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Secondary Complications (secondary + complications)
Selected AbstractsSubacute sclerosing panencephalitis: an updateDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 10 2010JOSE GUTIERREZ Subacute sclerosing panencephalitis (SSPE) is a chronic encephalitis occurring after infection with measles virus. The prevalence of the disease varies depending on uptake of measles vaccination, with the virus disproportionally affecting regions with low vaccination rates. The physiopathology of the disease is not fully understood; however, there is evidence that it involves factors that favour humoral over cellular immune response against the virus. As a result, the virus is able to infect the neurons and to survive in a latent form for years. The clinical manifestations occur, on average, 6 years after measles virus infection. The onset of SSPE is insidious, and psychiatric manifestations are prominent. Subsequently, myoclonic seizures usually lead to a final stage of akinetic mutism. The diagnosis is clinical, supported by periodic complexes on electroencephalography, brain imaging suggestive of demyelination, and immunological evidence of measles infection. Management of the disease includes seizure control and avoidance of secondary complications associated with the progressive disability. Trials of treatment with interferon, ribavirin, and isoprinosine using different methodologies have reported beneficial results. However, the disease shows relentless progression; only 5% of individuals with SSPE undergo spontaneous remission, with the remaining 95% dying within 5 years of diagnosis. [source] The mode of action of thiazolidinediones,DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue S2 2002Hans Hauner Abstract The thiazolidinediones (TZDs) or ,glitazones' are a new class of oral antidiabetic drugs that improve metabolic control in patients with type 2 diabetes through the improvement of insulin sensitivity. TZDs exert their antidiabetic effects through a mechanism that involves activation of the gamma isoform of the peroxisome proliferator-activated receptor (PPAR,), a nuclear receptor. TZD-induced activation of PPAR, alters the transcription of several genes involved in glucose and lipid metabolism and energy balance, including those that code for lipoprotein lipase, fatty acid transporter protein, adipocyte fatty acid binding protein, fatty acyl-CoA synthase, malic enzyme, glucokinase and the GLUT4 glucose transporter. TZDs reduce insulin resistance in adipose tissue, muscle and the liver. However, PPAR, is predominantly expressed in adipose tissue. It is possible that the effect of TZDs on insulin resistance in muscle and liver is promoted via endocrine signalling from adipocytes. Potential signalling factors include free fatty acids (FFA) (well-known mediators of insulin resistance linked to obesity) or adipocyte-derived tumour necrosis factor-, (TNF-,), which is overexpressed in obesity and insulin resistance. Although there are still many unknowns about the mechanism of action of TZDs in type 2 diabetes, it is clear that these agents have the potential to benefit the full ,insulin resistance syndrome' associated with the disease. Therefore, TZDs may also have potential benefits on the secondary complications of type 2 diabetes, such as cardiovascular disease. Copyright © 2002 John Wiley & Sons, Ltd. [source] European comparison of costs and quality in the prevention of secondary complications in Type 2 diabetes mellitus (2000,2001)DIABETIC MEDICINE, Issue 7 2002A. Gandjour Abstract Aims To compare the out-patient costs and process quality of preventing secondary complications in patients with Type 2 diabetes mellitus in France, Germany, Italy, The Netherlands, Sweden, Switzerland, and the UK. Methods A total of 188 European physician practices assessed annual services for one hypothetical average patient (cost evaluation) and 178 practices reported retrospective data on one or two real patients (quality evaluation) in 2000/2001. In countries with a detailed fee-for-service schedule (Germany, Italy, and Switzerland) reimbursement fees were used to approximate costs. These fee-for-service schedules were also used to develop index (average) fees for all countries, in order to measure resource utilization. The following process quality indicators were evaluated: control of HbA1c; control of lipids; urine test for (micro)albuminuria; control of blood pressure; foot examination; neurological examination; eye examination; and patient education. For each country an average quality rating was calculated by weighting the response to each quality indicator with the level of scientific evidence. Results Average quality ratings ranged from 0.40 in The Netherlands to 0.62 in the UK (0 = lowest rating; 1 = highest rating). Total annual costs for secondary prevention were higher in Switzerland than in Germany and Italy (EUR475, EUR381, and