Lymph node blast crisis in chronic myeloid leukemia mimicking T-immunoblastic lymphoma.

BACKGROUND: Chronic myeloid leukemia arises from a somatic mutation in a pluripotent stem cell. It generally terminates with a blastic crisis (BC). One third of BC are lymphoid, and most have a pre-B phenotype. Few cases of T-lymphoid BC have been reported. Here we describe a lymph node blast crisis mimicking T-immunoblastic lymphoma. METHODS: Bone marrow and lymph nodes were histologically examined by standard methods and by an immunoperoxidase technique. Cytogenetic studies were also performed on lymph node and blood cells. Analysis of T-cell receptor genes and BCR rearrangements were performed on DNA extracted from both frozen bone marrow and lymph-node cells. RESULTS: Lymph-node histology showed an infiltration by large lymphoid blasts, consistent with a diagnosis of immunoblastic lymphoma. Blast cells were CD2, CD7, TDT positive, and negative for myeloid and mature lymphoid antigens. The Ph1 chromosome was found in both bone marrow and lymph-node cells. BCR rearrangement was found in the DNA from both bone marrow and lymph-node cells. TCR genes were not rearranged. DISCUSSION: The present study provides strong evidence that the lymph-node blast crisis of CML can assume the morphological appearance of immunoblastic lymphoma and may retain the immunological phenotype and genetic features of early T cells with BCR rearrangements.     

Neutropenic typhlitis

Neutropenic typhlitis is an acute inflammation of the cecum occurring in neutropenic patients. Two cases are described, both presenting typical features of the disease. It is our experience that the treatment approach should consist of bowel rest, fluid therapy, and massive administration of broad spectrum antibiotics. In some cases, full recovery will follow. If abdominal signs persist, surgery should be deferred until hematologic convalescence occurs. At this time, cecostomy and drainage should be adequate. Only in very severe cases, with wide-spread necrosis, should a right hemicolectomy be performed.     

Helicobacter Pylori Infection is Not Related to Restenosis Following Angioplasty

Chronic inflammation is thought to be important in the pathogenesis of atherosclerosis. Helicobacter pylori (H. pylori) is a common chronic infection of humans that has been definitely linked to peptic ulcer. The evidence implicating H. pylori with atherosclerosis is controversial. We decided to investigate an effect of H. pylori infection on the restenosis after coronary angioplasty. Ninety four patients who underwent PTCA and a subsequent repeat angiography were included in the study. The indications for angiography and repeat PTCA were determined by the attending cardiologist. H. pylori serology was determined by ELISA. Sixteen (17.2%) of the patients developed restenosis. Of these 16, 12 (75%) were H. pylori seropositive versus 44 (56.4%) of the 78 patients who did not develop restenosis, p = 0.13. There was no difference between the H. pylori positive and negative patients with respect to cholesterol level, hypertension, diabetes or peptic disease. There appears to be no relationship between H. pylori and the development of restenosis following PTCA.     

Aberrant methylation of DAP-kinase in therapy-related acute myeloid leukemia and myelodysplastic syndromes

Death-associated protein kinase (DAP-kinase), a proapoptotic serine/threonine kinase, is a candidate tumor suppressor gene. We studied the methylation status of DAP-kinase of 194 bone marrow samples from 160 patients with acute myeloid leukemia (AML) and 34 with a myelodysplastic syndrome (MDS) at the time of initial diagnosis by polymerase chain reaction (PCR). Hypermethylation of DAP-kinase was present in 27.5% (44 of 160) of AML and in 47% (16 of 34) of MDS specimens and significantly correlated to loss of DAP-kinase expression (P =.008). It was significantly more frequent in AML secondary to therapy for other malignancies (s-AML; 14 of 29, 48.3%), as compared to de novo AML (30 of 131, 22.9%, P =.01). DAP-kinase hypermethylation in AML was associated with myelodysplastic changes in the bone marrow at the time of the initial diagnosis (P =.002) and with the presence of cytogenetic abnormalities (P =.02). Alteration in the apoptotic response due to the loss of DAP-kinase function may be an early event in the transformation pathway to secondary leukemia via myelodysplasia.     

A protocol for the management of pediatric type I open fractures

Background

The management of pediatric type I open fractures remains controversial. There has been no consistent protocol established in the literature for the non-operative management of these injuries.

Methods

A protocol was developed at our institution for the non-operative management of pediatric type I open forearm fractures. Each patient was given a dose of intravenous antibiotics at the time of the initial evaluation in the emergency department. The wound was then irrigated and a closed reduction performed in the emergency department. The patient was admitted for three doses of intravenous antibiotics (over approximately a 24-h period) and then discharged home without oral antibiotics.

Results

In total, 45 consecutive patients were managed with this protocol at our hospital between 2004 and 2008. The average age was 10 (range 4–17) years. The average number of doses of intravenous antibiotics was 4.06 per patient. Thirty patients (67 %) received cefazolin (Ancef®) as the treating medication and 15 patients received clindamycin (33 %). There were no infections in any of the 45 patients.

Conclusion

In this study we outline a consistent management protocol for type I open pediatric forearm fractures that has not previously been documented in the literature. Our results corroborate the those reported in the literature that pediatric type I open fractures may be managed safely in a non-operative manner. There were no infections in our prospective series of 45 consecutive type I open pediatric forearm fractures using our protocol. Using a protocol of only four doses of intravenous antibiotics (one in the emergency department and three additional doses during a 24-h hospital admission) is a safe and efficient method for managing routine pediatric type I open fractures non-operatively.     

Neuroimmunological function in parents of children suffering from cancer

The main aim of this study is to evaluate the relationship between depression and immunological function in parents of children with cancer. Thirty-two parents participated in the study. The parents completed the following assessments: a list of major stressful events in a Hemato-Oncology ward, beck depression inventory II (BDI-II), posttraumatic diagnostic scale (PDS) and quality of life (QOL) questionnaire. A single blood sample was drawn from parents for evaluation of cortisol levels and lymphocyte cell subgroups. The parents were divided into two groups: Those who suffered from depression as defined by BDI-II cutoff score of 14 (depressed parents (DP), n = 7), and non-depressed parents (non-DP, n = 25). In parents of children with cancer the DP group had statistically significantly higher stressful event scores, dysfunction scores (from the PDS) and CD8 percentage compared to the non-DP group. QOL, CD4 percentage and CD4/CD8 ratio were significantly lower in the DP group. The BDI scores significantly positively correlated with events and dysfunctional scores, and significantly negatively correlated with QOL scores and CD4/CD8 ratio. High psychiatric morbidity was found in parents of children with cancer. The findings of altered immunity in DP provide further evidence that the physiological response to stress and depression may alter immune functions.