Leukemia in Polycythemia Vera. Relationship to Splenic Myeloid Metaplasia and Therapeutic Radiation Dose

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1 Leukema n Polycythema Vera Relatonshp to Splenc Myelod Metaplasa and Therapeutc Radaton Dose JOHN H. LAWRENCE, M.D., D.SC, F.A.C.P., H. S. WINCHELL, M.D., PH.D., F.A.CP., and W. G. DONALD, M.D., F.A.C.P. Berkeley, Calforna Snce the ntal use of "PO* n our SUMMARY clnc n 1939 for the treatment of polycythema vera we have followed to termnaton 181 cases of the dsease treated wth "P or "P and X ray. Of these patents 45 of 181 (25%) developed sgnfcant splenc myelod metaplasa, and 26 of 181 (14%) developed an acute myelogenous leukema-lke state. Sxteen patents had both "acute leukema" and sgnfcant splenc myelopoess or myelod metaplasa (that s, 16 of 45 or 36% of all cases wth myelod metaplasa developed "acute leukema"), and 10 patents had only "acute leukema" but no sgnfcant splenc myelod metaplasa (that s, 10 out of 136 or 7% of all patents wthout myelod metaplasa developed acute leukema). Patents who faled to develop myelod metaplasa or acute leukema, or both, were older at the tme of onset and dagnoss than those wth these developments and dd not survve as long. The survval of patents who developed acute leukema was not sgnfcantly dfferent from patents who ded wth sgnfcant myelod metaplasa alone. The largest values of overall radaton exposure (both "P and X ray) tmes tme at rsk were receved by patents dyng wth splenc myelod metaplasa alone. The overall ncdence of acute leukema n ths seres of patents wth polycythema vera s 20 to 40 tmes greater than that expected for a populaton of "normal human subjects" exposed to smlar radaton doses and tmes at rsk. These data are consstent wth the hypotheses [1] that development of sgnfcant splenc myelod metaplasa and acute leukema-lke states are part of the evolutonary hstory of polycythema vera; [2] that myelod metaplasa usually precedes the appearance of acute leukema; and [3] that the ncdence of acute leukema n our patents treated wth **P may be prmarly a result of prolonged survval rather than radaton dose. SUBSEQUENT TO OUR frst use of 82 P0 4 for polycythema vera n 1939 t has become apparent that ths agent reduces morbdty and results n sgnfcant prolongaton of lfe over that of patents treated wthout myelosuppressve therapy (1, 2). Although the therapeutc benefts of 82 P n polycythema vera reman unchallenged, the hgh ncdence of acute leukema-lke states appearng late n the course of ths dsease has contnuously rased the queston of ts possble radaton nducton (3, 4). That radaton may ncrease the ncdence of leukema has been known for some tme (5, 6) and was well apprecated by us when we frst began usng radoactve sotopes n human dsease over 30 years ago (7-9). However, the lack of evdence that most patents could be controlled wth venesecton alone and the benefts attendant upon the management of polycythema vera patents wth 82 P justfed the possble rsks of such therapy. Snce radaton effects generally show some radaton dose-dependency, we correlated radaton dose wth presence of acute leukema at death n ths seres of 181 polycythema vera patents who had ded at the tme of ntaton of ths study. Receved August 2, 1968; accepted August 30, From the Donner Laboratory and Clnc and the Donner Pavllon, Unversty of Calforna, Berkeley, Calf. Ths study was supported by contract W eng-48, Atomc Energy Commsson, Washngton, D. C. Requests for reprnts should be addressed to John H. Lawrence, M.D., Donner Laboratory, Unversty of Calforna, Berkeley, Calf

