Rituximab-induced acute thrombocytopaenia in an African lupus patient: a case report

Drug-induced acute thrombocytopaenia (DITP) is a complication of various medications resulting in a platelet count <50 x 109/L from prior normal levels. It typically occurs within 1-2 weeks postadministration but can occur rapidly within 1-3 days with previous exposure. Rituximab (an anti-CD20 antibody) used to treat many autoimmune cytopaenias, has been reported to cause thrombocytopaenia mostly in lymphoma patients. Reports in lupus are rare possibly because of off-label use. We hereby highlight the case of a 39-year old African lady who developed acute thrombocytopenia 12 days post-rituximab. Frequent monitoring of blood counts will enhance identification and treatment of this complication

Aspects cliniques et évolutifs de la thrombopénie au service de Réani- mation Chirurgicale du Centre Hospitalier Universitaire Joseph Ravoahangy Andrianavalona, Antananarivo

Introduction : La découverte d'une thrombopénie en réanimation est une situation fréquente et la prise en charge est lourde. L'objectif de cette étude était d'évaluer les aspects cliniques et évolutifs de la thrombopénie dans un service de Réanimation Chirurgicale d'Antananarivo. Matériels et Méthodes : C'est une étude rétrospective, descriptive sur une période de 36 mois, réalisée au service de Réanimation Chirurgicale du Centre Hospi¬talier Universitaire Joseph Ravoahangy Andrianavalona Antananarivo, Madagascar, incluant les patients ayant présenté une thrombopénie à l'ad-mission. Nous avons analysé les caractères démographiques, les motifs d'admission, le taux de plaquettes à l'entrée et 72h après l'admission, le mécanisme et l'évolution des patients. Les données ont été saisies et analysées avec le logiciel Epi-Info 7.0. Résultats : Durant cette période, 386 patients sur 7021 admis ont présenté une thrombopénie soit 5,5% des patients. L'âge moyen était de 47,6±17,3 ans avec une prédominance mascu¬line (sex ratio de 2,1). Le taux moyen de plaquettes à l'admission était à 95,1±36,9 G/L. Le motif d'admission était dominé par le syndrome hémor¬ragique (46,1%) dont la majorité était une hémorragie digestive (88% des cas). Concernant le mécanisme, 84,1% ont été d'origine périphérique suite à un syndrome hémorragique et un hypersplénisme ; 5,2% étaient considérées comme d'origine centrale secondaire à des toxiques et une hémopa¬thie maligne et dans 10,7% des cas, l'origine était non identifiée. Le taux de mortalité était de 34,5% suite à un syndrome hémorragique et des dé¬faillances d'organes. La prise en charge est surtout faite de transfusion par du sang total frais ou du plasma riche en plaquettes à défaut de concentré de plaquettes, et de corticothérapie. Conclusion : La présence d'une thrombopénie en réanimation témoigne toujours la gravité d'une maladie. L'origine de la thrombopénie n'est pas toujours évidente mais sa connaissance détermine la suite de la prise en charge

The prevalence of HIV seropositivity and associated cytopenias in full blood counts processed at an academic laboratory in Soweto, South Africa

Background. The HIV epidemic in South Africa (SA) has had a substantial impact on laboratory services, at least partially owing to the well-described propensity to cytopenias in HIV-positive patients.Objectives. (i) To formally gauge the impact of HIV infection on the state sector haematology services in SA by determining the HIV seropositivity rate among full blood counts (FBCs) performed at a large academic state sector laboratory; and (ii) to document the prevalence of cytopenias among HIV-positive patients in this setting.Methods. Randomly selected FBCs submitted to the National Health Laboratory Service laboratory at Chris Hani Baragwanath Academic Hospital, Johannesburg, were extracted from the laboratory information system (LIS) and retrospectively reviewed. HIV test results and other pertinent information in the LIS were documented, as was the presence of any cytopenias.Results. HIV status was documented in 561 of 1 006 samples (55.8%), with 307 (54.7%) of these being HIV-positive. Of the HIV-positive patients, 63.2% had one or more cytopenia/s. Anaemia was present in 183/307 (59.6%) of the HIV-positive patients, and was severe (haemoglobin <8 g/dL) in 32/307 (10.4%). Multivariate linear regression analysis showed significant independent associations between the presence of anaemia and both immunological AIDS (iAIDS) (p<0.0001) and male sex (p<0.025), but not HIV viral load (VL) (p=0.33) or antiretroviral therapy (ART) exposure (p=0.70). Thrombocytopenia and neutropenia were present in 37/307 (12.1%) and 11/51 (21.6%) of the HIV-positive patients, respectively, with no statistically significant association between either of these cytopenias and iAIDS, exposure to ART or VL.Conclusions. The findings reflect the substantial impact of the HIV epidemic on state sector laboratory resources, particularly the haematology service

Characteristics and Mortality Rate of Neonates with Congenital Cytomegalovirus Infection

