Jaremo P.,The Vrinnevi Hospital |
Milovanovic M.,The Vrinnevi Hospital |
Buller C.,The Vrinnevi Hospital |
Nilsson S.,Linköping University |
Winblad B.,Karolinska Institutet
European Journal of Clinical Investigation | Year: 2013
Background: The current study investigates circulating eosinophils and neutrophils in Alzheimer's (AD) type dementia with respect to density (kg/L). The existence of β-amyloid plaques in the brain is a feature of AD. Sporadic scientific reports indicate that the disease affects circulating neutrophils. In contrast, numerous publications investigate inflammatory reactions in AD brains. Locally, the plaques evoke a substantial inflammatory response involving activated microglia and astrocytes. Methods: Subjects with probable AD (n = 39) were included and compared with elderly individuals (n = 22) lacking apparent memory problems. We sampled 10 mL venous blood in citrate. Granulocytes were separated according to density in linear Percoll™ gradients. Subsequently, the gradients were divided into density subfractions (n = 16). In every fraction, determination of eosinophil and neutrophil counts was carried out. Results: AD sufferers displayed less granulocytes in fractions nos. 13-15 containing light cells. For these fractions, the P-values proved to be (P < 0·001; not significant; P = 0·03) and (P = 0·01; P = 0·01; not significant), for eosinophils and neutrophils, respectively. Conclusions: The present work describes that less circulating light granulocytes are a feature of AD demented individuals. It is to hypothesize that it is a sign of impaired granulocyte turnover and cell damage. It is concluded that AD affects inflammatory cells in the periphery and that the behaviour of granulocytes in dementia is worthwhile further studies. © 2013 Stichting European Society for Clinical Investigation Journal Foundation.
PubMed | The Vrinnevi Hospital and Linköping University
Type: Journal Article | Journal: BMC family practice | Year: 2016
Chest pain assumed to be of non-coronary origin (NCCP) may be linked to enhanced mortality due to coronary heart disease (CHD). The aim of this study was to follow NCCP patients, as defined in primary care, with respect to mortality and long-term morbidity of CHD. We further examined if NCCP associates with risk factors for CHD.Patients consulting general practitioners (GPs) in 1998-2000 in three primary care centers in the southeast Sweden for chest pain regarded as NCCP were compared with controls matched for age, gender and residential area. Causes of death were gathered from registry data and death certificates. In 2005 a postal questionnaire was distributed to the survivors to collect demographic and clinical data. If participants had CHD diagnosed by a physician prior to inclusion they were excluded.Patients with NCCP (n=382) and population controls (n=746) did not differ with respect to mortality and incidence of CHD. The NCCP group reported more ongoing chest pain (OR 3.34 95% CI 2.41-4.62), they more often had elevated blood pressure (OR 1.86 95% CI 1.32-2.60), consumed more -blockers (p<0.001), aspirin (p=0.013), thiazides (p=0.004) and long-acting nitrates (p=0.002). They further had more remedies for acid-related disorders (p=0.014) and obstructive pulmonary disease (p<0.001).The study suggests that individuals with chest pain judged by GPs to be NCCP do not develop CHD more frequently than population controls. It is evident that NCCP often lasts for many years and that the condition associates with hypertension.
Jaremo P.,The Vrinnevi Hospital |
Eriksson-Franzen M.,The Vrinnevi Hospital |
Milovanovic M.,The Vrinnevi Hospital
Journal of Translational Medicine | Year: 2015
Objective: Platelets may well be significant in the pathogenesis of cerebral infarction. Platelets vary substantially according to gender. The scope of our current work is to establish if female and male stroke sufferers differ regarding platelet reactivity. Patients and methods: 73 Consecutive individuals stricken by acute ischemic cerebral infarction (31 females, 42 males) participated. All stroke subtypes were included. Platelet counts was determined electronically. Platelet reactivity i.e. the presence of surface-bound fibrinogen following provocation was analyzed with a flow cytometer. ADP (1.7 μmol/L) and a thrombin receptor agonist (TRAP-6) (57 μmol/L) were the agonists used. Results: Female stroke sufferers had higher platelet counts (p = 0.013) but their platelets were less reactive. The p values were (p = 0.038) and (p = 0.016) for ADP and TRAP-6, respectively. Conclusion: The current study demonstrates that women suffering acute cerebral infarction have less reactive platelets. It is concluded that gender affects platelets. Our study indicates that it may be beneficial to individualize platelet inhibition of stroke sufferers according to gender. © 2015 Järemo et al.
