Abdominal Aortic Aneurysm, Ciassification, 212, 213 Repair, 212 ABI, See Ankle-Brachial Index ACE Inhibitor, See Angiotensin-Con

Total Page:16

File Type:pdf, Size:1020Kb

Abdominal Aortic Aneurysm, Ciassification, 212, 213 Repair, 212 ABI, See Ankle-Brachial Index ACE Inhibitor, See Angiotensin-Con INDEX A lymphangiogenesis, 164, 194 Abdominal aortic aneurysm, plasmid DNA, 193, 194, 195, 198 cIassification, 212, 213 therapeutic angiogenesis, 191, 192 repair, 212 vasculogenesis, 189, 191 ABI, see Ankle-brachial index Angiography, see Catheter angiography; ACE inhibitor, see Angiotensin-converting Computed tomography angiography; enzyme inhibitor Magnetic resonance angiography Acidic fibroblast growth factor (aFGF), gene Angiotensin-converting enzyme (ACE) therapy critic al Iimb ischemia trials, inhibitor, 198 diabetes management, 162, 163 Acrocyanosis, presentation and management, hemostatic factor effects, 166 290 Ankle-brachial index (ABI), Acute limb ischemia (ALI), see also Arterial acute limb ischemia outcomes, 136, 137 embolism; Atheromatous embolism, continuous wave Doppler measurement, clinical presentation, 293, 295, 296, 299 64,65 diagnosis, 297, 298 intermittent cIaudication work-up, 39 differential diagnosis, 125, 297 interpretation, 65 epidemiology, 294 medial calcinosis, 63, 64, 69, 269 etiology, 293, 294 sensitivity and specificity, 22 instigating causes, 294, 295 Ankylosing spondylitis, large-vessel vasculitis laboratory studies, 297 and management, 333, 334 pathology, 295 Antiplatelet therapy, see specific agents physical examination, 295, 296 Aortoiliac disease, prognosis, 298 aneurysm, 212, 213 treatment, criticallimb ischemia management, pharmacotherapy, 298, 299 angioplasty, 107 surgery, 298 bypass grafting, 107, 108 Adventitial cysts, intermittent cIaudication les ion cIassification, 107 differential diagnosis, 43, 44 occIusive disease management, aFGF, see Acidic fibroblast growth factor aortofemoral bypass, 226, 227 ALI, see Acute limb ischemia axillofemoral bypass, 227-229 Amputation, endovascular therapy, 212 acute Iimb ischemia management, 138 Arginine, criticallimb ischemia management, 114 intermittent cIaudication management, Angiogenesis, 179, 180, 183 arteriogenesis relationship, 191 mechanism of action, 179 growth factors, Arrhythmia, perioperative medical gene therapy, see Gene therapy management, 256, 257 types, 189, 191 Arterial dissection, vascular endothelial growth factor, intermittent cIaudication differential 192-194 diagnosis, 46 347 348 Index peripheral blood flow effects, 64 physical measures, 131 Arterial embolism, see also Acute limb reperfusion injury, 134 ischemia, surgical revascularization versus atheroembolism, 81-82, 125,293-299 thrombolysis trials, 133, 134 clinic al presentation, 120 thrombectomy, 132, 133 detection, 64 thrombolysis, 131 etiology, timing,130 atrial fibrillation, 121, 122 vascular imaging, 127, 128 overview, 120 Arteriogenesis, overview, 191 patent foramen ovale, 121 Arteriovenous fistula (A VF), construction ventricular thrombi, 120, 121 for criticallimb ischemia management, intermittent claudication differential 237,238 diagnosis, 46, 47 Artery, sites, 122, 123 collateral arteries, see Collateral arteries Arterial thrombosis, see also Acute limb layers, 1,2 ischemia, location and structural variation, 56 catheter angiography, 88 medial calcification, 63, 69 classification of severity, 128-130 resistance of systems, 55, 56 clinical history, 123 size classification, 55 definition, 93 women, causes of occlusive disease, 281, 282 differential diagnosis, Arthritis, intermiUent claudication differential arterial trauma or dissection, 126 diagnosis, 41 atheroembolism, 125 Aspirin, hypercoagulable syndromes, 127 critic al limb ischemia management, 106, overview, 124, 125 111,112 popii te al artery aneurysm thrombosis, thrombus formation prevention, 167 126 Atherosclerosis, see also specific