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E Bruno

Publications and source records attributed to E Bruno.

At least 19 recordsLinked to original sources

Interleukin 10-induced thrombocytopenia in normal healthy adult volunteers: evidence for decreased platelet production.

Recombinant human interleukin 10 (rhuIL-10) inhibits the production of proinflammatory cytokines and has shown promise in the treatment of inflammatory bowel disease. Clinical trials have been accompanied by a reversible decline in platelet counts. We conducted a randomized, double-blinded, placebo-controlled, parallel group trial in 12 healthy volunteers to investigate the aetiology of rhuIL-10-induced thrombocytopenia. Eight volunteers received 8 microg/kg/d of rhuIL-10 subcutaneously, while four subjects received a placebo alone for 10 d. A reversible decline in the platelet counts from a mean of 275 x 10(9)/l to 164 x 10(9)/l was observed in the IL-10-treated cohort (P = 0.012). A fall in the haemoglobin mean levels was also observed in the IL-10-treated cohort from 13.7 to 11.7 g/dl (P = 0.011). No significant change was observed in the bone marrow cellularity or myeloid/erythroid ratio or in the number of megakaryocytes per high-powered field (HPF). A fall was observed in the number of megakaryocyte colony-forming units (CFU-MKs) after the administration of IL-10 compared with those receiving the placebo (P = 0.068). No difference in the change in granulocyte-macrophage CFUs (CFU-GMs), mixed lineage CFUs (CFU-GEMMs) or erythroid burst-forming units (BFU-Es) was observed when comparing the IL-10- vs. placebo-treated groups (P > 0.465). Serum cytokine levels of thrombopoietin (TPO). IL-6 and granulocyte-macrophage colony stimulating factor (GM-CSF) were not decreased following IL-10 administration. In fact, both TPO and GM-CSF appeared to be slightly increased in the serum. All subjects underwent In111-labelled platelet survival studies with liver/spleen scans to assess splenic sequestration prior to and then on day 7 of treatment. A significant reduction in splenic sequestration of platelets (P =0.012) was observed in the IL-10-treated group, but not in the placebo-treated subjects.

Adult↗

Ex vivo expansion of autologous bone marrow CD34(+) cells with porcine microvascular endothelial cells results in a graft capable of rescuing lethally irradiated baboons.

Hematopoietic stem cell (HSC) self-renewal in vitro has been reported to result in a diminished proliferative capacity or acquisition of a homing defect that might compromise marrow repopulation. Our group has demonstrated that human HSC expanded ex vivo in the presence of porcine microvascular endothelial cells (PMVEC) retain the capacity to competitively repopulate human bone fragments implanted in severe combined immunodeficiency (SCID) mice. To further test the marrow repopulating capacity of expanded stem cells, our laboratory has established a myeloablative, fractionated total body irradiation conditioning protocol for autologous marrow transplantation in baboons. A control animal, which received no transplant, as well as two animals, which received a suboptimal number of marrow mononuclear cells, died 37, 43, and 59 days postirradiation, respectively. Immunomagnetically selected CD34(+) marrow cells from two baboons were placed in PMVEC coculture with exogenous human cytokines. After 10 days of expansion, the grafts represented a 14-fold to 22-fold increase in cell number, a 4-fold to 5-fold expansion of CD34(+) cells, a 3-fold to 4-fold increase of colony-forming unit-granulocyte-macrophage (CFU-GM), and a 12-fold to 17-fold increase of cobblestone area-forming cells (CAFC) over input. Both baboons became transfusion independent by day 23 posttransplant and achieved absolute neutrophil count (ANC) >500/microL by day 25 +/- 1 and platelets >20,000/microL by day 29 +/- 2. This hematopoietic recovery was delayed in comparison to two animals that received either a graft consisting of freshly isolated, unexpanded CD34(+) cells or 175 x 10(6)/kg unfractionated marrow mononuclear cells. Analysis of the proliferative status of cells in PMVEC expansion cultures demonstrated that by 10 days, 99.8% of CD34(+) cells present in the cultures had undergone cycling, and that the population of cells expressing a CD34(+) CD38(-) phenotype in the cultures was also the result of active cell division. These data indicate that isolated bone marrow CD34(+) cells may undergo cell division during ex vivo expansion in the presence of endothelial cells to provide a graft capable of rescuing a myeloablated autologous host.

