ORIGINAL_ARTICLE
Prognostic value of magnetic resonance spectroscopy in patients with diffuse axonal injury: a systematic literature review
Introduction: Magnetic resonance spectroscopy (MRS) is an imaging technique that provides spectroscopic information about changes in biological markers. Studies suggest that MRS can be helpful in determining the prognosis of patients with diffuse axonal injury (DAI).Methods: The PubMed and Scopus databases were systematically searched in June 2015 using following search strategy: (“Magnetic resonance spectroscopy” OR MRS OR “MR spectroscopy”) AND [(“Diffuse axonal injury” OR DAI] AND Prognosis) to find relevant articles in which the prognostic value of MRS had been investigated in patients with traumatic DAI. All relevant information was extracted from the identified articles and used to synthesize the data for the purpose of this study.Result: In total, 19 articles were found in PubMed and 151 in Scopus. Of these, eight documents were selected for further data extraction following the application of the inclusion/exclusion criteria. The total number of patients who participated in the research studies described in the selected documents was 197. All of the selected documents showed that MRS can be used to quantitatively assess metabolite changes in patients with DAI.Discussion: The results of the studies indicate that MRS imaging as a sensitive method can quantitatively determine even small variations in metabolites. Any changes in the metabolite level of the brain after traumatic injury may be a useful predictor of a patient’s outcome; therefore, if the sensitivity of MRS is proven, this method can have prognostic value when employed with patients with DAI.Conclusion: Based on the results of this systematic review, MRS is a sensitive tool that is helpful in determining the prognosis of patients with DAI.
https://rcm.mums.ac.ir/article_6481_5235be3c33dddca3803c7514d560d7a5.pdf
2017-01-01
1
6
10.22038/rcm.2016.6481
Brain metabolite
Diffuse axonal injury
Prognosis
Traumatic brain injury
Ali
Shamsa
1
Department of Neurosurgery, Ghaem Hospital, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
LEAD_AUTHOR
Wolf JA, Stys PK, Lusardi T, et al. Traumatic axonal injury induces calcium influx modulated by tetrodotoxin-sensitive sodium channels. J Neurosci. 2001;21:1923-1930.
1
Adams JH, Graham DI, Murray LS, et al. Diffuse axonal injury due to nonmissile head injury in humans: an analysis of 45 cases. Ann Neurol. 1982;12:557-563.
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Adams JH, Doyle D, Ford I, et al. Diffuse axonal injury in head injury: definition, diagnosis and grading. Histopathology. 1989;15:49-59.
3
Meythaler JM, Peduzzi JD, Eleftheriou E, et al. Current concepts: diffuse axonal injury-associated traumatic brain injury. Arch Phys Med Rehabil. 2001;82:1461-1471.
4
Povlishock JT, Christman CW. The pathobiology of traumatically induced axonal injury in animals and humans: a review of current thoughts. J Neurotrauma. 1995;12:555-564.
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Garnett MR, Blamire AM, Rajagopalan B, et al. Evidence for cellular damage in normal-appearing white matter correlates with injury severity in patients following traumatic brain injury: A magnetic resonance spectroscopy study. Brain. 2000;123:1403-1709.
6
Garnett MR, Blamire AM, Corkill RG, et al. Early proton magnetic resonance spectroscopy in normal-appearing brain correlates with outcome in patients following traumatic brain injury. Brain. 2000;123:2046-2054.
7
Zink BJ. Traumatic brain injury outcome: concepts for emergency care. Ann Emerg Med. 2001;37:318-332.
8
Maas AI, Stocchetti N, Bullock R. Moderate and severe traumatic brain injury in adults. Lancet Neurol. 2008;7:728-741.
9
Armin SS, Colohan AR, Zhang JH. Traumatic subarachnoid hemorrhage: our current understanding and its evolution over the past half century. Neurol Res. 2006;28:445-452.
10
Holshouser BA, Tong KA, Ashwal S. Proton MR spectroscopic imaging depicts diffuse axonal injury in children with traumatic brain injury. AJNR Am J Neuroradiol. 2005;26:1276-1285.
11
Yeo RA, Phillips JP, Jung RE, et al. Magnetic resonance spectroscopy detects brain injury and predicts cognitive functioning in children with brain injuries. J Neurotrauma. 2006;23:1427-1435.
12
Liberati A, Altman DG, Tetzlaff J, et al. The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate health care interventions: explanation and elaboration. Annals Intern Med. 2009;151:W65-W94.
13
Kirov II, Tal A, Babb JS, et al . Diffuse axonal injury in mild traumatic brain injury: a 3D multivoxel proton MR spectroscopy study. J Neurol. 2013;260:242-252.
14
Babikian T, Marion SD, Copeland S, et al. Metabolic levels in the corpus callosum and their structural and behavioral correlates after moderate to severe pediatric TBI. J Neurotrauma. 2010;27:473-481.
15
Govind V, Gold S, Kaliannan K, et al. Whole-brain proton MR spectroscopic imaging of mild-to-moderate traumatic brain injury and correlation with neuropsychological deficits. J Neurotrauma. 2010;27:483-496.
16
Gasparovic C, Yeo R, Mannell M, et al. Neurometabolite concentrations in gray and white matter in mild traumatic brain injury: an 1H-magnetic resonance spectroscopy study. J Neurotrauma. 2009;26:1635-1643.
17
Yoon SJ, Lee JH, Kim ST, et al. Evaluation of traumatic brain injured patients in correlation with functional status by localized 1H-MR spectroscopy. Clin Rehabil. 2005;19:209-215.
18
Uzan M, Albayram S, Dashti SG, et al. Thalamic proton magnetic resonance spectroscopy in vegetative state induced by traumatic brain injury. J Neurol Neurosurg Psychiatry. 2003;74:33-38.
19
De Stefano N, Narayanan S, Francis SJ, et al. Diffuse axonal and tissue injury in patients with multiple sclerosis with low cerebral lesion load and no disability. Arch Neurol. 2002;59:1565-1571.
20
Heath DL, Vink R. Impact acceleration-induced severe diffuse axonal injury in rats: characterization of phosphate metabolism and neurologic outcome. J Neurotrauma. 1995;12:1027-1034.
21
Kirov II, Tal A, Babb JS, et al. Proton MR spectroscopy correlates diffuse axonal abnormalities with post-concussive symptoms in mild traumatic brain injury. J Neurotrauma. 2013;30:1200-1204.
22
Marmarou A, Foda MA, van den Brink W, et al. A new model of diffuse brain injury in rats. Part I: Pathophysiology and biomechanics. J Neurosurg. 1994;80:291-300.
23
Conzen M, Ebel H, Swart E, et al. Long-term neuropsychological outcome after severe head injury with good recovery. Brain Inj. 1992;6:45-52.
24
Sinson G, Bagley LJ, Cecil KM, et al. Magnetization transfer imaging and proton MR spectroscopy in the evaluation of axonal injury: correlation with clinical outcome after traumatic brain injury. AJNR Am J Neuroradiol. 2001;22:143-151.
25
Cummings JL. Frontal-subcortical circuits and human behavior. Arch Neurol. 1993;50:873-880.
26
Bayly PV, Cohen TS, Leister EP, et al. Deformation of the human brain induced by mild acceleration. J Neurotrauma. 2005;22:845-856.