diseases, popliteal artery cysts and entrapment, coprevalence of syndromes, 28, 29, 32, 243 126 definition, 1 vasculitis, 126 lesion classification and features, 2 vasospasm, 125 mortality, 1 Doppler velocimetry, 127 response to injury hypothesis, 5 echocardiography, 128 risk factors, 3-5, 25, 26 etiology, 123 Atherothrombosis, phases of development, follow-up and anticoagulation, 135 166, 167 laboratory tests, 128 A VF, see Arteriovenous fistula outcomes, B limb-related outcome, 136, 137 procedural mortality and morbidity, 137 Basic fibroblast growth factor (bFGF), recurrence, 137, 138 gene therapy, critical limb ischemia trials, physical examination, 124, 138 198 severity factors, 119, 120 intermittent claudication management, 180 sites, 123 Beh~et' s disease, large-vessel vasculitis and treatment, management, 332, 333 amputation, 138 bFGF, see Basic fibroblast growth factor angioplasty, 131, 132 Blood flow, velocity-pressure relationships, anticoagulation, 130, 131 60 approach by severity, 135, 136 Buerger's disease, see Thromboangiitis embolectomy, 132 obliterans fasciotomy, 134, 135 Buflomedil, intermittent claudication lesion, 135 management, 177, 183 Index 349 C Collateral arteries, CAD, see Coronary artery disease anatomy and hemodynamics, 62, 63 Cardiomyopathy, perioperative medical components, 61 management, 256 flow resistance, 61, 62 Camitine, intermittent claudication Composite graft, criticallimb ischemia management, 177, 178, 183 management, 238 Carotid artery, Computed tomography angiography (CT A), stenting, advantages, 86 complications, 204, 207 contrast agents, 86 contraindications, 207 image processing, 87, 89 indications, 205, 207 limitations, 86, 87 transluminal angioplasty, 204, 205 principles, 86 Catheter angiography, prospects, 90, 91 acute limb ischemia, 88 Coronary artery disease (CAD), chronic limb ischemia, 88, 90, 101, 102 peripheral arterial disease coprevalence, complications, 80-82 28,29,32,243,244 contrast agents, 76 revascularization surgery outcomes in film-screen versus digital subtraction peripheral arterial disease, angiography, 76, 77 balloon angioplasty, 245, 246 foot angiography, 80 coronary artery bypass surgery, 245 infrainguinal angiogram, 77, 79 retrospective studies, 244 large-vessel vasculitis, 335 stenting, 246 prospects, 90, 91 vascular surgery peri operative risks in Seldinger technique, 75 peripheral arterial disease patients, stenosis evaluation, 80 intraoperative management, suprainguinal angiography, 77 anesthesia, 257, 258 vasculitis and small vessel disease, 90 monitoring, 258 CA VA T AS trial, 205 mortality,244 Cerebrovascular disease, 23, 28-29, 95-96 perioperative medical management, Charcot foot, arrhythmias, 256, 257 causes,277 cardiomyopathy, 256 clinical presentation, 277 heart failure, 255, 256 fracture, 277 hypertension, 255 management, 277, 278 ischemie heart disease, 254, 255 pathophysiology,277 valvular heart disease, 256 Chelation therapy, intermittent claudication postoperative surveillance, 258, 259 management outcomes, 181 preoperative evaluation, Chronic limb ischemia, see Critical limb clinic al predictors, 247, 248 ischemia combining clinic al risk and testing, Cilostazol, 252 dosing, 176 complications, 253 intermittent claudication management, functional capacity, 248, 249 175-177,183 goals, 246, 247 mechanism of action, 175 long-term prognostic value, 254 side effects and precautions, 176, 177 surgical-specific risk, 249 women and peripheral arterial disease, 284 risk stratification testing, CLI, see Critical limb ischemia ambulatory electrocardiography, 251 Clopidogrel, dobutamine stress echocardiogram, cardiovascular event prevention, 167-169 250,251 dosing,168 echocardiography, 251, 252 safety, 168 myocardial perfusion imaging, 250 350 Index treadmill stress test, 249, 250 CT A, see Computed tomography angiography C-reactive protein (CRP), D giant cell arteritis levels, 324, 325 peripheral