Hebrew University-Hadassah Medical School Research Articles

Preface

Annals of the New York Academy of SciencesVolume 995, Issue 1 p. ix-xii Preface MARIT NILSEN-HAMILTON, Corresponding Author MARIT NILSEN-HAMILTON Department of Biochemistry, Biophysics, and Molecular Biology, Iowa State University, Ames, Iowa, USAAddress for correspondence: Marit Nilsen-Hamilton, Department of Biochemistry, Biophysics, and Molecular Biology, 3206 Molecular Biology Building, Iowa State University, Ames, IA 50011. Voice: 515-294-9996; fax: 515-294-0453. marit@iastate.eduSearch for more papers by this authorZENA WERB, ZENA WERB Department of Anatomy, University of California, San Francisco, California, USASearch for more papers by this authorELI KESHET, ELI KESHET Department of Molecular Biology, Hebrew University-Hadassah Medical School, Jerusalem, IsraelSearch for more papers by this author MARIT NILSEN-HAMILTON, Corresponding Author MARIT NILSEN-HAMILTON Department of Biochemistry, Biophysics, and Molecular Biology, Iowa State University, Ames, Iowa, USAAddress for correspondence: Marit Nilsen-Hamilton, Department of Biochemistry, Biophysics, and Molecular Biology, 3206 Molecular Biology Building, Iowa State University, Ames, IA 50011. Voice: 515-294-9996; fax: 515-294-0453. marit@iastate.eduSearch for more papers by this authorZENA WERB, ZENA WERB Department of Anatomy, University of California, San Francisco, California, USASearch for more papers by this authorELI KESHET, ELI KESHET Department of Molecular Biology, Hebrew University-Hadassah Medical School, Jerusalem, IsraelSearch for more papers by this author First published: 24 January 2006 https://doi.org/10.1111/j.1749-6632.2003.tb03204.xRead the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Volume995, Issue1TISSUE REMODELINGMay 2003Pages ix-xii RelatedInformation

Lifestyles of medical students in Jerusalem are “shocking”

The faculty of the Hebrew University Hadassah Medical School in Jerusalem was caught with their stethoscopes down after a survey showed that most new graduates don't practise what they're supposed to preach. Their smoking prevalence (25%) is only slightly less that that of the general population (28%), and most new graduates take little or no physical exercise. Most said that during their six years of medical studies, none or only a few of their teachers had advised them to stop smoking or to exercise. Of the Jerusalem medical school graduates surveyed, 67% thought the school should intensify its teaching of these subjects. A graduate of the medical school, Dr Tal Haimov, surveyed 83 of his 110 peers after being shocked …

Cysteine Residues Are Important for Functional Expression of the Na+/Ca2+ Exchanger NCX1 in HEK 293 Cells

Annals of the New York Academy of SciencesVolume 976, Issue 1 p. 89-89 Cysteine Residues Are Important for Functional Expression of the Na+/Ca2+ Exchanger NCX1 in HEK 293 Cells XIAOYAN REN, Corresponding Author XIAOYAN REN Department of Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem 91120, IsraelAddress for correspondence: Dr. Xiaoyan Ren, Department of Biochemistry, Hebrew University-Hadassah Medical School, Box 12272, Jerusalem 91120, Israel. Voice: 9772-2-6757510; fax: 972-2-6757061; renxiaovan@yahoo.com.Search for more papers by this authorJUDITH KASIR, JUDITH KASIR Department of Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem 91120, IsraelSearch for more papers by this authorHANNAH RAHAMIMOFF, HANNAH RAHAMIMOFF Department of Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem 91120, IsraelSearch for more papers by this author XIAOYAN REN, Corresponding Author XIAOYAN REN Department of Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem 91120, IsraelAddress for correspondence: Dr. Xiaoyan Ren, Department of Biochemistry, Hebrew University-Hadassah Medical School, Box 12272, Jerusalem 91120, Israel. Voice: 9772-2-6757510; fax: 972-2-6757061; renxiaovan@yahoo.com.Search for more papers by this authorJUDITH KASIR, JUDITH KASIR Department of Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem 91120, IsraelSearch for more papers by this authorHANNAH RAHAMIMOFF, HANNAH RAHAMIMOFF Department of Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem 91120, IsraelSearch for more papers by this author First published: 24 January 2006 https://doi.org/10.1111/j.1749-6632.2002.tb04721.xRead the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume976, Issue1CELLULAR AND MOLECULAR PHYSIOLOGY OF SODIUM-CALCIUM EXCHANGE: PROCEEDINGS OF THE FOURTH INTERNATIONAL CONFERENCENovember 2002Pages 89-89 RelatedInformation

Sidney Kark and John Cassel: social medicine pioneers and South African emigrés.

