy reduces arterial stiffness of SLE patients with baseline pathological PWV, who are mainly in the group of middle-aged patients. Further studies are needed to determine whether these patients would benefit from statin therapy in preventing cardiovascular events.

Metabolic syndrome is associated with decreased circulating endothelial progenitor cells and increased arterial stiffness in systemic lupus erythematosus.

OBJECTIVES: Metabolic syndrome (MetS) is highly prevalent in patients with systemic lupus erythematosus (SLE) and it has been associated with increased cardiovascular risk. We examined the contribution of MetS to inflammatory markers, arterial stiffness and circulating endothelial progenitor cells (EPCs) as surrogates of subclinical atherosclerosis. METHODS: Cardiovascular risk factors, SLE-specific factors and peripheral blood EPCs were assessed in 50 female SLE patients. MetS was defined according to the National Cholesterol Education Program Adult Treatment Panel III. Simultaneously, atherosclerosis was assessed by measuring the carotid-femoral pulse wave velocity (PWV) by doppler velocimetry. RESULTS: Beyond the factors included in the definition, SLE patients with MetS have a significantly higher serum level of uric acid (6.88 ± 2.20 vs 4.45 ± 1.17, p < 0.001) and some inflammatory biomarkers such as homocysteine, IL-8, sICAM-1 or complement molecules. The presence of MetS in our patients was closely linked with a significantly increased patient organ damage score (3.20 ± 1.97 vs 1.60 ± 1.67, p = 0.008), a decreased percentage of circulating EPCs (0.53 ± 0.24 vs 0.85 ± 0.57, p = 0.007) and an increased arterial stiffness (9.89 ± 2.40 vs 7.13 ± 1.51, p < 0.001). CONCLUSIONS: MetS may contribute to the development of atherosclerosis by significantly increasing inflammation levels and arterial stiffness and decreasing circulating EPCs. This finding would justify close monitoring of these patients.

Increased arterial stiffness is independently associated with metabolic syndrome and damage index in systemic lupus erythematosus patients.

OBJECTIVES: We evaluated whether traditional or non-traditional cardiovascular (CV) risk factors and systemic lupus erythematosus (SLE)-related risk factors were associated with pathological arterial stiffness measured by pulse wave velocity (PWV) adjusted for patients' age and blood pressure. METHOD: CV risk factors were measured in the 46 SLE female patients studied. Activity and organ damage were assessed by the SLE Disease Activity Index (SLEDAI) and the Systemic Lupus International Collaborative Clinics/American College of Rheumatology (SLICC/ACR) Damage Index, respectively. Other lupus-related parameters and information concerning treatment were recorded. Subclinical atherosclerosis was assessed by PWV calculated from pulse wave recording by Doppler, a non-invasive method to measure arterial stiffness. Multivariate logistic regression analysis was used to identify independent determinants of increased PWV. RESULTS: PWV was categorized as normal or pathological arterial stiffness following the reference values adjusted by age and blood pressure recently published by the European Society of Cardiology. Pathological PWV was associated with CV risk factors including homocysteine (p = 0.01), high-sensitivity C-reactive protein (hs-CRP; p = 0.03), uric acid (p = 0.01), and metabolic syndrome (p = 0.007). With regard to SLE-specific risk factors, a significant association was found between PWV and SLICC/ACR score (p = 0.006). Multivariate analysis showed that increased PWV was independently associated with metabolic syndrome [odds ratio (OR) 6.6, 95% confidence interval (CI) 1.2-38, p = 0.03] and SLICC/ACR score (OR 1.5, 95% CI 1-2.32, p = 0.05). CONCLUSIONS: We have found a close link between metabolic syndrome and SLICC/ACR score with increased aortic stiffness. These variables might be an indicator of subclinical atherosclerosis in SLE women without clinical evidence of atherosclerotic cardiovascular disease (CVD).

Biclonal gammopathies: Retrospective study of 47 patients. / Gammapatías biclonales: estudio retrospectivo de 47 pacientes.