arterial disease elevation, 25, Defibrotide, intermittent claudication 26, 165 management, 180, 183 statin effects on levels, 165 Diabetes, Criticallimb ischemia (CLI), amputation rates, 265 catheter angiography, 88, 90, 10 1, 102 angiotensin-converting enzyme inhibitor comorbidity, 95, 96 management, 162, 163 definition, 93 atherosclerosis acceleration, 162 differential diagnosis, 100, 101 atherosclerosis risk factor, 3 Doppler ultrasound, 101 Charcot foot, 277, 278 epidemiology, 97, 98 criticallimb ischemia risk factor, 94, 95 follow-up examination, 114 economic impact, 266 laboratory tests, 105 endothelial dysfunction, 11, 12 medical history, 98, 99 epidemiology, 161, 265 natural history, 96, 97 foot management, pathogenesis, 94 footwear, 274-276 physical examination, 99, 100 orthotics, 277 prevalence, 31 overview, 273 pulse volume recordings, 101 ulcer, risk factors, 94, 95 healing,274 surveillance, 112-114 pathophysiology of formation, 273, transcutaneous oxygen tension measurement, 274 101 glycemic control, 162 treatment, hemodynamic evaluation, 69 amputation, 114 medial artery calcification, 63, 69, 161 anticoagulation therapy, 112 peripheral arterial disease, aortoiliac disease, clinic al presentation and evaluation, angioplasty, 107 268,269 bypass grafting, 107, 108,226-229 pathological arterial changes, 267, 268 les ion classification, 107 prevalence studies, 27 aspirin, 106, 111, 112 prevention, 267 bed position, 105 risk factors, 24, 161-163, 268 foot care, 105 treatment, infrainguinal disease, antiplatelet agents, 270 angioplasty, 110, 111,233,234,236 footwear, 269, 270 bypass grafting, 109, 232-236 percutaneous transluminal lesion classification, 109 angioplasty, 270, 271 profundaplasty, 110, 231, 232 surgical revascularization, 271, 272 infrapopliteallesion classification, wound healing factors, 110, 111 abnormal cellular/inflammatory lumbar sympathectomy, 112 pathways, 266, 267 patient selection for surgery, 225, 239 peripheral neuropathy, 266 prospects, 114, 115 vascular disease and
Recommended publications
  • Journal of Turgut Ozal Medical Center
    OLGU SUNUMU/CASE REPORT J Turgut Ozal Med Cent 2015;22(3):193-6 Journal of Turgut Ozal Medical Center www.jtomc.org The Case of a Patient with Concomitant Popliteal Artery and Ascending Aortic Aneurysm Who Presented with the Blue Toe Syndrome Tevfik Güneş, İhsan Alur, Serkan Girgin, Bilgin Emrecan Pamukkale University, Faculty of Medicine, Department of Cardiovascular Surgery, Denizli, Turkey Abstract Popliteal artery aneurysms (PAAs) are rare though these aneurysms are the most frequently encountered peripheral arterial aneurysms. In this article, we present the treatment of a patient who simultaneously had bilateral popliteal artery and ascending aortic aneurysm but was admitted to the emergency room due to the blue toe syndrome. A 72-old-year female was admitted to the hospital with left lower extremity pain and cyanosis in her toe. Bilateral popliteal artery and ascending aortic aneurysm were observed on computed tomography. Aneurysmectomy and femoropopliteal bypass was performed primarily to the left popliteal artery owing to ischemia. Two months later, we performed valve and ascending aorta replacement followed by right popliteal aneurysmectomy and femoropopliteal bypass 16 months later. In conclusion, since other arterial aneurysms can be simultaneously observed with popliteal artery aneurysm, it is very important to scan whole main arterial system when PAA is evaluated. Key Words: Popliteal Artery; Aorta; Aneurysm; Embolism. Blue Toe Sendromu ile Başvuran Popliteal Arter ve Asendan Aort Anevrizmalı Hasta Özet Popliteal arter anevrizmaları (PAA) nadir görülen patolojilerdir, fakat periferik arter anevrizmaları arasında en sık karşılaşılanıdır. Bu yazıda blue toe sendromu ile başvuran bilateral popliteal arter ve asendan aort anevrizması saptanan hastanın aşamalı tedavisi sunulmaktadır.
