Extracapillary IgA nephropathy associated with infection with hepatitis C virus and hepatic cirrhosis

We describe a 36 year old man who was admitted to the hospital with dyspnea, edema of the lower limbs, arterial hypertension and oliguric renal failure. He had microhematuria and nephrotic range proteinuria, immunological tests were normal or negative. Renal biopsy revealed global (55%) or segmental glomeruloesclerosis, remaining glomeruli showed extracapillary proliferation (25%). Immunofluorescence study disclosed IgA mesangial deposits. He was also diagnosed as having liver cirrhosis with positive serology against hepatitis C virus. He was treated with dialysis, antihypertensive drugs and steroids with improvement of the renal function. However, ten months later maintenance hemodialysis became necessary. We emphasize two points: first IgA glomerulonephritis is rarely associated with hepatitis C infection, and second crescentic IgA nephropathy has been infrequently reported in liver cirrhosis.     

Beta-blockade and exercise capacity in patients with mitral stenosis in sinus rhythm

BACKGROUND AND AIM OF THE STUDY: The study aim was to determine whether beta-blocker treatment (atenolol) improves cardiopulmonary exercise performance and ventilatory response in patients with mitral stenosis in sinus rhythm. METHODS: A prospective study comparing the results of cardiopulmonary exercise tests (CPETs) was performed before and after atenolol therapy in 17 patients in NYHA classes I and II with mitral stenosis in sinus rhythm. Transthoracic echocardiography was performed pre-study, and left ventricular diameters, ejection fraction and mitral valve area monitored. CPETs (Naughton protocol) were performed by two different investigators before and after one-week atenolol therapy (50 mg/day). The second investigator was blinded to the result of the baseline test. O2 consumption, CO2 production, ventilatory parameters and respiratory exchange ratios were measured on line. RESULTS: Maximal O2 uptake (VO2max) did not differ significantly before and after beta-blockade (median 16.8 and 15.0 ml/kg/min, respectively. Median heart rate at rest (72 versus 55 beats/min; p = 0.0003) and during peak exercise (153 versus 105 beats/min; p = 0.0003), and anaerobic threshold (10 versus 8.9 ml/kg/min; p = 0.02) were lower with beta-blockade compared with the baseline state. Minute ventilation at maximum exercise (41 versus 40 l/min) and ventilatory equivalent for CO2 (34 versus 35) were unchanged with atenolol therapy, indicating no improvement in ventilatory performance. When patients were grouped into those in whom VO2max was improved with atenolol therapy (n = 7) and those in whom it was impaired (n = 10), there were no inter-group differences with respect to age, left ventricular function, severity of mitral stenosis, NYHA class and grade of beta-blockade reached. Four patients felt symptomatically worse during atenolol treatment (lower NYHA functional class). CONCLUSION: Beta-blockade does not improve exercise tolerance in patients with mitral stenosis in sinus rhythm. In addition, ventilatory performance does not change with treatment.     

Living morphogenesis of the ventricles and congenital pathology of their component parts

Living morphogenetic studies show that each definitive ventricle is constructed from different primitive cardiac segments, and each has its specific anatomical features. These ventricular segments are the atrioventricular junction; the primitive inlet segment, part of the primary heart tube, which initially provides the inlets of each ventricle; the primitive outlet segment, which gives rise to both ventricular outlets; and the apical trabeculated regions of the right and left ventricles which grow from the primary heart tube, respectively. In this review, we describe regional pathology based on the relationship of these primitive ventricular components. We propose that the abnormal morphogenesis of one of these segments gives origin to regional ventricular pathology. For example, abnormal embryogenesis of the atrioventricular canal produces malformations of the atrioventricular junctions, such as double inlet ventricle, absence of one atrioventricular connection, and straddling and overriding atrioventricular valves. Similarly, abnormal morphogenesis of the primitive outlet segment gives rise to malformations of the subarterial region of each ventricle, along with the valves guarding these vessels. The principal anatomical features of these malformations of the ventricular inlets and outlets are described, and their possible morphogenesis is discussed. Due to the fact that the apical trabeculated region of each ventricle arises from a separate primitive segment, each ventricle can be identified according to the pattern of its apical trabeculations. This feature is crucial in the elucidation of complex congenital pathology, such as discordant atrioventricular connections.     

Clinical features of idiopathic mitral valve prolapse]

This paper ask a question; is there a generalized defect of the connective tissue among subjects with primary mitral valve prolapse? Based on clinical methods it was found that paired subjects with and without primary mitral valve prolapse, are different in respect of an arbitrary score of joint hypermobility and phenotypic features. This is a statistically significant difference and suggest a possible molecular defect affecting connective tissue in people with primary mitral valve prolapse. Therefore, biochemical and molecular studies should be done to further characterize this abnormality.     

Pulmonary injuries and cytokine levels after the intraperitoneal administration of pancreatic homogenates in rats.

