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Protein-energy undernutrition is a very common problem among elderly patients. It is promoted by age-related decreases in the basal metabolic rate, physiological change in body composition, progressive dysphagia, physical and/or cognitive impairments, depression, socioeconomic factors, effects of drugs on absorption and utilization of nutrients, and other factors. Several studies suggest that nutritional support can lower the risk of adverse outcomes among undernourished elderly patients. Monitoring food intake in patients with dysphagia may be useful in deciding between oral supplementation or artificial nutrition. The decision to provide nutritional support and the route to be used will depend on the clinical conditions of the patient, the severity of the dysphagia, the expected course of any underlying diseases, and several other patient-specific considerations. In geriatric patients, the main objectives of this type of therapy are usually the maintenance of function and improvement of the quality of life.

Summary Protein-energy undernutrition is a very common problem among elderly patients. It is promoted by age-related decreases in the basal metabolic rate, physiological change in body composition, progressive dysphagia, physical and/or cognitive impairments, depression, socioeconomic factors, effects of drugs on absorption and utilization of nutrients, and other factors. Several studies suggest that nutritional support can lower the risk of adverse outcomes among undernourished elderly patients. Monitoring food intake in patients with dysphagia may be useful in deciding between oral supplementation or artificial nutrition. The decision to provide nutritional support and the route to be used will depend on the clinical conditions of the patient, the severity of the dysphagia, the expected course of any underlying diseases, and several other patient-specific considerations. In geriatric patients, the main objectives of this type of therapy are usually the maintenance of function and improvement of the quality of life.

We tested a set of commercially available probes to determine the feasibility and accuracy of FISH in the detection of abnormalities in 13 patients with Chronic Lymphocytic Leukemia (CLL) with a particular aggressive clinical disease. We utilized three different probes for the 13q12-14 region, one for the centromeric region of chromosome 12, one for the P53 gene at 17p13.1 and one for 3'-5' IGH at 14q32, covering the entire region of IGH, thus potentially allowing to detect more rearrangements. Conventional cytogenetic study showed a normal karyotype in 8/13 patients. FISH was able to detect chromosomal abnormalities in 10/13 pts (85%): +12 in 4 pts (38%); del 13q in 4 (38%); del 17p in 3 (35%); del of 5'-IGH in 1 (15%). In conclusion FISH confirmed its ability to improve the detection of cytogenetic abnormalities especially in patients with an aggressive disease.

Recurrent cytogenetic abnormalities are typically found in about one third of B-cell chronic lymphocytic leukemia patients (B-CLL) by standard cytogenetic analysis and their prognostic relevance is well known. We report a case of a B-CLL patient showing both trisomy 12 and a t(14;22)(q32;q11). Trisomy 12 is often associated with aggressive disease and resistance to chemotherapy, however, our patient is in good health and currently untreated after 7 years, suggesting in this case a relatively good prognosis and a questionable role for translocations involving the 14q32 locus.

Emergence of additional cytogenetic clones in chronic myelocytic leukemia (CML) patients who become Philadelphia chromosome–negative (Ph−) after α-interferon therapy (or more recently with imatinib mesylate) have been described. We report here a case of a novel t(6;7)(p21;q23) that developed in a CML patient in complete cytogenetic remission during imatinib therapy. In this case, fluorescence in situ hybridization and reverse transcriptase polymerase chain reaction showed a normal pattern for BCR and ABL genes, suggesting that a different and unrelated clone developed after the disappearance of the Ph chromosome.

CD34+/Ph+ cells are still detectable in chronic myeloid leukemia patients with sustained and prolonged complete cytogenetic remission during treatment with imatinib mesylate

Although trisomy 13 has been reported as a recurring abnormality in acute myelocytic leukemia [1], it has been rarely described in other hematological diseases, particularly in chronic myeloproliferative disorders. We report here a case of a 79-year-old male patient with idiopathic myelofibrosis showing a trisomy 13 at cytogenetic analysis upon diagnosis. The patient was referred to our division because of leukocytosis, anemia, and thrombocytopenia. Physical examination showed marked hepatomegaly and splenomegaly. A peripheral blood sample showed hemoglobin 9.6 g/dL, platelets 50 × 10/L, and white blood cells 60 × 10/L with 60% neutrophils, 10% lymphocytes, 20% myelocytes, 5% metamyelocytes, 5% monocytes, and rare erythroblasts. Poikilocytosis with dacryocytes was observed. Analysis of bone marrow biopsy showed hypercellularity and was consistent with a diagnosis of idiopathic myelofibrosis in the cellular phase. Cytogenetic analysis was performed with a Wright–Giemsa banding technique on a bone marrow aspirate. We examined metaphase cells from shortterm unstimulated cultures at 37 C in RPMI-1640 medium, supplemented with 10% fetal calf serum. Chromosomal abnormalities were described according to ISCN 1995 [2]. The karyotype showed 47,XY, 13[19]/46,XY[1]. As of writing, the patient was in good clinical condition, after being treated with hydroxyurea 1 g/d with stable disease at 6 months follow-up. Trisomy 13 is associated predominantly with undifferentiated acute myelocytic leukemia (AML, M0), but a few cases of myelodysplastic syndrome have been reported [3], with a highly variable prognosis: 4 months to 10 years of survival. Trisomy 13 affects predominantly older men and there is a possible association with previous chemoradiotherapy. No