    [Show full text]
  • Approach to Cyanosis in a Neonate.Pdf
    PedsCases Podcast Scripts This podcast can be accessed at www.pedscases.com, Apple Podcasting, Spotify, or your favourite podcasting app. Approach to Cyanosis in a Neonate Developed by Michelle Fric and Dr. Georgeta Apostol for PedsCases.com. June 29, 2020 Introduction Hello, and welcome to this pedscases podcast on an approach to cyanosis in a neonate. My name is Michelle Fric and I am a fourth-year medical student at the University of Alberta. This podcast was made in collaboration with Dr. Georgeta Apostol, a general pediatrician at the Royal Alexandra Hospital Pediatrics Clinic in Edmonton, Alberta. Cyanosis refers to a bluish discoloration of the skin or mucous membranes and is a common finding in newborns. It is a clinical manifestation of the desaturation of arterial or capillary blood and may indicate serious hemodynamic instability. It is important to have an approach to cyanosis, as it can be your only sign of a life-threatening illness. The goal of this podcast is to develop this approach to a cyanotic newborn with a focus on these can’t miss diagnoses. After listening to this podcast, the learner should be able to: 1. Define cyanosis 2. Assess and recognize a cyanotic infant 3. Develop a differential diagnosis 4. Identify immediate investigations and management for a cyanotic infant Background Cyanosis can be further broken down into peripheral and central cyanosis. It is important to distinguish these as it can help you to formulate a differential diagnosis and identify cases that are life-threatening. Peripheral cyanosis affects the distal extremities resulting in blue color of the hands and feet, while the rest of the body remains pinkish and well perfused.
    [Show full text]
  • Dermatologic Aspects of Fabry Disease ª the Author(S) 2016 DOI: 10.1177/2326409816661353 Iem.Sagepub.Com
    Original Article Journal of Inborn Errors of Metabolism & Screening 2016, Volume 4: 1–7 Dermatologic Aspects of Fabry Disease ª The Author(s) 2016 DOI: 10.1177/2326409816661353 iem.sagepub.com Paula C. Luna, MD1,2, Paula Boggio, MD2, and Margarita Larralde, MD, PhD1,2 Abstract Isolated angiokeratomas (AKs) are common cutaneous lesions, generally deemed unworthy of further investigation. In contrast, diffuse AKs should alert the physician to a possible diagnosis of Fabry disease (FD). Angiokeratomas often do not appear until adolescence or young adulthood. The number of lesions and the extension over the body increase progressively with time, so that generalization and mucosal involvement are frequent. Although rare, FD remains an important diagnosis to consider in patients with AKs, with or without familial history. Dermatologists must have a high index of suspicion, especially when skin features are associated with other earlier symptoms such as acroparesthesia, hypohidrosis, or heat intolerance. Once the diagnosis is established, prompt screening of family members should be performed. In all cases, a multidisciplinary team is necessary for the long-term follow-up and treatment. Keywords Fabry disease, angiokeratomas, lysosomal storage disorders Introduction Diffuse AKs are characterized by the presence of multiple lesions that affect more than 1 area of the skin. Although any Fabry disease (FD, also known as Anderson-Fabry disease or region of the skin can be affected, lesions usually localize to the angiokeratoma corporis diffusum [ACD]) is a rare X-linked bathing suit area (from the umbilicus to the upper thighs); this disease caused by the partial or complete deficiency of a lyso- phenotype is known as ACD.