INTRODUCTION: Our objective was to investigate the effects of the administration of pancreatic homogenates, with or without enzymatic activation, to healthy animals regarding cytokine serum levels and the development of pulmonary distress. MATERIAL AND METHODS: 106 male Wistar rats, divided into three groups, were studied: group A, intraperitoneal administration of homogenates activated with enterokinase; group B, homogenates without enterokinase; and group C, control group with administration of physiological saline solution. Each group was divided into 4 subgroups according to the time of sacrifice: 0, 2, 6 and 24 hours. We studied the pulmonary and pancreatic histology, serum parameters of renal and hepatic function, and serum levels of IL-1beta, IL-6 and TNFalpha. RESULTS: There was no mortality in any group. Pancreatic disorders in A and B groups were noted at 24 hours. These two groups had statistically significant higher transaminase serum levels than those of the control group, as well as statistically significant higher creatinine levels in group A. IL-1beta showed a statistically significant higher level at 6 h in both groups, A and B, but was higher in group A, which also exhibited significant pulmonary histologic damage with respect to controls at 6 h. CONCLUSIONS: The higher IL-1beta level in group A may result from production by peritoneal macrophages under the influence of homogenate enzymatic activation. This may be the reason for lung damage.     

Poor lymphocyte recovery following CD34-selected autologous peripheral blood stem cell transplantation for non-Hodgkin's lymphoma

Positive selection of CD34+ cells in autologous grafts, designed to deplete tumour cells, also results in T-cell depletion. To assess the reconstitution of the different lymphocyte subsets and of the T-cell repertoire diversity following autologous transplantation of selected CD34+ peripheral blood stem cells (PBSC), we analysed sequential blood samples in eight patients autografted for advanced B-cell non-Hodgkin's lymphoma in a phase I-II pilot study. Although natural killer cell recovery was rapid, T- and B-cell recovery was delayed with a median of 110/microliters CD4+, 175/microliters CD8+ T cells and 45/microliters B cells at 12 months post-transplant. The naive CD45RA+ T-cell compartment was profoundly deficient up to 12 months for both CD4+ and CD8+ subsets. A transient expansion of memory CD8+CD45RO+ T cells consisting of an increased percentage of CD57+CD28- cells occurred within the first 3 months post-transplant, but the memory CD4+CD45RO+ T cells remained far below the normal value. The CD8+CD28+ T-cell subset did not recover. Using multiplex PCR analysis of the T-cell receptor gamma locus, we found that the repertoire diversity improved at 12 months after being poor and oligoclonal during the first 3 months post-transplant. As shown by monoplex PCRgamma analysis of every VJ combination, despite T-cell depletion of the graft, mature T cells were carried over with the selected CD34+ PBSC and contributed to the T-cell recovery after transplantation.     

The incidence of Trypanosoma cruzi antibodies in patients with dilated myocardiopathy at the Instituto Nacional de Cardiología Ignacio Chávez]

Our objective was to measure the incidence of humoral immune response against Trypanosoma cruzi among patients with a definitive diagnosis of dilated cardiomyopathy at the Instituto Nacional de Cardiología "I. Chávez" over a year. Thirty seven patients were collected, 15 of them (40%) had antibodies against T. cruzi in two different tests, indirect immunofluorescence and ELISA, the presence of IgG antibody was confirmed through Western blot. There was not differences in clinical picture of cardiomyopathy nor on paraclinical studies. However, there was a significant difference in regard socio economical indexes between the group with positive anti T. cruzi antibodies. They had a predominant rural origin, poor housing and were aware of the vector bug. Also they recalled primary infection in their childhood--American trypanosomiasis could be on important etiologic factor for dilated cardiomyopathy in our country.     

Antiphospholipid arterial vasculopathy

We describe 3 relatively young patients who developed arterial occlusions in a limb requiring amputation. All 3 had antiphospholipid antibodies (APLA). In one, these appeared as part of the clinical and serologic spectrum of systemic lupus erythematosus and in the other 2 as a component of a primary antiphospholipid syndrome. Their arterial angiograms showed gradual narrowing of the arterial lumen and the histopathologic study showed striking intimal and medial proliferation as well as some increase in thickness of the adventitia. There was little evidence of thrombosis but in the 2 patients who were amputated early there was mononuclear cell infiltrate of the large arteries and in all 3 there was also leukocytoclastic vasculitis in the skin and/or muscle. We believe this represents a new form of vasculopathy, probably related to the presence of APLA, possibly triggered by the occurrence of vasculitis.     

Infectious endocarditis caused by Candida. Presentation of 3 cases and review of the literature

We present 3 patients with infective endocarditis due to Candida sp. They were not immunodeficient subjects, but they had major surgery, longterm antimicrobial therapy and prosthetic implants. Candida endocarditis is a difficult diagnosis for biological and technical. There is also poor results with and therapeutic reasons. The combined treatment with amphotericin B and 5-fluorocytosine, plus surgical removal of the infected tissue is recommended widely in the literature.