repens RTC Vol sao BRA (MCV) sb aK RARE Fl DW) ol Ae Bin) PH eee Saf Soe - SRR eS = Abstract ~ Classification of Anemias by Mean Corpuseular Volumne(MCV) and Red Cell Volume Distribution Width (RDW) Bog Yi Kim, MD., Chang Kon Kim, M.D., Hye S00 Lee, M.D., Sam Im Choi. M.D. Department of Clinteal Pathology, Chonbuk National University Hospital Chonju, Korea ‘To investigate the significance of classification of anemias by mean corpuscular volume (MCY) and red cell volume distribution width(RDW) in the complete blood count(CBC) of the peripheral blood obtained with a Coulter Counter Model $ Plus Tl, the authors performed this study. ‘Materials used in this study were 532 cases of inpatients and outpatients of Chon- ‘Duk Nationel University Hospital, including 144 cases of nonanemic group with nor- mal hemoglobin level and 388 cases of anemic group with low hemoglobin level(less than 14g/d) for mele, and less than 12 g/dl for female). Anemic group was dassified as causing disorder. mean levels of MCV and RDW were calculated in regard to every disorder, and analyzed. Results are as follows 1, Nonanemic group fad normal MCV and normal RDW (homogeneous normocytic), and among the anemic group, normal RDW were observed in chronic diseases such a diabetes, tuberculosis, chronic renal failure, and congestive heart failure, malignant solid tumor, infectious disease, such as salmonellosis and pneumonia, burn, posthemorrbagic state, and idiopathic thrombocytopenic parpura, Acute lymphocytic and myelocytic leukemia, chronic myelogeneous leukemia, chronic Liver diseases, cardiac diaeases as valvular disorder had normal MCV and high RDW (heterogeneous normocytic), 2, Iron deficiency anemia was heterogeneous microcytic(low MCV and high RDW) and aplastic anemia was homogeneous macrocstic(high MCV and normal RDW). 3, Disorders of anciaias with low MCV and normal RDW (homogenecus microcytic) and high MCV and high RDW (heterogenous mecrocytic) were not included in this study. SpyKea + 7a 1 108TH 4, MCH showed similar findings 28 MCV, and MCHC was within norma 1 limits ix all diseases, 20 these indices didn't have additional significance was not authorized Tn conclusion, we suggest that MCV and RDW are useful indicators for correct classification of anemias and these are helpful for the carly diagnosis and treatment ‘of anemias, 4 8 alald we dW) dala Fede Asia a Fas Vath MAGS 5S Waa oe ade 142 Viet, ATtede AaT ea CERO: volume of psckes red cole) 7} $& Qed Age 2 Le ade Uae a gues bly Ut wad Ue, late AMA, Sool TY LAE AA Seah a, “19 34 Ula WAL Te ANT EA ICV: sean corpascular volame)?3} -b4}4| 4 (retieale- enorhe] 470] 29 Anse, Yedda GU4e By, aap ale ASS aTAeaA SUA 24at+ Ad 424 Ava Wades = SAAS As| ALR Aedaesa aay ydada de and Bee e+ dA SD, AGT LAV IRDW: sod call volume dietrtbe- ‘ion wideh)®& “IQ 214) 01-149 theterozencity) Ute Ansy Paved eT TE 2 (anisocytosis)s} AEE LAAF (CV? contticient of variation) 24 EAL Adel, aS MOV A IE ¢ devas qAeTaduss wee Eee ARg 18 FEE DANI”. cle ANE AS APSA Ade Ae a Jia) £9 conlter counter Model S plus Te} sai) BIA BALTAACEC: complete bbl count)€ 0) £a]a} oie] EBM MCV St ROWS end dee Veen, $4 Daa amad xad bate avaae. A= a eel eae eld aa aA a PAT HIE FANS FEI4 VS WOT AES Moe BHA. Waa BaP eS ade AA WS Uos/dd, dae 12.00/dl=1e Salen, al ada tae we ale 4. EU UAEE 3 deel deh date meat Ye, FM, GM, WBA, SUAS 2) 4AM EA, A712) GaSe) See, Bite age Dida il, say ae 4 s4aael ola, Genta ses Adee w ol, 28s Sal Ia See] va, aS 29) bl da Fed dtgion, lat Bae 4 Natdde mda diddadad. ea ale Lada Wee oo, Aatee Ye 7 4, SAV GUNS Bd, FASTA MWA va, VIETA Vel of, ee eae! ANS] BM, 2a 21484 1, 229 Wie WTAGtast spa ae Ba AMSA BH Vea Coulter Counter Model § plus 1 (Coulter Rlectronies, Hialea, $1) So1SHHH. 9] Bal sty Ga esa Ate Av Mg dad Adee, wae cyanmethemoglobin ol 4s, AQTERAC) 2 Aye ARS AS TIS SAG A hae A AA ARS BI AAA FAA, Al Ts EAS AUF Aaeael(eed cell bisiokramel A a4 Movs} RDW2} alse ves}. 4, NOV AAG Aza WE impulses) 21k Sed AMF Fe ye] Ads, ROWE AF Ze 2B eda PIFG/oe4 #2 Seed o) AQF \Aszee Added Ay Ganeslan ee ESAFEM Hd AYA MCV ootIOfl 92 DW 19.61.27) Beh. leh BEATE (MICH: moan corpusealar hemoglobin), 3329). AAS (NCHC: mean corpuscular Kemoelohin concentration) 4¥7-$<(HCT: Lemasoerit)»| = MCV, REC aslz 2ala(Hebbel Ata sis} 20 Ada ay RBCxMCY, D HOTGs)= =tt=mi Ph RMaARMRETA CVD) Ses AELR Ae RDW)e) ett Sst FAR — wcrcagsay) =P aos 23 ALIS aol GE Vea PAE Tle zaas ah 1, BUFS(RBC) ARFEE ABTA 4740.7x Del Vl WA MRSE GPE 35x UL 2 AAS, 250 a4204 1a, 28, 2a Ta etd Qala 4a2 SaAe 25x ioyAl ds wala east. 2, a SNGICT) Bay ge Wad) alessio, WAS SA BRAY WIA BeADeA, Yo AL AAU, WII UG, 22, zee Fe yo ME UI Bee Dadts are Le AS Bae, 3, BRNBT Wale (NCH) ARART QHeAE dat] 91L6SpE a on) eee HAE IS P4a AL Ags oy Asad WA Aol 5,745.92 e A SAagia, WAWS Madde 20.048.07e 2 Brad qe ooh 4, SENET @eiats= (MCC) Beaat qqseee Gees) sh eks.relal geod ees ad Ba zea P42 TEL a. 5. HMACHSD) QB Bea lA CASE LED S/d A y UE QAGS a fel Ios/dL ela a aged, Saag wa, aaeed Ue, =F AMY SAAS ToCAL TS Qed BA. 6, UERRT SAMY) Agquy ge dae) gid sided, 1 ‘Tuble 1, Hematologic daa of anemic disorders( 1) Diagnosis amber. RECQ«1OY/aL) —_Kebte/éL) Hees) Nonesenie grout 1a a0? 11.626.9 ‘Anemie group 385 ‘Chronic disenee of diabetes, renal failure uberealosizete 18 31408 sobet 328.2 Malignant solid sumer ot 28.255.1 Chronie Tver disease 6 19.1202 Infections disease a 28.214.6 Cardiac diasease 6 Posthonorrbaie stato a Bam 4 Iiypothyroidion 1 Iron éelicieney anemia ~ ‘Aplastic anemia 7 ‘digpatbie thrombocytopenic purpura 8 Acute mysleegtie Teukemia RB ‘Acute Iymphoeytic leukemia 8 Chronic myelocytic leukemia 3 Myelotibrosis 1ein aE 2 6 TE Oe 1B 1987 — ‘Hable 2, Hematoloyle data of anemic disorder) Diasnesis weve MCH ps) NCHC(e/al) RDWI20) ‘Nonanersie group sik 78 310268 ahs. 514 Giron aitate of diabetes, Scual failure,Ceboreulosi eke, 67-6: 9.1 tosia.6 MoLes Malignant solid tumor 88.0101 15416 Chronie liver disease 0. 