Sidney Kark and John Cassel: social medicine pioneers and South African emigrés.

Nerve Root Inflammation Demonstrated by Magnetic Resonance Imaging in a Patient with Transient Neurologic Symptoms after Intrathecal Injection of Lidocaine

Received from the Department of Anesthesiology and Critical Care Medicine, Hebrew University Hadassah Medical School, Hadassah University Hospital, Jerusalem, Israel.TRANSIENT neurologic symptoms after intrathecal injection of lidocaine are common. The main symptoms are severe pain and dysesthesia in the buttocks and legs after recovery from spinal anesthesia. The symptoms typically resolve within 1 week. No definitive etiology has been established until now. We report findings on magnetic resonance imaging (MRI) of a patient with transient neurologic symptoms after spinal anesthesia with lidocaine that indicated a local inflammatory process as the possible etiology for this symptom.A 60-yr-old healthy male patient (American Society of Anesthesiologists physical status class I) underwent excision of a perineal condylomata under spinal anesthesia. Anesthesia was performed with the patient in the sitting position with a 27-gauge pencil-point spinal needle (te me na SARL, Bondy, France) and 50 mg hyperbaric lidocaine (AstraZeneca, London, United Kingdom). Dural puncture was achieved in the first attempt, and no paresthesias were elicited. The hyperbaric lidocaine was diluted with cerebrospinal fluid. The patient remained seated for 5 min and then was placed in the prone jackknife position. Intraoperatively, the patient was hemodynamically stable, and the postoperative course was uneventful. The patient was released home pain-free within several hours following the procedure.The next morning, the patient began to feel pain in his lower back radiating to his buttocks and legs. During the next few hours, the pain became severe, and the patient returned to the hospital.On admission, the patient was in extreme discomfort and complained of intractable pain in his buttocks and thighs. There was no tenderness or signs of inflammation at the site of the spinal injection. Neurologic examination revealed no motor, sensory, or muscle–tendon reflex abnormalities. The patient denied having severe back pain or a similar episode in the past. Due to the severe pain and the radicular findings, we performed an MRI (with and without Gd-DTPA contrast material [Magnetol, Soreq, Israel]), which ruled out an epidural or spinal hematoma, direct nerve injury, or an infectious process. There were no signs of pressure to the cord or the spinal roots due to bulging discs or degenerative changes. The only abnormal finding was enhancement of the mildly thickened cauda equina and the lumbosacral nerve roots on the postcontrast study (post Gd-DTPA), which are consistent with nonspecific inflammatory or infiltrative processes (figs. 1 and 2).Due to the severe pain, the patient was treated with intravenous morphine (patient-controlled analgesia), and the pain decreased gradually within several hours. The patient was released the next day with mild pain, which fully resolved the following day.The use of intrathecal lidocaine came under scrutiny in the past decade after an increasing number of reports of severe neurologic symptoms (transient neurologic symptoms, cauda equina syndrome) after spinal anesthesia with lidocaine. 1There is a lower incidence of these symptoms when other local anesthetics are used for spinal anesthesia. 2–4This supports the hypothesis that lidocaine has a neurotoxic effect, although other mechanisms, such as local anesthetics maldistribution, myofascial pain, and surgical positioning, have been proposed. 5–9The mechanism of this postulated lidocaine toxicity is unknown. An ischemic effect of lidocaine on the spinal cord was ruled out. 10The result of the MRI in this case showing enhancement of the cauda equina and the lumbosacral nerve roots may support the theory of a direct toxic effect of lidocaine. The MRI findings are suggestive of pial hyperemia or breakdown of the nerve root–blood barrier by a noninfectious inflammatory process. A similar picture can be found in patients with Guillain-Barré and Krabbe (demyelinating disorder) syndromes. 11–13In Guillain-Barré syndrome, the degree of enhancement correlates well with the severity of the disease. 14The enhancement of the cauda equine roots indicates breakdown of the blood–nerve barrier. In the present case, it suggests a chemical irritation due to intrathecal anesthetic. This breakdown may be the cause of the neurologic deficit or just another effect of the intrathecal anesthetic. Until now, no studies were performed to investigate findings in MRI in patients after spinal anesthesia with and without neurologic symptoms. It is therefore impossible to conclude definitely from this case that the findings in the MRI prove direct toxic effect of lidocaine. However, in regard to similar MRI findings in other neurologic disorders, it is suggestive that toxic effects of lidocaine are the cause of the transient neurologic syndrome.