27
Hardman JM, Manoukian A. Pathology of head trauma. Neuroimaging Clin N Am. 2002;12:175-187.
28
Mountford CE, Somorjai RL, Malycha P, et al. Diagnosis and prognosis of breast cancer by magnetic resonance spectroscopy of fine-needle aspirates analysed using a statistical classification strategy. Br J Surg. 2001;88:1234-1240.
29
Majós C, Bruna J, Julià-Sapé M, et al. Proton MR spectroscopy provides relevant prognostic information in high-grade astrocytomas. AJNR Am J Neuroradiol. 2011;32:74-80.
30
Shanmugalingam S, Thornton JS, Iwata O, et al. Comparative prognostic utilities of early quantitative magnetic resonance imaging spin-spin relaxometry and proton magnetic resonance spectroscopy in neonatal encephalopathy. Pediatrics. 2006;118:1467-1477.
31
da Silva LF, Höefel Filho JR, Anés M , et al. Prognostic value of 1H-MRS in neonatal encephalopathy. Pediatr Neurol. 2006;34:360-366.
32
ORIGINAL_ARTICLE
Effect of valproic acid on metabolic status and endocrine system in pediatric patients with epilepsy: systematic literature review
Introduction: Valproic acid (VPA) is an acidic compound that is commonly used as an anticonvulsant and mood-stabilizing agent in the treatment of epilepsy, mania and bipolar disorders as well as the prevention of migraine headaches. But, it can affect metabolic and endocrine system resulting in hormonal disturbances and incidence of some metabolic disease, especially in pediatric patients. In this study, we aimed to systematically review the literature wherein metabolic and endocrine effect of valproic acid has been studied in pediatric patients with epilepsy.Methods: To evaluate the relationship between VPA consumption and metabolic diseases, a systematic literature search was performed through searching for related documents in the PubMed and Scopus as two known databases using the following key terms “valproic acid”, “metabolic disease” and “pediatrics” in the title, keywords, and abstract of literatures. Data were then extracted and described.Result: Nearly 934 documents were collected and reviewed based on the main purpose of this study. Of the collected articles, 918 documents were excluded in several step by step processes of article selection, and only 16 relevant documents were included for further data assessment. The results showed that VPA can cause significant increase in plasma concentration of thyroid hormones and therefore increase the risk of metabolic disease in patients with epilepsy.Conclusion:The results of included documents in this review showed that VPA may induce metabolic and hormonal disturbances in pediatric patients, who were on treatment with VPA.
https://rcm.mums.ac.ir/article_6490_c7a69927e5a094e3207638a6688867ea.pdf
2017-01-01
7
13
10.22038/rcm.2016.6490
Endocrine system
Epilepsy
Metabolic disease
Pediatrics
Valproic acid
Sona
Sepahi
samanehsepahi@gmail.com
1
Iranian Academic Center for Education, Culture and Research, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Bamdad
Riahi-Zanjani
riahib@mums.ac.ir
2
Medical Toxicology Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Adel
Ghorani-Azam
3
Medical Toxicology Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
LEAD_AUTHOR
Bauer LA. Valproic Acid. Applied clinical pharmacokinetics. New York: McGraw-Hill New York; 2008.
1
Chaudhry N, Patidar Y, Puri V. Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes unveiled by valproate. J Pediatr Neurosci. 2013;8:135-137.
2
Labbe G, Pessayre D, Fromenty B. Drug-induced liver injury through mitochondrial dysfunction: mechanisms and detection during preclinical safety studies. Fundam Clin Pharmacol. 2008;22:335-353.
3
Price KE, Pearce RE, Garg UC, et al. Effects of valproic acid on organic acid metabolism in children: a metabolic profiling study. Clin Pharmacol Ther. 2011;89:867-874.
4
Wilffert B, Altena J, Tijink L, et al. Pharmacogenetics of drug-induced birth defects: what is known so far? Pharmacogenomics. 2011;12:547-558.
5
Sinclair DB, Berg M, Breault R. Valproic acid-induced pancreatitis in childhood epilepsy: case series and review. J Child Neurol. 2004;19:498-502.
6
Nicolai J, Gunning B, Leroy PL, et al. Acute hepatic injury in four children with Dravet syndrome: valproic acid, topiramate or acetaminophen? Seizure. 2008;17:92-97.
7
Mindikoglu AL, King D, Magder LS, et al. Valproic acid-associated acute liver failure in children: case report and analysis of liver transplantation outcomes in the United States. J Pediatr. 2011;158:802-807.
8
Wood JR, Nelson-Degrave VL, Jansen E, et al. Valproate-induced alterations in human theca cell gene expression: clues to the association between valproate use and metabolic side effects. Physiol Genomics. 2005;20:233-243.
9
Chang P, Walker MC, Williams RS. Seizure-induced reduction in PIP3 levels contributes to seizure-activity and is rescued by valproic acid. Neurobiol Dis. 2014;62:296-306.
10
Belcastro V, D’Egidio C, Striano P, et al. Metabolic and endocrine effects of valproic acid chronic treatment. Epilepsy Res. 2013;107:1-8.
11
Fang J, Chen S, Tong N, et al. Metabolic syndrome among Chinese obese patients with epilepsy on sodium valproate. Seizure. 2012;21:578-582.
12
Liberati A, Altman DG, Tetzlaff J, et al. The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate health care interventions: explanation and elaboration. Ann Intern Med. 2009;151:65-94.
13
Goldberg-Stern H, Yaacobi E, Phillip M, et al. Endocrine effects of valproic acid therapy in girls with epilepsy: a prospective study. Eur J Paediatr Neurol. 2014;18:759-765.
14
Turan MI, Cayir A, Ozden O, et al. An examination of the mutual effects of valproic acid, carbamazepine, and phenobarbital on 25-hydroxyvitamin D levels and thyroid function tests. Neuropediatrics. 2014;45:16-21.
15
Yilmaz U, Yilmaz TS, Akinci G, et al. The effect of antiepileptic drugs on thyroid function in children. Seizure. 2014;23:29-35.
16
Sonmez FM, Zaman D, Aksoy A, et al. The effects of topiramate and valproate therapy on insulin, c-peptide, leptin, neuropeptide Y, adiponectin, visfatin, and resistin levels in children with epilepsy. Seizure. 2013;22:856-61.
17
Kim SH, Chung HR, Kim H, et al. Subclinical hypothyroidism during valproic acid therapy in children and adolescents with epilepsy. Neuropediatrics. 2012;43:135-139.
18
Kanemura H, Sano F, Maeda Y, et al. Valproate sodium enhances body weight gain in patients with childhood epilepsy: a pathogenic mechanisms and open-label clinical trial of behavior therapy. Seizure. 2012;21:496-500.
19
Verrotti A, Manco R, Agostinelli S, et al. The metabolic syndrome in overweight epileptic patients treated with valproic acid. Epilepsia. 2010;51:268-273.
20
Abaci A, Saygi M, Yis U, et al. Metabolic alterations during valproic acid treatment: a prospective study. Pediatr Neurol. 2009;41:435-439.
21
Attilakos A, Katsarou E, Prassouli A, et al. Thyroid function in children with epilepsy treated with sodium valproate monotherapy: a prospective study. Clin Neuropharmacol. 2009;32:32-34.
22
Verrotti A, Laus M, Scardapane A, et al. Thyroid hormones in children with epilepsy during long-term administration of carbamazepine and valproate. Eur J Endocrinol. 2009;160:81-86.