Animals↗

CrkL and CrkII participate in the generation of the growth inhibitory effects of interferons on primary hematopoietic progenitors.

Interferons are potent regulators of normal and malignant hematopoietic cell proliferation in vitro and in vivo, but the signaling mechanisms by which they exhibit their growth inhibitory effects are unknown. We have recently shown that CrkL is engaged in Type I IFN signaling, as shown by its rapid tyrosine phosphorylation during engagement of the Type I IFN receptor. In the present study, we provide evidence that the related CrkII protein is also rapidly phosphorylated on tyrosine during treatment of U-266 and Daudi cells with IFNalpha or IFNbeta. We also show that both members of the Crk-family, CrkL and CrkII, are phosphorylated in an interferon-dependent manner in primary hematopoietic progenitors. Furthermore, inhibition of CrkL or CrkII protein expression by antisense oligonucleotides, reverses the inhibitory effects of IFNalpha or IFNgamma on the proliferation of normal bone marrow progenitor cells (colony forming units-granulocytic/monocytic [CFU-GM] and burst-forming units-erythroid [BFU-E]). Thus, both CrkL and CrkII are engaged in a signaling pathway (s) that mediates interferon-regulated inhibition of hematopoietic cell proliferation.

Adaptor Proteins, Signal Transducing↗

CD109 is expressed on a subpopulation of CD34+ cells enriched in hematopoietic stem and progenitor cells.

CD109 is a monomeric cell surface glycoprotein of 170 kD that is expressed on endothelial cells, activated but not resting T-lymphocytes, activated but not resting platelets, leukemic megakaryoblasts, and a subpopulation of bone marrow CD34+ cells. Observing an apparent association between CD109 expression and the megakaryocyte lineage (MK), we sought to determine whether CD109 was expressed on MK progenitors. In fetal bone marrow (FBM), a rich source of MK progenitors, CD109 is expressed on a mean of 11% of CD34- cells. Fluorescence activated cell sorting (FACS) of FBM CD34+ cells into CD109+ and CD109- fractions revealed that the CD34+CD109+ subset contained virtually all assayable MK progenitors, including the colony-forming unit-MK (CFU-MK) and the more primitive burst-forming unit-MK (BFU-MK). The CD34+CD109+ subset also contained all the assayable burst-forming units-erythroid (BFU-E), 90% of the colony-forming units-granulocyte/macrophage (CFU-GM), and all of the more primitive mixed lineage colony-forming units (CFU-mix). In contrast, phenotypic analysis of the CD34+CD109- cells in FBM, adult bone marrow (ABM) and cytokine-mobilized peripheral blood (MPB) demonstrated that this subset comprises lymphoid-committed progenitors, predominantly of the B-cell lineage. CD109 was expressed on the brightest CD34 cells identifiable not only in FBM, but also in ABM and MPB indicating that the most primitive, candidate hematopoietic stem cells (HSC) might also be contained in the CD109+ subset. In long-term marrow cultures of FBM CD34+ cells, all assayable cobblestone area forming cell (CAFC) activity was contained within the CD109+ cell subset. Further phenotypic analysis of the CD34+CD109+ fraction in ABM indicated that this subset included candidate HSCs that stain poorly with CD38, but express Thy-1 (CD90) and AC133 antigens, and efflux the mitochondrial dye Rhodamine 123 (Rho123). When selected CD34+ cells were sorted for CD109 expression and Rho123 staining, virtually all CAFC activity was found in the CD109+ fraction that stained most poorly with Rho123. CD34+ cells were also sorted into Thy-1 CD109+ and Thy-1 CD109+ fractions and virtually all the CAFC activity was found in the Thy-1+CD109+ subset. In contrast, the Thy-1-CD109+ fraction contained most of the short-term colony-forming cell (CFC) activity. CD109, therefore, is an antigen expressed on a subset of CD34+ cells that includes pluripotent HSCs as well as all classes of MK and myelo-erythroid progenitors. In combination with Thy-1, CD109 can be used to identify and separate myelo-erythroid and all classes of MK progenitors from candidate HSCs.

