Levels Of Platelet-associated Immunoglobulin Research Articles

Effects of low concentrations of benzene exposure on levels of platelet-associated antibodies and platelet parameters.

To evaluate the impact of exposure to low concentrations of benzene on the platelet-associated antibodies and platelet parameters. We carried out an analysis on 121 benzene-exposed workers and 110 healthy workers whose blood samples were collected and the levels of platelet-associated antibodies and platelet parameters were assessed. Benzene emissions were monitored over 5 years. Large-platelet cell ratios (P-LCR), platelet distribution width (PDW), and mean platelet volume (MPV) were significantly higher in benzene-exposed participants than in control participants. In participants who smoke cigarettes or drank alcohol, P-LCR, PDW, and MPV were more significantly elevated in the benzene-exposed group than in nonsmokers and nondrinkers. Platelet-associated immunoglobulin (PAIg) levels in benzene-exposed participants were higher than those in the control group, and PAIgA and PAIgM levels correlated with cumulative benzene exposure. Exposure to low concentrations of benzene can induce changes in PAIg levels and platelet parameters.

Increased Levels of Platelet-Associated Immunoglobulin G in a Patient With Pulmonary Adenocarcinoma

This report describes a rare case of thrombocytopenia with high levels of platelet-associated immunoglobulin G (PA-IgG) in a patient with an adenocarcinoma of the lung. After surgical resection, the platelet count gradually increased and the serum PA-IgG levels decreased to within normal reference ranges. These findings suggest a relationship between pulmonary adenocarcinoma and PA-IgG.

Significance of Laparoscopic Splenectomy in Patients with Hypersplenism

This study was aimed at investigating the efficacy and safety of minimally invasive laparoscopic splenectomy in patients with hypersplenism secondary to cirrhosis. While advances have been made in the treatment of liver cancer and chronic hepatitis, certain treatments such as radio frequency ablation (RFA) must often be discontinued due to thrombocytopenia caused by hypersplenism. Laparoscopic splenectomy is performed to treat diseases as idiopathic thrombocytopenic purpura, but is contraindicated for hypersplenism in many institutions. Few studies have thus examined the safety and efficacy of this approach. Efficacy and safety were retrospectively analyzed for laparoscopic splenectomies starting from January 2003. Relationships between postoperative increases in platelet count and thrombopoietin, platelet-associated immunoglobulin, excised spleen weight, and serum parameters were examined. Perioperative data of open splenectomies starting from January 1990 were compared with those of laparoscopic splenectomies. No laparoscopic cases were converted to open surgery in this series. Mean operative times of open and laparoscopic splenectomy were 205 and 173 min respectively. Mean blood losses were 750 and 359 ml (P < 0.05) and the mean weights of excised spleen were 460 and 525 g respectively. Postoperatively, no changes in liver function were noted, and platelet and leukocyte counts were significantly increased. Compared with preoperative platelet count, degree of increase at 2 weeks postoperatively did not correlate with preoperative thrombopoietin levels, but significantly correlated with levels of platelet-associated immunoglobulin and spleen volume (P < 0.05). Postoperative portal or splenic vein thrombosis (PSVT) was seen in 3 patients and these patients did not exhibit any clinical symptoms. Laparoscopic splenectomy is a safe technique for the treatment of hypersplenism and contributes to postoperative increases in platelet counts. Postoperative increases in platelet count seem to depend on platelet-associated immunoglobulin level and spleen weight, which may be valuable prognosticators.

Marked improvement of thrombocytopenia in a murine model of idiopathic thrombocytopenic purpura by pegylated recombinant human megakaryocyte growth and development factor.