2 764 LAWRENCE, WINCHELL, AND DONALD Annals of Internal Medcne MATERIALS AND METHODS In most cases studed, therapy and long-term follow-up were performed n assocaton wth the referrng physcan. Complete records were kept of all pertnent medcal nformaton throughout the patent's lfe. The decson as to what hematologc complcaton the patent had was made on the bass of both the patent's course and the fndngs at postmortem examnaton. Before 1949 the dagnoss of polycythema vera had been made on the bass of a sustaned elevaton of the red cell count n excess of 7 mllon cells/mm 8 wthout apparent cause and an assocated elevated whte cell count and splenomegaly. After 1949 all patents were dagnosed as havng polycythema vera on the bass of an ncreased crculatng red cell volume (exceedng 34 ml/kg body weght), a normal arteral oxygen saturaton, and, agan, excluson of those showng a cause for a secondary polycythema. The red cell volume was determned by usng *"P phosphate labelng of autologous red cells (10). Tumors assocated wth secondary erythrocytoss were excluded on the bass of complete medcal evaluaton (excluson of renal dsease, and so forth) durng clnc vsts, subsequent long-term follow-up of the patent's course, and fndngs ncludng postmortem examnaton. In each case one or more of the followng fndngs were present: an enlarged spleen, persstent thrombocytoss (n excess of 400,000/mm 8 by drect method), or leukocytoss (whte blood cells (WBC) n excess of 10,000/ mm 8 ). Sgnfcant splenomegaly (spleen tp extendng more than 3 cm beneath the costal margn), leukocytoss, and characterstc changes n red blood cells (RBC), WBC, and platelet morphology were noted before death n each case of sgnfcant splenc myelod metaplasa (for example, ansopoklocytoss, teardrop-shaped RBC, normoblasts, gant platelets, mmature granulocytes n perpheral blood). The presence of sgnfcant splenc myelod metaplasa was confrmed at the tme of postmortem examnaton on the bass of hstologc fndngs of myelopoess wth megakaryocytes clearly dentfable n the spleen. In recent years we attempted to dstngush ths state from chronc myelogenous leukema by performance of leukocyte alkalne phosphatase and chromosome studes. In those cases wth myelod metaplasa, where the determnatons were performed, leukocyte alkalne phosphatase was ether normal or elevated, and the Phladelpha chromosome was absent. All cases n ths category were placed wthn the "death wth sgnfcant splenc myelod metaplasa" group. Acute myelogenous leukema wth myelod metaplasa was the term appled to those cases wth leukocytoss and precedng sgnfcant splenc myelod metaplasa wth termnal fndngs of more than 20% blast cells n the crculatng blood. Patents n ths category usually had generalzed nfltraton of tssues by blast cells at postmortem examnaton. Generally, n these cases the perpheral blood contaned a spectrum of cells at varous levels of dfferentaton, from the mature granulocyte to the myeloblast. Acute myelogenous leukema wthout metaplasa was the term appled to those patents wthout precedng sgnfcant splenc myelod metaplasa who suddenly demonstrated varable numbers of myeloblasts n the perpheral blood wthout evdence of dfferentaton of these cells to more mature elements. Examnaton of bone marrow n such patents generally showed a preponderance of myeloblasts. In the seres reported here of 181 patents wth polycythema vera followed to death "P was the sole radaton modalty used n 123 cases. In the remanng cases both X ray and "P were used n therapy. (In all cases venesecton was used as supplemental therapy.) In 12 of ths latter group accurate measurement of X-ray dose was not avalable, and these cases were not used n analyss of radaton dose admnstered. Mllcures "P was converted to "equvalent R" exposure by use of the fgure suggested by Osgood (11) of 15R/mc. (Ths fgure s hgher than that used by us prevously (1)). When X ray was used n therapy, the maxmum radaton dose receved by a myelopoetc area (bone or spleen) was taken as the "equvalent R" exposure for the entre body. Thus, values for radaton exposure n "equvalent R" represent maxmum values. The product mllcure "P or "equvalent R M tmes months at rsk was obtaned by multplyng mllcures or "equvalent R" tmes the tme n months between admnstraton and death for each radaton exposure and summng all such values for each patent Values were calculated for the mean and the standard error of the mean for each parameter. The probablty that the value obtaned for a gven parameter n comparsons between groups of patents would be hgher or lower by chance alone (P values) was determned usng routne statstcal technques utlzng tables of Student's t dstrbuton.

