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Severe thrombocytopenia

secondary to alcohol use

Steven Peltz, MD

Preview were not identified. Red blood cells

Thrombocytopenia is commonly seen among alcoholic pa- were normochromic and mildly
tients admitted to the hospital. Dr Peltz reviews a severe case anisocytotic. An electrocardiogram
of the disorder and discusses the causes, treatment, and showed changes typical of hypoka-
prognosis. The patient described here is unique in having the lemia.
lowest platelet count ever reported for this condition. The patient was transferred to
a telemetry bed. Hypokalemia re-
solved over the next few hours after
A 42-year-old woman with a 20- chloride 60 mmol/L, carbon dioxide- administration of intravenous and
year history of alcohol abuse present- combining power 38 mmol/L, blood oral potassium chloride. Hypochlor-
ed to the emergency department. urea nitrogen 10 mgfdL, and creati- emia and hyponatremia resolved af-
After maintaining strict sobriety for nine 1 mgldL. Serum folate and vi- ter 3 days' infusion of normal saline
6 months, she had begun to drink tamin B12 levels were normal. Liver solution. During this time, the pa-
heavily during the preceding 2 enzyme levels were mildly elevated. tient's platelet count changed dra-
weeks. During this time she had Results of coagulation studies were matically. From 29,000/mm3 on ad-
been unable to eat and had vomited normal. White blood cell count was mission, it dropped to 14,000/mm3
copious amounts of dear liquid dai- 3
2,700/mm , hematocrit was 44.5%, on day 2, 12,000/mm3 on day 3,
ly, but she had no other complaints. and 8,000/mm3 on day 4. The
The patient had had her last drink count then rose to 16,000/mm3 on
12 hours before presentation and day 5, to 165,000/mm3 on day 6,
had been taking no medications or 3
to 325,000/mm on day 7, and to
illicit drugs. 567,000/mm on day 8, when the
The patient was admitted to the patient was discharged.
alcohol detoxification unit. Physical The patient's white blood cell
examination revealed her to be well • count increased to 6,000/mm3 by
nourished, alen, and fully oriented. day 3 and then remained constant
Hean rate was regular at 96 beats A PERPLEXING CASE throughout her hospital stay. With
per minute, and blood pressure was hydration, hematocrit fell to 31.5%
130/80 mm Hg without onhostatic by day 4 with a corresponding retic-
changes. There was no palmar ery- and platelet count was 29,000/mm3 • ulocyte fraction of2%. By day 8,
thema, spider telangiectases, or evi- Peripheral blood smear revealed a hematocrit had increased to 35.2%
dence of mucocutaneous bleeding. marked reduction in platelet num- and the reticulocyte fraction had in-
Ascites and hepatosplenomegaly ber and a mild decrement in average creased to 4%.
were absent. Neurologic examina- platelet size. Schistocytes, hyperseg- Results oflaboratory studies con-
tion showed no abnormalities. mented neutrophils, and target cells ducted 3 weeks after discharge were
Results of guaiac testing of the normal, including hematocrit of 40%
stool were normal. Serum chemistry and platelet count of 441,000/mm·1•
Steven Peltz, MD
values were as follows: sodium 124 Dr Peltz is a fellow in internal rnedicine, Bay- The patient denied alcohol use dur-
mmol/L, potassium 1.5 mmol/L, ley Seton Hospital, Staten Island, New York. ing this interval.