Adult↗

Impaired saccadic eye movement in diabetic patients: the relationship with visual pathways function.

The aim of this study was to evaluate whether a correlation existed between saccadic eye movements and visual pathways function in diabetic patients. Saccadic or fast Eye Movement System (EMS) and Visual Evoked Potentials (VEPs) were assessed in 20 insulin-dependent diabetic mellitus (IDDM) patients without long-term complications and in stable metabolic control and in 21 age-matched control subjects. In IDDM patients we observed significantly (p<0.01) longer EMS latency, while EMS velocity and accuracy were similar to those of controls; VEPs showed a significant delay in N75, P100, N145 latencies and significant reduction of N75-P100 and P100-N145 amplitudes. In IDDM patients no relationships between EMS and VEP parameters were found. In conclusion, EMS latency delay suggests an impairment of the saccadic eye movement system, while impaired VEPs may be ascribed to a dysfunction of the visual pathways. The lack of correlation between VEPs impairment and EMS latency delay suggests that in our IDDM patients the delay of saccadic latency cannot be exclusively related to a visual pathways dysfunction and could be ascribed to a diffuse neuronal involvement.

Adult↗

[Study on cell proliferation in nasal polyposis as predictive index of recurrence].

The purpose of the present research has been to identify a cellular parameter to be used as an index of increased cell proliferation and, therefore, the likelihood of recurrence. A total of 114 patients with bilateral nasal polyposis underwent naso-ethmoid dissection under endoscopy. Of these, 36 were affected by allergic rhinopathy, 6 bronchial asthma, 9 ASA syndrome and 9 diabetes mellitus; in addition 33 cases were classified as recurrences. The polyp material from each patient was analyzed using a Coulter XL cytofluorimeter, evaluating the cycles of approximately 10-20 thousand cells. The objective was to identify the nasal polyp activity status in the various patients, evaluating cell proliferation indicated by the percentage of cells in phase S and G2 + M. Of the 114 patients, 21 were ruled out of the study because of a high degree of cell debris. Cytofluorimetry made it possible to identify 3 groups based on the different percentage of cells in the genomic synthesis phase. In the first group (A) of 42 patients, the number of cells in the active phase ranged from 2.1% to 10%. The second group (B) of 21 patients showed a percentage in the 14.7-41.9% range. The third group (C) of 30 patients--all affected by recurrent polyps--showed a high percentage (25%-49.8%) of cells in the active phase. It is interesting to note that: 1. A full 91% of the allergic patients fell within group A. 2. Of the 9 patients with ASA, 7 were in the group with recurrences. 3. The 30 patients affected by recurrent polyps were all in group C and that of these 12 had more than one recurrence, expressing a higher percentage of active cells. The above appears to indicate that the cell parameter evaluated here cytofluorimetrically may be a new, simple, reliable index to predict nasal polyps recurrences.

Adult↗

Role of members of the Wnt gene family in human hematopoiesis.

