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Insulin Therapy with Personal Insulin Pumps and Early Angiopathy in Children with Type 1 Diabetes Mellitus  [PDF]
Joanna To?wińska,Barbara G?owińska-Olszewska,Artur Bossowski
Mediators of Inflammation , 2013, DOI: 10.1155/2013/791283
Abstract: Objective. Assessment of the effect of a treatment method change from multiple daily insulin injection (MDI) to continuous subcutaneous insulin infusion (CSII) on the development of early angiopathy in children with T1DM with or without retinopathy. Methods. The study pump group involved 32 diabetic children aged 14.8, with the initial HbA1c level of 8.3%, previously treated by MDI. The patients were examined before pump insertion and after 3 and 6 months of CSII. We assessed HbA1c level, carotid artery intima-media thickness (c-IMT), and flow-mediated dilatation (FMD) of the brachial artery. The pump group was compared to a group of eight teenagers with diagnosed nonproliferative retinopathy, treated with MDI. Results. HbA1c in the entire group was found to improve in the second and in the third examination. During 6 months of CSII, FMD increased and IMT decreased. Retinopathic adolescents had significantly thicker IMT and lower FMD compared to baseline results of the pump group. Treatment intensification in the retinopathy-free children enhanced these differences. Conclusions. CSII is associated with lower IMT and higher FMD. Whether on the long-run CSII is superior to MDI to delay the occurrence of diabetes late complications remains to be explained. 1. Introduction Insulin pump therapy in the form of continuous subcutaneous insulin infusion (CSII) was introduced in the 1970s and turned out to ensure better metabolic control of diabetes compared to traditional insulin therapy approaches. It is currently considered to be the optimal method of insulin administration, since it imitates the pancreatic activity in the best possible way, ensures precise dosage, and at the same time offers a high level of ease and comfort. Patients that experience the advantages are above all children and adolescents with type 1 diabetes mellitus (T1DM) [1–3]. Compared to the traditional methods of insulin therapy by means of multiple daily insulin injections (MDI), CSII can significantly decrease glycated hemoglobin (HbA1C), reduce 24-hour glucose variability, decrease incidence of severe hypoglycemia, and eliminate dawn phenomenon. Moreover, the use of CSII is associated with improved quality of life and precise insulin administration with respect to physical effort and diet [1, 4]. A long-term effect of CSII on the development of late complications of diabetes in the form of microangiopathy or macroangiopathy needs to be explained [5]. T1DM increases the risk of developing micro- and macrovascular complications which in turn will have a devastating impact on quality of
Diabetic angiopathy and angiogenic defects
Ling Xu, Keizo Kanasaki, Munehiro Kitada, Daisuke Koya
Fibrogenesis & Tissue Repair , 2012, DOI: 10.1186/1755-1536-5-13
Abstract: The epidemic of obesity-associated type 2 diabetes has prompted the need for strategies to prevent and treat diabetic complications [1]. In diabetes, diverse sets of organs are damaged. Such organ damage is certainly fundamentally associated with glucose metabolism defects. Therefore, normalizing blood glucose levels is essential for diabetic therapy [2-4]. However, recent evidence suggests that normalization of blood glucose levels is challenging in diabetes, and such intensive therapies in diabetic patients are associated with increased mortality risk, likely associated with frequent hypoglycemia [5]. To this end, patients enrolled in the intensive therapy group of the ACCORD trial, which employed intensive blood glucose lowering strategies aimed to normalize blood sugar levels, exhibited increased mortality [5]. Therefore, to prevent diabetic complications, additional therapeutic strategies are required in addition to those that target blood glucose normalization.Angiopathy is a term for vascular defects that are associated with angiogenic abnormalities [6]. Understanding the precise molecular mechanisms that lead to diabetic angiopathy is essential for designing new therapeutic strategies to treat diabetic complications. In this review, we focus on diabetic vascular defects and abnormal angiogenesis.Angiogenesis is characterized by new blood vessel formation from pre-existing vessels and is distinguished from vasculogenesis, which is de novo vessel formation from hematopoietic progenitor cells [7]. Angiogenesis is essential for proper development and organ homeostasis, such as placental and embryonic growth, collateral formation, wound healing, and granulation [8]. However, angiogenesis is not always healthy and is often associated with pathologic conditions, in which case it is referred to as pathologic angiogenesis [7]. Angiogenesis results from the balanced functions of pro- and anti-angiogenic molecules (Figure?1). Defects in the angiogenic balance may cause
Somatosensor Induced Potentials in Diagnosis of a Non-systemic Vertigo in Patients with a Dyscirculatory Encephalopathy  [PDF]
T.A. Davydova,A.V. Gustov,K.M. Belyakov
Sovremennye Tehnologii v Medicine , 2010,
Abstract: Aim of investigation is a study of the non-systemic vertigo mechanisms in patients with a dyscirculatory encephalopathy with a use of the somatosensor induced potentials.Materials and methods. 40 patients with a dyscirculatory encephalopathy of the I and II stages with a non-systemic vertigo at the age of 45—60 years are examined. An investigation of the somatosensor induced potentials from three levels: lumbar, cervical and cranial ones, was accomplished. A latency of cerebral components N20, P23, N30, P45 was assessed.Results. A trustworthy increase of the somatosensor induced potential component P45 latency testifies to the afferent way function insufficiency in a frontoparietal area.Conclusion. A verification of the non-systemic vertigo pathogenetic mechanisms in patients with a dyscirculatory encephalopathy permits to speak about the differentiated therapy expediency in a further elaboration.