3 Volume 70, No. 4 Aprl 1969 LEUKEMIA IN POLYCYTHEMIA VERA 765 TABLE 1. Age at Onset and Duraton of Dsease for Varous Categores of Deceased Patents wth Polycythema Vera Treated wth Radaton* Lack of Sgnfcant Splenc Myelod Metaplasa Before Death Sgnfcant Splenc Myelod Metaplasa (MM) Before Death No Leukema Termnal No Leukema Termnal (Uncompl- Acute (MM) Acute cated) (N = 126) Leukema (AL) (N = 29) Leukema (ALw/MM) (N= 10) (N = 16) Age at onset 57.9 ± =b ± ± 2.2 Age at dagnoss 59.7 =fc =fc ± ± 2.2 Duraton to death from onset 11.6 ± ± ± ± 1.3 Duraton to death from dagnoss 9.9 ± ± ± ± 1.2 * For each category values for the mean and standard error of the mean are gven. RESULTS Table 1 presents a comparson of the age at onset and the duraton of dsease between groups of patents wth polycythema vera treated wth 82 P and other radaton modaltes. Clncally, the patents were separated nto two major groups composed of those patents who had and had not demonstrated evdence of sgnfcant splenc myelod metaplasa. Under each of these major headngs the patents were further subdvded nto those who were judged to have developed a termnal acute leukemalke state and those who dd not show evdence of such a development. Of the patents lsted n Table 1, 45 of 181 patents (25%) developed sgnfcant splenc myelod metaplasa, and 26 of 181 (14%) developed an acute myelogenous leukema-lke state. Sxteen patents had both "acute leukema" and sgnfcant splenc myelod metaplasa (that s, 16 of 45 patents or 36% of all patents wth myelod metaplasa developed "acute leukema"), and 10 patents had only "acute leukema" but no sgnfcant splenc myelod metaplasa (that s, 10 of 136 or 7% of all cases wthout myelod metaplasa developed "acute leukema"). Patents who developed sgnfcant splenc myelod metaplasa or acute leukema before death were found to be younger at both the age of onset and dagnoss and to survve longer than patents who developed nether myelod metaplasa nor acute leukema (uncomplcated group). (See Table 4 for results of test of sgnfcance between groups.) In other words, those patents who faled to develop sgnfcant splenc myelod metaplasa or acute leukema before death were older at the tme of onset and dagnoss and faled to lve as long after onset of ther dsease as those patents who dd have these developments. Among the group of patents who developed sgnfcant splenc metaplasa before death, there was no sgnfcant dfference n terms of onset and duraton of dsease between those who developed acute leukema-lke states (acute leukema wth myelod metaplasa group) and those who ded wthout the development. Table 2 presents results summarzng the total dose for polycythema vera patents treated wth 82 P as the only source of radaton used n therapy. The dose s gven as cumulatve mllcures of 82 P and also the sum of the product of mllcures of 82 P admnstered tmes months at rsk (tme n months from 82 P admnstraton to death). The largest doses, expressed ether as total mllcures admnstered or as the product of mllcures tmes months at rsk, were receved by patents who developed sgnf-

4 766 LAWRENCE, WINCHELL, AND DONALD Annals of Internal Medcne TABLE 2. Radaton Dose for Deceased Polycythema Vera Patents Treated wth n P Radaton Alone* Lack of Sgnfcant Splenc Myelod Metaplasa Before Death Sgnfcant Sj >lenc Myelod Metaplasa (M] M) Before Death No Leukema Termnal Acute (Uncomplcated) Leukema (N = 92) (AL) (N = 8) No Leukema (MM) (N = 17) Termnal Acute Leukema (ALw/MM) (N = 6) Total Dose, mc Duraton to death from start of Total mllcure-months 25.4 =fc db 0.5 1,942 =fc ± ± 1.8 3,098 ± =fc =b 1.4 3,788 =fc =b ± 2.0 1,726 =fc 744 * For each category values for the mean and standard error of the mean are gven; mllcure-months