23
Rauchenzauner M, Haberlandt E, Scholl-Burgi S, et al. Effect of valproic acid treatment on body composition, leptin and the soluble leptin receptor in epileptic children. Epilepsy Res. 2008;80:142-149.
24
Rauchenzauner M, Haberlandt E, Scholl-Burgi S, et al. Adiponectin and visfatin concentrations in children treated with valproic acid. Epilepsia. 2008;49:353-357.
25
Cansu A, Serdaroglu A, Camurdan O, et al. The evaluation of thyroid functions, thyroid antibodies, and thyroid volumes in children with epilepsy during short-term administration of oxcarbazepine and valproate. Epilepsia. 2006;47:1855-1859.
26
Vainionpaa LK, Mikkonen K, Rattya J, et al. Thyroid function in girls with epilepsy with carbamazepine, oxcarbazepine, or valproate monotherapy and after withdrawal of medication. Epilepsia. 2004;45:197-203.
27
Guo C-Y, Ronen GM, Atkinson SA. Long-Term Valproate and Lamotrigine Treatment May Be a Marker for Reduced Growth and Bone Mass in Children with Epilepsy. Epilepsia. 2001;42:1141-1147.
28
Verrotti A, Domizio S, Angelozzi B, et al. Changes in serum lipids and lipoproteins in epileptic children treated with anticonvulsants. J Paediatr Child Health. 1997;33:242-245.
29
Komulainen T, Lodge T, Hinttala R, et al. Sodium valproate induces mitochondrial respiration dysfunction in HepG2 in vitro cell model. Toxicology. 2015;331:47-56.
30
Gokce S, Durmaz O, Celtik C, et al. Valproic acid-associated vanishing bile duct syndrome. J Child Neurol. 2010;25:909-911.
31
Larsen EP, Ostergaard JR. Valproate-induced hyperammonemia in juvenile ceroid lipofuscinosis (Batten disease). Seizure. 2014;23:429-434.
32
Knights MJ, Finlay E. The effects of sodium valproate on the renal function of children with epilepsy. Pediatr Nephrol. 2014;29:1131-1138.
33
Dhillon N, Hogler W. Fractures and Fanconi syndrome due to prolonged sodium valproate use. Neuropediatrics. 2011;42:119-121.
34
Bratton SL, Garden AL, Bohan TP, et al. A child with valproic acid-associated carnitine deficiency and carnitine-responsive cardiac dysfunction. J Child Neurol. 1992;7:413-416.
35
Verrotti A, D’Egidio C, Mohn A, et al. Antiepileptic drugs, sex hormones, and PCOS. Epilepsia. 2011;52:199-211.
36
Verrotti A, Loiacono G, Laus M, et al. Hormonal and reproductive disturbances in epileptic male patients: emerging issues. Reprod Toxicol. 2011;31:519-527.
37
Verrotti A, Agostinelli S, Parisi P, et al. Nonalcoholic fatty liver disease in adolescents receiving valproic acid. Epilepsy Behav. 2011;20:382-385.
38
Rauchenzauner M, Laimer M, Wiedmann M, et al. The novel insulin resistance parameters RBP4 and GLP-1 in patients treated with valproic acid: just a sidestep? Epilepsy Res. 2013;104:285-288.
39
Ogusu N, Saruwatari J, Nakashima H, et al. Impact of the superoxide dismutase 2 Val16Ala polymorphism on the relationship between valproic acid exposure and elevation of gamma-glutamyltransferase in patients with epilepsy: a population pharmacokinetic-pharmacodynamic analysis. PLoS One. 2014;9:e111066.
40
Coban D, Kurtoglu S, Akin MA, et al. Neonatal episodic hypoglycemia: a finding of valproic acid withdrawal. J Clin Res Pediatr Endocrinol. 2010;2:92-94.
41
ORIGINAL_ARTICLE
Effect of vitamin D supplementation on chronic liver disease: systematic literature review
Introduction: It is long known that vitamin D deficiency was common in patients with liver disease, but little is known on the therapeutic effects of vitamin D, especially in patients with chronic liver disease. In this study, we aimed to systematically review the literatures and study the evidences in which the effects of vitamin D supplementation had been investigated on the severity of chronic liver disease or liver cirrhosis.Methods: A systematic literature search was performed by using the following key terms “vitamin D supplementation” and “chronic liver disease” in the PubMed, Scopus and Google scholar to find relevant articles. After collecting the eligible documents, data were extracted and described based on the purpose of this review.Result: Of total 196 articles found, only 7 relevant documents with 518 studied patients were included. The results of this study showed that the levels of 25(OH) D were considerably lower in patients with chronic liver disease. Findings showed that vitamin D supplementation can rise up the mean serum level of 25(OH) D in patients with severe vitamin D deficiency, especially patients with liver cirrhosis.Conclusion:The results of this review showed that vitamin D deficiency is associated with the severity of liver disease and may have prognostic value in the assessment of liver disease. Also, it was shown that vitamin D supplementation may be helpful for the treatment of liver disease at least in certain groups of patients.
https://rcm.mums.ac.ir/article_7487_46fbd2152bc7a1ef8f6a7d643581fff6.pdf
2017-01-01
14
19
10.22038/rcm.2016.7487
Chronic hepatitis
Liver disease
Vitamin D
Vitamin D deficiency
Hooman
Mosannen Mozaffari
1
Department of Gastroenterology and Hepatology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Hosein Ali
Abbasi
abbasiha931@mums.ac.ir
2
Department of Gastroenterology and Hepatology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Ladan
Goshayeshi
goshayeshil@mums.ac.ir
3
Department of Gastroenterology and Hepatology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
LEAD_AUTHOR
Abbas
Esmaeelzadeh
esmaeelzadeha@mums.ac.ir
4
Department of Gastroenterology and Hepatology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Ali
Bahari
baharia@mums.ac.ir
5
Department of Gastroenterology and Hepatology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Ali
Mokhtarifar
mokhtarifara@mums.ac.ir
6
Department of Gastroenterology and Hepatology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Azita
Ganji
ganjia@mums.ac.ir
7
Department of Gastroenterology and Hepatology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Omid
Ghanaei
ghanaeio@mums.ac.ir
8
Department of Gastroenterology and Hepatology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Kambiz
Akhavan Rezayat
akhavanrk@mums.ac.ir
9
Department of Gastroenterology and Hepatology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Wacker M, Holick MF. Sunlight and Vitamin D: A global perspective for health. Dermatoendocrinol. 2013;5:51-108.
1
Miragliotta G, Miragliotta L. Vitamin D and infectious diseases. Endocr Metab Immune Disord Drug Targets. 2014;14:267-271.
2
Delvin E, Souberbielle JC, Viard JP, et al. Role of vitamin D in acquired immune and autoimmune diseases. Crit Rev Clin Lab Sci. 2014;51:232-247.
3
Bitetto D, Fabris C, Fornasiere E, et al. Vitamin D supplementation improves response to antiviral treatment for recurrent hepatitis C. Transpl Int. 2011;24:43-50.
4
Foroughi M, Maghsoudi Z, Ghiasvand R, et al. Effect of Vitamin D Supplementation on C-reactive Protein in Patients with Nonalcoholic Fatty Liver. Int J Prev Med. 2014;5:969-975.