    [Show full text]
  • Cocats 4 (Pdf)
    JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY VOL. 65, NO. 17, 2015 ª 2015 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION ISSN 0735-1097/$36.00 PUBLISHED BY ELSEVIER INC. http://dx.doi.org/10.1016/j.jacc.2015.03.017 TRAINING STATEMENT ACC 2015 Core Cardiovascular Training Statement (COCATS 4) (Revision of COCATS 3) A Report of the ACC Competency Management Committee Task Force Introduction/Steering Committee Task Force 3: Training in Electrocardiography, Members Jonathan L. Halperin, MD, FACC Ambulatory Electrocardiography, and Exercise Testing (and Society Eric S. Williams, MD, MACC Gary J. Balady, MD, FACC, Chair Representation) Valentin Fuster, MD, PHD, MACC Vincent J. Bufalino, MD, FACC Martha Gulati, MD, MS, FACC Task Force 1: Training in Ambulatory, Jeffrey T. Kuvin, MD, FACC Consultative, and Longitudinal Cardiovascular Care Lisa A. Mendes, MD, FACC Valentin Fuster, MD, PHD, MACC, Co-Chair Joseph L. Schuller, MD Jonathan L. Halperin, MD, FACC, Co-Chair Eric S. Williams, MD, MACC, Co-Chair Task Force 4: Training in Multimodality Imaging Nancy R. Cho, MD, FACC Jagat Narula, MD, PHD, MACC, Chair William F. Iobst, MD* Y.S. Chandrashekhar, MD, FACC Debabrata Mukherjee, MD, FACC Vasken Dilsizian, MD, FACC Prashant Vaishnava, MD Mario J. Garcia, MD, FACC Christopher M. Kramer, MD, FACC Task Force 2: Training in Preventive Shaista Malik, MD, PHD, FACC Cardiovascular Medicine Thomas Ryan, MD, FACC Sidney C. Smith, JR, MD, FACC, Chair Soma Sen, MBBS, FACC Vera Bittner, MD, FACC Joseph C. Wu, MD, PHD, FACC J. Michael Gaziano, MD, FACC John C. Giacomini, MD, FACC Quinn R. Pack, MD Donna M.
    [Show full text]
  • Diffuse Microvascular Pulmonary Thrombosis Associated with Primary Antiphospholipid Antibody Syndrome
    Eur Respir J 1997; 10: 727–730 Copyright ERS Journals Ltd 1997 DOI: 10.1183/09031936.97.10030727 European Respiratory Journal Printed in UK - all rights reserved ISSN 0903 - 1936 CASE STUDY Diffuse microvascular pulmonary thrombosis associated with primary antiphospholipid antibody syndrome M. Maggiorini*, A. Knoblauch**, J. Schneider+, E.W. Russi* Diffuse microvascular pulmonary thrombosis associated with primary antiphospholipid Depts of *Internal Medicine, and +Pathology, antibody syndrome. M. Maggiorini, A. Knoblauch, J. Schneider, E.W. Russi. ©ERS University Hospital, Zurich, Switzerland. Journals Ltd 1997. **Pneumology Division, Kantonsspital, St. ABSTRACT: Thromboembolism is a well-known complication of the hypercoag- Gallen, Switzerland. ulable state associated with anitphospholipid (aPL) antibodies. Acute respiratory Correspondence: M. Maggiorini failure (ARF) with diffuse pulmonary infiltrates has been reported in only a few Dept of Internal Medicine patients with aPL antibodies. University Hospital We describe a 49 year old patient with spiking fever, livedo reticularis, mild Ramistrasse 100 haemoptysis and ARF. Chest radiography revealed diffuse bilateral pulmonary infil- 8091 Zurich trates, and high resolution computed tomography (CT) revealed patchy distribu- Switzerland tion of areas of ground-glass attenuations. Pulmonary emboli were excluded with angiography. Lung biopsy revealed diffuse microvascular thrombosis, without cap- Keywords: Acute respiratory failure illaritis. High serum levels of anticardiolipin (aCL) antibodies
    [Show full text]
  • Occlusive Shrinkage of Ovation Endograft Presenting As Acute Lower Limb Ischemia
    Case Report AORTA, February 2017, Volume 5, Issue 1:21-26 Received: July 06, 2016 DOI: http://dx.doi.org/10.12945/j.aorta.2017.16.041 Accepted: October 28, 2016 Published online: February 2017 Occlusive Shrinkage of Ovation Endograft Presenting as Acute Lower Limb Ischemia Effective Endovascular Management Paolo Bianchi, MD1, Filippo Scalise, MD, FACC, FESC2, Andrea Mortara, MD3, Guido Lanzillo, MD, FECTS4, Giuseppe Scardina, MD3, Santi Trimarchi, MD, PhD5, Gianfranco Parati, MD, FESC6,7, Valerio Tolva, MD, PhD, FEBVS1,6* 1 Department of Vascular Surgery, Centro Cuore, Policlinico di Monza, Monza, Italy 2 Department of Interventional Cardiology, Centro Cuore, Policlinico di Monza, Monza, Italy 3 Department of Cardiology, Centro Cuore, Policlinico di Monza, Monza, Italy 4 Department of Cardiac Surgery, Centro Cuore, Policlinico di Monza, Monza, Italy 5 Department of Vascular Surgery, Policlinico San Donato IRCCS, San Donato Milanese, Italy 6 Department of Health Sciences, University of Milano-Bicocca, Milan, Italy 7 Istituto Auxologico Italiano IRCCS, San Luca Hospital, Milano, Italy Abstract shrinkage of proximal rings in the Ovation trivascular endograft. Angiographic and intravascular ultrasound The aim of this report is to describe the imaging and findings showed that covered stenting is effective and successful treatment of an acute shrinkage of the Ova- that the ring polymer is safely moldable. tion Abdominal Stent Graft System. The Ovation Prime Copyright © 2017 Science International Corp. system utilizes a polymer-filled sealing ring that is cast in situ at the margin of the aneurysm; however, the re- Key Words: sidual endograft inner volume after ring filling may re- duce volume and graft flow.