Population studies of sporadic cerebral amyloid angiopathy and dementia: a systematic review
Hannah AD Keage, Roxanna O Carare, Robert P Friedland, Paul G Ince, Seth Love, James A Nicoll, Stephen B Wharton, Roy O Weller, Carol Brayne
BMC Neurology , 2009, DOI: 10.1186/1471-2377-9-3
Abstract: To identify population-based studies assessing CAA and dementia, a previous systematic review of population-based clinicopathological studies of ageing and dementia was employed. To identify selected-sample studies, PsychInfo (1806–April Week 3 2008), OVID MEDLINE (1950–April Week 2 2008) and Pubmed (searched 21 April 2008) databases were searched using the term "amyloid angiopathy". These databases were also employed to search for any population-based studies not included in the previous systematic review. Studies were included if they reported the prevalence of CAA relative to a dementia classification (clinical or neuropathological).Four population-based studies were identified. They showed that on average 55–59% of those with dementia displayed CAA (of any severity) compared to 28–38% of the non-demented. 37–43% of the demented displayed severe CAA in contrast to 7–24% of the non-demented. There was no overlap in the range of these averages and they were less variable and lower than those reported in 38 selected sample studies (demented v non-demented: 32–100 v 0–77% regardless of severity; 0–50 v 0–11% for severe only).CAA prevalence in populations is consistently higher in the demented as compared to the non-demented. This supports a significant role for CAA in the pathogenesis of dementia.Alzheimer's disease (AD) is the most common type of dementia and is characterised pathologically by the intraneuronal accumulation of neurofibrillary tangles (NFT) containing tau and ubiquitin, and by the extracellular accumulation of amyloid-β (Aβ) in brain tissue and in artery walls as cerebral amyloid angiopathy (CAA). Many studies have correlated the severity of dementia in AD with the number and distribution of NFTs, the number of plaques of insoluble Aβ, and the levels of soluble Aβ in the brain [as reviewed by [1]]. Relatively few studies, however, have investigated the relationship between dementia and the key pathological change of CAA.CAA is the deposition of the a
Histopathological Evidence for Irradiation Angiopathy in Head and Neck Cancer  [PDF]
Nobuhiro Uwa, Hiroyuki Hao, Yoshitane Tsukamoto, Tomonori Terada, Kosuke Sagawa, Takeshi Mohri, Takashi Daimon, Hiroshi Doi, Yohei Sotsuka, Guillaume van Eys, Marie-Luce Bochaton-Piallat, Seiichi Hirota, Masafumi Sakagami
International Journal of Otolaryngology and Head & Neck Surgery (IJOHNS) , 2015, DOI: 10.4236/ijohns.2015.42020

Objective: To evaluate the incidence of cervical angiopathy caused by radiation therapy for head and neck cancer. Methods: Segments of 57 cervical arteries were obtained during surgery for head and neck malignant tumors and divided into two groups (irradiated group and non-irradiated group) based on the treatment prior to vascular resection. In order to evaluate vascular injury after radiation therapy, we examined the degree of medial atrophy, medial fibrosis, smooth muscle cell (SMC) differentiation in the media and intima, intimal hyperplasia and endothelial cell (EC) injury. Sections of arterial segments were stained with hematoxylin-eosin, Elastica van Gieson and Masson’s trichrome, and immunohistochemistry for α-smooth muscle actin (α-SMA), smoothelin, S100A4 and CD31 in the resected vessels was conducted. Results: The median interval between the completion of radiation therapy and vascular resection was nine months. No significant differences were observed between the two groups in terms of medial atrophy, medial fibrosis and intimal hyperplasia. The ratio of the smoothelin-positive area per α-SMA-positive area in the media and the S100A4-positive proportion in the intima, indicating the degree of differentiation of the medial SMC and dedifferentiation of the intimal SMC, respectively, showed no significant differences, despite the tendency toward a lower smoothelin-positive area per α-SMA-positive area in the media of the irradiated arteries. The EC coverage revealed on CD31 immunohistochemistry was significantly decreased, with mural thrombus adhesion, in the irradiated group. Conclusions: The ECs of small arteries are damaged by irradiation. Although we did not confirm the statistical significance of medial SMC dedifferentiation, a decreased expression of smoothelin tended to be observed in the media of the irradiated arteries. Our findings provide histopathological evidence of irradiation angiopathy in head and neck cancer and may help to improve the surgical safety of microvascular anastomosis and determine the treatment strategy for head and neck tumors.