2c 2 16116 Infestious disease Bhat 0.7 WAdL2 Cendiac fisoase ask as wads osthemorshagie state suck 82 seok.g 14.922 Bara oiak 74 58.5:hi. 8 10.081.2 Hypothyrordiom saz $22 1.2 Iron deficiency anemia ea at105 SL 546.2 21128 “Aplastic anemia 7,410.6 868818 1816 ie 81, 410.1 33.845.9 35.1428 AML 8,410.6 A. 3604.8 15.0.b9.1 ALL 95,0450.8 51.245.6 B84EL7 1att26 oun Bis 06 2.58.9 v0.9 wa.eti.e Mselolibrasis 78.3 at 35.2 Bt ‘Tublo 4, Claevificetion of anemic dinordere basnd on mean corputenlar volame(MCV) and red cell volume distribution width RDW) NV normal MCV low MCY low | NCV normal GY high MCV high DW normal KDW high KDW norwal «KDW tigh = REW normal © RDW Bish nletocyee (mlerorytic —(aermocytle —_(uormocytic _ (mmacrocyic— (macrozyt Iuemogencoss) emogencous) hemogchcoss) heterogeneous)" omogencous) _heterogercou: Heterozygous on eflelency Normal Chronic Aplastic anemia Folate ceficlency? Galisenia” anemia ITP Tiser disease Viena B Chronie disease Cardiae cissate deticioney'** (EB DN, CRE, Ate Cold agelttioins HY te) ALL. Malignancy CNT. Ipfectiows dissate Barly iron or ‘Salmonellos's, {olate deticiene faeuimonia eic.) stete* Burn Sileroblastic Posthemorrhasic + Reproduced from Beseman, JD. Gilmer, BD. Jr, and Gardner, PH, Improved classification of snemias by MCV and RDW. Qenqs ates deed tae 7 AUS 88 See(RDW) said RASA Wall A= 68.5-410.5 #ettoN, BMS Bole de ge 4 essa siz, 34294 994 dtd o1G106iLe es, Wagtde dea ae ae Soe e Pe SARL ae] att ‘mast 4, Oda, 3452, aeaeR, HOM, MASS, E4493 —6.0—ni RST AMCV) MRR RW) 2S Rin Po UNAS BDIIE Vols doh ada, Aaa, 4 WasiAd Ae Yo Fe waeal A= OMA, See Aas det Weta a Bas By 21a ONS} 1 BLL ERS Be Aad Sea sel glalel. 149) AAS ALt arid) Aa ee 9 4 q2.244 au, & MeVa ROWS goa. USE Lee Ba ble Bodh wa. S Weza A do) MCV 9 RDW 2 ad AAS AAATA dee ea 2 ass, 49%, a), $a 2 SNe Raged ae sj Fok gL 24, MOV ageloy ROW 2} rt JAAS AAOFA MBBS HAL Lee, AS PADD Soo at. ae MOVE a easiakt RDW 7} @7is}= aad alae a Aedt dage Wed Aes, MOVE Seal ERDW 44¢ Fadd ATE Weed AQSD8 Wa 431s le. ashy MCV be 42 DW} 44d Sada 24dt4 Weds MOV 3 RDW} wt Gries 24g lead NeSOn EU AE LaTed ean = ae 2 We $34a da ese ea Fade A ane Gg”, 2330 doze dA eaa 43db Jets eo wale ade aaa EWaHA, folic acid, vitomin BeE9 3 3dL AB, WAR, TAAET ARLES BFE 4 Hid AZAUTS A4ol ewe Aad WaRe Nabe ta Re adead dese ae indices Sa} ERR F Lea, se view min Ba 8 folic acid lea lt aaaTa Ne WIV osu, MCHC>st7s}e12, EAE BALE S59] io adsle caaTa, Aaa 302%)9\ 4, os} Go) ART ndlese ABT 4s, A RF E428 eoR ad Ado aad Ade dat S2eqetee4 waa dead Be EGS Fo) dev, Nad aes) Eade at AN 49512, cideroblansic anemia +} 31s) «13.51 1 4sbe Tad Ahlt ad AaTe Nae # Pos Wed dsedsisee agora Bat Hoe Bad Dt. le MCHE Move USE 27) AEM ULE aah ae, RICE A VTS ALY SEE Ada Fe monitore cg 4) Sook oe AY AAS WV Be) a} A460| Ash hereditary spheroeytosis a].Ash 2 BALE Me APE Aa A Yea BAR EATS Aa ols a eer Bez a EAA Ade we Aaa MCHE MOVs} = as7 AA ea MCHOe Aa Ae AAMAS