From www.bloodjournal.org by guest on May 24, 2017. For personal use only.

BLOOD The Journal oj Hematology

DECEMBER, 1962 YOL. XX, NO. 6
Leukocytic InclusionsDoble BodiesAssociated with
Platelet Abnormality (The May-Hegglin Anomaly)
Report of a Family and^Review of the Literature
By FRANK A. OSKI, J. LAWRENCE NAIMAN, DONALD M. ALLEN
AND Louis K. DIAMOND
IN 1911 DOHLE1 reported the presence of round blue-staining bodies in
the cytoplasm of leukocytes of patients with scarlet fever. They were tran-
sient in nature, appearing at the time of the exanthem and persisting only
for
as long as 6 days. These bodies, which now bear his ame, have
subsequently
been observed transiently in patients with other infectious diseases such as
erysipelas,2*3 diphtheria,2 typhus,3 tuberculosis,4 measles,3 and with severe
thermal burns.5
MayG in 1909 had noted similar leukocytic inclusions in a patient who was
otherwise well, but in this case the cytoplasmic bodies were persistent and
were associated with giant platelets. In 1945 Hegglin7 described the
presence
of Dhle bodies, also in association with giant platelets, in three members of
the same family, thus showing that this syndrome may be familial and is
likely
hereditary. In Hegglins report a father and his two sons had the anomaly in
association with chronic thrombocytopenia. Recently Wassmuth et al.8 and
Petz et al.17 have reported briefly on the second and third families with this
anomaly.
Because of the un usual nature of this condition and the scarcity of
reports
in the English literature, we will describe a fourth family with the May-
Hegglin anomaly.
CASE REPORT
A six-year-old white female was first seen at the Childrens Hospital
Medical Center in
September 1961, for evaluation of purpura of 2 months duration.
History revealed that the patient had been in good health until July 1961,
when
purpura and ecchymoses were first noted. A platelet count at that time was
142,000/mm3.
Ten days later, spontaneous bleeding from the nose and mouth and
hematuria were noted.
On admission to the local hospital the patients platelet count was
30,000/mm3. Treatment
with oral triamcinolone,0 48 mg. per day, was begun. No further bleeding
occurred at
From the Department of Pediatrics, Harvard Medical School, and the
Chdrens Hospi-
tal Medical Center, Boston, Mass.
 Supported in part hy a grant from the John A. Hartford Foundation, and by
a grant
from the National Institutes of Health (HTS 5255).
Submitted July 8, 1962; accepted for publication July 30, 1962.
Aristocort (Lederle Laboratories).
657
BLOOI>, VOL. 20, No. 6 (DECEMBKK), 1962
From www.bloodjournal.org by guest on May 24, 2017. For personal use only.
658
OSKI, NAIMAN, ALLEN AND DIAMOND
that time but new purpuric areas continued to appear and the platelet count
remained low.
In mid-August 1961, gradual tapering of the dose of triamcinolone was
begun, but
when it had been reduced to 40 mg. per day, spontaneous bleeding from the
nose and
mouth recurred and the triamcinolone was increased to 48 mg. per day.
Despite this high
level of steroid medication the platelet count remained low and the patient
continued to
have intermittent bleeding from the nose and mouth.
No history of recent infection or exposure to unusual drugs or toxins could
be elicited.
The family history was normal in all respects.
Physical examination revealed an alert, chubby girl with a marked
Cushingoid appear-
ance who was in no acute distress. Temperature 100 F., pulse 88 per minute,
respirations
20 per minute, blood pressure 95/65, weight 55 pounds (90th percentile),
height 44
inches (25th percentile).
Examination of the skin revealed extensive purpuric lesions 1-15 mm. in
diameter
over the entire body as well as the mucous membranes of the mouth.
Petechiae were
especially numerous over both cheeks, sharply coinciding in distribution with
the in-
creased adipose tissue in this regin. Severe dental caries were present. The
liver was palpa-
ble 3 cm. below the right costal margin. The spleen and lymph nodes were
not palpable.
The remainder of the physical examination was within normal limits.
Laboratory examinations: Hemoglobin 11.8 Gm. per cent, hematocrit 36
per cent,
red blood count 3,900,000/mm.3, MCV 92.4 cu. /x, MCH 28.0 xpg.y MCHC
30.8 per cent,
reticulocytes 8.0 per cent, platelets 6,000/mm.3, white blood count
19,600/mm.3 with a
differential of 60 per cent polymorphonuclear leukocytes, 19 per cent band
forms, 4 per
cent metamyelocytes, 12 per cent lymphocytes, 5 per cent monocytes, and
1 nucleated
red cell per 100 white blood cells. Bleeding time (Ivy) 30 minutes (normal 2-7
minutes).
Examination of the peripheral smear revealed that the few platelets
present were en-
larged and bizarre in shape with some platelets up to 8 x in diameter. The
leukocytes
contained Dhle bodies. This latter finding persisted in blood smears
repeated throughout
the 2-month hospital stay. Examination of a bone marrow asprate from the
iliac crest
revealed increased numbers of megakaryocytes with no platelet formation.
Dohle bodies
were found in the myelocytes, metamyelocytes, band forms, and
polymorphonuclear neutro-
phils and eosinophils of the bone marrow, but none were seen in the cells of
the lympho-
cytic or monocytic series. The erythroid elements appeared normal.
Urinalysis: pH 7.0, specific gravity 1.023, albumin 0, sugar 0, acetone 0,
many red blood
cells, many white blood cells. Urie culture contained more than one million
colonies of
Escherichia coli per mi. Stool guaiac 3 plus.
Non-protein nitrogen 33 mg. per cent, (18 mg. per cent 2 days later),
fasting blood
sugar 87 mg. per cent, electrolytes normal. All liver function tests were
normal. Five L.E.
preparations during the hospital stay were negative. Blood Hinton test
negative. Urie
ncgative for 5-hydroxy-indole acetic acid.
Hospital course (see fig. 1). The patient was placed on sulfisoxazole 0 for
her urinary
tract infection and started on prednisone, 40 mg. per day. Because of the
possibility that
prolonged high doses of steroid may have been suppressing platelet
production,9 the dose
of prednisone was tapered over a 10-day period to 5 mg. per day. The
platelet count did
not increase and the patient developed spiking temperatures to 104 F., new
petechiae and
purpura, and bleeding from the nose and mouth. Mltiple cultures of the
throat, urie,
and blood were negative.
Intravenous infusin of a suspensin of fresh platelets was followed by
fever and chills
and no elevation of platelet count 12 hours after administration. Oral
prednisone was re-
sumed at 40 mg. per day but fever and purpura continued. The patient
developed intense
frontal headaches, slight papilledema, and mild right hemiparesis,
suggesting intracranial
bleeding. In view of these symptoms, a splenectomy was performed on
October 9, 1961.
At no time prior to the splenectomy was the platients platelet count above
7,000/mm3.
The splenectomy was well tolerated and the patient did not require blood or
platelet
Gantrisin (Roche).
From www.bloodjournal.org by guest on May 24, 2017. For personal use only.
DHLE BODIES AND PLATELET ABNORMALITY 659

