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At least 127 records · Page 7Linked to original sources
PubMed1989

Is thrombopenia in cord blood indicative of intra-uterine sensitization?

The relation between platelet counts (PCT) and IgE was studied in cord blood from 136 European newborns. PCT was significantly lower (P = 0.0014) when cord-IgE was superior to 1.20 IU/ml (n = 29; 245,000/microliter) than when it was inferior to this value (n = 107; 284,080/microliter) which resulted in a significant negative Spearman rank correlation between PCT and cord-IgE (P = 0.002; rs = -0.25). A follow-up by questionnaire in 97 of the newborns revealed that those newborns who had developed definite atopy within 18 months of age had significantly (P = 0.002) lower PCT at birth (n = 8; 196,000/microliter) than those free of atopic symptoms (n = 61; 286,000/microliters). Further newborns to atopic mothers (n = 23; 245,000/microliters) had significantly (P = 0.014) lower PCT than newborns to non-atopic mothers (n = 74; 286,000/microliters). The lowest PCT was recorded when both the mother was atopic and the newborn had developed definite or probable atopy by the age of 18 months (n = 7; 175,000/microliters) as compared to atopy alone in mothers (n = 16; 276,000/microliters; P = 0.005), to atopy alone in infants (n = 9; 281,000/microliters; P = 0.005) and to non-atopic infants of non-atopic mothers (n = 65; 286,000/microliters; P = 0.0007). Significantly (P = 0.03) lower PCT amongst boys (n = 49; 259,000/microliters) compared with girls (n = 48; 294,000/microliters) was attributed to the higher incidence of elevated cord-IgE and infant atopy among boys.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1996

De novo 46,XX, dir dup (11)(q133.3-->q14.2) in a patient with mental retardation, congenital cardiopathy and thrombopenia.

A 31-year-old female is reported with mild to moderate mental retardation, facial dysmorphy, congenital cardiopathy, and mild thrombocytopenia as the most important clinical findings. Chromosome analysis in lymphocytes showed a de novo dir dup (11)(q13.3-->14.2), by both G-banding and FISH techniques. Previously reported constitutional duplications of 11q are mostly the result of unbalanced translocations involving chromosome 11q, and are associated with a partial monosomy or trisomy of the translocation partner chromosome. In case of an unbalanced translocation it is not clear which clinical findings result from the chromosome 11 duplication and which result from the abnormality on the translocation partner chromosome. This is the first report on a constitutional duplication of chromosome region 11q13.3-->14.2 without involvement of other chromosomes.

Adult↗
PubMed2004

FLI1 monoallelic expression combined with its hemizygous loss underlies Paris-Trousseau/Jacobsen thrombopenia.

Paris-Trousseau syndrome (PTS; also known as Jacobsen syndrome) is characterized by several congenital anomalies including a dysmegakaryopoiesis with two morphologically distinct populations of megakaryocytes (MKs). PTS patients harbor deletions on the long arm of chromosome 11, including the FLI1 gene, which encodes a transcription factor essential for megakaryopoiesis. We show here that lentivirus-mediated overexpression of FLI1 in patient CD34(+) cells restores the megakaryopoiesis in vitro, indicating that FLI1 hemizygous deletion contributes to the PTS hematopoietic defects. FISH analysis on pre-mRNA and single-cell RT-PCR revealed that FLI1 expression is mainly monoallelic in CD41(+)CD42(-) progenitors, while it is predominantly biallelic in the other stages of megakaryopoiesis. In PTS cells, the hemizygous deletion of FLI1 generates a subpopulation of CD41(+)CD42(-) cells completely lacking FLI1 transcription. We propose that the absence of FLI1 expression in these CD41(+)CD42(-) cells might prevent their differentiation, which could explain the segregation of the PTS MKs into two subpopulations: one normal and one composed of small immature MKs undergoing a massive lysis, presumably originating from either FLI1(+) or FLI1(-) CD41(+)CD42(-) cells, respectively. Thus, we point to the role of transient monoallelic expression of a gene essential for differentiation in the genesis of human haploinsufficiency-associated disease and suggest that such a mechanism may be involved in the pathogenesis of other congenital or acquired genetic diseases.

Antigens, CD↗
PubMed1999

[Severe mixed thrombopenia during interferon treatment for chronic viral hepatitis C].

BACKGROUND: Thrombocytopenia occurred in a woman given alpha interferon for chronic hepatitis C without cirrhosis. Both central thrombocytopenia, clearly demonstrated, and peripheral thrombocytopenia, probably of autoimunne origin, were involved. CASE REPORT: A 55-year-old woman with active chronic hepatitis C (Metavir score A2, F2) was given alpha interferon. One month after treatment onset, she developed thrombocytopenia (32 G/L). A second bone marrow aspirate and osteomedullary biopsy evidenced megalokaryocytes and the platelet count responded to polyvalent immunoglobulins. Five months after discontinuing interferon, the platelet count progressively returned to normal. DISCUSSION: Central thrombocytopenia is classically described in patients given interferon and usually appears during the first weeks of treatment. In our case, the central mechanism was clearly demonstrated by the bone marrow aspirate and osteomedullary biopsy findings at a time when the platelet count was 32 G/L. A peripheral immunological participation was more difficult to prove but was strongly suggested by the persistence of thrombocytopenia despite the interruption of the interferon and the efficacy of immunoglobulins.

Female↗