Discussion deficiency) can produce thrombocy- even afrer blood alcohol levels are
About 10.6 million adults in the topenia, and this seems to be the undetectable. Aggregation of plate-
United States are alcoholics, and 4.6 most frequent cause of platelet de- lets, release of thrombo:xane A2 , and
million youths are problem drink- pletion in hospitalized alcoholics. 4·9- 11 availability of platelet factor 3 can all
ers.1 Up to one thirdofhospitalized The mechanism whereby excessive be impaired during alcohol inges-
adults have medical problems related ingestion of alcohol decreases platelet tion.15 Platelet aggregation decreases
to alcohol. 2 Thrombocytopenia with production has not been fully clari- by 50% in response to adenosine
a platelet count below 100,000/mm3 fied. Alcohol may be directly toxic diphosphate, epinephrine, and colla-
occurs in 26% of alcoholic patients to the bone marrow, and a decrease gen in patients whose blood alcohol
admitted to hospitals because of in- in megakaryocyte count has been level remains near 300 mg/dL for 7
toxication, alcohol withdrawal, or found by some investigators. 12 Oth- days. 3Therefore, bleeding times are
complications of alcoholism. 1 ers have found an increased mega- prolonged in chronic alcoholics even
The three principal causes of karyocyte mass in the marrow asso- in the absence of thrombocytopenia.
this type of thrombocytopenia are ciated with decreased delivery of Bleeding times return to normal af-
splenomegaly, folic acid deficiency, platelets to the blood, a picture com- ter 2 to 3 weeks of abstinence and
and a direct toxic effect of alcohol on patible with ineffective thrombo- correlate with improved number and
platelet production, survival, and poiesis.1 function of platelets. 15
function (alcohol-induced thrombo- Alcohol also decreases platelet Alcohol-induced thrombocytope-
cytopenia). 3-1 Splenomegaly with re- survival time. One studi 3 using nia is seen in drinkers who consume
sultant sequestration of circulating platelets labeled with chromium 51 the equivalent of 1 to 2 pints of
platelets occurs in alcoholics with showed a reduction in platelet life whiskey daily for weeks or months,
cirrhosis. Total platelet mass is nor- span from a mean of 8.5 days to 6.6 or even during shott binges.4·10'11
mal, and thrombocytopenia tends to days in patients with normal platelet Platelet count typically increases in
be chronic and stable. counts and to 3.8 days in patients 2 to 5 days afrer cessation of drink-
Thrombocytopenia is common with thrombocytopenia. This differ- ing.3·8 This delay appears to be relat-
with megaloblastic hematopoiesis re- ence was attributed to accelerated ed to the time needed for megakary-
sulting from deficiency of folic acid platelet destruction and was not due ocytes to recover from toxic depres-
or vitamin B12 • Folate deficiency to folate deficiency, splenic seques- sion induced by alcohol. 11 After this
affectS up to 40% of hospitalized al- tration, disseminated intravascular delay, platelet count increases at a
coholic patients, but vitamin B12 de- coagulation, or the presence of an- rate of20,000/mm3to 60,000/mm3
ficiency is rare." Thrombocytopenia ti platelet antibodies. 3·14 It is believed each day and peak counts occur
in these patients is not severe and that by impairing platelet function, from 11 to 14 days afrer hospital ad-
is mostly attributed to ineffective alcohol may make platelets less able mission. 3Rebound thrombocytosis
thrombopoiesis. 7 After folic acid re- to survive repeated surface interac- with platelet counts greater than
placement, the platelet count rises tions and eventually lead to their 450,000/mm3occurs in one third of
within 4 to 7 days, and normal levels premature destruction. 14 alcoholic patien~ and may also be
are achieved afrer 1 or 2 weeks. 8 Chronically heavy ingestion of seen in those who are not thrombo-
Researchers have shown that alco- alcohol can exert a deleterious effect cytopenic at the time of admission. 4
hol per se (ie, independent of folate on platelet function that persists During rebound thrombocytosis,
continued on page 85



