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P Kolecki

Publications and source records attributed to P Kolecki.

At least 19 recordsLinked to original sources
PubMed2001

Argyria in the ED.

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Administration, Oral↗
PubMed2000

[High risk acute lymphoblastic leukaemia in children. Preliminary report after introducing a new version of New York (1997) protocol adjusted to the age of the patients. Report of the Polish Paediatric Leukaemia/Lymphoma Study Group].

The paper presents the experience of the Polish Paediatric Leukaemia/Lymphoma Study Group in the treatment of high-risk acute lymphoblastic leukaemia in children using a new version of the New York (1997-1999). Protocol with treatment intensity adjusted according to the age of the patients. From April 1997 to December 1999 a group of 49 children with leukocytosis ranging from 50 900/mm3 to 580 000/mm3 (median 122 000/mm3) and 6 children with leukocytosis below 50 000/mm3 and poor response to steroids were treated with this protocol. Children below 10 years (43 patients) were treated according to the previous protocol, children above 10 years (12 patients) were treated with intensified protocol (high doses of ARA-C in consolidation and intermediate doses of Mtx in maintenance). Induction was identical for all patients. Complete remission was achieved in 92.6% patients. There were 2 relapses. Six children died - 3 without remission, 2 due to a relapse, 1 due to treatment complications. The current opinions concerning classification of HRG-ALL and treatment possibilities in this group of children are discussed.

Adolescent↗
PubMed2000

[Results of treatment of children with chronic myelogenous leukaemia (CML) obtained by the Polish Paediatric Leukaemia/Lymphoma Study Group].

Retrospective analysis of 102 children with CML from 9 paediatric centres in Poland has been performed. A total number of 102 children: 58 boys and 44 girls aged 1-17 years (median 9.4 years old) with CML, treated in the period 1975-1999 were included in the study. Forty eight of 102 (47.1 %) children were treated with cytostatic drugs without IFN alpha: busulfan, hydroxyurea, 6-mercaptopurine or etoposide (VP-16). Fifty four of 102 (52.9%) patients were treated with interferon alpha (IFN alpha) after cytoreductive pretreatment. Thirty out of 102 (29.4%) patients underwent stem cell transplantation (SCT): 24 - matched related donor allo-BMT, 2 - matched unrelated donor allo-BMT, 1 - partially matched related donor T-cell depleted allo-PBPCT, 1 - syngeneic allo-BMT and 2 - autologous PBPCT. Overall survival analysis revealed that 46 of the 102 (45.1%) children remained alive: 5/35 (14.3%) children treated with cytostatics alone, 22/37 (59.5%) children treated with IFN alpha and 19/30 (63.3%) children treated with SCT. Among SCT survivors there are 10/17 (58.8%) children treated with IFN alpha prior to SCT and 9/13 (69.2%) children treated with cytostatics alone prior to SCT. The probability of 5-year survival is 0.51 in the group treated with SCT (median follow-up 58 months); 0.43 in the group treated with IFN alpha (median follow-up 53 months) and 0.23 in the group treated with cytostatics (median follow-up 31 months). Our data show, that BMT is the treatment of choice in CML in children. IFN alpha could be successfully applied as an alternative treatment for those, who do not have a suitable donor for allogeneic SCT. Better outcome in post BMT children, who were not treated with IFN alpha prior to SCT requires confirmation by studies on larger groups of patients. However, it seems to be justified to stop IFN alpha therapy at least 3 months before SCT. The main reason for unsuccessful treatment outcome in patients with CML in Poland remains the still insufficient access to MUD-BMT.

Adolescent↗
PubMed2000

[Results of the treatment of myelodysplastic syndrome (MDS)obtained by the Polish Paediatric Leukaemia /Lymphoma Study Group].

Sixty children with MDS treated in six centres of the Polish Paediatric Leukaemia/Lymphoma Study Group in the period 1975-1999 were included in the study. In 20 children RAEB-T, in 13 RA, in 21 RAEB and in 6 CMML were diagnosed. Our own and literature data showed that BMT is the best therapy for children with MDS. We need a new comprehensive protocol for the diagnosis and treatment of children with MDS in Poland.

Adolescent↗
PubMed1999

Delayed toxic reaction following massive bee envenomation.