vel DIA SA IIS ae Fe Bae. 3dv 2 SAAS MOVE WaNea ey eae TA MES Ge, aesy, thalessemis erate screcning 3} $9 AUF ALS VEse a) oe S2o1g4e teh ada tye Nev) sae 819 @, folic acid, vitamin Batwa) a7ial= $2 AT A REAM oe TATA F8-1 AA ASA Bade ALA OIF, we ZAe folie acid} Sela | etre MOV al Be Naa Raa aaa ah PANTY S4SaaT EN eda eee qAg S84 Hela le Aaeeds aeeR Adel 1Ghed, Wee ey, AES Ke sa, Mest sae ge AR aAa Ue Fe 08d AE det at ARE 4R8R24 19 BLE EGY Va NE SAU Ray 28, DAE WA ae HAI SU eet ave) ae tT Marae ABA Wadd ATA ALT 449) Ie AFae 2-30 Fa ET 2A ast Aada ated, ee Badd as atae Agdt Wen Qeaery add Srbsteirh son sataration | ahs) aha. 2a ASV Gudea ta, folate @ vie Be 4 PATE Mae AR Ate Bast ana aad. 29 SHAE wicteobe indices Q ae S ABZFACeyshropram)'%} LG DLA ASA GA OSs monitoring Her) S21 alex Eh, 28) coulter counters) AG ROWE VF, 24S Ceemoglobinepathien) 9 ait AS Ae 61eta aR $4 Was: thalassemia | sowaye? aw folic acid =4) ASA AR AA A AAAAD NEA 2 wsgal wel ol siat art. SE ANA Coulter Salus DE dag Bad a Adee We 7 724, oe 1888 RDW2 $9203 did de yas Cae e a) queues, Bessman-.¢ Coulter ZBL AGsg RDWE Sain acl uzeld 2, folie acid, 2 vit BoB, 244 $8, SC $e Se the Lassonia sai 2 al} Sra sles, aA 1 Ale SIA heteroryrous wor? thalastemia, aes ALBA WES asd RDWA Aaa Wa Shale}. Bossman SS lo] 2 DAE SAA 4 Be AES sled, ¢ at 244 la Bt A, folic acid, 9 vitamin 8.84 B9O¥ $30 Ut aasdds da, waa, Et ARECE LFF Aso) ASA UNS) aa a $4 MOVE Sage a4 ROWE wate w. ae) a8 aad le a ANTE ‘1a 1944 V4 Bane, Aes] ATES ZATES GA UGE s1gee we, thalass- emia mined Zale SL4e aaa Wee ag UGH At. MAE 2de Kayes} Alter») Jad Bg wh led, 2 PMA Aas aD Ate adele aaa, Bessmant02 =a fala Vasa So). atest Aut 219 aaa BAL ae Eaetste a, 24 Aad BAS S Be C trait DAE AYRDWE BAL hotorcaygous thalassemia 4 Ate AAUSLE Halt sade a4 ROW AL Ad] Ns) Vala Aa ash as ROW 7 BAER Boh. S14 WMA Bea, Vita SaaS MeV 2 RDW7 SF 24ol Ee Lash UR A pad seh LAT Sea) as ht MCVE Atea shew, 14 MCVsHe all WW) TAA ol ae WEE aaa ve AW. AA A MEE) ae ase RDW >} Goh) UAaSea fa Mas ROWS 4 wale 4202 a. QA LIGAT SRA, sold agulatinin lg, Aa Fabled S184 de Asay 1a4q MCV BQ RDW > MSs SAA AAEM aE Coulter 2-7 1B 198 counter} ASTE Ver ad) GALA pismon tation jl wolame thresholds) 222, A242 Se 1760148) suurious@ Aer ae AFA S Age gel ade Fa Be aol 4 oat AE AeA AAT Coulter counter 4] a4 ¥ paper Fol UehHe AES Bee 4a dae a4 BAe, a43\ 44 sella ead Baa) ARDW4 4UFE9 qezage MCV ge Ud ZALtsiesl HE See Bee 4244 Ad aed 1828 MOHCH 9 Aged = SALAS BFE A MNTAA SF Ree Av udosd 29ab Ad ae + aa, + HA devas AeaTeae 2a ea eel A MCV 9 ROWE 148 Ase S49 AEE U 2 2e8 shia 84a a Asa wale AA stdaa Qa aoe Coulter Counter Model § plus T4] AE URS qa azn ste AeaeTeAMeVs A UTHIBESEDWIE ld Ue Las 29918 Read AAAS Iss TSA QUAY AAT Bo} sols VASE AL HET Wels GAATE ee WEN LO B/llm\dy ibs 12.0e/Me) BE Bo MOVs} ROWS) 834 Sassi hist we a Saat 1, Jaz MOV ROWE BASEN aa APANIAA, LeeA 194 Is Bol 4, 2AG Bd UE YR, AS, LEAS ARR dana dase, ante, dasa aeaae, Sbt 