The hematopoietic system is derived from ventral mesoderm. A number of genes that are important in mesoderm development have been identified including members of the transforming growth factor-beta (TGF-beta) superfamily, the fibroblast growth factor (FGF) family, and the Wnt gene family. Because TGF-beta plays a pleiotropic role in hematopoiesis, we wished to determine if other genes that are important in mesoderm development, specifically members of the Wnt gene family, may play a role in hematopoiesis. Three members of the Wnt gene family (Wnt-5A, Wnt-2B, and Wnt-10B) were identified and cloned from human fetal bone stromal cells. These genes are expressed to varying levels in hematopoietic cell lines derived from T cells, B cells, myeloid cells, and erythroid cells; however, only Wnt-5A was expressed in CD34(+)Lin- primitive progenitor cells. The in vitro biological activity of these Wnt genes on CD34(+)Lin- hematopoietic progenitors was determined in a feeder cell coculture system and assayed by quantitating progenitor cell numbers, CD34(+) cell numbers, and numbers of differentiated cell types. The number of hematopoietic progenitor cells was markedly affected by exposure to stromal cell layers expressing Wnt genes with 10- to 20-fold higher numbers of mixed colony-forming units (CFU-MIX), 1.5- to 2. 6-fold higher numbers of CFU-granulocyte macrophage (CFU-GM), and greater than 10-fold higher numbers of burst-forming units-erythroid (BFU-E) in the Wnt-expressing cocultures compared with the controls. Colony formation by cells expanded on the Wnt-expressing cocultures was similar for each of the three genes, indicating similar action on primitive progenitor cells; however, Wnt-10B showed differential activity on erythroid progenitors (BFU-E) compared with Wnt-5A and Wnt-2B. Cocultures containing Wnt-10B alone or in combination with all three Wnt genes had threefold to fourfold lower BFU-E colony numbers than the Wnt-5A- or Wnt-2B-expressing cocultures. The frequency of CD34(+) cells was higher in Wnt-expressing cocultures and cellular morphology indicated that coculture in the presence of Wnt genes resulted in higher numbers of less differentiated hematopoietic cells and fewer mature cells than controls. These data indicate that the gene products of the Wnt family function as hematopoietic growth factors, and that they may exhibit higher specificity for earlier progenitor cells.

Adult↗

The Smad5 gene is involved in the intracellular signaling pathways that mediate the inhibitory effects of transforming growth factor-beta on human hematopoiesis.

Signals from transforming growth factor-beta (TGF-beta), a bifunctional regulator of the proliferation of hematopoietic progenitor cells, have been recently shown to be transduced by five novel human genes related to a Drosophila gene termed MAD (mothers against the decapentaplegic gene). We showed by reverse transcriptase polymerase chain reaction that the RNA from one homologue gene, Smad5, was present in the immortalized myeloid leukemia cell lines, KG1 and HL60, in bone marrow mononuclear and polymorphonuclear cells, as well as in purified CD34+ bone marrow cells. Therefore, we studied the role of this gene in the regulation of human hematopoiesis by TGF-beta. TGF-beta1 and TGF-beta2 significantly inhibited myeloid, erythroid, megakaryocyte, and multilineage colony formation as assayed in semisolid culture systems. The levels of Smad5 mRNA in CD34+ cells were decreased by antisense but not sense oligonucleotides to Smad5. Preincubation of CD34+ marrow cells with two sense oligonucleotides to Smad5 did not reverse the inhibitory effects of TGF-beta on hematopoietic colony formation. However, preincubation with two antisense oligonucleotides to Smad5 reversed the inhibitory effects of TGF-beta. These data show that the Smad5 gene is involved in the signaling pathway by which TGF-beta inhibits primitive human hematopoietic progenitor cell proliferation and that Smad5 antisense oligonucleotides can interrupt this signal.

Cell Division↗

Somatostatin release in response to glucose is impaired in chronic renal failure.

In order to evaluate somatostatin (SRIH) secretion in uremia, plasma SRIH concentrations were determined in basal conditions and after an oral glucose tolerance test (OGTT) in 14 non-dialysed patients with chronic renal failure (CRF), seven of whom had normal glucose tolerance (NGT) and seven impaired glucose tolerance (IGT). Plasma insulin, C-peptide and glucagon and blood glucose concentrations were also evaluated. The results were compared with those obtained in a group of age- and sex-matched normal subjects. In CRF patients, plasma SRIH fasting values (8.6 +/- 0.6 and 7.8 +/- 0.6 pmol/L in NGT and IGT patients, respectively) were comparable to those recorded in controls (7.7 +/- 0.5 pmol/L). SRIH response to OGTT, evaluated as area under curves (AUC) above basal, was similar in both groups of CRF patients (412.9 +/- 84.5 and 415.6 +/- 51.9 pmol/L per min), and significantly lower than in controls (660.1 +/- 58.5 pmol/L per min). Data indicate that chronic uremia induces a loss of SRIH secretory cell responsiveness to glucose. A possible effect of impaired SRIH secretion on glucose metabolism in CRF is discussed.

Adult↗

[Postural stabilization after otolithic repositioning for posterior semicircular canal canalization].