EUR283, respectively). Resource utilization was highest in Germany and lowest in the UK. Conclusions The overall quality of preventive services documented was found to be poor in the seven European countries studied. The UK rated as both the most effective and the most efficient country in providing secondary prevention in Type 2 diabetes. [source] Dysautonomia after severe traumatic brain injuryEUROPEAN JOURNAL OF NEUROLOGY, Issue 9 2010H. T. Hendricks Background:, Dysautonomia after traumatic brain injury (TBI) is characterized by episodes of increased heart rate, respiratory rate, temperature, blood pressure, muscle tone, decorticate or decerebrate posturing, and profuse sweating. This study addresses the incidence of dysautonomia after severe TBI, the clinical variables that are associated with dysautonomia, and the functional outcome of patients with dysautonomia. Methods:, A historic cohort study in patients with severe TBI [Glasgow Coma Scale (GCS) , 8 on admission]. Results:, Seventy-six of 119 patients survived and were eligible for follow-up. The incidence of dysautonomia was 11.8%. Episodes of dysautonomia were prevalent during a mean period of 20.1 days (range 3,68) and were often initiated by discomfort. Patients with dysautonomia showed significant longer periods of coma (24.78 vs. 7.99 days) and mechanical ventilation (22.67 vs. 7.21 days). Dysautonomia was associated with diffuse axonal injury (DAI) [relative risk (RR) 20.83, CI 4.92,83.33] and the development of spasticity (RR 16.94, CI 3.96,71.42). Patients with dysautonomia experienced more secondary complications. They tended to have poorer outcome. Conclusions:, Dysautonomia occurs in approximately 10% of patients surviving severe TBI and is associated with DAI and the development of spasticity at follow-up. The initiation of dysautonomia by discomfort supports the Excitatory: Inhibitory Ratio model as pathophysiological mechanism. [source] Serum N -acetyl-,- D -glucosaminidase profiles in type 1 diabetes secondary complications: causes of changes and significance of determination,JOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 4 2008V.B. Jovanovi Abstract The connection between changes in the activity of serum N -acetyl-,- D -glucosaminidase (NAG, E.C.3.2.1.30) and iso-enzymes and degree of secondary complications was analyzed in four groups of type 1 diabetic patients (n=69): without complications (n=22); with retinopathy (n=16); with retinopathy and polyneuropathy (n=13), and with retinopathy, neuropathy, and nephropathy (n=18). In all groups statistically significant higher (P<0.001) percent fraction of A form (83.84±6.09, 84.37±5.74, 81.76±6.02, 76.37±7.38%, resp.) and lower (P<0.001, P<0.01) fraction of B form (15.87±5.65, 15.66±5.74, 18.33±5.98, 23.63±7.38, resp.) in total NAG compared with the control (A=69.38±4.79%, B=30.61±4.78%) were found. The differences in A as well as B forms between diabetic groups were not statistically significant. Significant strong positive correlations between total NAG and glycemia (0.494,0.623), total NAG and A form (0.934,0.966), and A form and glycemia (0.512,0.638) were found in all groups. No correlation was found between the fractions of B and A forms, except in the fourth group. The A form of diabetic patients in the fourth group was more acidic compared with the control and other diabetic groups. It was concluded that the changes in serum NAG and iso-enzymic profiles in diabetes are the consequence of its increased exocytose, especially of the A form, in hyperglycemia and posttranslational modifications of iso-enzymes. The total activity of serum NAG and iso-enzymic profiles cannot be used for monitoring the development and distinction of type 1 diabetes secondary complications. J. Clin. Lab. Anal. 22:307,313, 2008. © 2008 Wiley-Liss, Inc. [source] Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 79JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2003U Del Carro Peripheral neuropathy is one of the most common secondary complications of diabetes mellitus, causing severe and prolonged morbidity. However, clinical and experimental studies have reported that careful glucose control may prevent, stabilize, and/or reverse neuropathy and other chronic diabetic complications. Unfortunately, insulin therapy does not prevent the development or progression of chronic lesions in the vessels, kidneys, eyes, or nerves of the diabetic patient. There is great interest in investigating other forms of endocrine replacement therapy, such as transplantation of the pancreas or of the islets of Langerhans (IT). Diabetic polyneuropathy (DP) evolution is characterized by progressive demyelination and axonal loss and is manifested by signs and symptoms on physical examination and abnormalities in nerve conduction studies (NCS). NCS provide reliable, noninvasive, objective measures of peripheral nerve function and constitute the most important technique for the evaluation of the