transfusions. There were no postoperative complications. The spleen

weighed 88 Gm. (nor-
mal). Pathologic examination showed evidence of congestin, hyperplasia,
and some min-
imal vascular intimal thickening. There was nothing to suggest lupus
erythematosus. Fol-
lowing splenectomy the patient was maintained on prednisone. In the early
postoperative
period the platelet count did nct rise above 9,000. Her steroid medication
was changed
from prednisone to oral hydrocortisone, 40 mg. per day, with no change in
the platelet
count. The hydrocortisone was gradually tapered and then discontinued. The
tapering and
withdrawal of the steroids was associated with a return of the fever to 104 F.
No cause
could be found for this and prednisone was reinstituted, but the fever and
thrombocyto-
penia continued. Prednisone was again discontinued and once more an
intensive but un-
revealing search was made for infeetion or evidence of systemic lupus
erythematosus or
other connective tissue disease.
Intravenous hydrocortisone in a dose of 200 mg. per day was begun.
Within 12 hours
the patient became afebrile and remained so throughout the rest of her
hospital stay.
Forty-eight hours after the intravenous hydrocortisone was begun the
platelet count was
55,000 and therapy was changed to oral hydrocortisone, 200 mg. per day.
During the
next week her platelet count rose to 196,000/mm.3 and the hydrocortisone
was decreased to
100 mg. per day.
The patient was discharged in good clinical condition on hydrocortisone,
100 mg. per
day. She has since been followed at frequent intervals as an outpatient and
the hydro-
cortisone has been slowly tapered to its present level (4/5/62) of 15 mg. per
day. As the
dosage was lowered, there was a gradual fall in platelets to 44,000/mm 3.
Since then it
has remained in the range of 80,000-100,000/mm3. There has been no
evidence of
petechiae or purpura, she has remained afebrile, and there is no evidence of
neurologic
sequelae.
Special studies: Additional studies were performed on the patient and the
remainder of
her family in an effort to characterize further this anomaly.
In table 1 are listed the hematologic findings in the available members of
the family.
It will be noted that both the patients mother and one of her two brothers
also had
Dhle bodies in their leukocytes. Their platelet counts were repeatedly
normal although
giant platelets were consistently present on Wright-stained smears. There
was no evidence
in their past medical history to suggest purpura or a bleeding tendency.
Complete blood
typing failcd to reveal any evidence of linkage of the May-Hegglin anomaly to
the blood
From www.bloodjournal.org by guest on May 24, 2017. For personal use only.
660
OSKI, NAIMAN, ALLEN AND DIAMOND
4-
n * 4-* )
a s es c S
anGi