Today the canal/cupulolithiasic pathogenesis of benign paroxysmal positional vertigo (BPPV) appears well defined; what is less clear is the origin of the postural "instability" often associated with rotatory vertigo. This form is less marked but still resists all know treatments. The purpose of the present study was to determine the actual postural arrangement of subjects suffering from canalolithiasis (CL) of the posterior semicircular canal (PSC) both before and after the positioning maneuver. In this case a personal method of spectral frequency analysis was used in an attempt to clarify the origin of the residual "instability" following otolithic repositioning. Static posturographic testing was performed on 20 patients with CL of the PSC and another 20 normal subjects of comparable age. In the present study the repositioning maneuver leads to a reduction in latero-lateral oscillation without any anterior-posterior variation. Such stabilization covers all the frequencies if a visual input is also present while it is limited to the lower frequencies when the visual content is lacking. In fact, in the latter case the subject maintains his posture using only vestibular and proprioceptive input. On the other hand, the anterior-posterior oscillations increase in all frequency ranges and this increase remains essentially unchanged after the repositioning maneuver. The authors feel that the anterior-posterior destabilization seen in CL of the PSC may stem from a proprioceptive-macular alteration linked to otolitic detachment rather than abnormal ampullar stimulation. The persistence and residual postural alterations found could, therefore, explain the persistent sense of instability that CL patients often complain of, even after the maneuvers which have encountered such success in controlling BPPV.

Adult↗

Thrombopoietin mobilizes CD34+ cell subsets into peripheral blood and expands multilineage progenitors in bone marrow of cancer patients with normal hematopoiesis.

Thrombopoietin (TPO), the primary regulator of megakaryocytopoiesis, also mediates biologic effects in vitro on hematopoietic cells more primitive than those committed to the megakaryocyte (MK) lineage. To assess the spectrum of hematopoietic effects of recombinant human (rh)TPO in vivo, we evaluated its proliferative effect on bone marrow (BM) progenitor cells, its maturation effect on BM MKs, and its mobilizing effect on peripheral blood (PB) progenitor cells during a phase I clinical laboratory investigation in which rhTPO was administered to cancer patients with normal hematopoiesis. Twelve patients received a single dose of rhTPO (0.3, 0.6, 1.2, or 2.4 microg/kg of body weight) prior to chemotherapy. BM and PB samples from these patients were analyzed 1 to 2 days before (baseline) and 7 days after rhTPO administration. At higher doses (1.2-2.4 microg/kg), rhTPO produced increased concentrations of primitive CD34+Thy-1+Lin-cells (mean 2.1-fold), CD34+mpl+ cells (mean 5.2-fold), CD34+CD41+CD14- promegakaryoblasts (mean 2.9-fold), and myeloerythroid colony-forming cells (mean threefold) in BM. No significant increases in the frequency of BM colony-forming unit (CFU)-MK were observed. Elevated numbers of both immature (2N-8N) and more mature (64N and 128N) CD41+ MKs were detected in BM, with modal ploidy remaining at 16N. Higher doses of rhTPO (1.2-2.4 microg/kg) also induced increased concentrations of CD34+ cell subsets in PB, including both primitive CD34+Thy-1+Lin- (mean 8.8-fold) and MK lineage-committed CD34+CD41+CD14- cells (mean 14.6-fold) as well as various myeloerythroid colony-forming cells (mean 3.6- to 5.5-fold). These results demonstrate that rhTPO given as a single dose not only promotes proliferation and maturation of cells of the MK lineage, but also expands the pool of BM primitive hematopoietic cells. In addition, rhTPO induces mobilization of hematopoietic progenitors into peripheral circulation. The extent to which such multilineage effects on human progenitor cells will contribute to clinical efficacy remains to be determined.

Adolescent↗

Human megakaryocyte progenitor cells.

