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BACKGROUND: Lupus nephritis (LN) is a common feature of systemic lupus erythematosus (SLE) and affects 50% of patients with SLE. Racial differences in incidence and prevalence have been well documented worldwide. In Australia, higher incidence and prevalence of SLE had been previously reported in Aboriginal and Torres Strait Australians compared with non-Indigenous Australians. AIM: To describe the differences in clinical features and lupus biomarkers between Aboriginal and Torres Strait Islander Australian and non-Indigenous Australian patients with LN. METHODS: We retrospectively identified all consecutive biopsy-proven LN patients in our institution and compared the clinical features and lupus biomarkers between Aboriginal and Torres Strait Islander Australians and non-Indigenous Australians. RESULTS: Of the 33 consecutive biopsy-proven LN patients, 26 self-identified as of Aboriginal and Torres Strait Islander descent. The estimated incidence of LN in Aboriginal and Torres Strait Islander Australian and non-Indigenous Australians were 5.08 and 0.47 per 100 000 patient-years respectively. Neurological manifestations (23.08% vs 0%), haematological manifestations (46.50% vs 16.67) and right-heart catheter proven pulmonary arterial hypertension (23.08% vs 0%) were more frequently observed among Indigenous Australian patients compared with non-Indigenous Australian patients. The incidence of positive extractable nuclear antigen was also higher among Indigenous Australian patients (84.62% vs 57.14%). CONCLUSION: The present study further supports the observation that lupus in Aboriginal and Torres Strait Islander Australians were of a 'distinct phenotype' compared with non-Indigenous Australians. Future research should be aimed at delineating the reason for this observed difference.
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Nefritis Lúpica , Humanos , Nefritis Lúpica/diagnóstico , Nefritis Lúpica/epidemiología , Australia/epidemiología , Estudios Retrospectivos , Aborigenas Australianos e Isleños del Estrecho de Torres , Biomarcadores , BiopsiaRESUMEN
We report a case of acute rheumatic fever with severe pancarditis occurring simultaneously with probable acute post-streptococcal glomerulonephritis in a previously well, Australian Aboriginal, 29-year-old male. These autoimmune streptococcal sequelae are usually considered pathogenetically distinct, and concurrence has not previously been reported from this high-burden setting. We hypothesize that a single type of infecting group A Streptococcus (Strep A) triggered both autoimmune sequelae. Salient features included mitral and aortic regurgitation that worsened during the acute illness, painful pericarditis, and high troponin; severe acute kidney injury with oliguria, hematuria, and macroalbuminuria; reduced complement (C3); and elevated streptococcal serology. The case highlights important diagnostic and management challenges. It also illustrates the serious morbidity impact of the complications of Strep A.
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Glomerulonefritis/etiología , Fiebre Reumática/complicaciones , Adulto , Antibacterianos/administración & dosificación , Antibacterianos/uso terapéutico , Antiinflamatorios/administración & dosificación , Antiinflamatorios/uso terapéutico , Ceftriaxona/administración & dosificación , Ceftriaxona/uso terapéutico , Floxacilina/administración & dosificación , Floxacilina/uso terapéutico , Cardiopatías/microbiología , Cardiopatías/patología , Humanos , Masculino , Prednisolona/administración & dosificación , Prednisolona/uso terapéutico , Fiebre Reumática/diagnóstico , Fiebre Reumática/tratamiento farmacológicoRESUMEN
Although new heptatis C virus treatments have increased efficacy and improved safety profiles, they also come with risk. We describe a 66-year-old white man with Child-Pugh A cirrhosis secondary to heptatis C virus genotype 3, who suffered from an acute kidney injury after treatment with sofosbuvir and daclatasvir. Kidney biopsy demonstrated evidence of acute tubular interstitial nephritis consistent with a drug reaction. A trial of steroid therapy was effective, and his creatinine continues to improve significantly. Our case is the first report in the literature that highlights potentially serious interstitial nephritis associated with sofosbuvir and daclatasvir use.
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BACKGROUND: Warfarin remains a widely used anticoagulant but application in the remote context is not well documented. This study aimed to assess in more detail whether warfarin is being utilised effectively in Australia's most isolated and remote areas. METHODS: Retrospective cohort analysis of 2013 captured international normalised ratio (INR) results from people engaged in long term warfarin usage within a number of remote Northern Australian communities. Assessment of monitoring, effectiveness of dosing and complication rates was undertaken. RESULTS: A cohort of 167 patients was established. On average, warfarin was utilised within therapeutic range 52% of the time. Monitoring frequency averaged 16 days. Major bleeding and thrombo-embolism occurred at rates of 5.8 and 4.1 per 100 patient years respectively. CONCLUSIONS: Therapeutic utilisation of warfarin in this setting is close to accepted rates but has room for improvement. Monitoring was acceptable and complication rates were not disproportionately high. This study indicates that warfarin is being used with reasonable safety and efficacy in remote regions, but further research is needed.