Cerebral amyloid angiopathy in the aetiology and immunotherapy of Alzheimer disease
Roy O Weller, Stephen D Preston, Malavika Subash, Roxana O Carare
Alzheimer's Research & Therapy , 2009, DOI: 10.1186/alzrt6
Abstract: Deposition of amyloid-beta (Aβ) in the walls of cerebral arteries and capillaries as cerebral amyloid angiopathy (CAA) has a prevalence of 90% to 96% in patients with Alzheimer disease (AD) [1] and is present in 30% of non-demented individuals over the age of 60 years [2]. CAA reflects an age-related failure of elimination of Aβ from the brain along perivascular lymphatic drainage pathways by which interstitial fluid (ISF) and solutes drain from the brain [3-5]. This failure may be a key factor in the aetiology of AD.Most organs have networks of lymphatic vessels that transport fluid, protein macromolecules, cells and particulate matter from tissue to lymph nodes. Lymphatic drainage along these vessels relies upon highly competent valves, an extrinsic pump action generated by external forces from surrounding tissues and an intrinsic pump generated by coordinated contractions of lymphatic muscle cells [6]. There are no conventional lymphatics in the brain. Instead, ISF and solutes drain out of the brain along narrow basement membranes in the walls of capillaries and arteries to lymph nodes in the neck [3,7], probably driven by an intrinsic pump powered by vascular pulsations [8]. The perivascular lymphatic drainage pathway for ISF and solutes from the brain is largely separate from the cerebrospinal fluid (CSF) [7,9]. With increasing age, the brain, with its almost unique lymphatic drainage system, develops problems with lymphatic drainage of Aβ and other amyloids and these problems are rarely seen in other organs. As a result, soluble and insoluble Aβs accumulate in vessel walls and in brain parenchyma.CAA in AD is a protein-elimination-failure arteriopathy (PEFA) [5,7] common to other forms of CAA in which a variety of amyloidogenic peptides accumulate in the walls of cerebral arteries. Non-Aβ forms of CAA tend to be hereditary in origin and are associated with intracerebral haemorrhage or dementia [10]. Mutated cystatin C is deposited in the walls of cerebral arte
Amyloid angiopathy of the floor of the mouth: a case report and review of the literature
Daniel D Kokong, Titus S Ibekwe, Clement A Okolo, Aliyu M Kodiya, James A Fasunla, Onyekwere GB Nwaorgu, Effiong EU Akang
Journal of Medical Case Reports , 2007, DOI: 10.1186/1752-1947-1-117
Abstract: Though the disease is usually fatal with a 5-year survival rate of 20%, there is still paucity of literature on this disease entity worldwide. Diagnosis has remained mostly at autopsy.A case of amyloid angiopathy involving the submandibular gland and floor of the mouth with an associated fatal bleed is reported. The purpose of this case report is to reiterate the importance of a high index of suspicion in the approach to the management of head and neck swellings.Amyloidosis is a rare disease characterised by the deposition of an insoluble extracellular fibrillar protein in various tissues of the body. It can be primary systemic, secondary systemic, localised, myeloma-associated or hereditary-familial. These categories constitute 56%, 8%, 9%, 26% and 1% respectively [1]. The primary systemic form affects mainly mesenchymal tissues such as the heart, tongue, and gastro-intestinal tract (GIT). The secondary form is however associated with destructive chronic inflammatory diseases such as tuberculosis, leprosy, rheumathoid arthritis, ankylosing spondylitis and osteomyelitis. This form affects primarily the kidneys, adrenals, liver and spleen. About 12% of myeloma patients develop amyloidosis [2].All types of amyloidosis consist of a major fibrillar protein derived from a precursor protein through conversion by cells suspected to be macrophages, though yet to be confirmed. These proteins define the type of amyloid in 95% of cases. In addition there are the minor fibrillar proteins that include a P-component derived from Serum Amyloid P-component (SAP), apolipoprotein E(apoE), heparan sulphate proteoglycan, glycosaminoglycans and some other glycoproteins which constitute the remaining 5%. About 20 different fibrils have been described in human amyloidosis, each with a different clinical picture.The disease has been called different names by various authors including paramyloidosis, malignant amyloidosis, essential amyloidosis, Wilds disease, Wild-Lubarschs disease, system
Intracranial Vertebrobasilar Artery Dissection Associated with Postpartum Angiopathy  [PDF]
James S. McKinney,Steven R. Messé,Bryan A. Pukenas,Sudhakar R. Satti,John B. Weigele,Robert W. Hurst,Joshua M. Levine,Scott E. Kasner,Lauren H. Sansing
Stroke Research and Treatment , 2010, DOI: 10.4061/2010/320627