Teratogen update: antithyroid drugs-methimazole, carbimazole, and propylthiouracil.

TeratologyVolume 65, Issue 1 p. 38-44 Teratogen UpdateFree Access Teratogen update: antithyroid drugs—methimazole, carbimazole, and propylthiouracil Orna Diav-Citrin, Orna Diav-Citrin The Israeli Teratogen Information Service, Israeli Ministry of Health, Jerusalem, IsraelSearch for more papers by this authorAsher Ornoy, Corresponding Author Asher Ornoy ornoy@cc.huji.ac.il> The Israeli Teratogen Information Service, Israeli Ministry of Health, Jerusalem, Israel Laboratory of Teratology, the Hebrew University Hadassah Medical School, Jerusalem, IsraelThe Israeli Teratogen Information Service, Laboratory of Teratology, The Hebrew University, Hadassah Medical School, PO Box 12272, Jerusalem, Israel 91120.Search for more papers by this author Orna Diav-Citrin, Orna Diav-Citrin The Israeli Teratogen Information Service, Israeli Ministry of Health, Jerusalem, IsraelSearch for more papers by this authorAsher Ornoy, Corresponding Author Asher Ornoy ornoy@cc.huji.ac.il> The Israeli Teratogen Information Service, Israeli Ministry of Health, Jerusalem, Israel Laboratory of Teratology, the Hebrew University Hadassah Medical School, Jerusalem, IsraelThe Israeli Teratogen Information Service, Laboratory of Teratology, The Hebrew University, Hadassah Medical School, PO Box 12272, Jerusalem, Israel 91120.Search for more papers by this author First published: 04 January 2002 https://doi.org/10.1002/tera.1096Citations: 77AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume65, Issue1January 2002Pages 38-44 ReferencesRelatedInformation

Traumatic wound dehiscence after cataract extraction

Purpose: To study the visual outcome and factors associated with it in patients with traumatic dehiscence of a cataract surgery wound. Setting: Department of Ophthalmology and the Brown School of Public Health and Community Medicine, The Hebrew University-Hadassah Medical School, Jerusalem, Israel. Methods: A retrospective observational study of 37 eyes of 37 consecutive patients with traumatic wound dehiscence of a cataract surgery wound was conducted. A complete ophthalmic evaluation was performed in all patients. Statistical analysis was done to identify factors associated with the best corrected visual acuity at the end of follow-up. Results: Patients had extracapsular cataract extraction (n = 29), intracapsular cataract extraction (n = 4), or lensectomy (n = 4). No patient had phacoemulsification via a small incision. A univariate analysis showed that factors associated with a worse visual outcome included the presence at presentation of hyphema ( P = .05), intraocular lens dislocation or loss ( P = .006), vitreous hemorrhage ( P = .0002), scleral rupture ( P = .001), a long interval from surgery to trauma ( P < .0001), and fall as the cause of trauma ( P < .0001). In a multivariate model, only a surgery-to-trauma interval longer than 8 weeks was associated with a worse visual outcome ( P < .0001). Visual acuity immediately after trauma was a poor predictor of final visual acuity. Conclusions: Visual outcome after traumatic wound dehiscence of a cataract surgery wound was strongly associated with the interval from surgery to trauma. Other factors were less reliable predictors of visual outcome. Traumatic wound dehiscence only moderately affected visual outcome after cataract surgery in most cases.