5
Nair S. Vitamin d deficiency and liver disease. Gastroenterol Hepatol (N Y). 2010;6:491-493.
6
Luong K, Nguyen LT. Theoretical basis of a beneficial role for vitamin D in viral hepatitis. World J Gastroenterol. 2012;18:5338-5350.
7
Webb AR. Who, what, where and when-influences on cutaneous vitamin D synthesis. Prog Biophys Mol Biol. 2006;92:17-25.
8
El Husseiny NM, Fahmy HM, Mohamed WA, et al. Relationship between vitamin D and IL-23, IL-17 and macrophage chemoattractant protein-1 as markers of fibrosis in hepatitis C virus Egyptians. World J Hepatol. 2012;4:242-247.
9
Baur K, Mertens JC, Schmitt J, et al. Combined effect of 25-OH vitamin D plasma levels and genetic vitamin D receptor (NR 1I1) variants on fibrosis progression rate in HCV patients. Liver Liver Int. 2012;32:635-643.
10
Grünhage F, Hochrath K, Krawczyk M, et al. Common genetic variation in vitamin D metabolism is associated with liver stiffness. Hepatology. 2012;56:1883-1891.
11
Ding N, Yu RT, Subramaniam N, et al. A vitamin D receptor/SMAD genomic circuit gates hepatic fibrotic response. Cell. 2013;153:601-613.
12
Tanaka A, Nezu S, Uegaki S, et al. Vitamin D receptor polymorphisms are associated with increased susceptibility to primary biliary cirrhosis in Japanese and Italian populations. J Hepatol. 2009;50:1202-1209.
13
Kitson MT, Sarrazin C, Toniutto P, et al. Vitamin D level and sustained virologic response to interferon-based antiviral therapy in chronic hepatitis C: a systematic review and meta-analysis. J Hepatol. 2014;61:1247-1252.
14
Yokoyama S, Takahashi S, Kawakami Y, et al. Effect of vitamin D supplementation on pegylated interferon/ribavirin therapy for chronic hepatitis C genotype 1b: a randomized controlled trial. J Viral Hepat. 2014;21:348-356.
15
Villar LM, Del Campo JA, Ranchal I, et al. Association between vitamin D and hepatitis C virus infection: a meta-analysis. World J Gastroenterol. 2013;19:5917-5924.
16
Abramovitch S, Dahan-Bachar L, Sharvit E, et al. Vitamin D inhibits proliferation and profibrotic marker expression in hepatic stellate cells and decreases thioacetamide-induced liver fibrosis in rats. Gut. 2011;60:1728-1737.
17
Song BJ, Rockey DC. Status of research on vitamin D supplementation in treating or preventing liver fibrosis. Liver Int. 2013;33:653-655.
18
Iruzubieta P, Teran A, Crespo J, et al. Vitamin D deficiency in chronic liver disease. World J Hepatol. 2014;6:901-915.
19
Liberati A, Altman DG, Tetzlaff J, et al. The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate health care interventions: explanation and elaboration. Ann Intern Med. 2009;151:W65-94.
20
Finkelmeier F, Kronenberger B, Zeuzem S, et al. Low 25-Hydroxyvitamin D Levels Are Associated with Infections and Mortality in Patients with Cirrhosis. PLoS One. 2015;10:e0132119.
21
Ladero JM, Torrejon MJ, Sanchez-Pobre P, et al. Vitamin D deficiency and vitamin D therapy in chronic hepatitis C. Ann Hepatol. 2013;12:199-204.
22
Atsukawa M, Tsubota A, Shimada N, et al. Efficacy of Alfacalcidol on PEG-IFN/ Ribavirin Combination Therapy for Elderly Patients With Chronic Hepatitis C: A Pilot Study. Hepat Mon. 2013;13:e14872.
23
Malham M, Peter Jorgensen S, Lauridsen AL, et al. The effect of a single oral megadose of vitamin D provided as either ergocalciferol (D(2)) or cholecalciferol (D(3)) in alcoholic liver cirrhosis. Eur J Gastroenterol Hepatol. 2012;24:172-178.
24
Corey KE, Zheng H, Mendez-Navarro J, et al. Serum vitamin D levels are not predictive of the progression of chronic liver disease in hepatitis C patients with advanced fibrosis. PLoS One. 2012;7:e27144.
25
Malham M, Jorgensen SP, Ott P, et al. Vitamin D deficiency in cirrhosis relates to liver dysfunction rather than aetiology. World J Gastroenterol. 2011 21;17:922-925.
26
Rode A, Fourlanos S, Nicoll A. Oral vitamin D replacement is effective in chronic liver disease. Gastroenterol Clin Biol. 2010;34:618-620.
27
Putz-Bankuti C, Pilz S, Stojakovic T, et al. Association of 25-hydroxyvitamin D levels with liver dysfunction and mortality in chronic liver disease. Liver Int. 2012;32:845-851.
28
Barchetta I. Could vitamin d supplementation benefit patients with chronic liver disease? Gastroenterol Hepatol (N Y). 2012;8:755-757.
29
Kitson MT, Roberts SK. D-livering the message: the importance of vitamin D status in chronic liver disease. J Hepatol. 2012;57:897-909.
30
DiCecco SR, Wieners EJ, Wiesner RH, et al. Assessment of nutritional status of patients with end-stage liver disease undergoing liver transplantation. Mayo Clin Proc. 1989;64:95-102.
31
Singal AK, Kamath PS, Francisco Ziller N, et al. Nutritional status of patients with alcoholic cirrhosis undergoing liver transplantation: time trends and impact on survival. Transpl Int. 2013;26:788-794.
32
Stokes CS, Grunhage F, Baus C, et al. Vitamin D supplementation reduces depressive symptoms in patients with chronic liver disease. Clin Nutr. 2016;35:950-957.
33
Jorde R, Sneve M, Figenschau Y, et al . Effects of vitamin D supplementation on symptoms of depression in overweight and obese subjects: randomized double blind trial. Clin Nutr. 2016;35:950-957.
34
Manson JE, Bassuk SS, Lee IM, et al. The VITamin D and OmegA-3 TriaL (VITAL): rationale and design of a large randomized controlled trial of vitamin D and marine omega-3 fatty acid supplements for the primary prevention of cancer and cardiovascular disease. Contemp Clin Trials. 2012;33:159-171.