Massive bee envenomation can produce both immediate and delayed toxic reaction. Signs and symptoms of immediate toxic reaction are fatigue, nausea, vomiting, hemolysis, kidney failure, and disseminated intravascular coagulation. The label "delayed toxic reaction" refers to a patient who is asymptomatic after a massive bee envenomation, with normal initial laboratory results, but later demonstrates laboratory evidence of hemolysis, coagulopathy, thrombocytopenia, rhabdomyolysis, liver dysfunction, and disseminated intravascular coagulation. The subject of this case report, a 66-year-old man, was stung more than 125 times in an attack by Africanized bees. He was initially asymptomatic, except for pain, and his laboratory findings were normal. The first signs of his fatal multi-organ-system failure were not apparent until 18 hours after envenomation. This experience has led the Good Samaritan Regional Poison Center in Phoenix, AZ, to recommend a 24-hour hospitalization for pediatric patients, older patients, and patients with underlying medical problems who are asymptomatic or who are experiencing only pain after an envenomation of 50 or more stings. Such patients have an increased risk of tissue injury, which may be delayed and which may be more effectively treated if identified early rather than on 12- to 24-hour follow-up. All other envenomated, asymptomatic patients or envenomated patients experiencing only pain who become symptomatic or who belatedly exhibit laboratory values consistent with hemolysis, thrombocytopenia, rhabdomyolysis, liver dysfunction, kidney failure, and disseminated intravascular coagulation within a 6-hour emergency department observation period should be admitted. Intravenous fluids, blood products, dialysis, and other intensive measures should be initiated if necessary.

Aged↗
PubMed1999

Metabolites of mercaptopurine in red blood cells: a relationship between 6-thioguanine nucleotides and 6-methylmercaptopurine metabolite concentrations in children with lymphoblastic leukemia.

Intracellular concentrations of 6-mercaptopurine metabolites, i.e. of 6-thioguanine nucleotides (6-TGN) and of 6-methylmercaptopurine metabolites (6-mMP) were analysed in red blood cells (RBC) of 19 children with acute lymphoblastic leukemia (ALL), the subjects of a maintenance chemotherapy of their first remission. Interpatient variations in concentrations of both metabolites were high; concentrations of 6-TGN varied from <60 to 833 pmol/8x10(8) RBC (median value, 144) and those of 6-mMP metabolites from <150 to 19000 pmol/8x10(8) RBC (median value, 3250). In two patients, 6-TGN appeared at concentrations below the limits of assay sensitivity, and 6-mMP metabolites were not detected. In another child the concentrations of both metabolites were at the limit of the assay sensitivity. In three other children the concentrations of both metabolites were below the median value of the group. In the analysed group of children, significant correlations were found between the white cell count (WBC) and RBC 6-TGN (r(s)=-0.72, P<0. 005) as well as between the neutrophil count and RBC 6-TGN (r(s)=-0.60, P<0.01). No significant correlation was found between the concentrations of 6-TGN and 6-mMP metabolites. The monitoring of concentrations of 6-TGN as well as of 6-mMP metabolites allows an early identification of patients who are at an increased risk of the disease relapse as indicated by the low levels of either 6-TGN itself or of its two metabolites.

Adolescent↗
PubMed1998

Inadvertent methamphetamine poisoning in pediatric patients.

With the increase in popularity of adult methamphetamine abuse in the state of Arizona, there has been an increase in the number of pediatric admissions from inadvertent methamphetamine poisoning. This report describes the signs and symptoms and the hospital course of pediatric patients inadvertently poisoned with methamphetamine. A nine-year retrospective chart review identified 18 pediatric patients poisoned only with methamphetamine. This review revealed that pediatric patients with methamphetamine poisoning commonly presented with the following signs and symptoms: tachycardia (18 patients), agitation (nine patients), inconsolable crying and irritability (six patients), and vomiting (six patients). The most common ancillary tests, excluding urine drug screens, used in formulating the diagnosis were computed tomography scans of the head (five patients) and lumbar punctures (three patients). Three patients received Centruroides sculpturatus antivenin intravenously. The most common complication of methamphetamine poisoning was rhabdomyolysis (two patients), and the average hospital stay for all patients was three days. This case series demonstrates that pediatric patients who ingest methamphetamine can present with signs and symptoms similar to those of an abdominal or neurologic pediatric emergency.

Adult↗
PubMed1995

Standard and intermediate risk acute lymphoblastic leukemia in Poland: a report of the Polish Children's Leukemia/Lymphoma Study Group.