was deterproducts of each dose of 82 P (mllcures) tmes months from admnstraton mned n each case as the sum of the to death. cant splenc myelod metaplasa but who dd not show sgns of acute leukema (myelod metaplasa group). The three other groups (uncomplcated, acute leukema, and acute leukema wth myelod metaplasa) had comparable total doses of 82 P expressed as mllcures. The patents who ded wth acute leukema but wthout sgnfcant splenc myelod metaplasa (acute leukema group) survved longer from the start of 82 P therapy and correspondngly had a larger value of "dose rsk" expressed as mllcures-months than dd the uncomplcated and acute leukema wth myelod metaplasa groups. Smlar fndngs are noted when all patents treated wth ether 82 P alone or 82 P and X ray are consdered (Table 3). In ths tabulaton both groups of patents who developed splenc myelod metaplasa (myelod metaplasa and acute leukema wth myelod metaplasa) receved larger doses than those patents who faled to develop splenc myelod metaplasa. Wthn each major category (presence versus absence of sgnfcant splenc myelod metaplasa) there was no sgnfcant dfference n radaton dose between those patents developng acute leukema and those not developng t. Table 4 shows tests of sgnfcance. The relatonshp between cumulatve death (plotted as percent dead on the ordnate) and tme after dagnoss (plotted n years on the abscssa) s shown n Fgure 1 for patents dyng of all causes and for patents n ths group who ded wth acute TABLE 3. Radaton Dose for Deceased Polycythema Vera Patents Treated wth a P and Other Radaton Modaltes* Lack of Sgnfcant Splenc Myelod Metaplasa Before Death Sgnfcant Splenc Myelod Metaplasa (MM) Before Death No Leukema (Uncomplcated) (N = 114) Termnal Acute Leukema (AL) (N= 10) No Leukema (MM) (N = 29) Termnal Acute Leukema (ALw/MM) (N= 16) Total Dose, R 545 =fc 73 Total R-monthj 36,882 db 4, =1=68 39,418 =fc 8,761 1,027 =fc ,255 =fc 16,309 1,386 =fc ,987 =fc 17,191 * For each category values for the mean and standard error of the mean are gven. The values for R-months were determned assumng each mllcure of tt P s equvalent to 15 R (9).

5 Volume 70, No. 4 Aprl 1969 LEUKEMIA IN POLYCYTHEMIA VERA 767 TABLE 4. Sgnfcance of Dfferences Between Values Gven n Tables 1, 2, and 3* Table Number/ Groupf Acute Leukema Myelod U ^complcated Category wth Myelod Metaplasa Metaplasa 1/Age at onset AL > ALw/MM <0.005 MM < /Age at dagnoss AL ALw/MM <0.005 MM < /Duraton to death from onset AL > ALw/MM MM < /Duraton to death from dagnoss AL ALw/MM MM < /Total dose, mc AL ALw/MM >0.400 MM < /Duraton to death from start of 82 P AL <0.005 ALw/MM >0.400 MM /Total mllcuremonths AL ALw/MM MM /Total dose, R AL ALw/MM AL /Total R-months AL ALw/MM MM * P values from Student's / test are lsted for comparsons between values n groups presented n Tables 1, 2, and 3. t AL = acute leukema; MM = myelod metaplasa; ALw/MM = acute leukema wth myelod metaplasa. leukema. The curves for both groups are roughly sgmodal n shape. In addton to the patents whose data are summarzed above, we have followed a seres of 15 patents wth polycythema vera who, usually, because of the relatve bengnty of ther dsease were managed ether wth phlebotomy alone (8 cases) or wth phlebotomy and alkylatng agents (7 cases). The medan survval from dagnoss to the present for ths group s 5 years. Two patents n ths group have ded so far, both showng sgnfcant splenc myelod metaplasa at postmortem examnaton. Of the 13 patents who are stll lvng and beng followed, 1 who had been controlled wth 2 to 4 venesectons per year for 21 years, now has sgnfcant splenc myelod metaplasa; another patent, who had been treated wth 2 to 6 phlebotomes per year for 4J years, has recently developed acute myeloblastc leukema. DISCUSSION In many patents wth polycythema vera the condton can be vewed as a progressve process n whch the ntal ncrease n the rate of erythropoess s followed by progressve reducton n red cell survval, ncompletely compensated for by ncrease n the rate of red cell producton (12). Durng the course of ths process the erythropoetc