35
ORIGINAL_ARTICLE
Effects of erythropoietin on neurological performance of patients with traumatic brain injury: a systematic literature review
Introduction: Previous studies have indicated that administering erythropoietin (EPO) can have a beneficial impact on the clinical outcomes of patients with severe traumatic brain injury (TBI). This review examines the possible therapeutic effects EPO can have neuronal functions, neurological performance, and neurological recovery. Methods: The PubMed and Scopus databases were systematically searched on the 5th June, 2015, using the following search strategy: (“traumatic brain injury” OR “brain trauma”) AND (erythropoietin OR EPO) to identify relevant articles in which the effect of erythropoietin on patients with TBI was assessed. No time limitation was defined as the inclusion criteria. All available studies were extracted and categorized based on the purpose of this study.Result: Of the 908 articles in total that were identified during the initial database search, 901 documents were excluded from further examination because they did not meet the predefined inclusion/exclusion criteria. The total number of patients enrolled in the selected literature was 798. Of these, the use of EPO failed to show significant improvement in 113 patients.Discussion: Previous studies have shown that EPO may represent a valuable neuroprotectant that is useful in the treatment of neonatal brain injury, neurodegeneration, and TBI. Studies on animal TBI models have also found that recombinant human erythropoietin (rhEPO) reduces the development of post-traumatic brain edema.Conclusion: EPO may represent a potential therapeutic approach for the treatment of TBI. In addition, it can improve the patients› recovery prospects and reduce in-hospital mortality and morbidity.
https://rcm.mums.ac.ir/article_6480_8b2c2b7400afa75bf7128cae96f99338.pdf
2017-01-01
20
25
10.22038/rcm.2016.6480
Erythropoietin
Neuronal function
Neuroprotective agent
Traumatic brain injury
Gholamreza
Bahadorkhan
1
Department of Neurosurgery, Ghaem Hospital, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Omid
Daneshvarfard
2
Department of Neurosurgery, Ghaem Hospital, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
LEAD_AUTHOR
Graham D, Gennarelli T. Pathology of brain damage after head injury. Head Injury. 4th ed. New York, NY: McGraw-Hill;2000.
1
Povlishock JT, Becker DP, Cheng CL. Axonal change in minor head injury. J Neuropathol Exp Neurol. 1983;42:225-242.
2
Katayama Y, Becker DP, Tamura T, et al. Massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury. J Neurosurg. 1990;73:889-900.
3
Murthy T, Bhatia P, Sandhu K, et al. Secondary brain injury: Prevention and intensive care management. Indian J Neurotrauma. 2005;2:7-12.
4
Xiong Y, Mahmood A, Chopp M. Emerging treatments for traumatic brain injury. Expert Opin Emerg Drugs. 2009;14:67-84.
5
Liberati A, Altman DG, Tetzlaff J, et al. The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate health care interventions: explanation and elaboration. Annals Intern Med. 2009;151:W-65-W-94.
6
Robertson CS, Hannay HJ, Yamal JM, et al. Effect of erythropoietin and transfusion threshold on neurological recovery after traumatic brain injury: a randomized clinical trial. JAMA. 2014;312:36-47.
7
Min K, Song J, Lee JH, et al. Allogenic umbilical cord blood therapy combined with erythropoietin for patients with severe traumatic brain injury: three case reports. Restor Neurol Neurosci. 2013;31:397-410.
8
Talving P, Lustenberger T, Inaba K, et al. Erythropoiesis-stimulating agent administration and survival after severe traumatic brain injury: a prospective study. Arch Surg. 2012;147:251-255.
9
Abrishamkar S, Safavi M, Honarmand A. Effect of erythropoietin on Glasgow Coma Scale and Glasgow Outcome Sale in patient with diffuse axonal injury. J Res Med Sci. 2012;17:51-56.
10
Nirula R, Diaz-Arrastia R, Brasel K, et al. Safety and efficacy of erythropoietin in traumatic brain injury patients: a pilot randomized trial. Crit Care Res Pract. 2010;2010.
11
Talving P, Lustenberger T, Kobayashi L, et al. Erythropoiesis stimulating agent administration improves survival after severe traumatic brain injury: a matched case control study. Ann Surg. 2010;251:1-4.
12
Shein NA, Grigoriadis N, Alexandrovich AG, et al. Differential neuroprotective properties of endogenous and exogenous erythropoietin in a mouse model of traumatic brain injury. J Neurotrauma. 2008;25:112-123.
13
Merelli A, Czornyj L, Lazarowski A. Erythropoietin: a neuroprotective agent in cerebral hypoxia, neurodegeneration, and epilepsy. Curr Pharm Des. 2013;19:6791-67801.
14
Traudt CM, Juul SE. Erythropoietin as a neuroprotectant for neonatal brain injury: animal models. Methods Mol Biol. 2013;982:113-126.
15
Xiong T, Qu Y, Mu D, et al. Erythropoietin for neonatal brain injury: opportunity and challenge. Int J Dev Neurosci. 2011;29:583-591.
16
Verdonck O, Lahrech H, Francony G, et al. Erythropoietin protects from post-traumatic edema in the rat brain. J Cereb Blood Flow Metab. 2007;27:1369-1376.
17
Byts N, Siren AL. Erythropoietin: a multimodal neuroprotective agent. Exp Transl Stroke Med. 2009;1:4.
18
Zhao J, Li G, Zhang Y, et al. The potential role of JAK2/STAT3 pathway on the anti-apoptotic effect of recombinant human erythropoietin (rhEPO) after experimental traumatic brain injury of rats. Cytokine. 2011;56:343-350.
19
Liao ZB, Jiang GY, Tang ZH, et al. Erythropoietin can promote survival of cerebral cells by downregulating Bax gene after traumatic brain injury in rats. Neurol India. 2009;57:722-728.
20
Hellewell SC, Yan EB, Alwis DS, et al. Erythropoietin improves motor and cognitive deficit, axonal pathology, and neuroinflammation in a combined model of diffuse traumatic brain injury and hypoxia, in association with upregulation of the erythropoietin receptor. J Neuroinflammation. 2013;10:156.
21
Jin W, Kong J, Lu T, et al. Erythropoietin prevents secondary brain injury induced by cortical lesion in mice: possible involvement of Nrf2 signaling pathway. Ann Clin Lab Sci. 2011;41:25-32.
22
Xiong Y, Mahmood A, Qu C, et al. Erythropoietin improves histological and functional outcomes after traumatic brain injury in mice in the absence of the neural erythropoietin receptor. J Neurotrauma. 2010;27:205-215.
23
Peng W, Xing Z, Yang J, et al. The efficacy of erythropoietin in treating experimental traumatic brain injury: a systematic review of controlled trials in animal models. J Neurosurg. 2014;121:653-664.
24
Kabadi SV, Faden AI. Neuroprotective strategies for traumatic brain injury: improving clinical translation. Int J Mol Sci. 2014;15:1216-236.
25
Nichol A, French C, Little L, et al. Erythropoietin in traumatic brain injury: study protocol for a randomised controlled trial. Trials. 2015;16:39.
26
ORIGINAL_ARTICLE
C4d and C3d immunohistochemical evaluation on formalin-fixed paraffin-embedded tissue for the diagnosis of bullous pemphigoid: systematic review of the literatures
Introduction: Several methods are available for the diagnosis of autoimmune bullous disease. Since the immunohistochemistry of complement component is easy and more accessible compared to other methods, it is thought that this technique as an efficient method can replace other difficult, and time-consuming procedures. Therefore, in this study we aimed to systematically review the literatures in which the diagnostic value of complement component 3d (C3d) and C4d had been investigated in bullous pemphigoid. Methods: A systematic search was conducted in the PubMed, Google scholar, and Scopus using following search method (((C3d OR C4d OR complement component 3d OR complement component 4d immunohistochemistry)) OR (C3d OR C4d marker OR complement component 3d OR complement component 4d marker)) AND (bullous pemphigoid OR cutaneous pemphigoid) to evaluate the diagnostic value of C3d and/or C4d for early and accurate detection of bullous pemphigoid on November 2015. Subsequently, the extracted data were described.Result: Total of 28 documents were collected and reviewed based on the purpose of this study. Of the collected articles, 21 documents were excluded in several steps of article selection process and only 7 relevant articles were included for data assessment. The results showed that the deposits of C3d and/or C4d in skin biopsies were found in 125 of 134 patients, indicating that immunohistochemistry is a reliable technique for the diagnosis of inflammatory skin diseases.Conclusion: The results of this review showed that C3d and/or C4d immunohistochemistry in skin biopsies is a reliable technique for the diagnosis of inflammatory skin diseases, particularly bullous pemphigoid.
https://rcm.mums.ac.ir/article_6822_0d3e22f1456c8019d0c3ecade1699585.pdf
2017-01-01
26
30
10.22038/rcm.2016.6822
Bullous pemphigoid
Complement Component 3d
Complement C4d
immunohistochemistry
Mahsa
Akbari Oryani
1
Department of Pathology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Masomeh
Safaei
safaeim911@mums.ac.ir
2
Department of Pathology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
LEAD_AUTHOR
Farzane
Farzam
3
Department of Pathology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Hadi
Razmara
4
Department of Pathology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Navid
Fathi
naveedfathee@yahoo.com
5
Department of Pathology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Yeh SW, Ahmed B, Sami N, et al. Blistering disorders: diagnosis and treatment. Dermatol Ther. 2003;16:214-223.