Tissue factor as a therapeutic target in coronary syndromes

T issue factor (TF), a low molecular weight (45kDa) membrane-bound glycoprotein, is a major regulator of coagulation and a critical determinant of thrombin generation in normal hemostasis and in atherothrombotic disease.1,2 Binding of TF to factor VIIa (FVIIa) is the first step in the extrinsic coagulation cascade. Normally, TF is located away from the luminal surface of blood vessels and outside the vasculature. The clinical consequences of inappropriately high intravascular expression of TFs are often catastrophic. Intraluminal TF activity can trigger the thrombogenic cascade that underlies the often-lethal thrombotic complications of atherosclerosis, the consumptive coagulopathy and hemorrhagic diathesis of systemic infections, and the prothrombotic state of cancer patients. In the uninjured vessel wall, TF is present on cells mainly in the adventitia and variably on cells of the media. It is usually not detectable on normal, healthy, endothelial cells.3 In human atherosclerotic vessels, TF is abundant, particularly within the acellular lipid core of the plaques and in the adjacent “shoulder region” close to the lumen where it is prominently expressed by monocyte-derived macrophages.3–5 Monocyte/macrophage-type cells play a major role in the development, progression, disruption, and thrombogenicity of atherosclerotic lesions.6 The relatively high TF content within the lipid-rich core is considered to be the principal underlying reason for the high thrombogenicity of this component of the plaque in human coronary arteries.7 Under “normal” conditions, intramural TF is not exposed to flowing blood. However, circumstances such as injury to the atherosclerotic arterial wall associated with disruption of the luminal surface and the fibrous cap results in exposure of TF to circulating factor VII/VIIa. The TF:FVIIa binding forms an enzymatic complex that proteolytically activates factor X to factor Xa, and factor IX to factor IXa, leading to thrombin generation followed by fibrin formation, platelet activation, and thrombosis. The proteolytic activity of this TF:FVIIa complex is tightly regulated by the endogenous inhibitor, TF pathway inhibitor (TFPI).8,9 TFPI forms a stable, inactive, quaternary complex consisting of TFPI, TF, FVIIa, and factor Xa, which inhibits the TF-dependent coagulation cascade.10 In normal arteries, the major pool of TFPI is found in the endothelium.11 Smooth muscle cells, megakaryocytes, platelets, freshly isolated monocytes, and macrophages also express TFPI.12,13 TFPI, although expressed predominantly in the normal vessel wall, is also enhanced in atherosclerotic vessels where it modulates TF activity.5 The complementary deoxyribonucleic acid of TFPI has been cloned and characterized, and TFPI has been synthesized by recombinant technology.14 The pathogenesis of restenosis after balloon angioplasty includes thrombosis at the site of vessel wall injury, acute elastic recoil, neointimal formation, and, in the long term, constrictive vessel wall remodeling. Thrombosis is the immediate consequence of angioplasty, stent implantation, or other forms of mechanical percutaneous coronary intervention. Similar in part to plaque erosion or rupture, deep arterial wall injury by the inflated balloon exposes subendothelial components to the flowing blood. Many of the exposed vessel wall components are thrombogenic, but in restenotic lesions, as with primary lesions, TF is probably the most thrombogenic. TF exposure and elaboration on the luminal surface, and factor X activation on the surface of platelets play pivotal roles in thrombus formation15,16 and thrombin generation, which facilitate smooth muscle cell proliferation, migration, and secretion of extracellular matrix—the principal pathogenetic components of neointima formation.17,18 Recently, it has been suggested that TF expression may play an important role in neointima formation not only through a coagulation-dependent mechanism, such as expansion of mural thrombus, but also through coagulation-independent mechanisms, such as direct acceleration of smooth muscle cell proliferation.19 Angioplasty is associated with a strikingly enhanced elevation of local TF expression in the adventitia and media during the first few days after injury.15,20 This has been shown to be persistent in some models even after 1 month.21 Balloon injury to the atherosclerotic arterial wall also has been shown to be associated with a marked increase in TF expression by circulating monocytes.22 Thrombus at the site of a disrupted atherosclerotic plaque is the principal cause of acute myocardial infarction, unstable angina, and sudden cardiac death. Plaque rupture has been shown to occur preferentially at sites of extensive lipid-rich pultaceous debris, which are separated from the lumen by a thin fibrous cap.23,24 The high TF content of the lipid-rich components is thought to account, in large part, for the high thrombogenicity of advanced lesions.4,25 From the Department of Cardiology, Bikur Cholim Hospital, and Department of Anatomy and Cell Biology, The Hebrew University–Hadassah Medical School, Jerusalem, Israel. Manuscript received August 2, 2000; revised manuscript received and accepted October 12, 2000. Address for reprints: Shmuel Banai, MD, Department of Cardiology, Bikur Cholim Hospital, P.O. Box 492, Jerusalem 91002, Israel. E-mail: banais@mail.netvision.net.il.

Bacterial superantigen antagonist rescues mice from toxic shock

Circumventing conventional wisdom, a team at the Hebrew University-Hadassah Medical School in Jerusalem, Israel, has designed a peptide antagonist of a staphylococcal enterotoxin which, in mice, prevents such toxins from triggering the excessive cellular immune response that leads to toxic shock.