6 768 LAWRENCE, WINCHELL, AND DONALD Annals of Internal Medcne FIGURE 1. Cumulatve deaths as a functon of duraton of dsease from tme of dagnoss, for patents wth polycythema vera treated wth radosotopes. Upper curve: 183 patents who ded from all causes. Lower curve: 26 of the 183 patents who ded wth acute leukema. One patent was stll lvng 30 years after dagnoss (lmt of tme scale), and he ded 38 years after dagnoss wth termnal acute leukema. bone marrow extends from ts normal central locaton (n vertebral bodes, pelvs, and proxmal femor and humer), down the shaft of the long bones and nto the dstal extremtes n assocaton wth progressve loss of such marrow from the central marrow cavtes (13). At varable tmes durng ths course, extramedullary erythropoess may appear, frst n the spleen and then n the lver (2, 12). Comparable changes appear to be occurrng n the whte cell seres. The number of whte cells appearng n the crculaton generally ncreases as the dsease progresses (12) n assocaton wth a varable ncrease n ther degree of "mmaturty." Durng the course of ths process, a sudden change n the number or state of dfferentaton of crculatng whte blood cells s often descrbed as a "leukemc" transformaton. Whether or not such "leukemc" transformatons n the course of polycythema vera are causally dentcal to clncally smlar leukemas occurrng wthout the pror presence of polycythema vera remans open to conjecture. Certanly the leukocytoss and splenomegally occurrng n polycythema vera patents wth myelod metaplasa smulatng chronc myelogenous leukema (CML) appear to dffer from that seen n classcal chronc myelogenous leukema. In the former the Phladelpha chromosome s generally absent, and the leukocyte alkalne phosphatase s normal or elevated. Future technques mght demonstrate smlar dfferences between the acute leukema-lke syndromes developng n polycythema vera and the more classcal forms of acute leukema. In order to analyze the effect of radaton dose on the ncdence of acute leukema n polycythema vera t s mportant to defne groups comparable wth respect to age at onset, dagnoss, duraton, and course but dfferng only n regard to radaton dose and presence or absence of acute leukema. Ideally, we would wsh to par patents n terms of comparable myeloknetcs, but, unfortunately, the only readly defned "sgnposts" n the evoluton of cell knetcs n polycythema vera are the development of sgnfcant splenc myelod metaplasa and the development of acute leukema (2). Therefore, we have classfed our patents nto groups dependent on the presence or absence of sgnfcant splenc myelod metaplasa or acute leukema. The fndngs that patents who ded wthout development of these hematologc complcatons were older at onset and dagnoss and lved for a shorter tme nterval than those who dd develop myelod metaplasa or acute leukema suggest that development of ether s part of the natural hstory of polycythema vera and that had these ndvduals who ded wthout these "complcatons" survved suffcently long wth ther dsease many of them would have developed such complcatons. Furthermore, our results suggest that the usual hematologc progresson n ths dsease nvolves development of sgnfcant myelod metaplasa before the appearance of an acute leukema-lke syndrome as evdenced by the hgh ncdence of sgnfcant splenc myelod metaplasa n the patents wth acute leukema.

