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Anti-D immunoglobulin in the treatment of idiopathic thrombocytopenic purpura.

Anti-D was evaluated in 8 RhD positive patients (6 males, 2 females) aged 2-21 years (mean 10 years) with Idiopathic Thrombocytopenic Purpura (ITP). Five patients with chronic ITP and 3 patients with acute ITP were administered Anti-D in the dosage of 50 micrograms/kg intramuscularly (IM) for 3 consecutive days. One patient of chronic ITP received two courses of Anti-D. Patients were followed up for 7 to 16 months (mean 9 months). All three cases of acute ITP had a complete response and are in remission between 3 to 12 months of follow up. Two of five cases of chronic ITP had a partial response. Rise in platelet count was observed within 72-124 hours, and duration of response varied between 10 to 15 days. None of these patients had any significant side effects of anti-D immunoglobulin therapy. Intramuscular administration of Anti-D is safe, effective and low cost alternative to IVIgG in the treatment of acute ITP.

Acute Disease↗

PubMedDate not supplied

Platelet function disorders in north India.

BACKGROUND: Platelet function disorders are a fairly common cause of bleeding manifestations. Although their relative types and incidence are well documented, data from India are lacking. METHODS: Between 1970 and 1991, we studied the clinical and laboratory features of 144 north Indian patients who presented to our hospital with a bleeding diathesis in whom coagulation disorders, von Willebrand's disease and a history of drug ingestion were absent. RESULTS: Isolated platelet factor 3 availability defect was the commonest (56 cases) followed by the thrombasthenias (49 cases), arachidonic acid pathway defect (26 cases), storage pool disease (8 cases) and the Bernard-Soulier syndrome (3 cases). Isolated platelet factor 3 deficiency was rare (2 cases). Two varieties of thrombasthenia were seen--the classical Glanzmann's (13 cases) and thrombopathic (36 cases). The latter was characterized by absent or sub-normal platelet aggregation with agonists along with a reduced (to less than 50% of normal) total platelet factor 3 content. This has not been reported from western countries. Patients with classical Glanzmann's thrombopathic thrombasthenia with absent platelet aggregation and isolated platelet factor 3 deficiency were severe bleeders. Their family history suggested an autosomal recessive transmission in Glanzmann's and thrombopathic thrombasthenia and a possible autosomal dominant transmission in isolated platelet factor 3 availability defect and isolated platelet factor 3 deficiency. CONCLUSION: The frequency of various types of platelet function disorders in Indians is similar to that in western populations except that the incidence of thrombopathic thrombasthenias is higher in India.

Adolescent↗