Megakaryocytopoiesis is a complex biological process involving a series of cellular events that is initiated with the pluripotent hematopoietic stem cell and eventually results in the biogenesis of platelets shed by mature megakaryocytes (MK). A hierarchy of human MK progenitor cells has been defined by means of studies of in vitro megakaryocytopoiesis. A number of in vitro clonal assays have been established that have aided in the characterization of each of these MK progenitor cells which can be distinguished by their cellular phenotype, physical characteristics, chemosensitivity, kinetics of colony formation, the size of the colonies that each progenitor cell subclass is capable of producing, and the cytokines required to induce such progenitor-cell-derived colony formation. The kinetics of appearance of these various classes of MK colonies derived from MK progenitor cells of differing proliferative capacity are consistent with a sequential developmental relationship between these various cellular subpopulations. The most primitive lineage-restricted MK progenitor cell identified to date is termed the high proliferative potential cell-MK (HPPC-MK). The HPPC-MK can be assayed from fetal but not adult human marrow, and in vitro it forms large unifocal pure MK colonies consisting of more than 300 cells (300 to 1,000). The burst forming unit-megakaryocyte is the most primitive MK progenitor cell that can be assayed from a variety of adult hematopoietic tissues, while the colony forming unit-megakaryocyte is the most differentiated MK progenitor cell still capable of forming pure MK colonies in vitro. Furthermore, a number of multipotent progenitor cells have been identified that are capable of producing colonies composed of multiple hematopoietic lineages of which MKs represent a minority component. A bipotent erythromegakaryocytic progenitor cell in human marrow has been carefully characterized that has the unique ability to form colonies composed exclusively of MKs and erythroblasts. This bipotent progenitor cell has been termed the burst-forming unit erythroid/MK and is indicative of the close linkage between features of the erythroid and megakaryocytic lineages. Recently the ex vivo incubation of CD34+ cells in the presence of a combination of cytokines has resulted in the generation of cell populations enriched for MKs and MK progenitor cells. Such an ex vivo generated product may serve as a source of a new generation of transfusion products capable of supporting thrombocytopenic patients.

Adult↗

Laryngeal metastasis from a signet ring cell carcinoma of the colon. A case report and review of the literature.

Secondary involvement of the larynx and pharynx by malignant neoplasms arising in contiguous structures is well known, but metastases to the larynx from distant tumors are rare. In the present paper a case of signet ring cell carcinoma of the transverse colon metastatic to the left pyriform sinus is reported. A review of the literature identifies 7 other published cases of metastases to the larynx from a colon carcinoma.

Aged↗

[Nasal reactivity in systemic lupus erythematosus].

The present study was prompted by the fact that alterations in nasal respiration were observed in patients with active Systemic Lupus Erythematosus (SLE). These alterations were most likely of a disreactive nature and, thus, could not be attributed to pathology-induced vasculitic alterations. The study was performed using the case/control method. Patients with active SLE were selected on the basis of reference symptoms (difficulty in nasal breathing) and the absence of any significant alteration in the rhinological objectives. Basal, positioning and evoked (cold water, 5 degrees C) rhinomanometry was performed in line with the standards suggested by the "Committee Report on Standardization of Rhinomanometry". Positional testing of the SLE patients revealed "paradoxical response" (66% in the supine decubitus, 50% homolateral and 56% controlateral). In addition there was a statistically significant (p < 0.05) increase in resistance vs. the control group both in the positional testing and upon cold water stimulation. The authors recognized that the rhinomanometric values found in the SLE patients--index of nasal mucosa disreactivity--confirm the presence of the distonic-vegetative alterations characteristic of aspecific vasomotor rhinopathy. In conclusion, the authors hypothesize on the pathogenic mechanisms behind the clinical and instrumental conditions revealed in light of the documented autonomic neuropathy present in SLE patients.

Adult↗

Plasma somatostatin response to an oral test meal in liver transplant patients.

