Results after the surgical treatment of anterior cervical hyperostosis causing dysphagia

Purpose

The objective of this study was to investigate the outcome of a case series of patients with dysphagia resulting from diffuse idiopathic skeletal hyperostosis (DISH) of the cervical spine who were treated surgically with resection and fusion.

Methods

A retrospective study was performed on all patients who presented (2005?2013) with complaints of dysphagia or respiratory compromise and who underwent anterior cervical osteophyte resection with fusion (polyether ether ketone cage and/or plate system) using an anterior approach. All patients were diagnosed with DISH and underwent preoperative esophageal and laryngoscopic examinations and a fluoroscopic swallowing study. Initial non-operative strategies were performed, including diet, change in head position during swallowing, non-steroidal anti-inflammatory drugs and pantoprazole.

Results

A total of six patients with DISH were included. The mean age was 67 ± 5 years. All patients were male and had symptoms of dysphagia and neck pain, one had simultaneous airway complaints, and another had regurgitation with a sleep disorder. All patients had significant improvements in dysphagia, respiratory complaints and regurgitation 6 weeks after surgery. The postoperative radiographs showed complete removal of the compressive structures. There were no postoperative complications. At the final follow-up (23 ± 8 months), the radiographic examinations showed no pathological regrowth, and the patients reported no recurrence of dysphagia.

Conclusion

Diffuse idiopathic skeletal hyperostosis may lead to osteophyte-associated pathologies of the aerodigestive tract. Preoperative investigations with esophageal and laryngoscopic examinations combined with fluoroscopic swallowing tests are essential. Surgical decompression through osteophytectomy and fusion is an effective management strategy in selected patients and should be considered when non-operative strategies have failed.

     

Mindfulness meditation training alters stress-related amygdala resting state functional connectivity: a randomized controlled trial

Recent studies indicate that mindfulness meditation training interventions reduce stress and improve stress-related health outcomes, but the neural pathways for these effects are unknown. The present research evaluates whether mindfulness meditation training alters resting state functional connectivity (rsFC) of the amygdala, a region known to coordinate stress processing and physiological stress responses. We show in an initial discovery study that higher perceived stress over the past month is associated with greater bilateral amygdala-subgenual anterior cingulate cortex (sgACC) rsFC in a sample of community adults (n = 130). A follow-up, single-blind randomized controlled trial shows that a 3-day intensive mindfulness meditation training intervention (relative to a well-matched 3-day relaxation training intervention without a mindfulness component) reduced right amygdala-sgACC rsFC in a sample of stressed unemployed community adults (n = 35). Although stress may increase amygdala-sgACC rsFC, brief training in mindfulness meditation could reverse these effects. This work provides an initial indication that mindfulness meditation training promotes functional neuroplastic changes, suggesting an amygdala-sgACC pathway for stress reduction effects.     

Ex vivo treatment of proliferating human cord blood stem cells with stroma-derived factor-1 enhances their ability to engraft NOD/SCID mice

Ex vivo proliferation of hematopoietic stem cells (HSCs) is important for cellular and gene therapy but is limited by the observation that HSCs do not engraft as they transit S/G(2)/M. Recently identified candidate inhibitors of human HSC cycling are transforming growth factor-beta(1) (TGF-beta(1)) and stroma-derived factor-1 (SDF-1). To determine the ability of these factors to alter the transplantability of human HSCs proliferating in vitro, lin(-) cord blood cells were first cultured for 96 hours in serum-free medium containing Flt3 ligand, Steel factor, interleukin-3, interleukin-6, and granulocyte colony-stimulating factor. These cells were then transferred to medium containing Steel factor and thrombopoietin with or without SDF-1 and/or TGF-beta(1) for 48 hours. Exposure to SDF-1 but not TGF-beta(1) significantly increased (> 2-fold) the recovery of HSCs able to repopulate nonobese diabetic/severe combined immunodeficiency mice. These results suggest new strategies for improving the engraftment activity of HSCs stimulated to proliferate ex vivo.     