OBJECTIVES: Biclonal gammopathies are characterized by the clonal proliferation of plasma cells or their B-lymphoid progenitors and are associated with the production of abnormal immunoglobulins (M proteins or paraproteins). There are no known studies that have analyzed this disease in Spain. We studied the underlying diseases, characteristics of paraproteins and the evolution of a series of patients with biclonal gammopathy. MATERIAL AND METHODS: We reviewed clonal gammopathies at the Department of Immunology of Hospital Puerta de Hierro in Madrid, between 1970 and 2011, selecting those patients with biclonal gammopathy in one reading. We collected data on the patient's epidemiology, underlying disease, associated diseases, therapies and paraprotein and immunoglobulin levels. RESULTS: Of the 1626 cases of clonal gammapathies, 47 were biclonal gammopathy (2.89%). The median follow-up was 2 years. The main associated condition was biclonal gammopathies of undetermined significance (BGUS). The most common paraprotein combination was IgG-IgG. Upon conducting a second paraprotein reading, 81% of the patients had lost at least 1 monoclonal component. A third of the patients had not undergone treatment. CONCLUSIONS: Biclonal gammopathy are fundamentally associated with biclonal gammopathies of undetermined significance. No biclonal gammopathies of undetermined significance evolved to a malignant disease. In a high percentage of patients, at least 1 of the 2 clonal components disappeared, sometimes spontaneously.

[Endobronchial inflammatory pseudotumor. A case report and review of the literature]. / Seudotumor inflamatorio endobronquial. Presentación de un caso y revisión de la literatura.

The endobronchial inflammatory pseudotumor is a little described variant of inflammatory lung pseudotumor, the growth of which is directed towards bronchial lumen. A case is presented and seventeen other well documented cases from the medical literature are reviewed. This variant has been frequently observed with clinical manifestations of obstructive respiration and atelectasis as a radiologic pattern allowing detection at an early age. Endoscopy does not usually confirm diagnosis; surgery and study of the specimen removed is therefore necessary.

[Prevalence of hepatitis C virus infection in patients with non-Hodgkin's lymphoma]. / Prevalencia de infección por el virus de la hepatitis C en pacientes con linfomas no hodgkinianos.

BACKGROUND: To know the prevalence of HCV infection in patients diagnosed with B-NHL in our area. PATIENTS AND METHOD: A group of patients diagnosed with B-NHL between 1998-99 were carefully reviewed (serological tests, HCV RNA, laboratory studies, toxicity, response to treatment and evolution) in a transversal study. RESULTS: Overall 9/77 (11.68%) of patients tested positive for HCV. Of the 9 patients HCV(+) showed abnormal elevated trans aminases in opposition with 10.3% of patients that tested seronegative. CONCLUSION: Compared with normal individuals, we have seen a higher prevalence of HCV in our B-NHL patients. It may be possible that HCV play a role in that lymphoma's pathogenesis.

[Hodgkin's disease in patients with infection caused by the human immunodeficiency virus. Study of 9 cases]. / Enfermedad de Hodgkin en pacientes con infección por el virus de la inmunodeficiencia humana. Estudio de 9 casos.

Nine young males with Hodgkin's disease (HD) and antibodies against the human immunodeficiency virus were evaluated. They had been diagnosed since 1984 in three Madrid hospitals: Hospital 12 de Octubre, Hospital Ramón y Cajal, and Clínica Puerta de Hierro. Eight patients were intravenous heroin abusers and one was homosexual. In 8 patients (88.8%) HD presented in advanced stages (III and IV), and in 5 cases (55.5%) the histology corresponded to mixed cell type. Four patients (44.4%) developed opportunistic infections. In the immunological study a reduction of CD4+ lymphocytes below 0.4 X 10(3)/l was found in 5 of 7 patients (71.4%), and an inversion of CD4+/CD8+ ratio in 6 of 7 patients (85.7%). The response to therapy was poor. Five patients died (55.5%). In 4, the direct cause of death was an opportunistic infection. The reasons why we think that HD in patients with HIV infections should be considered as indicating acquired immunodeficiency syndrome are discussed.

Young systemic lupus erythematosus patients with no hearing involvement: 10-year follow up.

OBJECTIVE: To evaluate patients with systemic lupus erythematosus and normal hearing over 10 years, compared with healthy controls. METHODS: Thirty patients diagnosed with systemic lupus erythematosus were evaluated in a prospective, descriptive study. Eight patients fulfilled the inclusion criteria, i.e. normal otoscopy, normal hearing, normal imaging and disease duration of less than one year. Eleven healthy companions of ENT patients were recruited as controls. RESULTS: At study commencement, the mean patient age was 32.75 years (range, 15-49 years) and there were no statistically significant audiometric differences between patients and controls. No statistically significant audiometric changes were found either within or between the patient and control groups at 10-year follow up. CONCLUSION: These results supply no evidence for progressive hearing loss in systemic lupus erythematosus patients with no hearing involvement at study commencement. Therefore, we recommend audiometric tests only for systemic lupus erythematosus patients complaining of hearing loss, or for other clinical purposes. It is conceivable that asymptomatic hearing loss could be observed over a more extended follow-up period (i.e. more than 10 years).