2a RSet weaeed teeae, MCY% a) ROW SnGlaaa aaee Aa ee geese y asie wee, Leet BqN, WNEE AY A9aa, sas Ad 2 ea 2. MCV 7 Boal ROW SACs 24 Taal ae WANS Ueagien, Mov 2 RDW7t BRGAA9, WALPADL TMS A ALE WV 3, MOV 7} Ya RDW7t 2ACELAS) 2a Adela} MCV RDW2} 25 B2i(e184 9) 4a) e2—Ai Ak RE RAAVATNICVI SD ae mARERR ARIE RWI) eee kel A — STA ae 2a hee. 4. MCHE MCV s} 29] 22 2¢ wala aoe MCHC E al ole 27 BANA E EOE Ae yd SIS 22 + Aste 148 B425 194 MOVs: RDWE ltt ad BEE Aes 197 SI} NAS Zriabe s}alaa) Baa adel Hee) Ase gas 1) Wintrobe, MM.+ Clinical homatotagy, Vel. T, th edition, Philadelphie, Lea asd Febiger, 5981 Hillman, RS, and Finch, CA. The mine By J Hematol 47-212, sed retiontcoste 1959 Bocamaa, J.D., Gilmer, PR Jr, and Gardner BH: Improved classification of axenies by MCW: Am J Clin Patho! 807222, 1989 Coulter Counter Model S Plus Il: Prodect reference marual, Hlatech, PL, Coulter Ele «tronics, 1982 Baner, J D+ Clinizal laboratory methods. oth edtson. St, Lows, Mosby, 1982 Conrad, M.E., and Crosby, WH: The vatural distory of iro deficiency indweed ay pltebo tomy. Blood 20:173, 1962 Herbert, Vi Experinestel melritional folate Ueficiency in men, Trans Assoc Am Physi clans 75:907, 1992 Gilmer, PR. Jr, and Koepke, JA: The reticulocyte, An abtroach to definition. Sow J Clin Pothol 68:262, 1976 Clarkeon, DR, and Moore, RM: Retielocyte anemies, Blood 48:669, 4) 5 6 n ® 9 tae in mutritional 1976 Klee, GG, Fairbanks, W.F., ond Pierre, RVs Rewtine ervtiracste meesurements in legaosts of iron deficiency anemia and the: lassemia minor, Am j Clin Pathol 68:870, 1676 Mentzer, WC: Differentiation of ios defie feney from thalessomia wait. Lancet 1:862, 1973 10 > 12) Bessman, J.D. 10 19) 19 2 B Ey ) ) > ) ae ant Jolson, BK: Brothro- ple colume distribution in normal and abuo. rmat subjects. Biocd 467369, 1977 England, JM, and Down, MD. Red call rolume distribution curve and the measurement of anisvestosis. Lancet 1:701, 1974 Hammersley, M.W., King, R-., and Sllltvant, RE: High ervthrocate distribution values and possibilities of hemogtobtnopathies. Am J Clix Pathol 75:70, 1981 Bessman, J.D. ond Feinstein, D. live asisocstesis as a discriminant between + Quastita iron deficiency and tholassemia minor, Blood 58:288, 1979 Bessman, J.D. Brythrapeiesis dering recavery from iron éeficieney: Normocstes and macro: fytes: Blood $0:985. 1977 Bessman, [.D.: Ersthropaiesis daring recovery fren macrocytie anemia: Macreeylen, norma ples. Blood §0:995, 1977 Pearson, HLA. O'Brien, RT, and Melntosh, Si: Screening Jor thalessemia trait by electro fe macsnromen) of mean corbuscaler volume N Eng J Med 288°551, 1973 Bessman, J.D. Foaluation of automated whole Wood phaietee counts end particteststug. Am J Clin Pathol 74:157, 1980 Bessmen, J.D. What's ax RDW? Am. J. Clin. Pathol 76:242, 1981 Keye, FJ., end Alter, BP: Red col! size Anon invasive evatie 1082. distribution analysis: ation of mecrocytesic. 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