Ten liver transplant patients were studied in basal conditions and after ingestion of a standard mixed test meal. Control groups included 10 normal subjects, 10 patients with nonalcoholic liver cirrhosis, and seven kidney transplant patients. Plasma somatostatin, blood glucose, and plasma insulin, C-peptide, and glucagon were determined before and 15, 30, 45, 60, 90, 120, and 180 minutes after the start of the meal. In liver transplant patients, basal somatostatin and insulin levels were significantly lower than in cirrhotics and were comparable to those recorded in controls and in kidney transplant patients. The time course of the somatostatin secretory response after the meal was similar in any group, but the increase, evaluated as the incremental area above baseline, was significantly higher in liver transplant patients than in controls and cirrhotics and comparable to that recorded in kidney transplant patients. Insulin incremental areas were also lower than in cirrhotics and comparable to those recorded in controls and kidney transplant patients. The data suggest that in liver transplant patients an increased somatostatin response to a meal may be related to a relative beta-cell secretory defect, which in turn seems consequent to immunosuppressive treatment.

Adult↗

The interaction between age and comorbidity contributes to predicting the mortality of geriatric patients in the acute-care hospital.

OBJECTIVE: To test the predictive power of comorbidity and of the interaction between age and comorbidity in geriatric patients with acute medical illness. DESIGN: Prospective observational study. SETTING: Medical and geriatric wards of an acute-care hospital. SUBJECTS: Three hundred and seventy patients over 70 years of age consecutively admitted in an 18-month period. MAIN OUTCOME MEASURE: In-hospital mortality. METHOD: On admission a multidimensional assessment was performed, and a comorbidity index and an age-comorbidity index developed on a comparable training population were calculated. The comorbidity index is based upon a scoring system that quantifies the prognostic weight of individual diseases, while the age-comorbidity index corrects the former for the age-related increase of the risk of death. The predictive power of variables univariately correlated with the outcome was tested by logistic regression. RESULTS: Death was independently predicted by clinical diagnosis of malnutrition (odds ratio = 1.87, confidence limits CL = 1.20-2.86), age-comorbidity index > 7 (odds ratio = 1.77, CL = 1.15-2.72), preadmission impairment in activities of daily living (odds ratio = 1.74, CL = 1.13-2.69), lymphocytopenia (odds ratio = 1.74, CL = 1.15-2.61). A weaker predictive model was obtained by substituting the comorbidity index for the index of age-comorbidity. Excluding comorbidity from the logistic regression greatly weakened the predictive model.

Acute Disease↗

Contribution of central neuropathy to postural instability in IDDM patients with peripheral neuropathy.

OBJECTIVE: To evaluate the contribution of central neuropathy on postural impairment observed in diabetic patients with peripheral neuropathy. RESEARCH DESIGN AND METHODS: Central sensory and motor nervous propagation, nerve conduction velocity, and static posturography were assessed in the following age-matched subjects: 7 IDDM patients with peripheral neuropathy (group DN), 18 IDDM patients without peripheral neuropathy (group D), and 31 control subjects (group C). Somatosensory-evoked potentials (SEPs) during tibial nerve stimulation were recorded, and the spine-to-scalp sensory central conduction time (SCCT) was evaluated. Motor-evoked potentials (MEPs) were recorded from leg muscles during magnetic transcranial brain stimulation, and the scalp-to-spine motor central conduction time (MCCT) was evaluated. The following posturographic parameters were calculated from the statokinesigram: trace length, trace surface, velocity of body sway with its standard deviation, and VFY (a parameter derived from the velocity variance and the anteroposterior mean position of the body). RESULTS: SCCT was significantly higher in the DN group than in the C and D groups (P < 0.001). MCCT was similar in all groups. Posturographic parameters were all significantly impaired in the DN group (P < 0.01). While posturographic parameters showed a direct relationship with some parameters of peripheral nerve conduction, no correlations were observed with SEP and MEP central conduction time. These results were also confirmed by logistic regression, which indicates peripheral neuropathy as the only implicating factor in postural instability (odds ratio 0.22, 95% CI 0.07-0.75) after data reduction by means of factor analysis. CONCLUSIONS: Although diabetic patients with peripheral neuropathy show a delay in central sensory conduction, postural instability may be fully explained by the presence of peripheral neuropathy.

Adult↗

[A rare case of angiolymphoid intramasseteric hyperplasia].

A white caucasian male 38-year-old has come to our Department with an intramasseterin neoformation. The histopathological report has been angiolymphoid hyperplasia. Surgical approach is discussed considering at the same time the peculiarity of this rare type of intervention.

Adult↗