We examined the stimulatory effect of pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) on platelet production in male (NZW x BXSB) F(l) (W/B F(1)) mice, a murine model of idiopathic thrombocytopenic purpura. A cohort of 19- to 25-week-old, severely thrombocytopenic male W/B F(1) mice were given PEG-rHuMGDF at different dosing schedules. Before and at various times after therapy, platelet counts, reticulated platelets, platelet lifespan, and levels of platelet-associated immunoglobulin G were measured. Analysis of megakaryocytic cells was performed. Treatment of male W/B F(1) mice with PEG-rHuMGDF (30 microg/kg/day) three times per week for several weeks resulted in sustained thrombocytosis, accompanied by increased megakaryocytopoiesis in both the bone marrow and spleen. The degree of the platelet response to PEG-rHuMGDF varied between individual mice, likely reflecting the heterogeneity of the disease. Production of new platelets in response to PEG-rHuMGDF was manifested by an increase in reticulated platelets. Levels of platelet-associated immunoglobulin G decreased inversely during periods of thrombocytosis. PEG-rHuMGDF therapy also improved thrombocytopenia in male W/B F(1) mice refractory to splenectomy. Platelet lifespan was not affected by PEG-rHuMGDF. Male W/B F(1) mice treated with pegylated murine MGDF, a homologue of PEG-rHuMGDF, had persistent thrombocytosis for at least 7 months, suggesting that antiplatelet antibody production was not enhanced. PEG-rHuMGDF therapy potently stimulated platelet production, effectively ameliorating thrombocytopenia in a murine model of idiopathic thrombocytopenic purpura.

Treatment with megestrol acetate improves human immunodeficiency virus-associated immune thrombocytopenia.

Splenic macrophage Fc gamma receptors participate in the pathophysiology of immune cytopenias, and in such disorders, the beneficial effects of glucocorticoids are in part mediated by decreased expression of macrophage Fc gamma receptors. In the animal model, progesterones, like glucocorticoids, inhibit expression of these receptors. Megestrol acetate (MA) is a progesterone frequently used for treating human immunodeficiency virus (HIV)-associated anorexia-cachexia. Twenty-eight patients with HIV-associated thrombocytopenia with shortened platelet survival and increased platelet-associated immunoglobulin G (IgG) who were being treated with MA for anorexia-cachexia were prospectively studied for a 6-month period to assess the potential role of progesterones in the treatment of immune thrombocytopenia. Treatment with MA for non-consecutive periods of 2 months and 1 month significantly increased platelet count and platelet survival without significant alteration of platelet-associated immunoglobulin levels. Of the 28 patients studied, 22 presented a complete response, 19 presented a complete response 1 month after finishing the MA treatment regimen, and 12 remained in complete response for a further month. Expression of Fc gamma receptors (Fc gamma RI and Fc gamma RII) by peripheral blood monocytes and the in vitro recognition of IgG-sensitized cells by monocytes were significantly decreased by the MA treatment. Decreased expression and functioning of these receptors significantly correlated with platelet counts and survival times, but no relationship was found with platelet-associated immunoglobulin, circulating immune complexes, body mass index, plasma HIV load, or CD4 lymphocyte levels. These results suggest that treatment with progesterones, like MA, may be an alternative therapy for immune cytopenias, with few side effects.

Treatment with liposome-encapsulated clodronate as a new strategic approach in the management of immune thrombocytopenic purpura in a mouse model

Immune thrombocytopenic purpura (ITP) is an autoimmune disease related to the presence of elevated levels of platelet-associated immunoglobulin, or autoantibodies. In recent years the importance of macrophage Fcγ receptors in the uptake of platelets in ITP has been confirmed. Although in patients with ITP the platelet destruction occurs in liver and spleen, in this present experimental mouse model the liver was the principal organ of sequestration of sensitized platelets. The uptake in the spleen, bone marrow, lung, and kidneys was negligible and not different from that in control animals. In addition, the trapped platelets did not return to circulation, and new cells derived from the platelet-storage pool or new thrombocytogenesis were necessary to restore the platelet count. The depletion of splenic and hepatic murine macrophages by liposome-encapsulated clodronate (lip-clod) was studied as a new strategy for ITP treatment. Lip-clod inhibits, in a dose-dependent manner, the antibody-induced thrombocytopenia. Moreover, lip-clod treatment rapidly restored (24 hours) the platelet count in thrombocytopenic animals to hematologic safe values, and despite additional antiplatelet antiserum treatment, mice were able to maintain this level of platelets at least up to 48 hours. The bleeding times in lip-clod–treated animals was not different from those in controls, demonstrating that the hemostasis was well controlled in these animals. The results presented in this study demonstrate that lip-clod treatment can be effective in the management of experimental ITP.