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Áreas de Influencia de Salud , Población Rural , Tromboembolia/prevención & control , Warfarina/administración & dosificación , Anciano , Anticoagulantes/administración & dosificación , Relación Dosis-Respuesta a Droga , Femenino , Estudios de Seguimiento , Servicios de Salud del Indígena , Humanos , Masculino , Persona de Mediana Edad , Morbilidad/tendencias , Northern Territory/epidemiología , Estudios Retrospectivos , Tromboembolia/epidemiología , Resultado del TratamientoRESUMEN
AIMS: The effect of statin treatment on ventricular arrhythmic complications is uncertain. We sought to test whether statins reduce the risk of ventricular tachyarrhythmia, cardiac arrest, and sudden cardiac death. METHODS AND RESULTS: We searched MEDLINE, EMBASE, and CENTRAL up to October 2010. Randomized controlled trials comparing statin with no statin or comparing intensive vs. standard dose statin, with more than 100 participants and at least 6-month follow-up were considered for inclusion and relevant unpublished data obtained from the investigators. Twenty-nine trials of statin vs. control (113 568 participants) were included in the main analyses. In these trials, statin therapy did not significantly reduce the risk of ventricular tachyarrhythmia [212 vs. 209; odds ratio (OR) = 1.02, 95% confidence interval (CI) 0.84-1.25, P = 0.87] or of cardiac arrest (82 vs. 78; OR = 1.05, 95% CI 0.76-1.45, P = 0.84), but was associated with a significant 10% reduction in sudden cardiac death (1131 vs. 1252; OR = 0.90; 95% CI 0.82-0.97, P = 0.01). This compared with a 22% reduction in the risk of other 'non-sudden' (mostly atherosclerotic) cardiac deaths (1235 vs. 1553; OR = 0.78, 95% CI 0.71-0.87, P < 0.001). Results were not materially altered by inclusion of eight trials (involving 41 452 participants) of intensive vs. standard dose statin regimens. CONCLUSION: Statins have a modest beneficial effect on sudden cardiac death. However, previous suggestions of a substantial protective effect on ventricular arrhythmic events could not be supported.
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Muerte Súbita Cardíaca/prevención & control , Paro Cardíaco/prevención & control , Inhibidores de Hidroximetilglutaril-CoA Reductasas/uso terapéutico , Taquicardia Ventricular/prevención & control , Anciano , LDL-Colesterol/sangre , Femenino , Humanos , Hipercolesterolemia/prevención & control , Hipolipemiantes/uso terapéutico , Masculino , Persona de Mediana Edad , Ensayos Clínicos Controlados Aleatorios como Asunto , Sesgo de SelecciónRESUMEN
Heart failure mortality is significantly increased in patients with baseline renal impairment and those with underlying heart failure who subsequently develop renal dysfunction. This accelerated progression occurs independent of the cause or grade of renal dysfunction and baseline risk factors. Recent large prospective databases have highlighted the depth of the current problem, while longitudinal population studies support an increasing disease burden. We have extensively reviewed the epidemiological and therapeutic data among these patients. The evidence points to a progression of heart failure early in renal impairment, even in the albuminuric stage. The data also support poor prescription of prognostic therapies. As renal function is the most important prognostic factor in heart failure, it is important to establish the current understanding of the disease burden and the therapeutic implications.