1
Mutasim DF. Therapy of autoimmune bullous diseases. Ther Clin Risk Manag. 2007;3:29-40.
2
Sagi L, Baum S, Agmon-Levin N, et al. Autoimmune bullous diseases the spectrum of infectious agent antibodies and review of the literature. Autoimmun Rev. 2011;10:527-535.
3
Bickle K, Roark TR, Hsu S. Autoimmune bullous dermatoses: a review. Am Fam Physician. 2002;65:1861-1870.
4
Cozzani E, Parodi A, Rebora A, et al. Bullous pemphigoid in Liguria: a 2-year survey. J Eur Acad Dermatol Venereol. 2001;15:317-319.
5
Gudi VS, White MI, Cruickshank N, et al. Annual incidence and mortality of bullous pemphigoid in the Grampian Region of North-east Scotland. Br J Dermatol. 2005;153:424-427.
6
Schmidt E, Zillikens D. Modern diagnosis of autoimmune blistering skin diseases. Autoimmun Rev. 2010;10:84-89.
7
Colbert RL, Allen DM, Eastwood D, et al. Mortality rate of bullous pemphigoid in a US medical center. J Invest Dermatol. 2004;122:1091-1095.
8
Roujeau JC, Lok C, Bastuji-Garin S, et al. High risk of death in elderly patients with extensive bullous pemphigoid. Arch Dermatol. 1998;134:465-469.
9
Damoiseaux J. Bullous skin diseases: classical types of autoimmune diseases. Scientifica (Cairo). 2013;2013:457982.
10
Liberati A, Altman DG, Tetzlaff J, et al. The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate health care interventions: explanation and elaboration. Ann Intern Med. 2009;151:W65-94.
11
Villani AP, Chouvet B, Kanitakis J. Application of C4d Immunohistochemistry on Routinely Processed Tissue Sections for the Diagnosis of Autoimmune Bullous Dermatoses. Am J Dermatopathol. 2016;38:186-188.
12
Velez AMA, Googe Jr PB, Howard MS. Immunohistochemistry versus immunofluoresence in the diagnosis of autoimmune blistering diseases. Our Dermatol Online. 2013;4:585-595.
13
Kwon EJ, Ntiamoah P, Shulman KJ. The utility of C4d immunohistochemistry on formalin-fixed paraffin-embedded tissue in the distinction of polymorphic eruption of pregnancy from pemphigoid gestationis. Am J Dermatopathol. 2013;35:787-791.
14
Zimmer V, Muller CS, Juengling B, et al. Esophageal intramural pseudodiverticulosis in mucous membrane pemphigoid: potential diagnostic utility of C4d immunohistochemistry. Dig Endosc. 2012;24:487.
15
Pfaltz K, Mertz K, Rose C, et al. C3d immunohistochemistry on formalin-fixed tissue is a valuable tool in the diagnosis of bullous pemphigoid of the skin. J Cutan Pathol. 2010;37:654-658.
16
Chandler W, Zone J, Florell S. C4d immunohistochemical stain is a sensitive method to confirm immunoreactant deposition in formalin-fixed paraffin-embedded tissue in bullous pemphigoid. J Cutan Pathol. 2009;36:655-659.
17
Magro CM, Dyrsen ME. The use of C3d and C4d immunohistochemistry on formalin-fixed tissue as a diagnostic adjunct in the assessment of inflammatory skin disease. J Am Acad Dermatol. 2008;59:822-833.
18
Haga H, Egawa H, Fujimoto Y, et al. Acute humoral rejection and C4d immunostaining in ABO blood type-incompatible liver transplantation. Liver Transpl. 2006;12:457-464.
19
Aguilera I, Sousa JM, Gavilan F, et al. Complement component 4d immunostaining in liver allografts of patients with de novo immune hepatitis. Liver Transpl. 2011;17:779-788.
20
Yang DH, Chang DM, Lai JH, et al. Usefulness of erythrocyte-bound C4d as a biomarker to predict disease activity in patients with systemic lupus erythematosus. Rheumatology (Oxford). 2009;48:1083-1087.
21
Kao AH, McBurney CA, Sattar A, et al. Relation of platelet C4d with all-cause mortality and ischemic stroke in patients with systemic lupus erythematosus. Transl Stroke Res. 2014;5:510-518.
22
Mehta N, Uchino K, Fakhran S, et al. Platelet C4d is associated with acute ischemic stroke and stroke severity. Stroke. 2008;39:3236-3241.
23
Navratil JS, Manzi S, Kao AH, et al. Platelet C4d is highly specific for systemic lupus erythematosus. Arthritis Rheum. 2006;54:670-674.
24
Kun GUO , GENG S-m. Detection of C3d expression in bullous pemphigoid. Chinese J Dermatol. 2012;45:364-365.
25
Khandpur S, Verma P. Bullous pemphigoid. Indian J Dermatol Venereol Leprol. 2011;77:450-455.
26
ORIGINAL_ARTICLE
Reflex epilepsy: a review
Interesting phenomena of reflex epileptic syndromes are characterized by epileptic seizures each one induced by specific stimulus with a variety of types. Simple triggers, which lead to seizures within seconds, are of sensory type (most commonly visual, most rarely tactile or proprioceptive stimuli). Complex triggers, which are mostly of cognitive type such as praxis, reading, talking, and music, usually induce the epileptic event within minutes. It should differ from what most epileptic patients report as provocative precipitants for seizures (such as emotional stress, fatigue, fever, sleep deprivation, alcohol, and menstrual cycle). The identification of a specific trigger is not only important for patients or their parents to avoid seizures, but also it might help neurologists to choose the most effective antiepileptic drug for each case. In addition, research in this area may possibly reveal some underlying pathophysiology of epileptic phenomena in the brain.In this review, we briefly introduce reported reflex epileptic seizures, their clinical features and management.
https://rcm.mums.ac.ir/article_6827_f6a20de7d612c6e1554f9ee5e98c5387.pdf
2017-01-01
31
34
10.22038/rcm.2016.6827
Reflex epilepsy
Reflex seizures
Triggers
Karim
Nikkhah
nikkhahk@mums.ac.ir
1
Department of Neurology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Mohammad Taghi
Farzadfard
farzadfardmt@mums.ac.ir
2
Department of Neurology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Fariborz
Rezaeitalab
rezaeetalab@yahoo.com
3
Department of Neurology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
LEAD_AUTHOR
Engle JR, Pedley TA. EPILEPSY, A Comprehensive Textbook. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2008.