Treatment with liposome-encapsulated clodronate as a new strategic approach in the management of immune thrombocytopenic purpura in a mouse model

AbstractImmune thrombocytopenic purpura (ITP) is an autoimmune disease related to the presence of elevated levels of platelet-associated immunoglobulin, or autoantibodies. In recent years the importance of macrophage Fcγ receptors in the uptake of platelets in ITP has been confirmed. Although in patients with ITP the platelet destruction occurs in liver and spleen, in this present experimental mouse model the liver was the principal organ of sequestration of sensitized platelets. The uptake in the spleen, bone marrow, lung, and kidneys was negligible and not different from that in control animals. In addition, the trapped platelets did not return to circulation, and new cells derived from the platelet-storage pool or new thrombocytogenesis were necessary to restore the platelet count. The depletion of splenic and hepatic murine macrophages by liposome-encapsulated clodronate (lip-clod) was studied as a new strategy for ITP treatment. Lip-clod inhibits, in a dose-dependent manner, the antibody-induced thrombocytopenia. Moreover, lip-clod treatment rapidly restored (24 hours) the platelet count in thrombocytopenic animals to hematologic safe values, and despite additional antiplatelet antiserum treatment, mice were able to maintain this level of platelets at least up to 48 hours. The bleeding times in lip-clod–treated animals was not different from those in controls, demonstrating that the hemostasis was well controlled in these animals. The results presented in this study demonstrate that lip-clod treatment can be effective in the management of experimental ITP.

High prevalence of anticardiolipin antibodies in hepatitis C virus infection: lack of effects on thrombocytopenia and thrombotic complications.

Hepatitis C virus (HCV) causes various extrahepatic immunologic abnormalities. Recently, an association between HCV infection and antiphospholipid syndrome, including thrombocytopenia, has been reported. However, the precise relationship between thrombocytopenia and anticardiolipin antibodies in patients with chronic HCV infection is not fully understood; likewise, the association of antiphospholipid syndrome and various liver diseases is not well understood. To evaluate the prevalence and importance of antiphospholipid antibodies in various chronic liver diseases, we determined the levels of anticardiolipin antibodies, platelet numbers, and levels of platelet-associated immunoglobulin G (PA-IgG) and thrombin-antithrombin III complex (TAT) in patients with chronic HCV infection, chronic hepatitis B virus (HBV) infection, and primary biliary cirrhosis (PBC). The prevalence of anticardiolipin antibodies in patients with HCV infection was significantly higher than that in control subjects or individuals with the other liver diseases examined. However, there was no significant correlation between anticardiolipin antibodies and platelet counts or TAT. The frequency of thrombotic complications was similar in anticardiolipin antibody-positive and -negative patients with chronic HCV infection. Further, sera from all but one anticardiolipin antibody-positive HCV patient were negative for phospholipid-dependent anti-beta2 glycoprotein I antibodies. Our results suggest that anticardiolipin antibodies are frequently found in patients with chronic HCV infection, but they do not appear to be of clinical importance. Immunologic disturbances induced by HCV or prolonged tissue damage in systemic organs as a result of the extrahepatic manifestations of HCV infection may induce the production of antibodies to various cardiolipin-binding proteins or phospholipids.

Assays for heparin-induced thrombocytopenia.

Tests for the presence of heparin-dependent antibodies (heparin-Ig) have evolved in parallel with improved understanding of the pathophysiology of heparin-induced thrombocytopenia (HIT). The first group of tests relied upon platelet aggregation or activation. Among tests in this group, the serotonin release assay has been reported to demonstrate the best performance characteristics. However, this test has not been widely adopted outside a few specialized laboratories owing to its complexity and need for radioactive materials. As a result, the less sensitive and specific platelet aggregation test is more commonly used for the diagnosis of heparin-Ig. The literature suggests that test sensitivity can be improved by the use of the patient's own platelets, platelets from selected donors known to be reactive in the assay, or washed platelets. Test specificity has been enhanced by the use of two point assays that include neutralization of the reaction by a high dose of heparin. A second group of assays have focused on detection of heparin-dependent binding of immunoglobulins to the platelet membrane. Most of these tests are hampered by the fact that platelets in patients with suspected HIT and in conditions that are in the differential diagnosis of HIT frequently express high levels of platelet-associated immunoglobulin. The most recent tests for heparin-Ig are based on the recognition that patient antibodies are directed against the heparin-PF4 complex. This has led to the development of the PF4/ heparin EIA assay. Because whole platelets are not used in this assay, problems related to under-reactivity or nonspecific reactivity are avoided. In addition, the ability of the test to predict clinical complications may be improved because the test can distinguish IgM from IgG heparin-Ig. Currently the laboratory diagnosis of heparin-Ig remains inexact. The sensitivity and specificity of laboratory assays cannot be firmly established. Much like the diagnosis of the phospholipid syndrome-where use of both the cardiolipin EIA and the lupus anticoagulant test offer overlapping advantages-the combination of the heparin-PF4 EIA plus either a test of platelet activation or a heparin-dependent antibody binding assay may prove to be a more sensitive and specific approach to the diagnosis of heparin-Ig. Despite the progress that has been made in the area of laboratory diagnosis of heparin-Ig, further improvement is needed. Heparin-induced thrombocytopenia is not rare and may be associated with devastating morbidity as well as mortality. Low-molecular-weight heparins usually cross-react with heparin-Ig. Therapy with Org 10172 appears to be the most promising alternative for patients with HIT. Because the clinical diagnosis is uncertain in sick hospitalized patients, further improvements in laboratory assays for heparin-Ig allowing earlier and more accurate diagnosis of patients at risk for HIT will be welcome.