7 Volume 70, No. 4 AprU 1969 LEUKEMIA IN POLYCYTHEMIA VERA 769 Presently avalable data ndcate that n man the probablty rate for development of leukema s 1 to 2 per mllon exposed populaton per roentgen per year averaged over the tme perod of 1 to 15 years after radaton exposure (14). The subjects n such prevous studes were not consdered at rsk durng the frst year after radaton exposure. In the present seres the average exposure dose tmes the total months at rsk subsequent to a gven dose of radaton was 44,852 R-months for all groups studed. Ths s equvalent to 3,738 R-years. Multplyng ths radaton exposure by 1 to 2 tmes 10-6 per R per year yelds an expected ncdence of leukema from radaton exposure alone n the present seres of approxmately 0.37% to 0.74% as opposed to 14% actually observed. One should note that n the present seres the patent was consdered to be at rsk from leukema mmedately after a gven radaton exposure, and, thus, ths calculated ncdence of radaton-nduced leukema for our patents would be expected to be a hgh estmate. Snce the observed ncdence of acute leukema n ths seres of polycythema vera patents treated wth radaton was roughly 20 to 40 tmes that expected other nonpolycythemc groups wthn the populaton exposed to onzng radaton, one must conclude ether that the appearance of acute lekema-lke states n patents wth polycythema vera s relatvely ndependent of radaton dose or that patents wth polycythema vera are more hghly susceptble to radaton-nduced acute leukema-lke states than other members of the populaton. (Smlar fndngs have been prevously reported by Osgood (15)). If the latter fndngs were the case then one would antcpate that those patents dyng wth an acute leukema-lke state would have larger values of the product, radaton dose tmes months at rsk, than comparable patents who faled to develop an acute leukemalke state.* In ths seres such was not the case. Indeed, the group that receved the hghest radaton dose was that n whch patents developed sgnfcant splenc myelod metaplasa before death but faled to develop acute leukema. These patents also had the longest survval from onset or dagnoss than any of the remanng three groups. Excellent results have been acheved usng radoactve phosphorus n the treatment of polycythema vera; the lfe expectancy s extended to nearly normal, and, furthermore, we do not see the hgh frequency of hemorrhage and of thromboblastc epsodes that are often observed when ths dsease s not adequately controlled (2, 16, 17). As for the queston of a possble ncrease n the ncdence of acute leukema n patents treated wth 82 P, our fndngs suggest that ths may be prmarly * For a group homogeneous wth respect to survval tme and susceptblty of acute leukema development from radaton exposure but dfferng wth respect to radaton dose, let: D equal the value of "equvalent R" exposure tmes tme at rsk defnng the th group; N equal the number of subjects n the th group; P equal the fractonal probablty of acute leukema development per equvalent R exposure per unt tme at rsk. Average radaton exposure tmes tme at rsk (R) for all patents n the group s equal to equaton 1 as follows: END LN Average radaton exposure tmes tme at rsk for patents n groups not developng acute leukema s equal to equaton 2 as follows: Z ND -PL ND 2 J N - P L ND It s clear the frst term n the numerator and the frst term n the denomnator n equaton 2 are dentcal to the numerator and denomnator, respectvely, n equaton 1. Snce D has nteger values greater than 1, t s also clear that ND 2 > ND. Thus, equaton 2 yelds values smaller than equaton 1. Consequently, the average radaton exposure tmes tme at rsk for patents falng to develop acute leukema must be lower than the values obtaned for the entre group. (Note that ths smplfed argument apples only when development of acute leukema does not nfluence survval as s the case n the present study n comparng patents havng myelod metaphasa wth those havng acute leukema and myelod metaplasa.