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BACKGROUND: Lowering LDL cholesterol with statin regimens reduces the risk of myocardial infarction, ischaemic stroke, and the need for coronary revascularisation in people without kidney disease, but its effects in people with moderate-to-severe kidney disease are uncertain. The SHARP trial aimed to assess the efficacy and safety of the combination of simvastatin plus ezetimibe in such patients. METHODS: This randomised double-blind trial included 9270 patients with chronic kidney disease (3023 on dialysis and 6247 not) with no known history of myocardial infarction or coronary revascularisation. Patients were randomly assigned to simvastatin 20 mg plus ezetimibe 10 mg daily versus matching placebo. The key prespecified outcome was first major atherosclerotic event (non-fatal myocardial infarction or coronary death, non-haemorrhagic stroke, or any arterial revascularisation procedure). All analyses were by intention to treat. This trial is registered at ClinicalTrials.gov, NCT00125593, and ISRCTN54137607. FINDINGS: 4650 patients were assigned to receive simvastatin plus ezetimibe and 4620 to placebo. Allocation to simvastatin plus ezetimibe yielded an average LDL cholesterol difference of 0·85 mmol/L (SE 0·02; with about two-thirds compliance) during a median follow-up of 4·9 years and produced a 17% proportional reduction in major atherosclerotic events (526 [11·3%] simvastatin plus ezetimibe vs 619 [13·4%] placebo; rate ratio [RR] 0·83, 95% CI 0·74-0·94; log-rank p=0·0021). Non-significantly fewer patients allocated to simvastatin plus ezetimibe had a non-fatal myocardial infarction or died from coronary heart disease (213 [4·6%] vs 230 [5·0%]; RR 0·92, 95% CI 0·76-1·11; p=0·37) and there were significant reductions in non-haemorrhagic stroke (131 [2·8%] vs 174 [3·8%]; RR 0·75, 95% CI 0·60-0·94; p=0·01) and arterial revascularisation procedures (284 [6·1%] vs 352 [7·6%]; RR 0·79, 95% CI 0·68-0·93; p=0·0036). After weighting for subgroup-specific reductions in LDL cholesterol, there was no good evidence that the proportional effects on major atherosclerotic events differed from the summary rate ratio in any subgroup examined, and, in particular, they were similar in patients on dialysis and those who were not. The excess risk of myopathy was only two per 10,000 patients per year of treatment with this combination (9 [0·2%] vs 5 [0·1%]). There was no evidence of excess risks of hepatitis (21 [0·5%] vs 18 [0·4%]), gallstones (106 [2·3%] vs 106 [2·3%]), or cancer (438 [9·4%] vs 439 [9·5%], p=0·89) and there was no significant excess of death from any non-vascular cause (668 [14·4%] vs 612 [13·2%], p=0·13). INTERPRETATION: Reduction of LDL cholesterol with simvastatin 20 mg plus ezetimibe 10 mg daily safely reduced the incidence of major atherosclerotic events in a wide range of patients with advanced chronic kidney disease. FUNDING: Merck/Schering-Plough Pharmaceuticals; Australian National Health and Medical Research Council; British Heart Foundation; UK Medical Research Council.
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Azetidinas/administración & dosificación , Enfermedades Cardiovasculares/prevención & control , LDL-Colesterol/efectos de los fármacos , Insuficiencia Renal Crónica/tratamiento farmacológico , Simvastatina/administración & dosificación , Adulto , Anciano , LDL-Colesterol/análisis , Intervalos de Confianza , Relación Dosis-Respuesta a Droga , Método Doble Ciego , Esquema de Medicación , Quimioterapia Combinada , Ezetimiba , Femenino , Estudios de Seguimiento , Humanos , Hipolipemiantes/administración & dosificación , Hipolipemiantes/efectos adversos , Pruebas de Función Renal , Masculino , Persona de Mediana Edad , Valores de Referencia , Diálisis Renal/métodos , Diálisis Renal/mortalidad , Insuficiencia Renal Crónica/diagnóstico , Insuficiencia Renal Crónica/mortalidad , Insuficiencia Renal Crónica/terapia , Medición de Riesgo , Índice de Severidad de la Enfermedad , Simvastatina/efectos adversos , Análisis de Supervivencia , Factores de Tiempo , Resultado del TratamientoRESUMEN
OBJECTIVE: To examine whether statins can reduce the risk of atrial fibrillation. DESIGN: Meta-analysis of published and unpublished results from larger scale statin trials, with comparison of the findings against the published results from smaller scale or shorter duration studies. DATA SOURCES: Medline, Embase, and Cochrane's CENTRAL up to October 2010. Unpublished data from longer term trials were obtained through contact with investigators. STUDY SELECTION: Randomised controlled trials comparing statin with no statin or comparing high dose versus standard dose statin; all longer term trials had at least 100 participants and at least six months' follow-up. RESULTS: In published data from 13 short term trials (4414 randomised patients, 659 events), statin treatment seemed to reduce the odds of an episode of atrial fibrillation by 39% (odds ratio 0.61, 95% confidence interval 0.51 to 0.74; P < 0.001), but there was significant heterogeneity (P < 0.001) between the trials. In contrast, among 22 longer term and mostly larger trials of statin versus control (105,791 randomised patients, 2535 events), statin treatment was not associated with a significant reduction in atrial fibrillation (0.95, 0.88 to 1.03; P = 0.24) (P<0.001 for test of difference between the two sets of trials). Seven longer term trials of more intensive versus standard statin regimens (28,964 randomised patients and 1419 events) also showed no evidence of a reduction in the risk of atrial fibrillation (1.00, 0.90 to 1.12; P = 0.99). CONCLUSIONS: The suggested beneficial effect of statins on atrial fibrillation from published shorter term studies is not supported by a comprehensive review of published and unpublished evidence from larger scale trials.