P* C Q* 0)
a O)C3 <D
C3 sa
>
E
3
es
H
d
H
J3
.si
ga
5 **
:0 %-i
Q
03
i
03
03
i
03
03
OI
03
i
03
a ^ *
j ^ ja S .a ^ es*' S
u H oT S S oT
3f Q Q 4- Q *4 ^
- i <4 u i rS H 8
8 W j. JO U -
^ < z* <
K
io
T
CD
><'
X
03
JO
C3
5
O

1
03
". i O 1 |
es TJ CD
oT co CD
i-H
g
00 lo 03 O O
S -
g H irj co
O IH H *-
H

& O t> p-
H

< <
D D
> IM 5
s c 0) O a; 5
1 .s o 5 o
*3 03 *-l t-i es
O CQ
From www.bloodjournal.org by guest on May 24, 2017. For personal use only.
DOHLE BODIES AND PLATELET ABNORMALITY 661
groups. Unfortunately the patients mother had no living relatives; therefore,
search for
other affected members vvas not possible.
Histochemical studies: To characterize further the Dhle bodies,
peripheral blood smears
were submitted to a number of special stains. Aside from a positive reaction
for ribo-
nuclec acid with methyl-green pyronine, stains for lipid (Sudan Black),
mucopolysac-
charide (Periodic Acid-Schiff), and desoxyribonucleic acid (Feulgen) were
negative.
To test the dual hypothesis that the Dhle bodies might represent
phagocytosed platelet
material and that the patients plasma contained a factor responsible for it,
the patients
leukocyte-free plasma was incubated with a suspensin of fresh normal white
cells and
platelets at 37 C. Wright-stained smears examined at periodic intervals for
12 hours
failed to reveal the presence of Dhle bodies or other phagocytosed partiles
in the normal
white blood cells.
Tlie mothers prothrombin consumption time and bleeding time were
normal.
Peripheral smears of 161 patients with thrombocytopenia that had been
seen at the
Childrens Hospital Medical Center in the past 5 years were carefully
reviewed and in
none were Dhle bodies seen.
DISCUSSION
This is the fourth report showing the familial nature of the May-Hegglin
anomaly. Our patient fulfills the criteria for classification as an example of
the May-Hegglin anomaly with Dhle bodies in her leukocytes in association
with giant platelets continuously for a period of 6 months in the absence of
severe infection or other known underlying cause. In addition, two members
of her family have also been found to have this anomaly on repeated
examina-
tions.
Dhle bodies are usually 1-2 fi in diameter (fig. 2). There is generally only
one in a cell but occasionally there may be more. There is no consistent
localiza-
tion within any particular area of the cytoplasm. With Wrights stain they
appear sky blue in color and are easily visible against the pinkish-gray cyto-
plasmic background. They are amorphous in shape but tend to be circular or
elliptical in outline.
The Dhle bodies are negative with fat and glycogen stains but appear
red
after staining with methyl-green pyronine, suggesting that they have a large
ribonucleic acid content. It has been demonstrated8,12 that after the cells are
incubated with ribonuclease the Dhle bodies no longer stain with the pyro-
nine, confirming that they are composed of ribonucleic acid. This has
suggested
that they represent areas of the cytoplasm that have failed to mature. Dhle
bodies may be observed in the myelocytes, metamyelocytes, band forms,
neutrophilic leukocytes, eosinophils and basophils. They are most easily and
most consistently seen in the neutrophilic leukocytes.
The platelets in the May-Hegglin anomaly show marked variations in size
and shape. Cigar-shaped and elliptical-shaped forms are common although
the
large round forms predomnate (fig. 3). Normal platelets may be as large as
4 /x in diameter15 while platelets as large as 15 /x have been observed8 in
this
condition. Although it is common to see large and bizarre platelet forms in
We are grateful to Dr. John Craig, Pathologist, Boston Lying-in Hospital,
for his
kind assjstance in the performance of these tests,
From www.bloodjournal.org by guest on May 24, 2017. For personal use only.
662 OSKI, NAIMAN, ALLEN AND DIAMOND
idiopathic thrombocytopenic States, the platelets in this condition are even
more striking. However, the size of the platelets in our family was not as
strik-
ing as that reported by others.** In addition, the platelets show uneven and
scant granulation, with eccentrically placed hyalomeres.
Including the present report, four families with the May-Hegglin anomaly