8 770 LAWRENCE, WINCHELL, AND DONALD Annals of Internal Medcne a result of prolonged survval rather than of radaton dose. It would help f we knew the ncdence of acute leukema among patents who have not been treated wth onzng radaton, but at the present tme ths s really not known. Untl recently, wth the advent of chemotherapeutc agents most patents wth polycythema vera have been treated wth roentgen radaton or 82 P, and, consequently, there are relatvely few reports n the lterature concernng large seres of patents who had not been treated wth some type of radaton. In our clnc we have a group of 15 patents who because of the relatve bengnty of ther dsease were treated wthout the use of onzng radaton, and t s noteworthy that n ths small group followed for a medan perod of 5 years after therapy, one patent who was treated only wth phlebotomy developed an acute myeloblastc leukema. Hanan and Russell's study (18) n 1965 compared survval and causes of death of an rradated group (107 patents treated wth X ray and radophosphorus) and a nonrradated group (117 patents treated wthout radotherapy), and they found no cases of acute leukema n ether group. They had used data from Perkns, Israels, and Wlknson (4) for ther nonrradated group, and n the latter's paper one patent wth polycythema vera treated wth venesecton alone ded of D Guglelmo's dsease (acute erythroblastc leukema). We have found sx addtonal cases cted n the lterature n whch patents wth polycythema vera who had not receved any radaton therapy developed an acute leukema. Rosenthal and Bassen (19) reported a case of erythroleukema n whch there was actve erythroblastc and leukoblastc nvolvement of the bone marrow before radaton therapy; Dameshek cted 2 such cases 1 among hs own seres of 50 patents and another that occurred among 100 patents treated at the Mayo Clnc (20); Wllams and Mendel (21) reported a case of polycythema vera termnatng wth myeloblastc leukema, the patent havng been treated only wth venesecton and low ron det; Renhard (22) reported 1 patent wth polycythema vera who had not receved radaton therapy of any sort who ded of acute myelocytc leukema; and Modan and Llenfeld (3) reported the development of acute leukema n a patent wth polycythema vera after phlebotomy and myleran therapy In addton to these cases already cted n the lterature, we have heard n dscussons wth and n letters from other physcans nterested n ths problem, of several unreported cases of acute leukema developng n patents treated wth myleran and alkaran. Apparently, these solated cases do not get nto the lterature. The ncdence of ths complcaton after varous forms of therapy, ncludng the varous chemotherapeutc agents, venesectons, and 82 P, s now beng studed at the natonal level (Natonal Insttutes of Health Polycythema Vera Study Group), but several years wll be requred to get the answer as to whether the ncdence of acute leukema and the prolongaton of lfe wth the use of chemotherapeutc agents, or venesectons, or both, wll be smlar to those observed wth the use of onzng radaton. Untl such knowledge s avalable we contnue to recommend that bengn cases of polycythema vera should be treated wth venesecton alone and that, when t s necessary to use 32 P or chemotherapy n combnaton wth venesecton n order to control the dsease adequately and prevent the occurrence of complcatons such as hemorrhage or thromboses, then the dosage of 82 P or of the chemotherapeutc agent should be kept as low as possble. REFERENCES 1. LAWRENCE, J. H.: Polycythema. Physology, Dagnoss and Treatment Based on 303 Cases, a Modern Medcal Monograph, Grune & Stratton, Inc., New York and London, WASSERMAN, L. R.: Polycythema vera ts course and treatment: relaton to myelod meta-

