Early predictors of dysphagia in ischaemic stroke patients

Background and purpose

Post-stroke dysphagia affects outcome. In acute stroke patients, the aim was to evaluate clinical, cognitive and neuroimaging features associated with dysphagia and develop a predictive score for dysphagia.

Methods

Ischaemic stroke patients underwent clinical, cognitive and pre-morbid function evaluations. Dysphagia was retrospectively scored on admission and discharge with the Functional Oral Intake Scale.

Results

In all, 228 patients (mean age 75.8 years; 52% males) were included. On admission, 126 (55%) were dysphagic (Functional Oral Intake Scale ≤6). Age (odds ratio [OR] 1.03, 95% confidence interval [CI] 1.00–1.05), pre-event modified Rankin scale (mRS) score (OR 1.41, 95% CI 1.09–1.84), National Institutes of Health Stroke Scale (NIHSS) score (OR 1.79, 95% CI 1.49–2.14), frontal operculum lesion (OR 8.53, 95% CI 3.82–19.06) and Oxfordshire total anterior circulation infarct (TACI) (OR 1.47, 95% CI 1.05–2.04) were independently associated with dysphagia at admission. Education (OR 0.91, 95% CI 0.85–0.98) had a protective role. At discharge, 82 patients (36%) were dysphagic. Pre-event mRS (OR 1.28, 95% CI 1.04–1.56), admission NIHSS (OR 1.88, 95% CI 1.56–2.26), frontal operculum involvement (OR 15.53, 95% CI 7.44–32.43) and Oxfordshire classification TACI (OR 3.82, 95% CI 1.95–7.50) were independently associated with dysphagia at discharge. Education (OR 0.89, 95% CI 0.83–0.96) and thrombolysis (OR 0.77, 95% CI 0.23–0.95) had a protective role. The 6-point “NOTTEM” (NIHSS, opercular lesion, TACI, thrombolysis, education, mRS) score predicted dysphagia at discharge with good accuracy. Cognitive scores had no role in dysphagia risk.

Conclusions

Dysphagia predictors were defined and a score was developed to evaluate dysphagia risk during stroke unit stay. In this setting, cognitive impairment is not a predictor of dysphagia. Early dysphagia assessment may help in planning future rehabilitative and nutrition strategies.     

Tumor detectability and conspicuity comparison of standard b1000 and ultrahigh b2000 diffusion-weighted imaging in rectal cancer

Abdominal Radiology - To compare tumor detectability and conspicuity of standard b = 1000 s/mm2 (b1000) versus ultrahigh b = 2000 s/mm2 (b2000)...     

Frequent aberrant promoter hypermethylation of O6-methylguanine-DNA methyltransferase and death-associated protein kinase genes in immunodeficiency-related lymphomas

Aberrant promoter hypermethylation is a mechanism of tumour suppressor gene inactivation. We explored aberrant promoter hypermethylation of multiple genes in 88 human immunodeficiency virus (HIV)-non Hodgkin lymphomas (NHL), 25 post-transplant lymphoproliferative disorders (PTLD) and five common variable immunodeficiency (CVI)-related NHL. Twenty-six of 79 (32.9%) HIV-NHL, eight of 14 (57.1%) PTLD and two of five (40.0%) CVI-NHL showed aberrant hypermethylation of O6-methylguanine-DNA methyltransferase (MGMT). Aberrant hypermethylation of death-associated protein-kinase (DAP-K) occurred in 70 of 84 (83.3%) HIV-NHL, 19 of 25 (72.0%) PTLD and three of five (60.0%) CVI-NHL. These data implicate MGMT and DAP-K hypermethylation in lymphomagenesis of immunodeficient hosts. In particular, promoter hypermethylation of DAP-K represents the most frequent molecular alteration yet identified in immunodeficiency-related lymphomas.     

Effects of montelukast treatment and withdrawal on fractional exhaled nitric oxide and lung function in children with asthma

BACKGROUND: Leukotriene receptor antagonists (LTRAs) reduce fractional exhaled nitric oxide (Feno) concentrations in children with asthma, but the effect of LTRA withdrawal on Feno and lung function is unknown. We aimed to study the effect of treatment and withdrawal of montelukast, a LTRA, on airway inflammation as reflected by Feno and lung function in children with asthma. METHODS: A double-blind, randomized, placebo controlled, parallel group study was undertaken in 14 atopic children with mild persistent asthma who were treated with oral montelukast (5 mg/d for 4 weeks) and 12 atopic children with mild persistent asthma who received matching placebo. A follow-up visit was performed 2 weeks after montelukast or placebo withdrawal. RESULTS: Montelukast reduced Feno concentrations by 17% (p = 0.067), an effect that was more pronounced (35%) [p = 0.0029] when children with seasonal atopy who were exposed to relevant allergens during the treatment phase were excluded from analysis (n = 3). Compared to those at the end of treatment, Feno concentrations were increased 2 weeks after montelukast withdrawal (p = 0.023) concomitant with a reduction in absolute FEV(1) values (p = 0.011), FEV(1) percentage of predicted values (p = 0.006), FEV(1)/FVC ratio (p = 0.002), and forced expiratory flow at 25% to 75% of FVC values (p = 0.021). These changes were not observed in the placebo group. CONCLUSIONS: LTRAs reduce Feno concentrations in children with asthma, and withdrawal can result in increased Feno values and worsening of lung function in children with asthma.     

