Correspondence THE PLATELETS IN GLANDULAR FEVER ANIJ IDIOPATHIC THROMIIOCYTOPENIC PURPURA Chanarin et al (1077) report that autoimmunity to platelets can be shown in both glandular fever (GF) and idiopathic thrombocytopenic purpura (ITP). This link between ITP and GF even when the platelet count is normal is also considered by Dixon & Rosse (1975) and is of great interest to us because we have other evidence suggesting a link and perhaps a common immunological process in these tw-o disease states. The heparin thrombin clotting time (HTCT) of platelet poor plasma measures the total heparin neutralizing activity (HNA) of the plasma. A short HTCT indicates an excess of HNA and vice versa. This non-specific test is thought largely to depend on a platelet factor 4-like activity and may thus reflect the degree of platelet factor 4 (PF4) released or otherwise liberated from the platelets into the plasma in v i m . Because the HTCT uses the patient's plasnia as substrate a sensitive thrombin clotting time is always carried out to check whether the substrate reacts normally to thrombin. For example, there is little plasma HNA in aplasia when there are few circulating platelets and conversely there is much HNA in the plasma from patients with thrombosis when platelets are presumably activated and may also undergo the release reaction (O'Brien et af, 1975); yet such platelets can apparently continue to circulate in a degranulated and 'exhausted' state (Reimers et al, 1976). Thirty available patients with sero-positive and hacmatological evidence of GF were studied sequentially and a platelet count, the HTCT and a dilute thrombin clotting time were also measured. Twenty-three apparently healthy age-matched controls were studied in parallel. Table I shows that the mean H T C T of the GF patients (61.6 s) is very significantly different from the controls (25.9 s). The thrombin clotting time of the GF groups w a s on average 3 . 5 s longer than the controls. This difference of 3.5 s possibly reflecting a slight change in the reactivity of the substrate might diminish the significance of the difference in the HTCTs but could hardly account for a mean difference of 3 5 s. During the same period 16 patients with ITP were similarly studied. Most were young and had an acute short attack of ITP preceded by an infection. Few adults with sub-acute or chronic ITP were included (this may represent a different disease entity). Again it will be seen that the HTCT is pathologically prolonged (Table I) and this is in agreement with a preliminary report (O'Brien et al, 1974). TABLE 1. Heparin thrombin clottiiig time (HTCT) and thrombin clotting time (Th.CT) in glandular fever (GF) and Idiopathic thrombocytoperuc purpura (ITP) with the means, range in parentheses and the standard error NO.

Age

GF patients

30

21

Controls ITP patients

23

21

16

(3-72) (16-28) 23 ( 3 - 6 0 )

count x

Platelet

io9/1

HTCT

(5)

61.6+27.2** (16-328)f81.34 249 (105-340)f62.39 25.95+ 7.8** 24 (5-70) f 19.69** 56.75f 14.85

201

* Prelative to controls