    [Show full text]
  • Erythromelalgia Misdiagnosed As Cellulitis
    CONTINUING MEDICAL EDUCATION Erythromelalgia Misdiagnosed as Cellulitis LT Mark Eaton, MC, USNR; LCDR Sean Murphy, MC, USNR GOAL To understand erythromelalgia OBJECTIVES Upon completion of this activity, dermatologists and general practitioners should be able to: 1. Describe the clinical presentation of erythromelalgia in patients. 2. Explain the pathophysiology of erythromelalgia. 3. Discuss the treatment options for erythromelalgia. CME Test on page 32. This article has been peer reviewed and is accredited by the ACCME to provide continuing approved by Michael Fisher, MD, Professor of medical education for physicians. Medicine, Albert Einstein College of Medicine. Albert Einstein College of Medicine designates Review date: December 2004. this educational activity for a maximum of 1 This activity has been planned and implemented category 1 credit toward the AMA Physician’s in accordance with the Essential Areas and Policies Recognition Award. Each physician should of the Accreditation Council for Continuing Medical claim only that credit that he/she actually spent Education through the joint sponsorship of Albert in the activity. Einstein College of Medicine and Quadrant This activity has been planned and produced in HealthCom, Inc. Albert Einstein College of Medicine accordance with ACCME Essentials. Drs. Eaton and Murphy report no conflict of interest. The authors report off-label use of aspirin, gabapentin, heparin, lidocaine patches, misoprostol, serotonin reuptake inhibitors, ticlopidine, topical capsaicin, tricyclic antidepressants, and warfarin for the treatment of erythromelalgia. Dr. Fisher reports no conflict of interest. This case report examines the presentation of a Treatments target symptom alleviation, as well as patient with erythromelalgia that was misdiag- diagnosis and treatment of causative factors.
    [Show full text]
  • Erythromelalgia Presentation and Outcome in 168 Patients
    STUDY Natural History of Erythromelalgia Presentation and Outcome in 168 Patients Mark D. P. Davis, MB, MRCPI; W. Michael O’Fallon, PhD; Roy S. Rogers III, MD; Thom W. Rooke, MD Objective: To describe the demographics, presenta- male, and 46 (27.4%) were male. At presentation, the pa- tion, and outcome in patients with erythromelalgia—a tients’ mean age was 55.8 years (age range, 5-91 years). rare and poorly understood clinical syndrome defined by Symptoms had been present since childhood in 7 pa- the triad of red, hot, painful extremities. tients (4.2%). Six patients (3.6%) had a first-degree rela- tive with erythromelalgia. Symptoms were intermittent Design: Retrospective medical record review with fol- in 163 patients (97.0%) and constant in 5 (3.0%). Symp- low-up by survey questionnaire. toms predominantly involved feet (148 patients [88.1%]) and hands (43 patients [25.6%]). Kaplan-Meier sur- Setting: Large tertiary care medical center. vival curves revealed a significant decrease in survival com- pared with that expected in persons of similar age and Subjects: Patients with erythromelalgia examined at the of the same sex (P,.001). After a mean follow-up of 8.7 Mayo Clinic, Rochester, Minn, between 1970 and 1994. years (range, 1.3-20 years), 30 patients (31.9%) re- ported worsening of, 25 (26.6%) no change in, 29 (30.9%) Intervention: The medical records of 168 patients were improvement in, and 10 (10.6%) complete resolution of analyzed. Follow-up data, which consisted of answers to the symptoms. On a standard health status question- 2 survey questionnaires or the most recent information naire, scores for all but one of the health domains were in the medical record from patients still alive and death significantly diminished in comparison with those in the certificates or reports of death for those deceased pa- US general population.