have been described. In addition, three isolated cases have also been re-
ported.0lft*11 Table 2 summarizes the data in all cases reported to date.
From our data and that of Hegglin, Wassmuth, and Petz, it appears that
this ancmaly follows an autosomal dominant mode of inheritance.
We agree with Davidscn10 that the patient reported by Leitner10 probably
dees nct represent a true case of the syndrcme inasmuch as the patient was
acutely ill with an apparent septicemia that was accompanied by thrombocy-
topenia, a hemolytic anemia and an apparent leukemoid reaction. No
autopsy
was performed and no family members were found to have this anomaly
when
studied. Since Dohle bodies may appear in toxic States, their presence in the
patient described by Leitner is not surprising and does not in itself constitute
sufficient evidence for including this patient with the others who have been
demonstrated to have the anomaly permanently.
Excluding the report of Leitner from the tabulation, it is noted that nine of
the 24 cases reported have had thrombocytopenia in association with their
morphologic abnormality. Although no member of the kindred reported by
Wassmuth was found to have thrombocytopenia at the time of study, the
possibility, as shown in our patient, that this is transitory in nature and was
not evident at the time of their examinations cannot be excluded. In
Hegglins
family all members had thrombocytopenia; in Wassmuths there was none.
It is of interest that in our family one member, the patient, has had thrombo-
cytopenia and two do not. The exact reason for this variable but increased
incidence of thrombocytopenia in this condition is not apparent but there are
several theoretical possibilities. The first is that the syndrome consists of
Dohle bodies, giant platelets, and thrombocytopenia, and that there is
variable
expressivity of the latter in different families. An alternative explanation is
that the abnormal platelet morphology refleets a disturbance of
megakaryocyte
or platelet metabolism which under the stress of ill-defined trigger factors,
such as infections, drugs, or toxins, results in thrombocytopenia.
We wish to thank Dr. R. Sheets for supplying us with slides from his
family with the
May-Hegglin anomaly.
Fig. 2.Pal blue Dohle body in cvtoplasm of neutrophil of patient with
the
May-Hegglin anomaly (peripheral smear, Wright stain).
Fig. 3.Giant platelet in peripheral blood smear of patient with the Mav-
Hegglin anomaly. (Similar abnormal platelets were present in the affected
relatives
who had normal platelet counts.)
Fig. 4.For contrast, a neutrophil from a patient with the Chedik-Higashi
svndrome, showing several large irregular cvtoplasmic inclusions. (The
tvpical slate-
green color is appreciated better in the original blood smears.) (Peripheral
smear,
Wright stain.)
From www.bloodjournal.org by guest on May 24, 2017. For personal use only.
DOHLE BODIES AND PLATELET ABNORMALITY
663
Figs. 2-4.See legends, facing page.

Summary of All Cases of the May-Hegglin

Table 2.- Anomaly Reported to Date
Propositu Dohle Giant
s Bodie Platelet Platelet Clinical
Author, Year Agre Sex s s Count Findings Outcome Family Studies
May, R.G 24 f prese present not known, not known not performed
1909 nt ap- transient
peared edema
normal and
on erythema
smear of legs
Hcgglin, R.7 50 m prese present 10,000- purpura died 14 two sons with t
1945 nt 30,000 yrs. anomaly,
after both
diag- thrombocytope
nosis, 30 other memb
cause of kin-
unknow ship found to b
n normal
Leitner, S., et 45 m prese present 50,000 pneumona, died patients moth
al.10 nt purpura, shortly sister, and
1954 anemia after three childr
ad- found to
mission be normal
, no
autopsy
Scholer, V., et 30 m prese present 25,000- No evidence unknown not performed
al.11 nt 110,000 of
1960 illness
Wassmuth, D., (not prese present normal No evidence not stated thirteen memb
et al.8 state nt of of 3 gen-
1961 d) illness erations fou
(abstract) to have
the anomaly
males, 4
females, ag
4-73; all
well
Petz, A., et al.17 (not prese not mild No evidence not stated father and 2 so
1960 state nt stated thrombo- of found to
(abstract) d) cytopenia illness have the
anomaly; al
well