Mechanism of anti- and pro-oxidant effect of azide on pentachlorophenol metabolite-induced toxicity: [formula omitted], Smadar Levy and Mordechai Chevion〈BR〉Department of Cellular Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel〈BR〉

Recent findings on the photophysical investigations of several cofacial bisporphyrin dyads for through space singlet and triplet energy transfers raised several serious questions about the mechanism of the energy transfers and energy migration in the light harvesting devices, notably LH II, in the heavily studied purple photosynthetic bacteria. The key issue is that for simple cofacial or slipped dyads with controlled geometry using rigid spacers or spacers with limited flexibilities, the fastest possible rates for singlet energy transfer for three examples are in the 10 × 109 s−1 (i.e. just in the 100 ps time scale) for donor–acceptor distances approaching 3.5–3.6 Å. The reported time scale for energy transfers between different bacteriochlorophylls, notably B800∗ → B850, is in the picosecond time scale despite the long Mg⋯Mg separation of ∼18 Å. Such a short rate drastically contrasts with the well accepted Förster theory. This article reviews the modern knowledge of the structure, bacteriochlorophyll a transition moments, and photophysical processes and dynamics in LH II, and compares these parameters with the recently investigated model bisporphyrin dyads build upon octa-etio-porphyrin chromophores and rigid and semi-rigid spacers. The recently discovered role of the rhodopin glucoside residue called carotenoid will be commented as the possible relay for energy transfer, including the possibility of uphill processes at room temperature. In this context, the concept of energy migration, called exciton, may also be affected by relays and uphill processes. Also, it is becoming more and more apparent that the presence of an irreversible electron transfer reaction at the reaction center, i.e. electron transfer from the special pair to the phyophytin macrocycle and so on, renders the rates for energy transfer and migration more rapid precluding all possibility of back transfers.

Mechanism of protection by deferoxamine against tetrachlorohydroquinone-induced biological damage: [formula omitted] and Mordechai Chevion, Department of Cellular Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem 91120, ISRAEL

Mechanism of protection by deferoxamine against tetrachlorohydroquinone-induced biological damage: [formula omitted] and Mordechai Chevion, Department of Cellular Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem 91120, ISRAEL

Hydroxyl radical production by pentachlorophenol metabolites and H2O2: An organic fenton reaction?: [formula omitted] and Mordechai Chevion. Department of Cellular Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem 91120, ISRAEL

Hydroxyl radical production by pentachlorophenol metabolites and H2O2: An organic fenton reaction?: [formula omitted] and Mordechai Chevion. Department of Cellular Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem 91120, ISRAEL

Prognosis of Benign Congenital Hypotonia

Twenty five children diagnosed with benign congenital hypotonia (BCH) between infancy and 2 years of age were examined at 6 to 8 years of age and compared to 26 controls, matched for sex, age, and weight, in a study at the School of Occupational Therapy, Hebrew University-Hadassah Medical School, and Child Development Institute, Jerusalem.

Modified Hirt procedure for rapid purification of extrachromosomal DNA from mammalian cells.

Modified Hirt procedure for rapid purification of extrachromosomal DNA from mammalian cells.

Outcome of Children Born to Epileptic Mothers Treated With Carbamazepine During Pregnancy

Department of Anatomy and Cell Biology and the Jerusalem Institute of Child Development, Hebrew University Hadassah Medical School and Ministry of Health, Jerusalem, Israel. Arch Dis Child 1996:75:517-520.

Mast cells, eosinophils and fibrosis

We have presented results that increase our understanding of the roles MC and EOS play in modulating fibrotic processes. In vitro studies have provided clear-cut evidence for the direct involvement of these two inflammatory cells in enhancing proliferation, and either enhancing or decreasing collagen synthesis in human fibroblasts isolated from different anatomical locations. In addition, we have shown that MC and EOS interactions can also take part in modulating fibrosis. In vivo studies in murine and human cGVHD showed that MC activation is detrimental, and that MC stabilization therapy may be helpful in treating the fibrotic outcome of this disease. Much is still obscure. It is, for example, important to define the MC and EOS mediators involved in the modulation of fibroblast properties, and their pattern of influence, keeping in mind the ultimate goal of defining new therapeutic targets for the treatment of fibrotic diseases.

Immunogenic proteins in the body and faecal material of the human body louse, Pediculus humanus, and their homology to antigens of other lice species.