As a result of the low proliferative index, only 50% of chronic lymphocytic leukemia cases are adequate for cytogenetic analysis. Of these, about half have clonal abnormalities. The application of fluorescence in situ hybridization (FISH) to CLL has substantially enhanced our ability to detect chromosomal aberrations; the incidence of a number of recurring abnormalities has been established, providing new insights into the pathogenesis of this disease with a direct impact on the prognosis.

Recurring chromosomal abnormalities such as der(22), 8, i(17q), and 19 (i.e., karyotype evolution) have been described during the accelerated and/or blastic phase of chronic myelocytic leukemia (CML-BP). Deletion of the long arm of chromosome 20 is a recurring abnormality in clonal myeloid disorders, which are found in approximately 10%–30% of polycythemia vera patients and 5% of myelodysplastic syndrome (MDS) patients, and is only rarely reported in acute myelocytic leukemias (AMLs) [1] and not described in CML. We report here a case of involvement of chromosomes 20 and 21 in a 45-year-old male patient with CML that progressed to a blastic phase after 9 months of treatment with interferon-α plus oral cytosine arabinoside. A peripheral blood cell count showed the following: white blood cells, 2.4 × 10/L; hemoglobin, 10.5 g/dL; platelets, 74. × 10/L. Bone marrow cells from unstimulated 24to 48-hour cultures in

Whereas hyperdiploidy is a frequent cytogenetic abnormality in acute lymphoblastic leukemia, tetraploidy is rarely observed in acute myeloblastic leukemia (AML), in which gains and losses of whole chromosomes do occur frequently [1–4]. A 76-year-old man was admitted to our division with dyspnea and weakness. Peripheral blood cell analysis showed white blood cell count 29.6 × 10/mL with 90% blast cells, hemoglobin 9.4 g/dL, and platelets 55 × 10/mL. Physical examination findings were normal, except for liver enlargement. Bone marrow examination confirmed a diagnosis of AML M5a with 90% blast cells. Leukemic cells

Although the success of imatinib mesylate therapy represents an exciting advance in targeted cancer therapy, it has still to be determined whether responses to this p210 inhibitor in chronic myeloid leukemia (CML) patients will be durable. In fact most of clinical studies agree on the evidence of a persistent molecular disease in the majority of treated patients and altough the absolute level of bcr-abl transcript may vary over the treatment, yet a molecular complete response is of rare observation. In addition, discontinuation of imatinib exerts always in rapid loss of response. In accordance to this the persistence of malignant progenitors in patients in complete cytogenetic response (CCR) after short term imatinib treatment, has been recently demonstrated. In particular, Bathia et al. showed in 12/15 patients studied after a median time of 10 months of imatinib treatment a median of 11% of residual CML CD34+ progenitors in the bone marrow (by FISH Dual Fusion bcr/abl analysis)while only 3/15 patients had no detectable residual CD34+ cells. Less is known about residual Ph+/CD34+ cells surviving after a prolonged therapy with this targeting drug. Thus, we evaluated the amount of bone marrow residual CD34+ cells in 17 CML patients in stable CCR after a long lasting treatment with imatinib. At the time of evaluation, the patients were on conventional dose (400mg) Imatinib for a median time of 48 months (range 36–58 months) having achieved a CCR status (conventionally defined as the complete absence of t(9;22) on caryotypic analysis) within 3 to 6 months of treatment. However all of them still showed molecular disease as detected by nested RT-PCR. Bone marrow CD34+ cell-enriched populations were selected from mononuclear cells using immunomagnetic column separation and were evaluated after cytospin by FISH using a bcr-abl Dual Color Extra Signal Probe(LSI bcr-abl ES, Vysis), that is able to detect bcr-abl fusion in interphase nuclei with a false positive signal rate close to 0. A minimum of 100 CD34+ nuclei per each sample were evaluated. Interestingly, in 8/17 patients no Ph+/CD34+ cells were detected, while in the remaining 9/17 patients a median of 2% (range 0.5–11%) of bcr-abl positive progenitors were still observed. In this small selected serie of patients prolonged treatment with imatinib appears to be correlated with a lower, yet detectable, amount of residual bone marrow Ph+/CD34+ cells when compared to previously published data. This result could be partly explained with the different specificity and sensitivity of the probe used (bcr/abl ES