Oski, F., et al. 6 f prese present 1,000- severe presently patients moth
1962 nt 220,000 purpura thrombocy and brother
- affected; bo
topenic well
From www.bloodjournal.org by guest on May 24, 2017. For personal use only.
DHLE BODIES AND PLATELET ABNORMAUTY 665
FAMILY PEDIGREE

Of the many leukocytic anomalies that have been described, the only one
that might be confused with the May-Hegglin anomaly is that seen in the
Chedik-Higashi syndrome.1'*14 However, when blood smears from the two
conditions are compared, the morphologic and staining differences between
the two types of granulocytic inclusions are readily apparent (figs. 2 and 4).
In the Chedik-Higashi anomaly (fig. 4) the cytoplasm of the neutrophilic
leukocytes contains numerousl;i 15 giant, coarse granules that appear
refractile
and stain greenish-gray with Wright s stain. Some of the lymphocytes contain
inclusions as well, generally single and staining red or the color of the
nuclear
chromatin. The granules of the eosinophils have been described as giant in
size. Platelet morphology is generally normal but thrombocytopenia may de-
velop terminally.
The clinical picture in the two conditions is also quite dissimilar. In the
May-Hegglin anomaly the patient is generally well, while patients with the
Chedik-Higashi anomaly may have repeated pyogenic infections, photo-
phobia, pal optic fund, excessive sweating, disturbances of pigmentation,
hepatosplenomegaly, lymphadenopathy, and generally die from this poorly
understood condition.
At present, one can only speculate on the relationship between the abnor-
mal platelet morphology and the development of thrombocytopenia in the
May-Hegglin anomaly. Although this anomaly may easily be overlooked in
the clinically well patient, it appears more than coincidence that 9 of 24
cases described to date had thrombocytopenia in association with their
anomaly. The relationship between the Dohle bodies and the platelet defect
is equally obscure.
All patients with thrombocytopenic purpura should be examined for this
anomaly. Although this defect is apparently rare, with further observations
it is hoped that this anomaly will be better defined as to incidence, course,
and prognosis. In addition, family studies are worthwhile in all such patients.
SlJMMARY
A six-year-old girl with thrombocytopenia was found to have the May-
Hegglin anomaly, consisting of Dohle bodies in the leukocytes in association
From www.bloodjournal.org by guest on May 24, 2017. For personal use only.
666
OSKI, NAIMAN, ALLEN AND DIAMOND
with giant platelets. This was also observed in the patients mother and
brother
who had normal platelet counts. The familial nature of this anomaly is again
confirmed, and the world literature reviewed. Its morphologic and clinical
features are contrasted with those seen in the leukocytes of the Chedik-
Higashi anomaly.
SUMMARIO IN INTERLINGUA
Esseva trvate que un puera de sex annos de etate con thrombocytopenia
habeva le anormalitate de May-Hegglin, consistente de corpores de Dhle
in le leucocytos in association con plachettas gigante. Isto esseva etiam ob-
srvate in le matre e le fratre del patiente le quales habeva normal numera-
tiones plachettal. Se corrobora le natura familial de iste anormalitate. Le
pertinente litteratura mundial es revstate. Le characteristicas morphologic e
clinic del condition es contrstate con dios vidite in le leucocytos del anor-
malitate de Chedik-Higashi.
ADDENDUM
At present (September 1962) the patient is clinically very well. Her plate-
let count is 240,000/mm.3 The hydrocortisone was discontinued in June.
REFERENCES
1. Dhle, V.: Leukoeyteneinschlusse bei
Scharlach. Zentralbl. Bakt. 61:63,
1911.
2.Kolmer, J. A.: Leucocytic inclusin
boches with special reference to
scarlet fever. Am. J. Dis. Child. 4:1,
1912.
3.McEwen, W.: An investigaron con-
cerning Dhles leucocytic inclusin
bodies in scarlet fever and other