9 Volume 70, No. 4 Aprl 1969 LEUKEMIA IN POLYCYTHEMIA VERA 771 plasa and leukema. Bull. NY Acad. Med. 30: 343, MODAN, B., LILIENFELD, A. M.: Polycythema vera and leukema the role of radaton treatment. Medcne (Bat.) 44: 305, PERKINS, J., ISRAELS, M. C. G., WILKINSON, J. F.: Polycythema vera: clncal studes on a seres of 127 patents managed wthout radaton therapy. Quart. J. Med. 33: 499, COURT BROWN, W. M., ABBOTT, J. D.: The ncdence of leukema n ankylosng spondylts treated wth X-rays. Lancet 1: 1283, FURTH, J., UPTON, A. C: Leukemogeness by onzng radaton. Acta Radol. 116 (suppl.): 469, LAWRENCE, J. H., HAMILTON, J. G., ERF, L. A., PECHER, C.: Recent advances n clncal medcne wth the ad of artfcally prepared radoactve sotopes. /. Cln. Invest. 20: 436, HAMILTON, J. G., LAWRENCE, J. H.: Recent clncal developments n the therapeutc applcaton of radophosphorus and radoodne. /. Cln. Invest. 21: 624, ERF, L. A., LAWRENCE, J. H.: Clncal studes wth the ad of rado-phosphorus. III. The absorpton and dstrbuton of rado-phosphorus n the blood of, ts excreton by and ts therapeutc effect on patents wth polycythema vera. Ann. Intern. Med. 15: 276, BERLIN, N. I., LAWRENCE, J. H., GARTLAND, J.: Blood volume n polycythema as determned by ^P labeled red blood cells. Amer. J. Med. 9: 747, OSGOOD, E. E.: The relatve dosage requred of total body X-ray vs. ntravenous ^P for equal effectveness aganst leukemc cells of the lymphatc seres or granulocytc seres n chronc leukema. /. Nuc. Med. 6: 421, POLLYCOVE, M., WlNCHELL, H. S., LAWRENCE, J. H.: Classfcaton and evoluton of patterns of erythropoess n polycythema vera as studed by ron knetcs. Blood 28: 807, VAN DYKE, D., LAWRENCE, J. H., ANGER, H. O.: Whole body marrow dstrbuton studes n polycythema vera. Battelle-Northwest Symposum on Myeloprolferatve Dsorders n Anmals and Man. In press, CRONKITE, E. P., MOLONEY, W., BOND, V. P.: Radaton leukemogeness. Amer. J. Med. 28: 673, OSGOOD, E. E.: Contrastng ncdence of acute monocytc and granulocytc leukemas n M P- treated patents wth polycythema vera and chronc lymphocytc leukema. /. Lab. Cln. Med. 64: 560, CALABRESI, P., MEYER, O. O.: Polycythema vera. I. Clncal and laboratory manfestatons. Ann. Intern. Med. 50: 1182, CHIEVITZ, E., THIEDE, T.: Complcatons and causes of death n polycythema vera. Acta Med. Scand. 172: 513, HALNAN, K. E., RUSSELL, M. H.: Polycythema vera: comparson of survval and causes of death n patents managed wth and wthout radotherapy. Lancet 2: 760, ROSENTHAL, N., BASSEN, F. A.: Course of polycythema. Arch. Intern. Med. (Chcago) 62: 903, DAMESHEK, W.: Physopathology and course of polycythema vera as related to therapy. JAMA 142: 790, WILLIAMS, M., MENDEL, J.: Polycythema vera termnatng wth myeloblastc leukema. Blood 9: 189, REINHARD, E.: Crtcal evaluaton of the harmful effects and dangers of radoactve sotope therapy. Proceedngs, 6th Congress Internatonal Socety of Hematology, Grune & Stratton, Inc., New York, 1956, pp

10 ANSWERS TO QUESTIONS OF THE MONTH IN THIS ISSUE OF THE ANNALS Page 706. Pulmonary Dsease 275: D Reference: MYERS, C. E.: Anthracolco-tuberculoss as seen n a general hosptal. Ds. Chest 44: 469, Page 712. Infectous Dsease and Allergy 343: B Reference: LEVINE, B. B., REDMOND, A. P., FELLNER, M. J., Voss, H. E., LEVYTSKA, V.: Penclln allergy and the heterogeneous mmune responses of man to benzylpenclln. /. Cln. Invest. 45: 1895, Page 722. Gastroenterology 402: D Reference: GRACE, N. D., MUENCH, H., CHALMERS, T. C.: The present status of shunts for portal hypertenson n crrhoss. Gastroenterology 50: 684, Page 734. Renal Dsease and Electrolytes 533: B; 534: D References: ROBIN, E. D.: Abnormaltes of acd-base regulaton n chronc pulmonary dsease wth specal reference to hypercapna and extracellular alkaloss. New Eng. J. Med. 268: 1249, SCHWARTZ, W. B., HAYS, R. M., POLAR, A., HAYNIE, G. D.: Effects of chronc hypercapna on electrolyte and acd-base equlbrum. II. Recovery wth specal reference to nfluence of chlorde ntake. /. Cln. Invest. 40: 1238, Page 750. Cardovascular Dsease 700: C Reference: FOWLER, N. O.: n The Heart, edted by HURST, J. W., LOGUE, R. B., McGraw-Hll Book Co., New York, 1966, pp

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