Antiplatelet antibody testing in thrombocytopenic pregnant women

OBJECTIVE: The purpose of the study was to attempt to distinguish pregnant women with gestational thrombocytopenia from those with idiopathic immune thrombocytopenia by eight different platelet antibody assays. STUDY DESIGN: Sera from pregnant women with presumed gestational thrombocytopenia ( n = 160) and idiopathic immune thrombocytopenia ( n = 90) were prospectively tested for indirect and platelet-associated immunoglobulins G and M and complement C3, as well as for serotonin release. After the results were analyzed, a subset of patients were subsequently analyzed for circulating antiplatelet antibody directed against platelet membrane glycoprotein GPIIb/IIIa. RESULTS: Indirect immunoglobulin G was significantly greater in the 85 women with idiopathic immune thrombocytopenia than in the 129 women with gestational thrombocytopenia ( p < 0.001). Platelet-associated immunoglobulin G was elevated in the majority of women, both those with gestational thrombocytopenia and those with idiopathic immune thrombocytopenia. There were also no statistically significant differences in the values for platelet-associated C3 or indirect immunoglobulin M and C3. Levels of platelet-associated immunoglobulin M showed a tendency to be higher in women with gestational thrombocytopenia ( p = 0.04), as did the values in the serotonin release assay ( p = 0.06). CONCLUSION: Our data demonstrate that patients with gestational thrombocytopenia had surprisingly high levels of platelet-associated immunoglobulin despite mild thrombocytopenia. Comparison of a relatively large number of patients with idiopathic immune thrombocytopenia and gestational thrombocytopenia indicates that women with idiopathic immune thrombocytopenia cannot be distinguished from those with gestational thrombocytopenia by means of one or more of the prototypic platelet antiglobulin tests currently in use. Our preliminary data with glycoprotein-specific assays indicate that they may be more useful. (AM J OBSTET GYNECOL 1996;174:1014-8.)

Hypertension and Diabetes Mellitus Increase the Risk of Haemorrhage in Chronic Idiopathic Thrombocytopenic Purpura

The risk factors for haemorrhage in chronic idiopathic thrombocytopenic purpura (ITP) remain poorly understood. We classified 49 patients with chronic ITP into two groups on the basis of the presence (n = 11) or absence (n = 38) of hypertension and/or diabetes mellitus, and then analyzed their clinical and immunological characteristics. The patients with hypertension and/or diabetes were older than those without these complications. There were no significant differences between the two groups with regard to platelet count or the levels of platelet-associated immunoglobulin G, platelet-associated immunoglobulin M, and platelet-associated C3. Positivity for anti-glycoprotein IIb/IIIa and anti-glycoprotein Ib autoantibodies was also similar. However, severe purpura and a poor response to prednisolone were far more common in the patients with hypertension and/or diabetes. We conclude that ITP complicated by hypertension and/or diabetes may be resistant to prednisolone and thus require more careful treatment.

The significance of platelets with increased RNA content (reticulated platelets). A measure of the rate of thrombopoiesis.