    [Show full text]
  • Aspirin Responsive Thrombotic Complications in Thrombocythemia Vera. a Novel Platelet-Mediated Arterial Thrombophilia
    Aspirin Responsive Thrombotic Complications in Thrombocythemia Vera. A Novel Platelet-Mediated Arterial Thrombophilia Jan Jacques MICHIELS Department of Hematology, Hemostasis, Thrombosis and Vascular Research, University Hospital Antwerp, Belgium and MPD Center Europe, Goodheart Institute, Rotterdam, NETHERLANDS ABSTRACT Erythromelalgia is the main, pathognomonic and presenting symptom in patients with Essential Thrombocyt- hemia and thrombocythemia associated with Polycythemia Vera. Complete relief of erythromelalgic and acrocya- notic pain is obtained with the cyclooxygenase inhibitors aspirin and indomethacin, but not with sodiumsalicylate, dipyridamol, sulfinpyrozone and ticlopedine indicating that platelet-mediated cyclooxygenase metabolites are ne- cessary for erythromelalgia to develop. Local platelet consumption in erythromelalgic areas became evident by the demonstration of arteriolar fibromuscular intimal proliferation and occlusions by platelet-rich thrombi in skin bi- opsies, by the findings of shortened platelet survival times, significant higher levels of platelet activation markers ß-thromboglobulin (ß-TG), thrombomoduline and increased urinary thromboxane B2 excretion in thrombocythe- mia patients suffering from erythromelalgia. Aspirin treatment of erythromelalgia in thrombocythemia patients re- sulted in disappearance of the erythromelalgic, thrombotic signs and symptoms, correction of the shortened plate- let survival times, and significant reduction of the increased levels of ß-TG, PF IV, thrombomodulin and urinary
    [Show full text]
  • Antiphospholipid Antibodies and Multiple Organ Failure in Critically Ill Cancer Patients
    CLINICS 2009;64(2):79-82 CLINICAL SCIENCE ANTIPHOSPHOLIPID ANTIBODIES AND MULTIPLE ORGAN FAILURE IN CRITICALLY ILL CANCER PATIENTS Jorge I. F. Salluh,I,II Márcio Soares,I Ernesto De Meis,III, IV doi: 10.1590/S1807-59322009000200003 Salluh JIF, Soares M, De Meis E. Antiphospholipid antibodies and multiple organ failure in critically ill cancer patients. Clinics. 2009;64:79-82. OBJECTIVES: To describe the clinical outcomes and thrombotic events in a series of critically ill cancer patients positive for antiphospholipid (aPL) antibodies. DESIGN: Retrospective case series study. SETTING: Medical-surgical oncologic intensive care unit (ICU). Patients and Participants: Eighteen patients with SIRS/sepsis and multiple organ failure (MOF) and positive for aPL antibodies, included over a 10-month period. INTERVENTIONS: None MEASUREMENTS AND RESULTS: aPL antibodies and coagulation parameters were measured up to 48 hours after the occur- rence of acrocyanosis or arterial/venous thrombotic events. When current criteria for the diagnosis of aPL syndrome were applied, 16 patients met the criteria for “probable” and two patients had a definite diagnosis of APL syndrome in its catastrophic form (CAPS). Acrocyanosis, arterial events and venous thrombosis were present in eighteen, nine and five patients, respectively. Sepsis, cancer and major surgery were the main precipitating factors. All patients developed MOF during the ICU stay, with a hospital mortality rate of 72% (13/18). Five patients were discharged from the hospital. There were three survivors at 90 days of follow-up. New measurements of lupus anticoagulant (LAC) antibodies were performed in these three survivors and one patient still tested positive for these antibodies.