severity of DP in clinical trials. Several research groups have demonstrated that skin biopsy with measurement of intraepidermal nerve fiber density is another method minimally invasive and repeatable that provides direct pathologic evidence of axonal damage in diabetic neuropathy. Fifty-one consecutive IDDM patients with or without end stage renal disease were enrolled at the moment of islet (Is), kidney (KD), kidney-pancreas (KP) or kidney-islet (KI) transplantation. Patients underwent skin biopsy punch, neurologic examination and neurophysiological investigation. Particularly, 20 pts underwent KP tx, 16 KD tx, 10 islet tx and 5 KI. The patients were comparable for duration of diabetes, dialysis (when present), age, lipid profile. In half of the patients a follow-up of 2 years has been reached. After KP tx, and partially with KI, a complete normalization of glycometabolic control has been achieved, with statistically lower HbA1c in comparison with KD group (KP = 6.2; 0.1% vs. KD = 8.4; 0.5%; p < 0.01). In the KI/Is group, a long-term restoration of islet endocrine function has been achieved, with insulin independence. When this has been lost, a persistent secretion of C-peptide was shown for a long period of time. This was correlated with a global improvement quality of life and vascular structure. Preliminary results will be presented. [source] Molecular Modeling Of The Aldose Reductase-Inhibitor Complex Based On The X-Ray Crystal Structure And Studies With Single-Site- Directed MutantsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2000S.B. Singh Aldose reductase (AR) has been implicated in the etiology of the secondary complications of diabetes. This enzyme catalyzes the reduction of glucose to sorbitol using nicotinamide adenine dinucleotide phosphate as an essential cofactor. AR has been localized at the sites of tissue damage, and inhibitors of this enzyme prevent the development of neuropathy, nephropathy, retinopathy, and cataract formation in animal models of diabetes. The crystal structure of AR complexed with zopolrestat, a potent inhibitor of AR, has been described. (1) We have generated a model of the AR-inhibitor complex based on the reported C alpha coordinates of the protein and results of a structure-activity relationship study using four structurally distinct classes of inhibitors, recombinant human AR, and four single-site-directed mutants of this enzyme. The effects of the site-directed mutations on residues within the active site of the enzyme were evaluated by average interaction energy calculations and by calculations of carbon atom surface area changes. These values correlated well with the IC50 values for zopolrestat with the wildtype and mutant enzymes, validating the model. On the basis of the zopolrestat-binding model, we have proposed binding models for 10 other AR inhibitors. Our models have enabled us to gain a qualitative understanding of the binding domains of the enzyme and how different inhibitors impact the size and shape of the binding site. [source] Progenitor cell trafficking in the vascular wallJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 2009M. HRISTOV Summary., Adult endothelial as well as smooth muscle progenitor cells are engaged in the complex pathophysiology of atherosclerosis including primary remodeling with development and progression of atherosclerotic plaques as well as secondary complications associated with ischemia, endothelial damage, neointimal growth and transplant arteriosclerosis. These adult vascular precursor cells correspond to similar embryonic stem cell-derived progeny and are primarily located in bone marrow and peripheral blood. Recently, specific investigation on their recruitment emerged as a novel fundamental in the pathogenesis of arterial remodeling, plaque stability and angiogenesis. This multifaceted process of mobilization and homing is regulated by numerous chemokines, adhesion molecules and growth factors that guide and control the trafficking of vascular progenitor cells to the arterial wall after injury or during ischemia. [source] Lower limb replantations: Indications and a new scoring systemMICROSURGERY, Issue 5 2002Bruno Battiston M.D. The need for reconstruction of lower limb amputations is increasing, due to high-energy trauma in road accidents and work-related injuries. The indication for lower limb replantation is still controversial. Compared with upper limb replantations, indications are more select due to the frequent complications in lower limb salvage procedures, such as severe general complications or local complications such as necrosis, infections, nonunions, the need for secondary lengthening, or other reconstructive procedures. The satisfactory results given by artificial prosthesis, such as quicker recovery time and fewer secondary procedures, also contribute to the higher degree of selection for lower limb replantation candidates. Since 1993, we have replanted 14 amputations