Studies on the mechanism of accumulation of cholesterol in the gallbladder mucosa. Evidence that sterol 27-hydroxylase is not a pathogenetic factor

BACKGROUND/AIMS: Cholesterolosis is characterized by accumulation of esterified cholesterol in human gallbladder mucosa. The present study aimed at investigating possible pathogenetic factors for cholesterolosis. The hypothesis was tested that a reduced sterol 27-hydroxylase or an increased amount of ACAT-1 enzyme may be of importance. METHODS: Gall bladder mucosa and bile were obtained from patients with cholesterol gallstones undergoing cholecystectomy (30 with and 43 without cholesterolosis). RESULTS: In cholesterolosis, the gall bladder mucosa was characterized by a several-fold increase in esterified cholesterol and normal content of free cholesterol. The amount of ACAT-1 protein, measured by immunoblotting, was similar in patients with and without cholesterolosis. The level of 27-hydroxycholesterol in gallbladder mucosa was elevated sevenfold as compared with cholesterol in patients with cholesterolosis. Most (87%) of this oxysterol was esterified and the accumulation is most probably secondary to the higher total amount of cholesterol in the cells. Patients with cholesterolosis had normal levels of both sterol 27-hydroxylase mRNA (real time polymerase chain reaction) and protein (immunoblotting). The enzymatic activity of the sterol 27-hydroxylase in gallbladder mucosa was normal or increased in cholesterolosis. CONCLUSIONS: The pathogenesis of cholesterolosis may be multifactorial, but is not caused by reduced efflux of cholesterol due to a defect sterol 27-hydroxylase mechanism.     

Seroconversion to hepatitis C virus antibodies in patients with acute posttransfusion non-A,non-B hepatitis in Sweden

Summary Seventy-four patients in 1978 and 316 in 1986, all transfused during open-heart surgery in Stockholm, Sweden, were studied prospectively for the development of posttransfusion non-A, non-B (NANB) hepatitis, seroconversion to hepatitis C virus antibodies (anti-HCV) (C-100), time lag to seroconversion to anti-HCV and outcome of posttransfusion NANB/C hepatitis. Anti-HCV was tested up to six months after transfusions in patients from 1978 and up to one year after transfusions in patients from 1986. Fifty-four percent of the patients who developed posttransfusion NANB hepatitis seroconverted to anti-HCV, 7/15 (47%) in 1978 and 8/13 (62%) in 1986. Four (27%) of the 15 patients who seroconverted to anti-HCV were anti-HCV reactive within one week, 12 (80%) within eight weeks and all within 18 weeks after the onset of hepatitis. The ELISA optical density/cut-off (OD/CO) ratio was above 4.0 in all patients with hepatitis C who seroconverted. One transfused patient with normal serum aminotransferase levels throughout follow-up seroconverted after six months. He had a temporary positive anti-HCV reactivity with a maximal ELISA OD/CO ratio for anti-HCV of only 1.2, which became negative three years later. Development of chronic hepatitis was noticed in 9/15 (60%) patients who seroconverted to anti-HCV and in 5/13 (38%) patients with posttransfusion NANB hepatitis who did not seroconvert.

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Anti-HBC-Serokonversion bei Patienten mit akuter Non-A, Non-B-Hepatitis nach Transfusion in Schweden