    [Show full text]
  • Early-Onset Osteoarthritis, Charcot-Marie-Tooth Like Neuropathy, Autoimmune Features, Multiple Arterial Aneurysms and Dissection
    Early-Onset Osteoarthritis, Charcot-Marie-Tooth Like Neuropathy, Autoimmune Features, Multiple Arterial Aneurysms and Dissections: An Unrecognized and Life Threatening Condition Me´lodie Aubart1, Delphine Gobert2, Fleur Aubart-Cohen3, Delphine Detaint1,4,5, Nadine Hanna6, Hyacintha d’Indya6, Janine-Sophie Lequintrec4, Philippe Renard4, Anne-Marie Vigneron4, Philippe Dieude´ 7,8, Jean-Pierre Laissy8,9, Pierre Koch9, Christine Muti4, Joelle Roume4, Veronica Cusin4, Bernard Grandchamp8, Laurent Gouya4,10, Eric LeGuern11, Thomas Papo2,8, Catherine Boileau6,10, Guillaume Jondeau1,4,8* 1 INSERM U698, Hoˆpital Bichat, Paris, France, 2 AP-HP, Hoˆpital Bichat, Service de Me´decine Interne, Hoˆpital Bichat, Paris, France, 3 AP-HP, Service de Me´decine Interne, Hoˆpital Pitie´-Salpe´trie`re, Paris, France, 4 AP-HP, Hoˆpital Bichat, Centre de re´fe´rence pour les syndromes de Marfan et apparente´s, Service de Cardiologie, Paris, France, 5 AP-HP, Hoˆpital Bichat, Service de Cardiologie, Paris, France, 6 AP-HP Ge´ne´tique mole´culaire, Boulogne, France, 7 AP-HP, Hoˆpital Bichat, Service de Rhumatologie, Hoˆpital Bichat, Paris, France, 8 Universite´ Denis Diderot, Paris 7, UFR de Me´decine, Paris, France, 9 AP-HP, Hoˆpital Bichat, Service de Radiologie, Paris, France, 10 Universite´ Versailles SQY, UFR des Sciences de la Sante´, Guyancourt, France, 11 AP-HP, De´partement de Ge´ne´tique, Hoˆpital Pitie´-Salpe´trie`re, Paris, France Abstract Background: Severe osteoarthritis and thoracic aortic aneurysms have recently been associated with mutations in the SMAD3 gene, but the full clinical spectrum is incompletely defined. Methods: All SMAD3 gene mutation carriers coming to our centre and their families were investigated prospectively with a structured panel including standardized clinical workup, blood tests, total body computed tomography, joint X-rays.
    [Show full text]
  • Overlap Syndromes
    ABC ofRheumatology RAYNAUD'S PHENOMENON, SCLERODERMA, AND OVERLAP SYNDROMES David A Isenberg, Carol Black Raynaud's phenomenon Several rheumatological conditions are linked to impaired peripheral circulation. These abnormalities may take various forms, including chilblains, acrocyanosis, and Raynaud's phenomenon. This last condition, described by the French clinician Maurice Raynaud in 1862, occurs in up to 5% of an otherwise healthy population, but may be a link between certain autoimmune rheumatic diseases. Raynaud's disease refers to the development of trophic changes as a result of microcirculatory damage and prolonged local ischaemia. Fortunately, gangrene is relatively rare, and, because patients are often young, recovery may be remarkable. Disturbances of peripheral circulatory system Chilblains-Painful, burning or itching erythematous lesions of hands or feet (rarely ulceration) precipitated by damp and cold (especially if inadequate clothing worn) Acrocyanosis-Persistent cold, blue, and rather sweaty appearance,. usually of hands Well defined blanching of skin characteristic of Raynaud's phenomenon-Episodic, clearly demarcated two or three phase Raynaud's phenomenon. colour change-white (ischaemia), then often blue (stasis), then red (reactive hyperaemia)-of fingers and sometimes toes (rarely nose, tongue, or ears) in response to cold or, less often, emotion Prevalence of Raynaud's phenomenon in autoimmune Raynaud's phenomenon as a predictor ofautoimmune rheumatic disease rheumatic diseases Over 90% ofpatients with Raynaud's phenomenon are female and, Rheumatoid arthritis <5% at the time of presentation, are often aged under 25. Up to 5% of Systemic lupus erythematosus 20-30% patients presenting with the condition eventually develop an Sjogrens syndrome 20-30% disease. The of abnormal nail fold Myositis 25% autoimmune rheumatic presence Scleroderma >95% capillaries (detected by capillaroscopy) and antinuclear antibodies are of particular value in predicting this development.
    [Show full text]