aChE and BuChE inhibition by rivastigmin have no effect on peripheral insulin resistance in elderly patients with Alzheimer disease.

BACKGROUND: Insulin resistance (IR) may play a role in most pathogenic processes that promote the development of Late Onset Alzheimer Disease (LOAD). This study was designed to determine the interaction between inhibition of both butyrylcholinesterase (BuChE) and acetylcholinesterase (AChE) with rivastigmine and peripheral insulin resistance (IR) in LOAD. METHODS: Seventy-Nine consecutive elderly patients, 31 late onset AD and 48 non-demented patients were evaluated. IR was calculated with HOMA. All of the patients were evaluated through comprehensive geriatric assessments at baseline and in the 6th and 12th months. RESULTS: End of the study, compared to the baseline values, there was a significant increase in the 6th month in both MMSE and IADL scores (t =2.200, p = 0.036 for MMSE and t =2.724, p= 0.011 for IADL, respectively). Rivastigmine was improved both the scores of MMSE and IADL in elderly patients with LOAD, but there was no significance or correlation between HOMA scores and cognitive status. CONCLUSION: In conclusion, inhibition of both BuChE and AChE with rivastigmine was improved the cognition without affecting on the peripheral IR in the elderly patients with LOAD by HOMA. Due to the complexity of disease pathogenesis, it is too early to make general comments, and further longitudinal and long-term studies on this issue are needed.

The relationship between body mass index and incidental mild cognitive impairment, Alzheimer's disease and vascular dementia in elderly.

OBJECTIVE: To examine the association between body mass index (BMI) and cognitive decline (CD) due to Mild Cognitive Impairment (MCI), Alzheimer's Disease (AD), and Vascular Dementia (VaD). DESIGN AND SETTING: The subjects aged ≥ 65 years were recruited prospectively from the Geriatrics Clinic of Gulhane Medical School, between 2004 and 2008 years. PARTICIPANTS: 1302 patients were included in the study. MEASUREMENTS: Cognitive status, clinical diagnosis of CD (MCI, AD, and VaD) and clinical and environmental risk factors were evaluated by comprehensive geriatric assesment. Finally, the subjects were categorized into two groups according to having CD or not. RESULTS: 905 (69.5%) subjects were not having CD whereas 397 (30.5%) patients with CD. Of the patients with CD, 140 (10.4%) had MCI, 227 (16.9%) AD, and 30 (2.2%) VaD. After adjustment for confounding with a model for multiple regression analysis, age (OR=1.054; CI:1.027-1.083; p < 0.001) and family history of dementia (OR=1.662; CI:1.038-2.660; p=0.034) were found to be independent risk factors for CD. Also, overweight (OR=0.594; CI:0.370-0.952; p=0.03) and obese (OR=0.396; CI:0.242-0.649; p < 0.001), and high education level (OR=0.640; CI:0.451-0.908; p=0.012) were found to be independent protective factors for CD. CONCLUSIONS: We found the risk of CD decreases in overweight and obese elderly. The results indicate that the primary prevention should not only consider risk factors, but must also take anthropometric data into consideration in order to identify persons at high risk for CD.

Trospium and cognition in patients with late onset Alzheimer disease.

OBJECTIVES: Cholinesterase inhibitors for the treatment of Alzheimer's Disease (AD) and antimuscarinic agents for the treatment of urge urinary incontinence (UUI) may reduce the potential effect of each other in the patients with both diseases. Trospium has a relatively low lipophilicity and low CNS penetration, and galantamine, a cholinesterase inhibitors, has also allosterically modulates nicotinic cholinergic receptors. This study was designed to evaluate the effects of dual use of trospium and galantamine for 6 months in the elderly patients with AD and UUI. SETTING/PARTICIPANTS: One hundred and seventy eight elderly patients: 99 UUI patients (Group I, treated with trospium), 43 AD patients (Group II, treated with galantamine) and 36 AD and UUI patients (Group III, treated with galantamine and trospium) were evaluated by geriatric assessments, the Global Perception Index (GPI), Patients' Satisfaction Question (PSQ), Estimated Patients' Improvement (EPI), nocturia and pads/day at baseline and in the 6th month. RESULTS: Trospium increased the satisfaction of the patients in Groups I and III according to the EPI, PSQ, GPI, number of nocturia and pads/day. Decreasing in the GDS score was significant in the Group I and III (p < 0.05). Decreasing in the ADL score was significant in the Group III (p < 0.05). The MMSE scores were not significantly changed in the all groups during the 6 months. CONCLUSION: Consequently, we have thought that a combination of trospium and galantamine could be recommended for the management of the elderly patients with UUI and AD, which are common problems in the elderly.