some patients may be at increased present. Worsening thrombocytope- effect of alcohol on production,
risk of thromboembolic phenome- nia may signal another cause that ne- survival time, and function of
na.IG cessitates further evaluation, includ- platelets. Platelet count begins to
Leukopenia and anemia, like ing bone marrow examination. rise after 2 to 5 days' abstinence
thrombocytopenia, have been ob- fiom alcohol. The condition is
served in hospitalized alcoholics. 17 generally benign, and clinically
The causes include folate deficiency Summary significant hemorrhage is rare. Rllll
and a toxic effect of alcohol on bone
marrow. Reticulocytosis and a rise in Thrombocytopenia in hospital- Address for correspondence: Steven Peltz,
leukocyte count characteristically oc- ized alcoholics may be caused by MD, Department of Medicine, Bayley
cur with cessation of alcohol inges- splenomegaly; folate deficiency, Seton Hospital, 75 Vanderbilt Ave, Staten
tion and resumption of a normal and, most frequently, a direct toxic Island, NY 10304.
diet. 6 There is, however, no correla-
tion between thrombocytopenia and
the presence or severity of anemia or
leukopenia. 3 References
1. Centers fur Disease Conttol. Trends in mor- 10. Ryback R, Desfurges J. Alcoholic thrombo-
In alcoholics, the clinical signifi- tality from cirrhosis and alcoholism: United States, cytopenia in three inpatient drinking alcoholics.
cance of thrombocytopenia is not 1945-1983. JAMA 1986;256(24):3337-8 Arch Intern Med 1970;125(Mar):475-7
2. West LJ, Maxwell DS, Noble EP, et al. Alco- 11. Cowan DH, Hines JD. Thrombocytopenia
certain but it rarely causes serious holism. Ann Intern Med 1984;100(3):405-16 of severe alcoholism. Ann Intern Med 1971 ;74(1):
bleeding. 11 ' 18 If bleeding does occur, 3. Cowan DH. Effect of alcoholism on hemosta- 37-43
sis. Semin Hematol1980;17(2):137-47 12. Sullivan LW, Liu YK, Talariro L, et al. Alco-
thrombocytopenia would be expect- 4. Lindenbaum J, Hargrove RL Thrombocy- hol-induced thrombocytopenia in man. (Abstr) J
ed to worsen it and make it less re- topenia in alcoholics. Ann Intern Med 1968;68(3): Clin Invest 1968;47(1):95a
526-32 13. Cowan DH. Thrombokinecic studies in alco-
sponsive to treatment. Alcoholics 5. Wtlson]H. Alcoholic thrombocytopenia: a hol-related thrombocytopenia. J Lab Clin Med
with cirrhosis of the liver may have brief review. J Okla State MedAssoc 1980;73(1): 1973;81(1):64-76
13-7 14. Cowan DH. The platelet defect in alcoholism.
an increased tendency to hemor- 6. Lindenbaum]. Folate and vitamin B12 defi- Ann NY Acad Sci 1975;252:328-41
rhage because of coexistent coagula- ciencies in alcoholism. Semin Hematol1980;17(2): 15. Mikhailidis DP, Jenkins WJ, 8arradas MA,
119-29 et al. Platelet function defects in chronic alcohol-
tion defects; however, no significant 7. Wmttobe MM, Lee GR, Boggs DR, et al. ism. BMJ 1986;293(20 Sep):715-8
change in coagulation occurs with Clinical hematology. 8th ed. Philadelphia: Lea & 16. Haselager EM, VreekenJ. Rebound throm-
Febiger, 1981:1112 bocytosis after alcohol abuse: a possible factor in the
alcohol ingestion in the absence of 8. Jadcson DP. Management of thrombocytope- pathogenesis of thromboembolic disease. Lancet
cirrhosis. 3 nia. In: Colman RW, Hirsh}, Marder VJ, et al, eds. 1977;1{8015):774-5
Hemostasis and thrombosis: basic principles and 17. Sullivan LW, Herbert V. Suppression of he-
Most hospitalized alcoholics with clinical practice. 2d ed. Philadelphia: JB Lippincott, matopoiesis by ethanol. J Clin Invest 1964;43(11 ):
thrombocytopenia can be treated ex- 1987:531 2048-62
9. Post RM, Desfurges JR Thrombocytopenia 18. Eichner ER, Hillman RS. The evolution of
pectantly after folic acid supplemen- and alcoholism. Ann Intern Med 1968;68(6): anemia in alcoholic patients. Am J Med 1971;
tation is begun. Thrombocytopenia 1230-6 50(Feb):218-32
caused by folate deficiency and di-
rect alcohol toxicity can be expected
to subside after 2 to 5 days of absti- Readers are invited to submit brief reports of perplexing cases related to primary medi-
nence. If thrombocytopenia remains cal care. Address submissions to: Manuscript Administrator, POSTGRADUATE MEDICINE,
consistent, hypersplenism may be 4530 W 77th St, Minneapolis, MN 55435.