1
Italiano D, Ferlazzo E, Gasparini S, et al. Generalized versus partial reflex seizures: a review. Seizure. 2014;23:512-520.
2
Wolf P, Koepp M. Reflex epilepsies. Handb Clin Neurol. 2012;107:257-276.
3
Kasteleijn-Nolst Trenité DG, Pinto D, Hirsch E, et al. photosensitivity, visual induced seizures and pileptic syndromes. In: Roger J, Bureau M, Dravet C, et al., editors. Epileptic syndromes in infancy, Childhood and adolescence. 4th ed. Montrouge: John Libbey Eurotext; 2005.p. 395-422.
4
Sandhya M, Bharath RD, Panda R, et al. Understanding the pathophysiology of reflex epilepsy using simultaneous EEG-fMRI. Epileptic Disord. 2014;16:19-29.
5
Carballosa-Gonzalez MM, Muñoz LJ, López-Alburquerque T, et al. EEG characterization of audiogenic seizures in the hamster strain GASH:Sal. Epilepsy Res. 2013;106:318-325.
6
Ilik F, Pazarli AC. Reflex Epilepsy Triggered by Smell. Clin EEG Neurosci. 2015;46:263-265.
7
Blauwblomme T, Kahane P, Minotti L, et al. Multimodal imaging reveals the role of γ activity in eating-reflex seizures. J Neurol Neurosurg Psychiatry. 2011;82:1171-1173.
8
Herrick CE, Jeavons PM, Harding GF. Proceedings: Study of a photosensitive family. Electroencephalogr Clin Neurophysiol. 1975;39:428.
9
Baykan B, Matur Z, Gürses C, et al. Typical absence seizures triggered by photosensitivity. Epilepsia. 2005;46:159-163.
10
Oguni H, Hayashi K, Awaya Y, et al. Severe myoclonic epilepsy in infants--a review based on the Tokyo Women’s Medical University series of 84 cases. Brain Dev. 2001;23:736-348.
11
Ikeda H, Imai K, Ikeda H, et al. Lamotrigine is favourable for startle-induced seizures. Epileptic Disord. 2011;13:277-383.
12
Wolf P, Inoue Y. Complex reflex epilepsies: reading epilepsy and praxis induction. In: Roger J, Bureau M, Dravet C, et al, editors. Epileptic syndromes in infancy, Childhood and adolescence. 4th ed. Montrouge: John Libbey Eurotext; 2005.p.347-358.
13
Engel J Jr. A proposed diagnostic scheme for people with epileptic seizures and with epilepsy: report of the ILAE Task Force on Classification and Terminology. Epilepsia. 2001;42:796-803.
14
Aguglia U, Tinuper P, Gastaut H. Startle-induced epileptic seizures. Epilepsia. 1984;25:712-720.
15
Faught E. Lamotrigine for startle-induced seizures. Seizure. 1999;8:361-363.
16
Labate A, Barone R, Gambardella A, et al. Startle epilepsy complicating aspartylglucosaminuria. Brain Dev. 2004;26:130-133.
17
Caraballo R, Semprino M, Cersósimo R, et al. Hemiparetic cerebral palsy and startle epilepsy. Rev Neurol. 2004-31;38:123-127.
18
Stern J. Musicogenic epilepsy. Handb Clin Neurol. 2015;129:469-477.
19
Maguire MJ. Music and epilepsy: a critical review. Epilepsia. 2012;53:947-961.
20
Ferlazzo E, Zifkin BG, Andermann E, et al. Cortical triggers in generalized reflex seizures and epilepsies. Brain. 2005;128:700-710.
21
Nevler N, Gandelman-Marton R. Acute provoked reflex seizures induced by thinking. Neurologist. 2012;18:415-417.
22
Brick JF, Gutrecht JA, Ringel RA. Reflex epilepsy and nonketotic hyperglycemia in the elderly: a specific neuroendocrine syndrome. Neurology. 1989;39:394-399.
23
Satishchandra P. Hot-water epilepsy. Epilepsia. 2003;44 1:29-32.
24
Grosso S, Farnetani MA, Francione S, et al. Hot water epilepsy and focal malformation of the parietal cortex development. Brain Dev. 2004;26:490-493.
25
Satishchandra P, Dilipkumar S, Subbakrishna DK, et al. Intermittent clobazam prophylaxis in hot water epilepsy is safe and effective: a prospective study. Epilepsy Res. 2014;108:1238-1242.
26
Ilik F, Pazarli AC. Reflex Epilepsy Triggered by Smell. Clin EEG Neurosci. 2014.
27
Xue LY, Ritaccio AL. Reflex seizures and reflex epilepsy. Am J Electroneurodiagnostic Technol. 2006;46:39-48.
28
Iriarte J, Sánchez-Carpintero R, Schlumberger E, et al. Gait epilepsy. A case report of gait-induced seizures. Epilepsia. 2001;42:1087-1090.
29
ORIGINAL_ARTICLE
Different methods for assessment of nutritional status in newborn infants based on physical and anthropometric indexes: a short review article
Several complications during childhood is associated with nutritional status of infants at birth. Therefore, nutritional status of newborns must be evaluated properly after birth. Assessment of the nutritional status of neonates based on anthropometric and physical indices is simple and inexpensive without the need for advanced medical equipment. However, no previous studies have focused on the assessment methods of the nutritional status of infants via anthropometric and physical indices. This study aimed to review some of the key methods used to determine the nutritional status of neonates using anthropometric and physical indices. To date, most studies have focused on the diagnosis of fetal malnutrition (FM) and growth monitoring. In order to diagnose FM, researchers have used growth charts and Ponderal index (PI) based on anthropometric indices, as well as Clinical Assessment of Nutritional (CAN) Score based on physical features. Moreover, in order to assess the growth status of infants, growth charts were used. According to the findings of this study, standard intrauterine growth curves and the PI are common measurement tools in the diagnosis of FM. Furthermore, CAN score is widely used in the evaluation of the nutritional status of neonates. Given the differences in the physical features of term and preterm infants, this index should be adjusted for preterm neonates. Longitudinal growth charts are one of the most prominent methods used for monitoring of the growth patterns of infants.
https://rcm.mums.ac.ir/article_7520_b441b54252637151ff3bca2e11a4c6be.pdf
2017-01-01
35
38
10.22038/rcm.2016.7520
fetal
Growth Chart
Infant
Malnutrition
Newborn
Ali Asghar
Rashidi
ali.rashidi.1749@gmail.com
1
Department of Nutrition, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Abdolreza
Norouzy
rashidiaa931@mums.ac.ir
2
Department of Nutrition, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
LEAD_AUTHOR
Bahare
Imani
3
Department of Pediatrics, NICU Dr.Sheikh Hospital, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Mohsen
Nematy
4
Department of Nutrition, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Mohammad
Heidarzadeh
heidarzadehm1@mums.ac.ir
5
Department of Pediatrics, Tabriz University of Medical Sciences, Director of Department of Neonatal Health, Ministry of Health and Medical Education, Tabriz, Iran.