diseases. J. Path. & Bact. 18:456,
1913-1914.
4. Bachman, R. W., and Lucke, B. H.:
The differential blood count, the
Arneth formula and Dhles [sic] in-
clusin bodies in pulmonary tuber-
culosis. N. Y. J. Med. 107:492, 1918.
5. Weiner, W., and Topley, E.: Dhle
bodies in the leukocytes of patients
with bums. J. Clin. Path. 8:324, 1955.
6.May, R.: Leukoeyteneinschlusse.
Deutsches Arch. klin. Med. 96:1,
1909.
7.Hegglin, R.: Simultaneous constitutional
changes in neutrophils and platelets.
Helvet. med. acta 12:439, 1945.
8. Wassmuth, D. R., DeGroote, B. A.,
Hamilton, H. E., and Sheets, R. F.:
An anomaly of granulocytes and
platelets: A newly established hered-
itary entity. J. Lab. & Clin. Med. 58:
969, 1961 (abstract).
9. Cohn, P., and Gardner, F. H.: The
thrombocytopenic effect of sustained
high dosage prednisone therapy in
thrombocytopenic purpura. New Eng-
land J. Med. 265:611, 1961.
10. Leitner, S. J., Neumark, E., and Heeres,
P. A.: Panmyclopathy with Dhle
bodies, thrombocytopenia and eryth-
roblastosis (Hegglins syndrome).
Acta haemat. 11:321, 1954.
11. Scholer, V. H., Im Hof, H., and Schns,
M.: Beobachtungen an einem weiter-
en Trager der May-Hegglinschen
Anomalie der Leukocyten und Blut-
plttchen. Schweiz. med. Wchnschr.
44:1269, 1960.
12. Hansson, H., Linell, F., Nilsson, L. R.,
Sderhjelm, L., and Undritz, E.: Foha
haemat. N. S. 3:152, 1959, cited by
Davidson, W.: Inherited variations
in leucocytes. Brit. M. Bull. 17:190,
1961.
13. Chedik, M.: Nouvelle anomalie leuco-
cytaire de caractre constitutionnel
et familial. Rev. hmat. 7:362, 1952.
14. Donohue, W. L., and Bain, H. W.:
From www.bloodjournal.org by guest on May 24, 2017. For personal use only.
DOHLE BODIES AND PLATELET ABNORMALITY
Chedik-Higashi syndrome: A lethal
familial disease with anomalous in- 16.
clusions in the leukocytes and con-
stitntional stigmata: Report of a case
with necropsy. Pediatrics 20:416, 17.
1957.
15. Wintrobe, M. M.: Clinical Hematology,
5th ed., Philadelphia, Lea & Febiger,
667
1961, p. 224.
Davidson, W.: Inherited variations in
leukocytes. Brit. M. Bull. 17:190,
1961.
Petz, A., Smith, I., and Nelson, N.: The
May-Hegglin anomaly: A study of
 three cases. Clin. Res. 8:215, 1960
(abstract).
Frank A. Oski, M.D., Trainee in Pediatric Hematology, Chilr
drens Hospital Medical Center, Boston, Mass.
Donald M. Alien, M.D., Instructor in Pediatrics, Harvard
Medical School; Associate Physician, Childrens Hospital Med-
ical Center, Boston, Mass.
Lotiis K. Diamond, M.D., Associate Professor of Pediatrics,
Harvard Medical School, and Director, Hematology Research
Laboratories, Childrens Hospital Medical Center, Boston,
Mass.
J. Lawrence Naiman, M.D., Trainee in Pediatric Hematology,
Childrens Hospital Medical Center, Boston, Mass.
From www.bloodjournal.org by guest on May 24, 2017. For personal use only.
1962 20: 657-667
Leukocytic InclusionsDohle BodiesAssociated with Platelet
Abnormality (The May-Hegglin Anomaly): Report of a Fami1y and Review of
the Literature
FRANK A. OSKI, J. LAWRENCE NAIMAN, DONALD M. ALLEN and LOUIS K.
DIAMOND

Updated information and services can be found at:

http://www.bloodjoumal.org/content/20/6/657.full.html
Articles on similar topics can be found in the following Blood collections
Information about reproducing this article in parts or in its entirety may be
found online at:
http://www.bloodjournal.org/site/misc/rights.xhtml#repub_requests
Information about ordering reprints may be found online at:
http://www.bloodjournal.org/site/misc/rights.xhtml#reprints
Information about subscriptions and ASH membership may be found online
at:
http://www.bloodjournal.org/site/subscriptions/index.xhtml
Blood (print ISSN 0006-4971, online ISSN 1528-0020), is published weekly by
the American Society of
Hematology, 2021 L St, NW, Suite 900, Washington DC 20036.
Copyright 2011 by The American Society of Hematology; all rights reserved.