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Microsoft word - ojha et al pdf
Universal Journal of Medicine and Dentistry Vol. 1(3) pp. 034-036, March, 2012 Available online http://www.universalresearchjournals.org/ujmd Copyright 2012 Transnational Research Journals
Case Report
Acute severe thrombocytopenia in a young male; Case report and review of literature Abhishek Ojha1, Nishtha Sareen2 Greg Savino3, and Manouchkathe Cassagnol4
1MBBS Ravindra Nath Tagore Medical College, India
2MBBS Long Island Jewish Medical Center (Department of Medicine
3 St. John’s University College of Pharmacy and Allied Health Professions
4 St. John’s University College of Pharmacy and Allied Health Professions (Clinical Pharmacy Practice Department);
Long Island Jewish Medical Center (Department of Pharmacy Services)
A 42 year old male presented to the emergency department (ED) complaining of progressive oral mucosal bleeding, rectal bleeding and diffuse petechiae over 72 hours. He denied any other systemic symptoms. On presentation to our ED, he had diffused multiple petechiae on his torso and bilateral lower extremities. His medical history was significant for sarcoidosis diagnosed 3 years ago for which he was not on any medications. 3 weeks prior to this presentation, he had noticed spots in his left visual field and upon examination was found to have retinal hemorrhages. As a part of the work up, serum IgM (Immunoglobulin M) was positive for toxoplasmosis and he was given a 2 week course of trimethoprim/sulfamethoxazole (TMPSMX). His visual symptoms had resolved at the time of his presentation to ED. His vital signs were stable. Initial blood work revealed a platelet count of 3,000 cells/µL. He always had normal platelet count before. Given both worsening toxoplasmosis and sarcoidosis could have caused thrombocytopenia, a thorough work up was undertaken. A repeat serum toxoplasmosis IgM was negative. His serum Angiotensin Converting Enzyme (ACE) level was elevated to 87, serum Lactate Dehydrogenase (LDH) and Liver Function Tests (LFTs) were within goal. Human Immunodeficiency Virus (HIV) and Hepatitis screen were both negative. Chest X ray revealed hilar lymphadenopathy and patchy opacity right upper lobe, consistent with known sarcoid disease. Computed Tomography (CT) Chest revealed numerous upper lobe peri-bronchial pulmonary nodules, right paratracheal, bilateral hilar and subcarinal lymphadenopathy. On day 2 of hospitalization, the platelet count further decreased to nadir of 1,000 cells/µL. Due to the worsening thrombocytopenia, the patient was transferred to the Medical Intensive Care Unit (MICU) where he was given two doses of 70 mg intravenous immune globulin (IVIG) along with a single 40 mg dose of intravenous dexamethasone. By day 4, his platelet count increased to 17,000 cells/µL. On day 5 of hospitalization the platelet count increased to 78,000 cells/µL and he was discharged later that day. Two days after discharge the platelets normalized to 285,000 cells/µL. No further complications were noted after discharge. Key Words: bleeding, thrombocytopenia, sulfamethaxazole-trimethoprim, sarcoidosis DISCUSSION
Thrombocytopenia is often defined as a platelet count
be attributed including, but not restricted to systemic
≤100,000cells/µL or a reduction from baseline of greater
infections, alcohol intoxication, vitamin B 12 deficiency,
than 50%. There are multiple etiologies, to which it can
severe liver dysfunction, hereditary conditions (Fanconi’s/
Thrombocytopenic Purpura, Disseminated Intravascular
*Corresponding author Email:[email protected], Tel: 718-
Coagulopathy, Systemic Lupus Erythematosus,
the hospital where he was found to have a platelet count
of <5,000 cells /µL. He was administered 1mg/kg of oral
prednisolone daily for 2 weeks, over which his
thrombocytopenia associated with either sarcoidosis or
thrombocytopenia resolved. He was discharged with an
toxoplasmosis does exist and is typically accounted for
additional four weeks of oral prednisolone to be tapered
by case reports (Tuon et al., 2008 and Larner et al., 1990
and was said to remain well after treatment.