Zusammenfassung 74 Patienten, die 1978, und 316 Patienten, die 1986 während offener Herzchirurgie in Stockholm, Schweden, Transfusionen erhielten, wurden in eine prospektive Studie aufgenommen und im Hinblick auf das Auftreten einer Non-A, Non-B-Posttransfusions-hepatitis, Serokonversion für Hepatitis C Virus-Antikörper (anti-HCV, C-100), Zeitspanne bis zur Serokonversion für anti-HCV und Verlauf der NANB/C-Posttransfusionshepatitis untersucht. Bei Patienten, die 1978 transfundiert worden waren, wurden Untersuchungen auf anti-HCV bis zu sechs Monate nach der Transfusion und bei 1986 Transfundierten bis zu einem Jahr nach Transfusion durchgeführt. Eine Serokonversion zu anti-HCV trat bei 54% der Patienten mit NANB-Posttransfusions-hepatitis ein, 7/15 (47%) der Patienten aus dem Jahr 1978 und 8/13 (62%) aus dem Jahr 1986. Die Serokonversion zu anti-HCV trat bei vier der 15 Patienten (27%) schon innerhalb einer Woche ein, bei 12 (80%) innerhalb acht Wochen und bei allen innerhalb 18 Wochen nach Beginn der Hepatitis. Bei den Patienten mit Hepatitis C, die eine Serokonversion entwickelten, lag der Quotient von ELISA Meßwert zu Grenzwert (Optical density/ Cut-off, OD/CO) in allen Fällen über 4,0. Ein Patient, bei dem nach der Transfusion stets normale Serum- Aminotransferase-Spiegel vorlagen, zeigte nach sechs Monaten eine Serokonversion. Er war vorübergehend anti-HCV positiv, der ELISA OD/CO- Quotient für anti-HCV betrug maximal 1,2; nach drei Jahren war er seronegativ. Bei neun der 15 Patienten (60%) war eine chronische Hepatitis nach Serokonversion für anti-HCV zu beobachten. Unter den 13 Patienten mit NANB-Posttransfusionshepatitis, die keine Serokonversion zeigten, entwickelten fünf eine chronische Hepatitis (38%).

     

Reconstitution after transplantation with T-lymphocyte-depleted HLA haplotype-mismatched bone marrow for severe combined immunodeficiency.

Severe combined immunodeficiency (SCID) is potentially correctable by bone marrow transplantation if a patient has a suitable histocompatible donor. In the absence of an HLA-matched donor, lethal graft-versus-host disease (GVHD), which is mediated by alloreactive donor T cells, may occur. In an attempt to prevent GVHD in one SCID patient lacking a matched donor, we treated maternal haplomismatched bone marrow with a unique nonmitogenic T-cell-specific monoclonal antibody (anti-T12) and complement to remove mature T cells. Despite the removal of greater than 99% mature T cells, the child developed significant life-threatening GVHD, which was terminated by a 5-day course of intravenous anti-T12. Subsequently, immune reconstitution occurred by 6 wk: the mature circulating T cells proliferated in response to soluble and allo-antigens in vitro and provided help for B-cell immunoglobulin synthesis. The patient was removed from a protective environment and discharged without evidence of further infection. Both HLA and chromosomal analyses showed that the circulating cells in the patient were of maternal origin. More importantly, the maternal T cells were no longer reactive with recipient cells. Mixing experiments indicated that the state of tolerance that resulted in this chimera was not due to active suppression. We conclude that HLA-mismatched transplantation for SCID can be undertaken if mature alloreactive donor T lymphocytes are depleted before and after bone marrow grafting.     

Heart-type fatty acid-binding protein permits early risk stratification of pulmonary embolism.

AIMS: We investigated the value of a novel early biomarker, heart-type fatty acid-binding protein (H-FABP), in risk stratification of patients with acute pulmonary embolism (PE). METHODS AND RESULTS: We prospectively included 107 consecutive patients with confirmed PE. The endpoints were (i) PE-related death or major complications and (ii) overall 30-day mortality. Overall, 29 patients (27%) had abnormal (>6 ng/mL) H-FABP levels at presentation. Of those, 12 (41%) had a complicated course, whereas all patients with normal baseline H-FABP had a favourable 30-day outcome (OR, 71.45; P<0.0001). At multivariable analysis, H-FABP (P<0.0001), but not cardiac troponin T (P=0.13) or N-terminal pro-brain natriuretic peptide (P=0.36), predicted an adverse outcome. Evaluation of a strategy combining biomarker testing with echocardiography revealed that patients with a negative H-FABP test had an excellent prognosis regardless of echocardiographic findings. In contrast, patients with a positive H-FABP test had a complication rate of 23.1% even in the presence of a normal echocardiogram, and this rose to 57.1% if echocardiography also demonstrated right ventricular dysfunction (OR vs. a negative H-FABP test, 5.6 and 81.4, respectively). CONCLUSION: H-FABP is a promising early indicator of right ventricular injury and dysfunction in acute PE. It may help optimize risk stratification algorithms and treatment strategies.