PubMed | The Vrinnevi Hospital
Type: | Journal: Journal of translational medicine | Year: 2015
Platelets may well be significant in the pathogenesis of cerebral infarction. Platelets vary substantially according to gender. The scope of our current work is to establish if female and male stroke sufferers differ regarding platelet reactivity.73 Consecutive individuals stricken by acute ischemic cerebral infarction (31 females, 42 males) participated. All stroke subtypes were included. Platelet counts was determined electronically. Platelet reactivity i.e. the presence of surface-bound fibrinogen following provocation was analyzed with a flow cytometer. ADP (1.7 mol/L) and a thrombin receptor agonist (TRAP-6) (57 mol/L) were the agonists used.Female stroke sufferers had higher platelet counts (p = 0.013) but their platelets were less reactive. The p values were (p = 0.038) and (p = 0.016) for ADP and TRAP-6, respectively.The current study demonstrates that women suffering acute cerebral infarction have less reactive platelets. It is concluded that gender affects platelets. Our study indicates that it may be beneficial to individualize platelet inhibition of stroke sufferers according to gender.
PubMed | The Vrinnevi Hospital
Type: Journal Article | Journal: Platelets | Year: 2013
Stroke is worldwide a leading cause of death and disability. Its etiology is regarded as heterogeneous. Platelets are implicated in its pathophysiology, but our understanding of their specific role is incomplete. Only sparse and conflicting information exists about platelet reactivity and activity in acute stroke. Some scientists take the view that platelets activate in conjunction with acute cerebral infarctions. Others put forward evidence corroborating the contrary notion. Increased soluble P-selectin as a sign of platelet and/or endothelial activity seems to be a feature of the disease. The latter point of view is opposed by other researchers. Due to these conflicting opinions, this study is devoted to platelet characteristics in acute cerebral infarctions. We studied subjects (n=72; age 7410(SD) years; 31 females) having acute stroke. As controls served atrial fibrillation (AF) patients (n=58; age 697(SD) years; 12 females) subject to electrical cardioversion, a flow cytometer was put to use for measuring platelet reactivity and activity. After agonist provocation, both platelet bound P-selectin and fibrinogen were employed as estimates of platelet reactivity. Dilutions of a thrombin-receptor-activating peptide (TRAP-6) (74 and 57mol/l) (P-selectin and fibrinogen) and ADP (8.5 and 1.7mol/l) (fibrinogen only) were put to use as platelet agonists. Membrane-bound P-selectin without agonist stimulation served as a measure of invivo platelet activation. Soluble P-selectin, as determined from a commercial ELISA, was used to assess platelet and/or endothelial activity. In acute stroke neither platelet-bound P-selectin nor fibrinogen after stimulation, i.e. reactivity, differed from AF controls. In contrast, lower platelet activity as judged from surface attached and circulating P-selectin without agonist stimulation proved to be a feature of cerebral infarctions. The p-values were p<0.001 and p<0.01, respectively. It is concluded that acute stroke is not associated with platelet reactivity platelets circulate less activated during the disease. It is evident that the mechanisms reflecting platelet reactivity and activity being investigated in this study play minor roles in stroke pathophysiology. New powerful platelet inhibitory drugs are currently introduced. To avoid major bleeding studies on platelet, behavior in acute stroke are necessary before including these medications in stroke treatment protocols.