Direct flow cytometric measurement of nucleic acid content in individual platelets is possible using the fluorescent dye Thiazole Orange (Becton-Dickinson, San Jose, CA). When applied to studies of thrombocytopenic patients, platelets with elevated nucleic acid content ("reticulated platelets") can be identified and quantitated. Labeling of these platelets is saturable and is abolished by treatment with RNAse. It has been suggested that, similar to the erythrocyte reticulocyte response to anemia, the number of these platelets appearing in the circulation may provide an estimate of the rate of thrombopoiesis. The authors studied 229 thrombocytopenic patients, measuring both reticulated platelets and platelet-associated immunoglobulin. The results show that for the subset of patients with normal levels of platelet-associated immunoglobulin, the average absolute number of reticulated platelets is independent of platelet count and remains in the normal range. For those with elevated levels of platelet-associated immunoglobulin, the absolute number of reticulated platelets increases in patients who are moderately thrombocytopenic (60 to 100 x 10(9)/L) but decreases to normal or subnormal levels as thrombocytopenia worsens. The latter finding has been duplicated in studies of mice made thrombocytopenic by injection of anti-platelet antiserum. These results are consistent with the hypothesis that reticulated platelets are subject to peripheral destruction at the same rate as mature platelets, and that in the severely thrombocytopenic patient their level may decrease despite an appropriate marrow thrombopoietic response.

T-cell-dependent immunity and thrombocytopenia in rats infected with Plasmodium chabaudi

Normal, splenectomized, and athymic Fischer rats were infected with Plasmodium chabaudi. In normal rat infections, acute-phase infection resolved rapidly and completely. In splenectomized rats, infection resulted in high parasitemia and ultimately death. In nude rats, parasite growth was reduced compared with normal rats, and a persistent parasitemia (between 20 and 45%) was observed for several months. Complete resolution of the infection was achieved after adoptive transfer of T lymphocytes, even when transfer occurred during the course of infection. These results indicated that an acquired, T-lymphocyte-dependent immunity was necessary for the complete recovery observed in normal rats. In normal rats, thrombocytopenia and splenomegaly occurred during infection. By contrast, in nude rats, both of these pathological manifestations were only observed after thymus grafting. Thrombocytopenia was also absent in the splenectomized animals. Despite an increase in platelet-associated immunoglobulin levels during the infection, thrombocytopenia was not transferred by injection of infected rat serum to normal recipients. It has been concluded that the nude rat infection can be regarded as a novel and useful model for studying the T-cell-dependent effector and pathological mechanisms and to investigate the anti-P. chabaudi immune response.

Alpha interferon therapy in the treatment of idiopathic thrombocytopenic purpura

Treatment of patients with idiopathic thrombocytopenic purpura (ITP) varies according to the severity of the condition, the patient's age and the phase of the disease. The mainstay of treatment is corticosteroid therapy, with splenectomy for non-responding patients. For the 5%–10% of patients with refractory disease and bleeding problems, intravenous immunoglobulins are often used. Danazol achieves a response in about 30%–40% of refractory patients. At our centre, we have now treated 13 patients with interferon alfa-2b, all of whom had severe steroid-unresponsive ITP of various durations. All patients received 12 injections of 3 million units (MU) interferon subcutaneously three times a week. The platelet count rose significantly in 10 patients after interferon therapy and in one patient during therapy. Three patients had a complete response and eight a partial response. One complete responder relapsed at 5 months but again responded to retreatment with interferon. Responses were similar in splenectomized and non-splenectomized patients, and platelet-associated immunoglobulin levels remained essentially unchanged. Based on a compilation of data from this and other studies, the positive response rate (platelets at least 30–200 × 10 9/L for at least 6 weeks) is 69% ( 22 32 patients). The future role and dosage of interferon in ITP remains to be determined and particularly in direct comparison with intravenous IgG therapy.

Effect of danazol in immune thrombocytopenic purpura.

Danazol and vinblastine are effective in many patients with chronic immune thrombocytopenic purpura (ITP). To evaluate the mechanism of action of these drugs, we studied six consecutive patients with chronic ITP treated with danazol and one treated with vinblastine. All the patients responded clinically without a notable change in the level of platelet-associated IgG. Instead, the clinical response to therapy was associated with a decrease in the number of monocyte binding sites for monomeric IgG (Fc receptors). In one patient, clinical relapse was associated with a spontaneous 2.7-fold increase in the number of monocyte Fc (IgG) receptors, without a change in the level of platelet-associated immunoglobulin. A decrease in the number of monocyte Fc (IgG) receptors following vinblastine infusion was associated with a clinical remission. We conclude that the clinical course of ITP may be influenced by the expression of monocyte or macrophage Fc (IgG) receptors. Danazol and vinblastine may mediate their clinical effect, at least in part, by influencing the number of available Fc (IgG) receptors on phagocytic cells.