Medical and Veterinary EntomologyVolume 10, Issue 1 p. 105-107 Immunogenic proteins in the body and faecal material of the human body louse, Pediculus humanus, and their homology to antigens of other lice species K. Y. MUMCUOGLU, Corresponding Author K. Y. MUMCUOGLU Department of Parasitology, Hebrew University-Hadassah Medical School, Jerusalem, IsraelDepartment of Parasitology, Hebrew University-Hadassah Medical School, P.O. Box 12272, 91120 Jerusalem, IsraelSearch for more papers by this authorD. BEN-YAKIR, D. BEN-YAKIR Department of Parasitology, Hebrew University-Hadassah Medical School, Jerusalem, IsraelSearch for more papers by this authorS. GUNZBERG, S. GUNZBERG Department of Parasitology, Hebrew University-Hadassah Medical School, Jerusalem, IsraelSearch for more papers by this authorJ. O. OCHANDA, J. O. OCHANDA *Department of Biochemistry, University of Nairobi, KenyaSearch for more papers by this authorR. GALUN, R. GALUN Department of Parasitology, Hebrew University-Hadassah Medical School, Jerusalem, IsraelSearch for more papers by this author K. Y. MUMCUOGLU, Corresponding Author K. Y. MUMCUOGLU Department of Parasitology, Hebrew University-Hadassah Medical School, Jerusalem, IsraelDepartment of Parasitology, Hebrew University-Hadassah Medical School, P.O. Box 12272, 91120 Jerusalem, IsraelSearch for more papers by this authorD. BEN-YAKIR, D. BEN-YAKIR Department of Parasitology, Hebrew University-Hadassah Medical School, Jerusalem, IsraelSearch for more papers by this authorS. GUNZBERG, S. GUNZBERG Department of Parasitology, Hebrew University-Hadassah Medical School, Jerusalem, IsraelSearch for more papers by this authorJ. O. OCHANDA, J. O. OCHANDA *Department of Biochemistry, University of Nairobi, KenyaSearch for more papers by this authorR. GALUN, R. GALUN Department of Parasitology, Hebrew University-Hadassah Medical School, Jerusalem, IsraelSearch for more papers by this author First published: January 1996 https://doi.org/10.1111/j.1365-2915.1996.tb00091.xCitations: 6AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume10, Issue1January 1996Pages 105-107 RelatedInformation

P-A3-19 Protein volume & compressibility are decreased by macromolecular cosolvents: Almagor A, Priev A, Gavish B, and Yedgar S. Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel 91120

P-A3-19 Protein volume & compressibility are decreased by macromolecular cosolvents: Almagor A, Priev A, Gavish B, and Yedgar S. Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel 91120

P-H5-29 Red blood cell aggregation by dextran in plasma: Wajnblum D, Barshtein G, Yedgar S. Department of Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel 91120

P-H5-29 Red blood cell aggregation by dextran in plasma: Wajnblum D, Barshtein G, Yedgar S. Department of Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel 91120

Appearance of White Urine During Propofol Anesthesia

To the Editor: We have noticed the appearance of white urine in a small number of patients during prolonged surgical procedures under intravenous general anesthesia with propofol, fentanyl, and muscle relaxants. Propofol, due to its phenol group, can produce changes in the color of the urine [1,2]. We have observed white urine in four patients receiving propofol anesthesia. Of these, three had an uneventful postoperative course, while one developed pulmonary edema before the end of radical neck dissection surgery, which we attributed to a venous air embolism. This patient went on to have a complete recovery. No diminution in renal function was observed in any of these patients. We think that the vehicle of the propofol emulsion (whose composition is similar to that of Intralipid Trademark [Kabi Pharmacia AB, Stockholm, Sweden]) is responsible for the color change of the urine. The only supportive reference found is a case report of lipiduria after Intralipid Trademark infusion in a boy after abdominal trauma [3]. In this case report, renal function was normal as well. Changes in renovascular hemodynamics and endothelial abnormalities have been reported after short-term induced hypercholesterolemia in animals. This is most probably due to the effect of oxidized low-density lipoproteins on endothelial cell membranes increasing nitric oxide and prostaglandin production [4]. There was no evidence of trauma to the kidney during surgery in our patients. Matot et al. [5] found that there is 60% uptake of propofol by the lung after its first pass and only 40% (approximately) when it is used in combination with fentanyl. It is possible that the combination of propofol and an opiate alters the pharmacokinetics of propofol such that the plasma concentration of both propofol and its vehicle is higher than expected. Joseph Nates, MD Alexander Avidan, MD Yaacov Gozal, MD Morris Gertel, MD, FRCP Department of Anesthesiology and Critical Care Medicine, Hadassah University Hospital, Hebrew University Hadassah Medical School, Jerusalem 91120, Israel