A total of 527 children with acute lymphoblastic leukaemia (ALL) from the most frequent risk groups: standard risk group (SRG) and intermediate risk group (IRG) were treated between 1987 and 1991 according to an intensified treatment program (based on the BFM protocol) including the use of an intermediate dose of methotrexate in the IRG. A comparison of the treatment results in this group from 513 children treated between 1981 and 1987 indicates that the chance for a 6 year event-free survival has increased to 73% (previously 55%).

Antineoplastic Agents↗
PubMed1985

Chronic lymphocytic leukemia B-lymphocytes forming SRBC-rosettes not due to an anti-SRBC activity of monoclonal surface immunoglobulin.

A case of chronic lymphocytic leukemia is described in which large numbers of peripheral blood lymphocytes expressed immunoglobulin on their membrane and rosetted spontaneously with sheep red blood cells (SRBC) at 4 degrees C. They also showed weak staining with a heterologous antiserum against T-cells as well as with a monoclonal antibody (OKT11) with specificity for an epitope associated with the SRBC-receptor, but failed to react with other T-lineage-restricted monoclonal antibodies. The B-cell origin of the leukemic cells was documented by the presence of light-chain-restricted monoclonal surface immunoglobulin, reactivity with various monoclonal anti-B-cell reagents, presence of Ia-like antigens, their capability to synthesize intracytoplasmic immunoglobulin on exposure to phorbol ester TPA, their lack of response to T-cell mitogen PHA, and their inability to help or suppress the allogeneic B-cell response upon PWM stimulation. Extensive blocking studies with both specific antisera and Forsmann antigen-rich guinea pig kidney extracts, which did not prevent SRBC-rosetting, lend support to the hypothesis that SRBC-rosette formation in this case was not attributable to an anti-SRBC affinity of the surface immunoglobulin on the cells. This case will be discussed in relation to the recent finding of SRBC-rosette expression on some cultured chronic lymphocytic leukemia B-lymphocytes.

Aged↗
PubMed1984

Ph1 positive blast crisis of chronic myeloid leukaemia exhibiting features characteristic of early T blasts.

Leukaemic cells from a patient in the blast crisis of chronic myeloid leukaemia were subjected to a surface marker analysis using a panel of monoclonal antibodies recognizing differentiation antigens of myeloid (MY7, MY906, VIM D5, M phi P9), erythroid (VIE G4), megakaryocyte (AN51), T-lymphoid (WT1, 10.2, OKT3, OKT4, OKT6, OKT8, OKT11A) and B-lymphoid cells (B1, B2, Y29/55), common ALL-antigen (VILA1), non-lineage-restricted antigens (OKT9, OKT10), monomorphic HLA-DR determinants (7.2) as well as TdT. When the patient entered his first blast crisis, his blasts expressed a phenotype corresponding to an immature myeloid cell (7.2+, MY7+, My906+, VIM D5-). Ph1-chromosome-positive blasts from this patient's first relapse had completely changed their surface marker characteristics: they had become TdT-positive and exhibited surface features characteristic of early T blasts (WT1+, 10.2+, OKT9+, OKT10+, 7.2-, OKT6-). Together, these features provide evidence that myeloid cells may share a common precursor with T cells.

Adult↗
PubMed1984

Monoclonal antibodies recognizing T-cells (Leu 1) and transferrin receptor (OKT 9) crossreact with malignant B-cells of distinct differentiation stages.

The present study was carried out to determine the reactivity of Leu 1 and OKT 9 mouse monoclonal antibodies with B-cell samples obtained from 99 patients suffering from non-Hodgkin lymphomas of various B-type entities classified according to the Kiel-nomenclature. It could be demonstrated that both antibodies--previously known to display anti-T-cell reactivity--cross-react with several types of malignant B-cell. Leu 1 shows preference for membrane IgM and mouse erythrocyte receptor-bearing cells, whereas OKT 9 was expressed on malignant B-cells reflecting the terminal phase of B-cell ontogeny.

Antibodies, Monoclonal↗
PubMedDate not supplied

Isolated venlafaxine-induced serotonin syndrome.

Serotonin syndrome is a potentially fatal complication of serotonergic drug therapy. Usually, serotonin syndrome occurs with the concomitant use of two serotonergic drugs; this case report describes a patient with a classic presentation of serotonin syndrome induced solely by a venlafaxine overdose. Emergency physicians need to be aware that the serotonin syndrome may occur not only with serotonergic drug combinations but also with overdoses of a single potent serotonergic agent such as venlafaxine.

Adult↗