AUTHOR
Ali
Taghipour
taghipoura@mums.ac.ir
6
Department of Biostatistics and Health Sciences Research Center, School of Health, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Korkmaz A, Teksam Ö, Yurdakök M, et al. Fetal malnutrition and its impacts on neonatal outcome in preterm infants.Turk J Pediatr. 2011;53:261-268.
1
Neel N, Alvarez J. Risk factors of fetal malnutrition in a group of Guatemalan mothers and neonates. Bol Oficina Sanit Panam. 1991;110:93-107.
2
Fall CH. Fetal malnutrition and long-term outcomes. Nestle Nutr Inst Workshop Ser. 2013;74:11-25.
3
Joosten KF, Hulst JM. Malnutrition in pediatric hospital patients: current issues. Nutrition. 2011;27:133-137.
4
Kim S, Fleisher BM, Sun JY. The Long-term Health Effects of Fetal Malnutrition: Evidence from the 1959-1961 China Great Leap Forward Famine. Health Econ. 2016
5
Nair L, Nair M, Chacko D. Markers of fetal onset adult diseases. Indian Pediatr. 2009;46:s48-s54.
6
Adebami OJ, Owa J. Comparison between CANSCORE and other anthropometric indicators in fetal malnutrition. Indian J Pediatr. 2008;75:439-442.
7
Borisut P, Kovavisarach E. Standard intrauterine growth curve of Thai neonates delivered at Rajavithi hospital. J Med Assoc Thai. 2014;97:798-803.
8
Fenton TR, Kim JH. A systematic review and meta-analysis to revise the Fenton growth chart for preterm infants. BMC Pediatr. 2013;13:59.
9
Schaffrath Rosario A, Kurth BM. Regional differences in the prevalence of overweight and obesity at school entry in Germany : reality or artifact?. Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz. 2009;52:643-646.
10
de Onis M, Onyango AW. WHO child growth standards. Lancet. 2008;371:204.
11
Niklasson A, Engström E, Hård A-L, et al. Growth in very preterm children: a longitudinal study. Pediatr Res. 2003;54:899-905.
12
Bertino E, Spada E, Occhi L, et al. Neonatal anthropometric charts: the Italian neonatal study compared with other European studies. J Pediatr Gastroenterol Nutr. 2010;51:353-361.
13
Gaillard R, Jaddoe VW. Assessment of fetal growth by customized growth charts. Ann Nutr Metab. 2014;65:149-155.
14
Organization WH. Physical status: The use of and interpretation of anthropometry, Report of a WHO Expert Committee. World Health Organ Tech Rep Ser. 1995;854:1-452.
15
Dhanorkar A, Bagdey P, Humne A, et al. Detection and comparison of foetal malnutrition by CANSCORE and other methods with birth weight as a gold standard. Healthline. 2014;5:24-28.
16
Ezenwa BN, Ezeaka VC, Iroha E, et al. Determination of Fetal malnutrition in preterm newborns. J Food Nutr Sci. 2013;1: 50-56.
17
Pereira-da-Silva L, Virella D. Is intrauterine growth appropriate to monitor postnatal growth of preterm neonates? BMC Pediatr. 2014;17;14:14.
18
Groveman SA. New Preterm Infant Growth Curves Influence of Gender and Race on Birth Size. (Master’s Thesis), Drexel University, Philadelphia, PA, 2008.
19
Nanoti G, Kamal S. Clinical Assessment of Foetal Malnutrition using’CAN Score’in Full Term Neonates. International Journal of Neurology and Neurosurgery. 2015;7:49.
20
Soundarya M, Basavaprabhu A, Raghuveera K, et al. Comparative Assessment of Fetal Malnutrition by Anthropometry and CAN Score. Iran J Pediatr. 2012;22:70-76.
21
Walther F, Ramaekers L. The ponderal index as a measure of the nutritional status at birth and its relation to some aspects of neonatal morbidity. J Perinat Med. 1982;10:42-47
22
Verhoeff FH, Brabin BJ, van Buuren S, et al. An analysis of intra-uterine growth retardation in rural Malawi. Eur J Clin Nutr. 2001;55:682-689.
23
Lubchenco LO, Hansman C, Boyd E. Intrauterine growth in length and head circumference as estimated from live births at gestational ages from 26 to 42 weeks. Pediatrics. 1966;37:403-408.
24
Singhal V, Agal P, Kamath N. Detection of Fetal Malnutrition by CAN Score at birth and its comparision with other methods of determining intrauterine growth. Indian J Clin Prac. 2012;22:576-582.
25
Olsen IE, Lawson ML, Meinzen-Derr J, et al. Use of a body proportionality index for growth assessment of preterm infants. J Pediatr. 2009;154:486-491.
26
Kramer MS, Olivier M, McLean FH, et al. Impact of intrauterine growth retardation and body proportionality on fetal and neonatal outcome. Pediatrics. 1990;86:707-713.
27
Crane J, Kopta M. Comparative newborn anthropometric data in symmetric versus asymmetric intrauterine growth retardation. Am J Obstet Gynecol. 1980;138:518-522.
28
Mei Z, Grummer-Strawn LM, Pietrobelli A, et al. Validity of body mass index compared with other body-composition screening indexes for the assessment of body fatness in children and adolescents. Am J Clin Nutr. 2002;75:978-985.
29
Korkmaz A, Teksam O, Yurdakök M, et al. Fetal malnutrition and its impacts on neonatal outcome in preterm infants. Turk J Pediatr. 2011;53:261-268.
30
Deodhar J, Jarad R. Study of the prevalence of and high risk factors for fetal malnutrition in term newborns. Ann Trop Paediatr. 1999;19:273-277.
31
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ORIGINAL_ARTICLE
Risks associated with preeclampsia: possible mechanisms
Findings have shown that low serum 25-hydroxy vitamin D level is a possible risk factor for incidence of preeclampsia during pregnancy. Vitamin D has important effects on multiple biological pathways, including angiogenesis. Some studies have shown that vitamin D deficiency is highly prevalent among women suffering from preeclampsia, influencing immune modulation and vascular function. Evidence has shown that an imbalance of pro-antigenic and anti-angiogenic proteins can be considered as a possible etiological factor in the development of preeclampsia. Besides, there is a series of studies linking the renin–angiotensin aldosterone system (RAAS) with preeclampsia. In this article, we review the current studies evaluating the association between maternal vitamin D status and vascular health, metabolism, placental immune function and the risk of preeclampsia. We provided evidence of the different factor involved in the metabolism of vitamin D and vitamin D receptor (VDR) expression, gene regulations, immune function, and chronic disease when vitamin D is used optimally.
https://rcm.mums.ac.ir/article_8234_8f9f53d1cb9acb7de38d7d21aa1dd84f.pdf
2017-01-01
39
44
10.22038/rcm.2017.13735.1156
Preeclampsia
Vascular Endothelial Growth Factor (VEGF)
Vitamin D
Bentolhoda
Sahebnasagh
hoda.sahebnasagh@gmail.com
1
Department of Community Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran.
AUTHOR
Mohammad Javad
Hosseinzadeh-Attar
mhosseinzadeh@tums.ac.ir
2
Department of Clinical Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran.
LEAD_AUTHOR
Amrollah
Sharifi
a.sharifi1983@gmail.com
3
Golestan Research Center of Gastroenterology and Hepatology- GRCGH, Golestan University of Medical Sciences, Gorgan, Iran.
AUTHOR
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