Short-Duration Prednisolone in Children with Nephrotic Syndrome Relapse: A Noninferiority Randomized Controlled Trial

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Coronary Artery Disease Manifestations in HIV: What,How, and Why

Understanding why persons with human immunodeficiency virus (HIV) have accelerated atherosclerosis and its sequelae, including coronary artery disease (CAD) and myocardial infarction, is necessary to provide appropriate care to a large and aging population with HIV. In this review, we delineate the diverse pathophysiologies underlying HIV-associated CAD and discuss how these are implicated in the clinical manifestations of CAD among persons with HIV. Several factors contribute to HIV-associated CAD, with chronic inflammation and immune activation likely representing the primary drivers. Increased monocyte activation, inflammation, and hyperlipidemia present in chronic HIV infection also mirror the pathophysiology of plaque rupture. Furthermore, mechanisms central to plaque erosion, such as activation of toll-like receptor 2 and formation of neutrophil extracellular traps, are also abundant in HIV. In addition to inflammation and immune activation in general, persons with HIV have a higher prevalence than uninfected persons of traditional cardiovascular risk factors, including dyslipidemia, hypertension, insulin resistance, and tobacco use. Antiretroviral therapies, although clearly necessary for HIV treatment and survival, have had varied effects on CAD, but newer generation regimens have reduced cardiovascular toxicities. From a clinical standpoint, this mix of risk factors is implicated in earlier CAD among persons with HIV than uninfected persons; whether the distribution and underlying plaque content of CAD for persons with HIV differs considerably from uninfected persons has not been definitively studied. Furthermore, the role of cardiovascular risk estimators in HIV remains unclear, as does the role of traditional and emerging therapies; no trials of CAD therapies powered to detect clinical events have been completed among persons with HIV.     

Electroencephalographic and imaging profile in a subacute sclerosing panencephalitis (SSPE) cohort: a correlative study.

OBJECTIVE: There are only a few studies correlating diverse radiological and EEG features of subacute sclerosing panencephalitis (SSPE). The objective of the study was to (a) describe EEG profile and (b) correlate it with the clinical and imaging data of patients with confirmed SSPE. METHODS: This study was conducted at a University teaching hospital in south India and involved 58 patients (M:F=37:21, age: 12.3, SD 4.8 years) of SSPE. Diagnosis of SSPE was based on the characteristic clinical manifestations, and raised IgG (1:625) anti-measles antibody in cerebrospinal fluid (CSF) by ELISA in all the patients. Scalp EEGs were recorded on 16 channel machines using standard parameters and procedures. The EEG, clinical and imaging data were reviewed. RESULTS: EEGs were frequently abnormal: typical (37) and atypical (21). Diffuse slowing of background activity (BGA) was noted in 46 records being asymmetrical in six. Periodic complexes were periodic (32), quasi-periodic (21) or a-periodic (4). Periodic complexes (PC) (amplitude: 370.7, SD 171.2 microV; duration - 1.7, SD 2.0 s; inter-complex interval: 8.4, SD 9.2s) were symmetrical in 39 and asymmetrical in 19. CT (32) and MRI (23) scans were normal in 16 patients while others had white matter (15), cerebral edema (8), cerebral atrophy (8), basal ganglia (2), and thalamic (2) changes. There was an independent association of frontally dominant slowing of BGA (p=0.04) and typical PCs (p=0.03) with the diffuse cerebral edema on imaging. White matter changes correlated with slowing of BGA (p=0.04), but not with typical PC (p=0.16). CONCLUSIONS: This study provides valuable insight into the structural and clinical correlates of EEG changes in SSPE. SIGNIFICANCE: Irrespective of the incidence of occurrence of SSPE in a community, a clinician should be aware of the wide spectra of EEG findings. This study also discusses the possible underlying structural and clinical correlates.     

Left ventricular mass regression following aortic valve replacement with mechanical valves

Objective The degree of Left Ventricular Mass Index (LVMI) regression following aortic valve replacement correlates with long-term survival. This study aims to assess the extent of LVMI regression at 3 months following aortic valve replacement (AVR) with different types and sizes of mechanical valves in rheumatic aortic valve disease. Methods The LVMI regression was studied in 34 consecutive patients, undergoing elective AVR for rheumatic aortic stenosis and/or regurgitation. They were grouped in A and B, matched in age, body surface area and pre-operative LVMI, receiving respectively a tilting disc and a bileaflet mechanical valve. The LVMI was calculated by M-mode echocardiography using the Devereux' formula pre-operatively and three months post-operatively. The trend of LVMI reduction was compared between the two groups and amongst the patients with stenotic, regurgitant and mixed aortic valve, pathologies; and receiving different sizes of valves. Results The mean preoperative LVMI was 199g±79.5 g/m². At three months post aortic valve replacement, the mean LVMI was 130g±49.0 g/m². There was a significant reduction of LVMI post-operatively (p=0.001) at three months follow-up. The extent of LVMI regression following surgery amongst the groups A and B did not vary significantly (p=0.92). The extent of LVMI regression did not vary significantly in patients with different aortic valve pathology nor with different sizes of the valves implanted. Conclusions There is a significant early LVMI regression following aortic valve replacement in rheumatic aortic valve disease. The type and the size of the mechanical prosthesis or the rheumatic pathology do not appear to influence this regression.     

Psoriasis in childhood and adolescence: evaluation of demographic and clinical features

BACKGROUND: The present study was aimed to define the gender ratio, familial occurrence, age of onset, precipitating factors, clinical types, nail and joint involvement of psoriasis in childhood and adolescence in Turkey. METHODS: A total of 61 children with psoriasis under 18 years old were evaluated retrospectively, for age, gender, age of disease onset, family history, concomitant disease, the clinical type of psoriasis, clinical localization, nail and joint involvement and treatment modalities. RESULTS: Of the patients, 23 (37.70%) were boys and 38 (62.30%) were girls. Mean age was 9.28 +/- 4.02 years in girls and 11.18 +/- 3.85 years in boys (9.96 +/- 4.03 years in all children). Mean age at the onset of the disease was 6.81 +/- 4.11 years in girls and 7.03 +/- 4.28 years in boys (6.89 +/- 4.14 years in all patients). In 14 (23%) cases, a positive family history was detected. The most frequent probable triggering factors were upper respiratory tract infections (14.8%) and positive throat culture for A group ss-hemolytic streptococcus (21.3%). Frequency of emotional stress and psychiatric morbidity were 54% and 9.8%, respectively. The most frequent localizations at onset were trunk (44.3%), extremities (54.0%), and scalp (36.0%). Three children (4.9%) had a history of dissemination from psoriatic diaper rash. In total, 51 (83.6%) patients presented with psoriasis vulgaris, eight (13.1%) with generalized pustular psoriasis, and the remaining two (3.3%) with erythrodermic psoriasis. CONCLUSION: The incidence of psoriasis among dermatological patients in childhood and adolescence was 3.8%. The disease tends to appear earlier in girls than boys. The authors suggested that stress and upper respiratory infections are the most important triggering factors in childhood and adolescence psoriasis.     

Does prophylactic sotalol and magnesium decrease the incidence of atrial fibrillation following coronary artery bypass surgery: a propensity-matched analysis

Background  

Atrial fibrillation can occur in up to 40% of patients undergoing coronary surgery.     

Enteritis necroticans in Port Moresby--report of three cases

Three cases of enteritis necroticans seen at Port Moresby General Hospital are described. All three cases proved diagnostic problems and in all three the diagnosis was made only at laparotomy. While the condition is uncommon in Port Moresby, these cases indicate that it must now be considered earlier rather than later.