and 2010). This patient had both of these conditions
In a similar case, a 54 year old woman (Yamreudeewong,
previously diagnosed, but was recently started on
et al., 2002) developed blood blisters in her mouth and
TMP/SMX. The chronology of events during his drug
petechiae on her hands after 9 days of therapy with
therapy provided the greatest indication that TMP/SMX
TMP/SMX 160mg/800mg. A complete blood count
was the most credible causative agent of his
revealed a platelet count of 2,000cells/µL and TMP/SMX
thrombocytopenia. The Naranjo Nomogram for Causality
was discontinued. Treatment consisted of a transfusion of
(Naranjo et al., 1981) yielded a score of 6, making
two units of platelets along with oral prednisone 60mg
TMP/SMX a probable cause of this adverse drug event.
given twice daily. After 1 day of treatment (and TMP/SMX
Hence, TMP/SMX was discontinued and he was
discontinuation) the patient’s platelets increased to 7,000
The incidence of drug-induced thrombocytopenia,
manifestations had gradually resolved over the hospital
excluding heparin, has been estimated to be 10 cases
course. By day 5 of hospitalization, platelets were
per 1,000,000 persons, in the general population, per
110,000 cells/µL. The patient was discharged and 10
year (Dipiro et al. 2008). Well over 100 medications have
days of oral prednisone was tapered to discontinuation.
been found to induce thrombocytopenia and a number of
Two weeks later her platelet count was 351,000 cells/µL.
mechanisms have been proposed5 including 1) direct
In a third report, a 40 year old male developed an
toxicity reactions, 2) hapten-type immune reactions, 3)
erythematous rash on his face after 5 days of TMP/SMX
platelet-reactive autoantibodies and 4) drug-dependent
80mg/400mg treatment (Kocak et al 2006)., TMP/SMX was
autoantibodies. Most commonly, an immunologic reaction
withdrawn and levofloxacin was initiated to treat the
is seen and occurs when the offending drug binds to
condition, but the condition progressed to the oral
certain platelet glycoproteins, forming an antigenic
mucosa, trunk and extremities. Antihistamines and
complex. Antibodies are then generated and bind to
steroids did not work well in the patient. Platelet count
these complexes. This results in an increased peripheral
was 133,000 cells/dL and most other laboratory values
lysis of platelets through complement activation or
were below normal range. The patient was diagnosed
circulating macrophages (Dipiro et al. 2008). Although
with neutropenia (WBC, 700 cells/dL; ANC, 200 cells/dL)
TMP/SMX is considered to be an effective and well
and erythroderma. Despite continued steroid therapy,
tolerated therapeutic antibiotic, rare and serious side
whole blood, red cell concentrates, thrombocyte
effects have been established even with normal dosages.
transfusions and filgrastim, laboratory results on day 8 of
hospitalization revealed a platelet count of 4,000 cells/dL.
Three days later the patient died despite continued ther
Review of literature
In our patient, platelet levels on admission were
3,000cells/µL. Platelet transfusions yielded no increase in
To date, there have been 3 cases of thrombocytopenia
the patient’s platelet count, but may have acted as a
due to oral trimethoprim/sulfamethoxazole (MEDLINE
supplement to counteract platelet lysis by drug
search from January 1965 to July 2010). The three
dependent antibodies. Platelet levels dropped to
similar case reports of severe thrombocytopenia possibly
1,000cells/µL by day 2 of hospitalization and the patient
precipitated by oral TMP/SMX administration are
was administered dexamethasone. While corticosteroid
summarized in tabular format (table 1) (DiPiro et al., 2008
therapy was also seen in the other three cases with
beneficial outcomes, due to the severity of our patient’s
Generally, TMP/SMX thrombocytopenia reactions occur
thrombocytopenia, intravenous immune globulin (IVIG)
approximately 5 to 9 days after exposure. The onset time
was also initiated. IVIG is thought to exert its activity in
seen in our patient was approximately 7 days, which
the reticuloendothelial system through blockade of the Fc
coincides with other reports. Primary treatment entails
receptor on macrophages, disallowing antibody binding
discontinuation of the offending agent and supplementary
and thus platelet phagocytosis (Immune Globulin 2010) .