of the lower limb in 12 patients, including 2 bilateral cases. Although survival of the replanted segment was obtained in all patients, 5 cases were subsequently amputated for severe secondary complications. Of the remaining 9 cases, evaluated by means of Chen criteria, 7 had good results (3 Chen I and 4 Chen II), 1 sufficient (Chen III), and 1 poor (Chen IV). The best results were obtained in young patients. Our experience led us to examine the necessity for careful, objective patient selection. We developed a score evaluation system by modifying the international classifying method for severe limb traumas (mangled extremity severity score, or MESS system). This relatively simple system, based on the retrospective study of our cases, considers several parameters (patient's age, general conditions, level and type of lesion, time of injury, and associated lesions), giving each one a score. The total score gives the indication for replantation, predicts the functional outcome, and facilitates decision-making. © 2002 Wiley Liss, Inc. MICROSURGERY 22:187,192 2002 [source] IL-10 and the resolution of infections,THE JOURNAL OF PATHOLOGY, Issue 2 2008CM Filippi Abstract Chronic viral infections pose serious health concerns, as secondary complications such as immunodeficiencies and cancers are common. Treating such infections with conventional vaccine approaches has proved to be difficult. Studies in animals and humans suggest that vaccine failure is probably due to exhaustion of antiviral T cell responses, which occurs in a number of chronic infections. Attempts to elucidate the causes of impairment of antiviral immunity have pointed to a role for the immunomodulatory cytokine IL-10 in the ability of viruses to establish persistence. Induction of IL-10 production by the host during chronic infection appears to be one of the viral means to alter the class of the antiviral immune response and induce generalized immune suppression. Recent work by us and others suggests that it is possible to resuscitate antiviral immunity by interfering with the IL-10 signalling pathway. Targeting IL-10 thus constitutes a promising alternative to conventional vaccine strategies which have not proved to be successful in treating chronic infections. In addition, sterile cure may be achieved with minimal side-effects by combining agents that alter the IL-10 signalling pathway with other compounds, such as antiviral drugs or interferon, but also agents neutralizing other crucial elements of T cell exhaustion, such as PD-1. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] Dysregulation of the Cytokine Network in the Uterus of the Diabetic RatAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 6 2001SERGE PAMPFER Insulin-dependent (type 1) diabetes is an auto-immune disorder that produces secondary complications in numerous non-immunological systems. Changes in the synthesis and action pattern of several cytokines have been associated with the development of these alterations. Based on the clinical facts that the pregnant and non-pregnant functions of the reproductive system are also disrupted by diabetes, our laboratory has decided to concentrate its research activities on the hypothesis that cytokines may be implicated in the uteropathy and embryopathy associated with the metabolic disorder. This review article summarizes our major findings concerning the synthesis of TNF-, and IL-1, in the uterus of diabetic rats, and in cultures of rodent uterine cells upon their exposure to high concentrations of glucose. The paper also reviews evidence that both the peri-implanting embryo and the epithelial cell layer lining the uterine lumen are targets for the deleterious influence of excess TNF-,. If confirmed in the uterus of diabetic patients, these observations may explain how cytokines contribute to the dysregulation of crucial reproductive events like menstruation and embryo implantation in humans. [source] Has Time Come for New Goals in Human Islet Transplantation?AMERICAN JOURNAL OF TRANSPLANTATION, Issue 6 2008R. Lehmann The enthusiasm regarding clinical islet transplantation has been dampened by the long-term results. Concerns about the associated risks of life-long immunosuppression and the striking imbalance between potential recipients and available donor pancreata warrant changes in some of the current goals. Islet transplantation will never be a cure of type 1 diabetes in the majority of patients with no secondary complications, but is a valid option for a limited number of patients with brittle diabetes waiting for an organ or after organ transplantation. Furthermore, insulin independence should not be the main goal of islet transplantation, but avoidance of severe hypoglycemia and good glycemic control, which can be achieved with a relatively small functional beta-cell mass. Therefore, initially one islet infusion is sufficient. Retransplantation at a later time point remains an option, if glucose control