| 1. |
- Békássy, Albert, et al.
(author)
-
Arterial occlusion due to Listeria meningoencephalitis in an immunocompromised boy
- 1987
-
In: Scandinavian Journal of Infectious Diseases. - : Informa UK Limited. - 1651-1980 .- 0036-5548. ; 19:4, s. 485-489
-
Journal article (peer-reviewed)abstract
- Sequential CAT scan studies of the brain were performed in a 7-year-old boy with Listeria monocytogenes serotype 1 meningoencephalitis. The infection occurred while he was receiving maintenance chemotherapy for T-cell non-Hodgkin lymphoma. A lesion in the right hemisphere during the infection resulted in an excessive enlargement of the right ventricle 10 months later, most probably caused by arterial occlusion.
|
|
| 2. |
- Heim, Sverre, et al.
(author)
-
A new specific chromosomal rearrangement, t(8;16) (p11;p13), in acute monocytic leukaemia
- 1987
-
In: British Journal of Haematology. - 0007-1048. ; 66:3, s. 323-326
-
Journal article (peer-reviewed)abstract
- The translocation t(8;16) (p11;p13) was found as the sole deviation from the normal karyotype in three patients with acute monocytic leukaemia. The bone marrow morphology was strikingly similar in the two cases where smears were available for re-evaluation: the leukaemic cells showed signs of differentiation, and active erythrophagocytosis was a particularly conspicuous feature. We suggest that t(8;16) (p11;p13) represents a new consistent abnormality in acute monocytic leukaemia, specifically associated with the differentiated subtype (M5b) and with pronounced phagocytic activity by the leukaemic monocytes.
|
|
| 3. |
- Heim, Sverre, et al.
(author)
-
New structural chromosomal rearrangements in congenital leukemia
- 1987
-
In: Leukemia. - 1476-5551. ; 1:1, s. 16-23
-
Journal article (peer-reviewed)abstract
- The karyotypic abnormalities and clinical data on three patients in whom acute leukemia was diagnosed within the first 6 months of life are presented. The four structural chromosomal rearrangements detected in the bone marrow from these patients, i.e., t(7;12)(q36;p13) and t(1;19)(q11;q11) in case 1, t(2;10;11;12)(q21q31;p13;q13;q24) in case 2, and t(11;19)(q23;p13) in case 3, have not previously been associated with congenital leukemia. Acquired chromosomal changes have until now been reported in only 31 leukemic infants in this age group. Of the total material, 18 patients had acute lymphoblastic leukemia and 16 had acute nonlymphocytic leukemia. The by far most frequently recorded cytogenetic aberration has been t(4q;11q), seen in 14 cases of lymphoblastic leukemia. Although t(4q;11q) has not been found in a single patient with acute nonlymphocytic leukemia, these leukemias have often had other rearrangements involving the same region of 11q. Hence, genetic material around 4q21 may be active in lymphocytic differentiation, whereas gene(s) in 11q23 may be important in the neoplastic process in a less cell-type specific manner and perhaps particularly vulnerable to neoplastic rearrangement in fetal life. The finding of four cases out of 34 with translocations between 11q23 and chromosome 19 indicates that this rearrangement might characterize a specific cytogenetic subgroup of leukemia in the very young.
|
|
| 4. |
- Moëll, Christian, et al.
(author)
-
Disturbed pubertal growth in girls treated for acute lymphoblastic leukemia
- 1987
-
In: Pediatric Hematology & Oncology. - : Informa UK Limited. - 1521-0669 .- 0888-0018. ; 4:1, s. 1-5
-
Journal article (peer-reviewed)abstract
- Pubertal growth was studied in 10 girls previously treated for acute lymphoblastic leukemia. The average age at menarche was 12.2 years, which is significantly lower (p less than 0.01) than the expected 13.1 years. Compared with normal girls, these girls showed a subnormal (p less than 0.05) peak height velocity during the second year before menarche. The remaining growth before menarche as well as the total postmenarchal growth was close to the normal average. The average final standing height was 1 SD less than what would be expected from their height 1 year after the cessation of therapy. A relative growth hormone deficiency in combination with early onset of puberty could account for this loss in final height.
|
|
