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Severe Systemic Disease (severe + systemic_disease)
Selected AbstractsInduction of the vascular endothelial growth factor pathway in the brain of adults with fatal falciparum malaria is a non-specific response to severe diseaseHISTOPATHOLOGY, Issue 2 2010Isabelle M. Medana Medana I M, Day N P J, Roberts R, Sachanonta N, Turley H, Pongponratn E, Hien T T, White N J. & Turner G D H (2010) Histopathology,57, 282,294 Induction of the vascular endothelial growth factor pathway in the brain of adults with fatal falciparum malaria is a non-specific response to severe disease Aims:, Pathological or neuroprotective mechanisms in the brain in severe malaria may arise from microvascular obstruction with malaria-parasitized erythrocytes. This study aimed to investigate the role of hypoxia and induction of the vascular endothelial growth factor (VEGF) pathway in the neuropathophysiology of severe malaria. Methods and results:, Immunohistochemistry was performed on post mortem brain tissue sections from 20 cases of severe malaria and examined for the expression of transcriptional regulators of VEGF [hypoxia-inducible factor-1 alpha (HIF-1,), HIF-2,], DEC-1, VEGF, VEGF receptors 1 and 2, and the activated, phosphorylated VEGF receptor 2 (pKDR). HIFs showed limited protein expression and/or translocation to cell nuclei in severe malaria, but DEC-1, which is more stable and regulated by HIF-1,, was observed. There was heterogeneous expression of VEGF and its receptors in severe malaria and non-malarial disease controls. pKDR expression on vessels was greater in malaria cases than in controls but did not correlate with parasite sequestration. VEGF uptake by malaria parasites was observed. Conclusions:, VEGF and its receptor expression levels in severe malaria reflect a non-specific response to severe systemic disease. Potential manipulation of events at the vasculature by the parasite requires further investigation. [source] Iridovirus infections in finfish , critical review with emphasis on ranavirusesJOURNAL OF FISH DISEASES, Issue 2 2010R J Whittington Abstract Viruses in three genera of the family Iridoviridae (iridoviruses) affect finfish. Ranaviruses and megalocytiviruses are recently emerged pathogens. Both cause severe systemic disease, occur globally and affect a diversity of hosts. In contrast, lymphocystiviruses cause superficial lesions and rarely cause economic loss. The ranavirus epizootic haematopoietic necrosis virus (EHNV) from Australia was the first iridovirus to cause epizootic mortality in finfish. Like other ranaviruses, it lacks host specificity. A distinct but closely related virus, European catfish virus, occurs in finfish in Europe, while very similar ranaviruses occur in amphibians in Europe, Asia, Australia, North America and South America. These viruses can be distinguished from one another by conserved differences in the sequence of the major capsid protein gene, which informs policies of the World Organisation for Animal Health to minimize transboundary spread of these agents. However, limited epidemiological information and variations in disease expression create difficulties for design of sampling strategies for surveillance. There is still uncertainty surrounding the taxonomy of some putative ranaviruses such as Singapore grouper iridovirus and Santee-Cooper ranavirus, both of which cause serious disease in fish, and confusion continues with diseases caused by megalocytiviruses. In this review, aspects of the agents and diseases caused by ranaviruses are contrasted with those due to megalocytiviruses to promote accurate diagnosis and characterization of the agents responsible. Ranavirus epizootics in amphibians are also discussed because of possible links with finfish and common anthropogenic mechanisms of spread. The source of the global epizootic of disease caused by systemic iridoviruses in finfish and amphibians is uncertain, but three possibilities are discussed: trade in food fish, trade in ornamental fish, reptiles and amphibians and emergence from unknown reservoir hosts associated with environmental change. [source] Psoriasis: a possible risk factor for development of coronary artery calcificationBRITISH JOURNAL OF DERMATOLOGY, Issue 2 2007R.J. Ludwig Summary Background, Psoriasis is a chronic inflammatory skin disorder affecting about 2% of white-skinned individuals. Epidemiological data on the prevalence and degree of coronary artery calcification (CAC) as an indicator for cardiovascular diseases in patients with psoriasis are contradictory. Objectives, To study the prevalence and degree of CAC as an indicator for cardiovascular diseases in 32 patients with psoriasis matched for age, sex and risk factors to an equally sized control population. Methods, Noncontrast-enhanced 16-row spiral computed tomography was performed in patients and controls. Results, We found a significantly increased prevalence (59·4% vs. 28·1%, P = 0·015) and severity (CAC score according to Agatston 3·7 vs. 0·0, P = 0·019) of CAC in patients with psoriasis. Multiple linear regression calculations identified psoriasis as a likely independent risk factor for CAC. Conclusions, Our results point towards the potentially systemic nature of the inflammatory processes underlying the pathogenesis of psoriasis, which may therefore be considered a potentially severe systemic disease. [source] Langerhans cell histiocytosis in a premature baby presenting with skin-isolated disease: case report and literature reviewACTA PAEDIATRICA, Issue 12 2008Shraga Aviner Abstract Langerhans cell histiocytosis (LCH) in premature babies is extremely rare as is a vesicular skin rash, while gastrointestinal involvement is associated with a poor outcome. We report a case of LCH in