deteriorates. Efforts to improve islet transplantation should no longer focus on islet isolation and immunosuppression, but rather on the low posttransplant survival rate of islets caused by activation of the coagulation pathway and the limited oxygen delivery to the islets. Transplantation of smaller islets be it naturally small or size tailored reaggregated islets has the potential to facilitate these processes. [source] Extensive venous/lymphatic malformations causing life-threatening haematological complicationsBRITISH JOURNAL OF DERMATOLOGY, Issue 3 2007J. Mazereeuw-Hautier Summary Background, Large venous/lymphatic slow-flow malformations (SFM) can be associated with a coagulopathy resulting in thrombosis and haemorrhage. Such potentially life-threatening complications of SFM have been reported only rarely. Objectives, To better define the clinical characteristics of haematological complications associated with SFM, to highlight the importance of recognition and to discuss the management of these difficult-to-treat patients. Patients and methods, A cohort of six children who presented with massive SFM associated with serious haematological complications was seen between January 1980 and June 2005 in the Department of Paediatric Dermatology, Great Ormond Street Hospital for Children, London, U.K. (tertiary referral centre for vascular anomalies). Clinical and haematological characteristics were recorded. Results, Patients were aged 1,20 years. All suffered with recurrent episodes of pain, localized skin necrosis and bleeding. All had intravascular coagulopathy and life-threatening complications. These included brain haemorrhage, massive bleeding from the uterus and colon, large and extensive thromboses of the deep vessels in the abdomen and pelvis and severe haemoptysis. One patient died suddenly at the age of 20 years from pulmonary thromboembolism and thrombosis within the deep vessels of the vascular malformation. The youngest patient underwent a leg amputation to remove the huge vascular malformation due to the major risk of complications and lack of limb function. Three of the patients underwent anticoagulation treatment and showed improvement in their coagulopathy. Conclusions, It is essential that patients with extensive SFM have their coagulation screened regularly to detect intravascular coagulopathy. This may progress to disseminated vascular coagulopathy and a serious risk of thrombosis and haemorrhage. Such patients require early anticoagulation in an attempt to prevent these secondary complications. [source] A prospective cohort study determining the prevalence of thrombotic events in children with acute lymphoblastic leukemia and a central venous line who are treated with L-asparaginase,CANCER, Issue 2 2003Results of the Prophylactic Antithrombin Replacement in Kids with Acute Lymphoblastic Leukemia Treated with Asparaginase (PARKAA) Study Abstract BACKGROUND Thrombotic events (TEs) are serious secondary complications in children with acute lymphoblastic leukemia (ALL) who receive L-asparaginase (ASP) therapy; however, the prevalence of TEs has not been established. The primary objective of the Prophylactic Antithrombin Replacement in Kids with Acute Lymphoblastic Leukemia Treated with Asparaginase (PARKAA) Study was to determine the prevalence of TEs. The secondary objective was to detect any association of TEs with the presence of congenital or acquired prothrombotic disorders. METHODS Children with ALL were screened for TEs at the end of ASP treatment using bilateral venograms, ultrasound, magnetic resonance imaging, and echocardiography. Symptomatic TEs were confirmed by appropriate radiographic tests. All tests were read by a blinded central adjudication committee. RESULTS Twenty-two of 60 children had TEs, a prevalence of 36.7% (95% confidence interval, 24.4,48.8%). TEs were located in the sinovenous system of the brain in 1 patient, the right atrium in 3 patients, and the upper central venous system in 19 patients. TEs detected by venography resulted in 1) 25,100% occlusion, with 1 in 3 patients showing occlusion of > 75% of the greatest vessel dimension, and 2) the presence of collaterals in 60% of patients, with 40% categorized as major. No children with TEs were positive for factor V Leiden or prothrombin gene 20201A, and four of eight children with antiphospholipid antibodies had a TE. CONCLUSIONS The prevalence of TEs is exceedingly high in this population, and it is likely that the extent of occlusion is likely clinically significant. No trend was seen toward an association between TEs and the presence of congenital prothrombotic disorders. A trend was seen toward an association between TEs and antiphospholipid antibodies. Carefully designed clinical trials of primary prophylaxis for the prevention of TEs are required in this patient population. Cancer 2003;97:508,16. © 2003 American Cancer Society. DOI 10.1002/cncr.11042 [source] | ||||||||||||||||||||||