Background. Cytomegalovirus (CMV) infection is a common congenital infection in neonates. Clinical presentation and laboratory findings in CMV-infected infants in a setting where HIV is prevalent are not well characterised. Objective. To determine the characteristics and survival to hospital discharge of neonates with congenital CMV infection. Methods. In this retrospective; case-control study; hospital records of neonates; tested for CMV in the first 3 weeks of life from January 2004 to December 2008; were reviewed for maternal and neonatal characteristics; clinical presentation; laboratory findings and inpatient mortality. Comparisons were made between CMV-infected and CMV-uninfected neonates in those infants who were tested for CMV.Results. Among the CMV-infected; 91 were of low birth weight; 83 were preterm and 29 were small for gestational age. The CMV-infected neonates were more likely to present with hepato/splenomegaly compared with uninfected neonates (p=0.02). Thrombocytopenia was more severe in CMV-infected neonates (p=0.004). Congenital CMV-infected neonates were more likely to be HIV-exposed (p=0.003) and HIV-infected (p=0.02). Mortality before hospital discharge was significantly higher in congenital CMV-infected neonates (p=0.01) and in those with HIV co-infection (p=0.02). The male gender was a significant independent predictor of inpatient mortality (odds ratio: 23; 95 confidence interval 1.19 - 445.698; p=0.04). Conclusion. Neonates presenting with hepato/splenomegaly and severe thrombocytopenia are most likely to be CMV-infected. Neonates with congenital CMV are more likely to be co-infected with HIV. The co-infection of CMV and HIV is associated with a high mortality rate; especially in male neonates

Platelet abnormalities in experimental malaria

Several abnormalities of platelet haemostatic function that have been previously described; are summarized in this article. These include hypersensitivity to agonists such as adenosine diphosphate (ADP); adrenaline and arachidonic acid; increased loss of platelet lactate dehydrogenase (LDH); and enhanced platelet production of thromboxane A2 (TXA2) found with enhanced but delayed prostacyclin (PGI2) production. Other features include marked reduction (by 36-62) of total platelet sialic acid associated with shortened platelet life span. It was also observed that platelets thathad interacted even for only one minute with Plasmodium falciparum-infected erythrocytes in culture; when challenged immediately afterwards with optimal concentration of ADP; had lost the usual platelet refractoriness after interaction with sub-optimal ADP concentration. The significance of this novel finding has not been investigated further. These platelet changes which were also observed in the human disease; suggest that a hypercoagulable state associated with platelet activation exists in acute P. falciparum infection in man; a feature that was not previously described and appreciated. Its significance has not been investigated. However; it explains the relative rarity of bleeding complication that is sometimes described in the disease in man. Some of the changesdescribed also suggest that additional mechanism(s) of platelet destruction in addition to those previously postulated; may occur in the infection. They also suggest that other therapeutic modalities may be available

Platelet abnormalities in experimental malaria: a review

Several abnormalities of platelet haemostatic function that have been previously described; are summarized in this article. These include hypersensitivity to agonists such as adenosine diphosphate (ADP); adrenaline and arachidonic acid; increased loss of platelet lactate dehydrogenase (LDH); and enhanced platelet production of thromboxane A2 (TXA2) found with enhanced but delayed prostacyclin (PGI2) production. Other features include marked reduction (by 36-62) of total platelet sialic acid associated with shortened platelet life span. It was also observed that platelets thathad interacted even for only one minute with Plasmodium falciparum-infected erythrocytes in culture; when challenged immediately afterwards with optimal concentration of ADP; had lost the usual platelet refractoriness after interaction with sub-optimal ADP concentration. The significance of this novel finding has not been investigated further. These platelet changes which were also observed in the human disease; suggest that a hypercoagulable state associated with platelet activation exists in acute P. falciparum infection in man; a feature that was not previously described and appreciated. Its significance has not been investigated. However; it explains the relative rarity of bleeding complication that is sometimes described in the disease in man. Some of the changesdescribed also suggest that additional mechanism(s) of platelet destruction in addition to those previously postulated; may occur in the infection. They also suggest that other therapeutic modalities may be available

L'incompatiblite foeto-maternelle anti-plaquettaire: a propos de 238 gestantes a Cotonou

En Afrique l'incompatibilite foeto-maternelle est le plus souvent percue sous l'angle des incompatibili-tes erythrocytaires. Cette incompatibilite peut aussi se manifester par une destruction des plaquettes sensibilisees par les anticorps (Ac) d'une mere soit auto immunisee; soit allo-immunisee contre des antigenes (Ag) plaquettaires fotaux transmis par le pere mais absents chez la mere.Sur une periode de 8 mois; 238 gestantes de moins de 7 mois de grossesse ont ete suivies : 109 parmi elles sont phenotypees pour les Ag plaquettaires specifiques et toutes ont subi des tests de depistage et d'identification d'anticorps anti-plaquettaires par la technique du MAIPA. Durant cette periode; les enfants nes de meres immunisees ont ete examines a la recherche d'une thrombopenie et de signes cliniques de spoliation sanguine.Les genotypes les plus frequemment rencontres sont : HPA-1a/1a (81;65) ; HPA-5a/5a (62;39) ; HPA-3a/3b (52;3) ; HPA-3a/3a (41;28) et HPA-5a/5b (35;78)79;2des gestantes ont developpe des auto-Ac contre le complexe glycoproteique IIb IIIa. La fre-quence de l'auto-immunisation semble inversement proportionnelle a la gestite. Chez quatre gestan-tes (1;7) dont 3 primigestes; des allo-Ac sont detectes contre l'Ag HPA-5b.Des 4 enfants nes de meres immunisees dans la periode de suivi; aucun n'a pose de probleme clini-que. Par contre 2 ont ete thrombopeniques des la naissance (109 et 9 G/L) mais leurs nombres de plaquettes se sont spontanement normalises au 3eme jour de naissance