The role of ace gene polymorphism in the development of angioedema secondary to angiotensin converting enzyme inhibitors and angiotensin II receptor blockers.

BACKGROUND: Angiotensin Converting Enzyme inhibitors (ACEi) may cause angioedema, with an incidence of 0.1 % to 1 %, which may be life-threatening. ACEi induce angioedema by increasing the levels of bradykinin. Angiotensin II receptor blockers (ATRB), have a pharmacological profile similar to ACEi. The polymorphism of the ACE gene is based on the presence or absence of a 287-bp element on intron 16 on chromosome 17. The plasma level of ACE is related to gene polymorphism. ACE level in genotype DD is double that in genotype II. OBJECTIVE: The aim of this study was to investigate whether the relationship between ACE gene polymorphism and ACEi induced angioedema is present or not. METHODS: ACE gene polymorphism was investigated in patients with angioedema due to the use of ACEi or ATRB (n:32, group 1), in patients receiving ACEi or ATRB without angioedema (n:46, group 2), and healthy controls (n:96, group 3). RESULTS: ID polymorphism was the most frequent genotype in all groups, without any significant difference among the groups (p:0.868). ACE gene polymorphism was not related with the drugs used (ACEi or ATRB), localisation of angioedema, and female sex, in group 1. CONCLUSION: Our results showed that ACE gene polymorphism has no effect on ACEi or ATRB induced angioedema.

The role of ace gene polymorphism in the development of angioedema secondary to angiotensin converting enzyme inhibitors and angiotensin II receptor blockers

Background: Angiotensin Converting Enzyme inhibitors (ACEi) may cause angioedema, with an incidence of 0.1 % to 1 %, which may be life-threatening. ACEi induce angioedema by increasing the levels of bradykinin. Angiotensin II receptor blockers (ATRB), have a pharmacological profile similar to ACEi. The polymorphism of the ACE gene is based on the presence or absence of a 287-bp element on intron 16 on chromosome 17. The plasma level of ACE is related to gene polymorphism. ACE level in genotype DD is double that in genotype II. Objective: The aim of this study was to investigate whether the relationship between ACE gene polymorphism and ACEi induced angioedema is present or not. Methods: ACE gene polymorphism was investigated in patients with angioedema due to the use of ACEi or ATRB (n:32, group 1), in patients receiving ACEi or ATRB without angioedema (n:46, group 2), and healthy controls (n:96, group 3). Results: ID polymorphism was the most frequent genotype in all groups, without any significant difference among the groups (p:0.868). ACE gene polymorphism was not related with the drugs used (ACEi or ATRB), localisation of angioedema, and female sex, in group 1. Conclusion: Our results showed that ACE gene polymorphism has no effect on ACEi or ATRB induced angioedema

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The plasma levels of soluble P-selectin in subjects with prediabetes.

Prediabetes has been associated with an increased risk of cardiovascular disease and mortality. Soluble P-selectin (sP-selectin) is an index of platelet activation and also a risk factor for future vascular events. sP-selectin levels were investigated in prediabetic subjects who had no confounding factors such as hypertension, obesity or dyslipidaemia. sP-selectin, hsCRP levels and HOMA-IR indexes were measured in 40 prediabetic subjects (n = 24 for IFG and n = 16 for IGT) and age-, sex- and BMI-matched 40 healthy controls. sP-selectin levels in prediabetic subjects were not significantly different compared with those in controls (p = 0.12). Prediabetic group had similar hsCRP (p = 0.29), higher HOMA-IR indexes (p < 0.001) and lower HDL cholesterol levels (p = 0.001) when compared with healthy controls. The power of the study was 0.93 for sP-selectin, 0.7 for hsCRP and 1.0 for HOMA. Our data suggest that sP-selectin may not contribute to the prothrombotic state as well as the accelerated atherogenesis associated with prediabetes.