Intensive plasma exchange therapy in ten patients with idiopathic thrombocytopenic purpura.

Intensive plasma exchange therapy with fresh-frozen plasma as the replacement fluid was used to manage ten patients, five with acute and five with chronic immune thrombocytopenic purpura (ITP). Therapy was started because of severe hemorrhage (1 case), failure to respond to steroid therapy (6 cases), or steroid dependence (3 cases). After a median of four exchanges over 6 days (median total volume removed, 11.7 liters), initial responses, defined as a platelet count greater than 100,000 per microliter at the end of the exchange series, were observed in 80 percent of the patients treated. Two adolescents, ages 16 and 17 years, with chronic ITP failed to respond to plasma exchange therapy and subsequently responded to splenectomy. Prolonged remissions of 9 months and greater than 2 years were observed in two patients with acute ITP; in patients with chronic ITP, no prolonged remissions occurred. Neither pre-exchange levels of platelet-associated immunoglobulin G (PAIgG) nor circulating immune complexes predicted the response to plasma exchange, although serially determined PAIgG levels correlated with the severity of ITP and response, or lack of response, to plasma exchange. We conclude that intensive plasma exchange merits further study in patients with acute ITP unresponsive to steroid therapy to determine if the need for splenectomy is reduced. In selected patients with chronic ITP, exchange therapy may provide short-term adjunctive benefit.

Intravenous immunoglobulin administration in the treatment of severe chronic immune thrombocytopenic purpura

Human immunoglobulin was administered intravenously to nine adult patients having severe chronic immune thrombocytopenia purpura. The response in three patients was an increase in the platelet count to greater than 50,000/mm 3, a hemostaticly adequate level. Response was associated with a pretreatment platelet-associated immunoglobulin level of more than 5,000 molecules per platelet, and successful treatment resulted in a decrease in that level. In those patients with pretreatment platelet-associated immunoglobulin levels less than 5,000 molecules per platelet, there was neither a significant decrease in that level nor an increase in their platelet count. Immunoglobulin infusion may prove useful for selected patients with severe chronic Immune thrombocytopenia.

Platelet associated IgM in acute idiopathic thrombocytopenic purpura. High-dose intravenous IgG compared to prednisolone

An ELISA test for platelet associated immunoglobulins was performed at disease onset in 36 consecutive patients with acute idiopathic thrombocytopenic purpura. All case histories were later reviewed. Platelet associated IgM was elevated in 91% of the patients, correlating with platelet associated IgG. It was found that neither platelet associated IgG nor IgM levels could predict duration of thrombocytopenia or the transition to chronic disease observed in three patients. High-dose intravenous IgG given to six patients had a significantly better antithrombocytopenic effect than oral prednisolone in eleven patients. Platelet associated immunoglobulin levels were reduced after IgG treatment, suggesting a possible interference with the binding of antibodies or immune complexes to platelets. IgG, IgM, platelets, prednisolone, thrombocytopenia

Acquired storage pool deficiency with increased platelet-associated IgG: Report of five cases

Acquired abnormalities of platelet aggregation have been reported with increasing frequency. We studied five patients (including two with systemic lupus erythematosus and one with compensated chronic idiopathic thrombocytopenic purpura) in whom platelet aggregation responses to collagen, epinephrine and ADP are impaired; in all cases, we found that levels of platelet-associated immunoglobulin G (IgG) were increased. In all five patients substances stored in platelet-dense granules (ATP, ADP, serotonin and calcium) were diminished. The content of the α-granule substance, β-thromboglobulin, was also decreased in most cases, whereas the levels of two secretable acid hydrolase enzymes (β-glucuronidase and β-N-acetyl glucosaminidase) were within normal limits. These findings are similar to those observed in subtypes of congenital storage pool deficiency. However, in contrast to the congenital disorder, a membrane-bound (nonsecretable) acid phosphatase was also decreased in the patients with acquired storage pool deficiency. These findings suggest that impaired platelet aggregation on an acquired basis may, in some patients, be due to immune platelet damage resulting in a distinctive type of platelet storage pool deficiency.