Abstract: Background. Cervicocephalic arterial dissection (CCAD) is rare in the postpartum period. To our knowledge this is the first reported case of postpartum angiopathy (PPA) presenting with ischemic stroke due to intracranial arterial dissection. Case. A 41-year-old woman presented with blurred vision, headache, and generalized seizures 5 days after delivering twins. She was treated with magnesium for eclampsia. MRI identified multiple posterior circulation infarcts. Angiography identified a complex dissection extending from both intradural vertebral arteries, through the basilar artery, and into both posterior cerebral arteries. Multiple segments of arterial dilatation and narrowing consistent with PPA were present. Xenon enhanced CT (Xe-CT) showed reduced regional cerebral blood flow that is improved with elevation in blood pressure. Conclusion. Intracranial vertebrobasilar dissection causing stroke is a rare complication of pregnancy. Eclampsia and PPA may play a role in its pathogenesis. Blood pressure management may be tailored using quantitative blood flow studies, such as Xe-CT. 1. Case Report A 41-year-old pregnant woman with no other past medical history presented to a community hospital with pre-eclampsia at 36-week gestation. She had a systolic blood pressure (SBP) of 160?mmHg with proteinuria but no neurologic signs or symptoms. Twins were delivered by emergent Cesarean section under spinal anesthesia without apparent complications. She was discharged home on hospital day 5. The following day she developed a severe headache, blurred vision, and SBP > 160?mmHg. She had a generalized tonic-clonic seizure in the emergency department. She was orotracheally intubated for airway protection, treated with magnesium sulfate, levetiracetam, and labetalol. She had no further clinical seizures. A noncontrast CT of the head was normal. After extubation the following day, she became lethargic, and her mental status rapidly declined. MRI of the brain showed several areas of acute infarction in the posterior circulation. She was transferred to our neurological intensive care unit (NeuroICU) for further evaluation on the third day of hospitalization. On presentation to our facility, she was lethargic and opened her eyes only to repeated tactile stimulation. She was oriented to name, could follow simple commands, and was severely dysarthric with incomprehensible speech. She had a right homonymous hemianopia, disconjugate gaze, and was quadriparetic. She was treated with a magnesium infusion, intravenous levetiracetam, aspirin 325?mg daily, and a nicardipine
Screening for Familial APP Mutations in Sporadic Cerebral Amyloid Angiopathy  [PDF]
Alessandro Biffi,Anna Plourde,Yiping Shen,Robert Onofrio,Eric E. Smith,Matthew Frosch,Claudia M. Prada,James Gusella,Steven M. Greenberg,Jonathan Rosand
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0013949
Abstract: Advances in genetic technology have revealed that variation in the same gene can cause both rare familial and common sporadic forms of the same disease. Cerebral amyloid angiopathy (CAA), a common cause of symptomatic intracerebral hemorrhage (ICH) in the elderly, can also occur in families in an autosomal dominant pattern. The majority of affected families harbor mutations in the Beta amyloid Peptide (Aβ) coding region of the gene for amyloid precursor protein (APP) or have duplications of chromosomal segments containing APP.
Cerebral amyloid angiopathy: A clinicopathological study of three cases  [cached]
Panicker Jalesh,Nagaraja D,Chickabasaviah Yasha
Annals of Indian Academy of Neurology , 2010,
Abstract: Cerebral amyloid angiopathy (CAA) is an important cause for intracerebral hemorrhage (ICH), yet often goes undiagnosed in the absence of histological examination of the blood vessels in the clot. In this study, we report three patients who presented with ICH. Two patients had no risk factors for bleed, whereas one patient had systemic hypertension. Tissue for analysis was obtained during hematoma evacuation in two patients and necropsy in the third. Histopathology in all three patients revealed severe degree of amyloid angiopathy with extensive amyloid deposits in the vessel walls, which was diagnostic of CAA. Both medium- and small-sized leptomeningeal and cortical vessels were affected. The vascular amyloid deposits stained with Congo red and displayed characteristic birefringence under polarizing light. In addition, vessels also showed fibrinoid necrosis and vascular endothelial proliferation. Immunohistochemistry demonstrated beta-amyloid peptide in all three cases-the protein most commonly involved in sporadic CAA. Senile plaques with amyloid cores were present in all areas, whereas neurofibrillary tangles were restricted to the medial temporal region in the autopsied case. CAA is an important cause for intracerebral bleed and may be a contributory factor even when other risk factors for ICH are present. Areas of hemorrhage tend to correlate with severity of CAA changes.
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