Vascular endothelial growth factor and monocyte chemoattractant protein-1 in Behçet's patients with venous thrombosis.

OBJECTIVE: Vascular lesions can involve both arterial and venous systems which are often the major causes complicating the disease course of Behçet's disease (BD). Vascular endothelial growth factor (VEGF) is a stimulant of angiogenesis secondary to ischemia while monocyte chemoattractant protein 1 (MCP-1) is induced by shear stresses leading to vascular collateral development. MCP-1 has been also shown to contribute to the recanalization of venous thrombi. Tumor necrosis factor-alpha (TNF-alpha) is known to play a major role in the pathogenesis of BD. Furthermore, up-regulation of secreted MCP-1 and VEGF was observed following stimulation with TNF-alpha. In view of the above functions of VEGF, MCP-1 and TNF-alpha, we hypothesized that these factors may be important in the pathogenesis of thrombosis seen in BD. METHODS: A total of 36 patients with a diagnosis of BD were studied. BD patients were separated into 3 groups with respect to vascular involvement. Group BD-AT (n = 9) with acute thrombosis, BD-CT (n = 12) with chronic thrombosis and BD-MC (n = 15) with mucocutaneous involvement only. The control group (group H) was comprised of 20 healthy persons. In addition, patients with acute, DC-AT (n= 11) and patients with chronic DC-CT (n = 9) thrombosis without BD served as disease controls. Serum measurements of VEGF MCP-1 and TNF-alpha were performed by quantitative sandwich ELISA. The acute phase reactants, including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were also measured. RESULTS: The levels of VEGF were significantly higher in the patients in group BD-AT than either in group BD-CT or BD-MC (p = 0.03 and p < 0.001, respectively). However, no significant difference was found for VEGF levels of thrombotic patients regarding the cause (BD-AT vs. DC-AT, p = 0.063; BD-CT vs. DC-CT, p = 0.084) or the stage of thrombosis (DC-AT vs. DC-CT, p > 0.05). Both BD patients and disease controls with acute thrombosis had significantly higher levels of MCP-1 as compared to corresponding chronic thrombosis patients (BD-AT vs. DC-CT; p < 0.001; DC-AT vs. DC-CT, p < 0.001). Patients with BD and disease controls had significantly higher serum TNF-alpha level when compared with healthy subjects. No significant difference with respect to serum TNF-alpha level was noted when patient subgroups with BD and disease controls were compared with each other Serum levels of VEGF, MCP-1, and TNF-alpha were not found to be correlated with either ESR or CRP (p > 0.05). CONCLUSIONS: Increased levels of VEGF and MCP-1 detected in BD thrombosis suggest the possible role of those angiogenic cytokines in the pathogenesis. Although not specific for BD, detection of VEGF or MCP-1 levels seems to serve as an assay for differentiation of BD patients with acute thrombosis from chronic.

Observations on edema formation and resolution in Gleich syndrome: essential role of the kidneys in effective arterial blood volume regulation.

Gleich syndrome is clinically present with episodes of angioedema, hypereosinophilia, oliguria, and weight gain due to fluid retention which may be sudden and remarkable, sometimes increasing to 10-20% of the baseline weight. The purpose of this study was to evaluate body fluid regulation and hormonal responses during the episode of angioedema and during the recovery phase in a patient with Gleich syndrome. A 24-year-old male was referred to our hospital for further evaluation of recurrent attacks of swellings of face, upper arms, and legs, marked weight gain, and oliguria. On first admission, the patient was in a remission phase, and the initial physical examination showed no abnormalities. Underlying disorders causing edema, such as heart, kidney, and liver diseases, and the recognized causes for hypereosinophilia, such as allergy, parasites, and collagen diseases, were ruled out. After 2 months, since his course was monitored, the patient was hospitalized. During days 10-19, he developed pronounced nonpitting edema of face, upper arms, and legs. Constant leukocytosis and hypereosinophilia, oliguria, and marked weight gain were also noted. A clinical remission was observed without any medication: intensive diuresis, loss of weight, regression of edema, and decreased eosinophil and leukocyte counts within 2 weeks. Physiological mechanisms during edema and resolution are discussed. In conclusion, our patient represents a suitable model for the protection of effective arterial blood volume because of the absence of underlying disorders causing edema. The kidneys play an essential role in the effective arterial blood volume regulation.