treatment modalities should be utilized (DiPiro et al.,
Improvement in clinical manifestations and platelet count
occurred over the next two days. By day 5, steroid
Papaioannides et al. 2003, reported a case of a 58 year
therapy was still in place and platelets reached 78,000
old male who discontinued TMP/SMX 160mg/800mg
cells/µL. The patient was discharged on day 5 with no
therapy 2 days before completion of a 10 day course due
to easy bruising. The subsequent development of
widespread purpuric lesions and rhinorrhagia led him to
036. Univers. J. Med. Dent. Table (1): Case Reports of Trimethoprim/Sulfamethoxazole Induced Severe Thrombocytopenia Age/ Gender TMP/SMX Dose Initial Clinical Platelet Frequency Signs/Symptoms Manifestation Co-trimoxazole Induced Acute 58/Male Thrombocytopenic Purpura 12 Thromboctopenia 54/Female Possibly Associated TMP/SMX Therapy 13 Trimethoprim-Sulfamethoxazole Hematologic Disorders 14 CONCLUSION
Koda-Kimble et al (2008). "Drug-Induced Thrombocytopenia." Applied
Therapeutics: The Clinical Use of Drugs. 9th ed. Philadelphia: Lippincott Williams and Wilkins. 87(7): 9-87
Presentation with thrombocytopenia has a very broad
Toxoplasmosis (2009)." Division of Parasitic Diseases. Centers for
differential and could pose a diagnostic dilemma in a
patient with underlying multiple comorbidities. Medication
2009.Web.21June2010.<http://www.dpd.cdc.gov/dpdx/HTML/Frames
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/SZ/Toxoplasmosis/body_Toxoplasmosis_serol1.htm>
Tuon et al. (2008). "Acute Immune-mediated Thrombocytopenic
carefully in any young patient presenting with low
Purpura Related to Toxoplasma Gondii Infection." International
platelets. Also, practitioners should educate patients on
Journal of Infectious Diseases 12(6 ): 671-72
the side effects of prescribed medications and monitor
Gurkan et al.(2003). "Immune Thrombocytopenic Purpura Associated
their blood levels routinely for any life threatening
with Brucella and Toxoplasma Infections." Am. J. Hematol. 74(1): 52-54.
complication as thrombocytopenia. Continual self
monitoring in combination with the monitoring of platelets
<http://www3.interscience.wiley.com/cgi-
when indicated may aid in early recognition of
thrombocytopenia and can reduce more serious
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(1990):31719.PubMedCentral.3Feb.1990.Web.23June2010.<http://w
underlying mechanism responsible for drug-induced
ww.ncbi.nlm.nih.gov/pmc/articles/PMC1661928/?tool=pubmed>.
thrombocytopenia, especially in patients receiving various
Naranjo et al.(1981). “A Method for Estimating the Probability of
Adverse Drug reactions.” Clinical Pharmacology and Therapeutics 30 (1981):
medications.2,4 Clinicians should use laboratory findings,
<http://www.nature.com/clpt/journal/v30/n2/pdf/clpt1981154a.pdf>.
evidence from recent reports and the temporal
DiPiro et al (2008). "Treatment: Drug-Induced Thrombocytopenia."
relationship to aid in causal determination of such events.
Pharmacotherapy: A Pathophysiologic Approach. 7th ed. New York:
Papaioannides et al(2003). "Co-trimoxazole Induced Acute
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