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Article Review/Hyperlink
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Yamamoto S, Koide M, Matsuo M, Suzuki S, Ohtaka M, Saika S,
Matsuo T
Heparin-induced thrombocytopenia in dialysis patients
Am J Kidney Dis
(Jul) 28:82-85 1996

Heparin-induced thrombocytopenia (HIT) is an important
complication of heparin therapy. Its incidence in hemodialysis
patients, who receive heparin thrice weekly, is unknown. The
objective of this study was to determine its incidence and to
characterize its subtypes. Of 154 hemodialysis patients, six
(3.9%) developed HIT. The diagnosis was suspected by clotting of
the extracorporeal circuit in the presence of thrombocytopenia.
Five had anti-platelet factor 4-heparin complex antibody detected
by ELISA and were diagnosed with immunologic HIT (of note only
three of these had heparin-induced platelet aggregation in an in
vitro assay; see comment). The etiology in the other patient is
not clear (this patient had a positive platelet aggregation test
but negative antibodies). Heparin was discontinued and an
alternate anticoagulant (either argatroban or nafamstat mesilate)
used. In conclusion, the incidence of HIT in hemodialysis
patients appears to be 4-5%, and can be diagnosed in most
patients by the ELISA assay.
Comment:
HIT is clinically suspected when thromobocytopenia
occurs with or without thrombosis in patients receiving heparin.
Diagnosis is usually made by a positive platelet aggregation test
in which the ability of heparin to aggregate platelets incubated
in platelet rich plasma is assessed. There appears to be two
forms of HIT: a mild early onset thrombocytopenia, possibly due
to non-immunologic mechanisms, and a more severe delayed-onset
immunologically mediated disease which is often associated with
clinical thrombosis. Diagnosis of inmmunologically-based HIT can
be made by ELISA (as in this paper), by platelet aggregometry or
by platelet serotonin release. ELISA is a more sensitive test
than is platelet aggregometry but ELISA gives in more false positive
results.
We initially reported HIT in two hemodialysis patients with
thrombocytopenia (Leehey DJ et al. Int J Artif Organs 10: 37-39,
1987). Yamomoto et al report an incidence of HIT of 3.9% (6/154
patients) in their hemodialysis unit; however, testing was
performed only when HIT was clinically suspected. When all
patients in a chronic hemodialysis facility are screened, the
prevalence of heparin-dependent antibodies is lower (1.5%) and
not different from that in patients treated with short-term
continuous heparin (Kappers-Klunne M, et al. Blood 1995;
86:900a).
Treatment of HIT generally involves discontinuation of heparin,
although this may not always be necessary, especially after
thrombocytopenia has resolved. In patients in whom heparin
cannot be discontinued, heparin in combination with low dose
aspirin may be helpful in prevention of thrombosis (Hall AV et
al. Clin Nephrol 1992; 38: 86-9 and HL Messmore, Hines/Loyola
Medical Center, personal communication). Use of low-molecular
weight heparin (LMWH) will not in general be of use once HIT has
developed, since such patients also generally react to LMWH (HL
Messmore, personal communication). Another option (although not
available in the U.S.) is the use of danaparoid (Org 10172;
Organon), which is a low-molecular weight heparanoid consisting
of a mixture of sulfated glycosaminoglycans including heparan
sulfate, dermatan sulfate, and chondroitin sulfate which rarely
cross reacts with heparin. This heparanoid has been used
successfully in hemodialysis patients with HIT (Greinacher A et
al, Nephrol Dial Transplant 1993; 8: 1176-7).
(David J. Leehey, M.D., Loyola University at Chicago)
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