a premature baby presented with isolated vesiculo-papulo-macular skin lesions and insidiously developed gastrointestinal symptoms, haematological and severe pulmonary involvement. We also reviewed a few cases of LCH in premature babies in the English language medical literature. LCH in preterm babies appears to be a severe systemic disease, usually lethal in-utero or post delivery. Conclusion: Careful observation should be applied to newborns with skin-only Langerhans cell histiocytosis in order to identify in time progression to potentially fatal systemic disease. [source] Congenital systemic Langerhans cell histiocytosis presenting as hydrops fetalisACTA PAEDIATRICA, Issue 12 2005Cheuk H Lee Abstract Congenital Langerhans cell histiocytosis (LCH) encompasses a wide spectrum of disease involvement and severity. Congenital "self-healing" cutaneous LCH represents one end of the spectrum, whereas the case we encountered represents the other extreme. A rare case of congenital LCH with severe multiorgan involvement presenting as hydrops fetalis is described in this report. Hydrops fetalis has not previously been associated with congenital LCH. The overall clinical features of this infant closely mimicked those of disseminated congenital infection, and he ran a fulminant and rapidly fatal course. Conclusion: A high index of suspicion is required to diagnose congenital LCH in the early neonatal period. Hydrops fetalis is an ominous sign and probably reflects severe systemic disease compromising the well-being of the fetus. [source] Testosterone Supplementation Therapy for Older Men: Potential Benefits and RisksJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 1 2003David A. Gruenewald MD Serum testosterone levels decline gradually and progressively with aging in men. Many manifestations associated with aging in men, including muscle atrophy and weakness, osteoporosis, reduced sexual functioning, and increased fat mass, are similar to changes associated with testosterone deficiency in young men. These similarities suggest that testosterone supplementation may prevent or reverse the effects of aging. A MEDLINE search was performed to identify studies of testosterone supplementation therapy in older men. A structured, qualitative review was performed of placebo-controlled trials that included men aged 60 and older and evaluated one or more physical, cognitive, affective, functional, or quality-of-life outcomes. Studies focusing on patients with severe systemic diseases and hormone deficiencies related to specific diseases were excluded. In healthy older men with low-normal to mildly decreased testosterone levels, testosterone supplementation increased lean body mass and decreased fat mass. Upper and lower body strength, functional performance, sexual functioning, and mood were improved or unchanged with testosterone replacement. Variable effects on cognitive function were reported, with improvements in some cognitive domains (e.g., spatial, working, and verbal memory). Testosterone supplementation improved exercise-induced coronary ischemia in men with coronary heart disease, whereas angina pectoris was improved or unchanged. In a few studies, men with low testosterone levels were more likely to experience improvements in lumbar bone mineral density, self-perceived functional status, libido, erectile function, and exercise-induced coronary ischemia with testosterone replacement than men with less marked testosterone deficiency. No major unfavorable effects on lipids were reported, but hematocrit and prostate specific antigen levels often increased. Based on these results, testosterone supplementation cannot be recommended at this time for older men with normal or low-normal testosterone levels and no clinical manifestations of hypogonadism. However, testosterone replacement may be warranted in older men with markedly decreased testosterone levels, regardless of symptoms, and in men with mildly decreased testosterone levels and symptoms or signs suggesting hypogonadism. The long-term safety and efficacy of testosterone supplementation remain uncertain. Establishment of evidence-based indications will depend on further demonstrations of favorable clinical outcomes and symptomatic, functional, and quality-of-life benefits in carefully performed, long-term, randomized, placebo-controlled clinical trials. J Am Geriatr Soc 51:101,115, 2003. [source] Dynamics of bacterial growth and distribution within the liver during Salmonella infectionCELLULAR MICROBIOLOGY, Issue 9 2003Mark Sheppard Summary Salmonella enterica causes severe systemic diseases in humans and animals and grows intracellularly within discrete tissue foci that become pathological lesions. Because of its lifestyle Salmonella is a superb model for studying the in vivo dynamics of bacterial distribution. Using multicolour fluorescence microscopy in the mouse typhoid model we have studied the interaction between different bacterial populations in the same host as well as the dynamic evolution of foci of infection in relation to bacterial growth and localization. We showed that the growth of Salmonella in the liver results in the spread of the microorganisms to new foci of infection rather than simply in the expansion of the initial ones. These foci were associated with independently segregating bacterial populations and with low numbers of bacteria in each infected phagocyte. Using fast-growing and slow-growing bacteria we also showed that the increase in the number of infected phagocytes parallels the net rate of bacterial growth of the microorganisms in the tissues These findings suggest a novel mechanism underlying growth of salmonellae in vivo with important consequences for understanding mechanisms of resistance and immunity. [source] | ||||||||||