The multicenter trial SAKK 37/95 of cladribine, cyclophosphamide and prednisone in the treatment of chronic lymphocytic leukemias and low-grade non-Hodgkin's lymphomas

A multicenter trial was performed to confirm the therapeutic efficacy and the toxicity profile of the combination of cladribine, cyclophosphamide and prednisone in low-grade non-Hodgkin's lymphoma (NHL) and chronic lymphocytic leukemia (CLL). Twenty-three adults with previously treated (61%) or untreated (39%) NHL International Working Formulation A or Binet B and C CLL were administered cladribine 0.1 mg/kg/day as a subcutaneous bolus for 5 days, intravenous cyclophosphamide 500 mg/m2 on day 1, and oral prednisone 40 mg/m2 on days 1-5, every 4 weeks. Unexpected early hematological toxicities led to dose modifications for pretreated patients who received cladribine for 3 days only up to a maximum of five courses. Responses were observed in 75%, with 7 patients obtaining a complete clinical and hematological response. Median duration of complete response was 9 months. Median time to progression or relapse was 31 months. Myelosuppression and infections were dose limiting whereas posttreatment complications, including fatalities, resulted from infections. Median overall survival time from trial entry was 60 months. Activity of the combination of cladribine, cyclophosphamide and prednisone was confirmed. However, in the specific setting of a multicenter trial, unexpected fatal infectious episodes occurred in pretreated patients. Great caution is thus required in these susceptible patients and the routine use of corticosteroids should probably be abandoned.     

Double partial trisomy 9q34.1-->qter and 21pter-->q22.11: FISH and clinical findings.

We describe a patient with double trisomy 9q34.1-->qter and 21pter-->q22.1 resulting from 3:1 segregation of a maternal balanced translocation. The patient shows a clinical syndrome similar to that observed in patients with duplication of the chromosome 9q distal region, while no signs of trisomy 21 were observed. The use of high resolution banding and FISH were of fundamental importance for the cytogenetic diagnosis and for definition of the breakpoints on both chromosomes 9 and 21.     

Severe pelvic organ prolapse treated by vaginal native tissue repair: long-term analysis of outcomes in 146 patients

Aims

The aim of this study was to assess the effectiveness and safety of vaginal native tissue repair (VNTR) as a surgical treatment for severe pelvic organ prolapse (POP) and, second, to evaluate the impact on the quality-of-life (QoL) and sexual function.

Methods

Women with symptomatic POP (≥III stage according to POP Quantification System) with or without stress urinary incontinence (SUI) underwent VNTR. The clinical stage, 3-day voiding diary, and urodynamic testing were evaluated in the preoperative and postoperative times, respectively. The International Consultation on Incontinence Questionnaire–Urinary Incontinence Questionnaire Short Form (ICIQ–UI SF), the Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire short form (PISQ-12), and the prolapse quality-of-life questionnaire (P-QoL) were administered.

Results

One hundred forty-six patients were recruited. The median follow-up was 48 months (36–63). Fifty-two women (36%) had a previous hysterectomy, and 16 (11%) had a previous prolapse/continence surgery. Preoperatively, 135 (92.5%), 109 (74.7%), and 98 (67.1%) patients had anterior, central, and posterior descent ≥III stage, respectively. Thirty-two patients (22%) had concomitant diagnosis of SUI. Median operative time was 85 min (37–154), and median postoperative hospital stay was 2 days (2–4). No intraoperative severe complications occurred. At the long-term follow-up, the subjective cure rate for prolapse was 97.3% and the objective cure rate was 91.1%. A significant improvement of ICIQ-UI SF, the P-QoL, and the PISQ-12 was recorded at the follow-up (p?<?0.001).

Conclusion

VNTR is effective, safe, and durable and improves POP-related symptoms and sexual function.

     

Creutzfeldt-Jakob disease (CJD) with a mutation at codon 148 of prion protein gene: relationship with sporadic CJD

Creutzfeldt-Jakob disease (CJD), the most common human prion disease, includes sporadic (s) and familial (f) forms. Regardless of etiology, both forms are thought to share the pathogenic mechanism whereby the cellular prion protein (PrP(C)) converts into its pathogenic isoform (PrP(Sc)). While PrP(C) conversion is thought to be random in sCJD, conversion in fCJD is facilitated by the congenital presence of mutated PrP. Differences in PrP genotype (PRNP) and in conversion circumstances lead to PrP(Sc) with distinct characteristics that elicit different disease phenotypes. Here, we describe a case of fCJD with a substitution of histidine (H) for arginine (R) at codon 148 (R148H) and heterozygosity of the methionine/valine (M/V) polymorphic codon 129, with the 129M allele coupled with the mutation. The disease phenotype and all major characteristics of PrP(Sc) of fCJD(R148H) were virtually indistinguishable from those of sCJDMV2, which has features different from those of any other sCJD. Therefore, despite the differences in etiology, PRNP, and conversion process, the two forms of PrP(Sc) had similar characteristics. Furthermore, comparison of fCJD(R148H) with a recently reported case carrying R148H and homozygosity at codon 129 suggests that codon 129 coupled with the mutation as well as that located on the normal allele can modify major phenotypic and PrP(Sc) features of fCJD(R148H).