• IMA sites
  • IMAJ services
  • IMA journals
  • Follow us
  • Alternate Text Alternate Text
עמוד בית
Mon, 29.04.24

Search results


August 2006
A. Primov-Fever, Y.P. Talmi, A. Yellin and M. Wolf
 Background: Intubation and tracheostomy are the most common causes of benign acquired airway stenosis. Management varies according to different conceptions and techniques.

Objectives: To review our experience with cricotracheal resection and to assess related pitfalls and complications.

Methods: We examined the records of all patients who underwent CTR[1] in a tertiary referral medical center during the period January 1995 to April 2005.

Results: The study included 61 patients (16 women and 45 men) aged 15–81 years. In 17 patients previous interventions had failed, mostly dilatation and T-tube insertion. Complete obstruction was noted in 19 patients and stenosis > 70% in 26. Concomitant lesions included impaired vocal cord mobility (n=8) and tracheo-esophageal fistula (n=5). Cricotracheal anastomosis was performed in 42 patients, thyrotracheal in 12 and tracheotracheal in 7. A staged procedure was planned for quadriplegic patients and for three others with bilateral impaired vocal cord mobility. Restenosis occurred in six patients who were immediately revised with T-tube stenting. Decanulation was eventually achieved in 57 patients (93.4%). Complications occurred in 25 patients, the most common being subcutaneous emphysema (n=5). One patient died of acute myocardial infarction on the 14th postoperative day.

Conclusions: CTR is a relatively safe procedure with a high success rate in primary and revised procedures. A staged procedure should be planned in specific situations, namely, quadriplegics and patients with bilateral impaired vocal cord mobility. 


 





[1] CTR = cricotracheal resection


June 2006
D. Prais, Y. Raviv, D. Shitrit, A. Yellin, G. Sahar, D. Bendayan, Y. Yahav, O. Efrati, N. Reichart, H. Blau, I. Bakal, G. Buchman, M. Saute, B. Vidne and M.R. Kramer
 Background: Lung transplantation is a well-established therapeutic option for end-stage lung disease in cystic fibrosis. Although it confers a clear survival advantage, outcome differs among centers according to local experience, patient selection, transplantation procedure, and postoperative care.

Objectives: To evaluate the national Israeli experience with lung transplantation in patients with CF[1].

Methods: We reviewed the medical charts of all CF patients who underwent lung transplantation between January 1996 and June 2005 at the two Israeli centers that performed this procedure.

Results: Eighteen transplantations were performed in 17 patients. Mean patient age at transplantation was 25.3 ± 9.1 years, and mean duration of follow-up in survivors (n=14) was 37.2 months (range 1–113 months). The actuarial survival rate was 88% at 1 year and 74% at 5 years. Pulmonary function, expressed as percent of predicted normal forced expiratory volume in 1 sec, improved from 22.4 ± 8.1% to 76 ± 16.8% at one year after transplantation. Bronchiolitis obliterans syndrome was diagnosed in 5 patients (29%), of whom 2 died and 2 are currently candidates for retransplantation. Median time to onset of BOS[2] was 34.2 months (range 17–64 months).

Conclusion: In Israel, the early and intermediate-term results of lung transplantation for cystic fibrosis are encouraging. BOS remains a major complication that threatens long-term outcome.


 





[1] CF = cystic fibrosis

[2] BOS = bronchiolitis obliterans syndrome


March 2006
H. Schayek, M. Krupsky, P. Yaron, A. Yellin, D.A. Simansky and E. Friedman

Background: The contribution of the abnormal DNA mismatch repair system to non-small cell lung cancer tumorigenesis is controversial and has not been reported in Jewish Israeli patients. Similarly, the involvement of 3p deletions in NSCLC[1] in the same population has not been assessed.

Objectives: To assess the contribution of the DNA-MMR[2] system to NSCLC pathogenesis by analyzing microsatellite instability, and evaluate loss of heterozygosity at 3p rates in Israeli NSCLC patients.

Methods: Paired DNA from tumorous and non-tumorous tissue was extracted, and genotyping for MSI[3] determination was carried out using the five Bethesda markers and for determining LOH[4] two 3p markers were used. Genotyping was performed using polymerase chain reaction amplification and size separation on an ABI semiautomatic DNA sequencer, and the allelic patterns of tumorous and non-tumorous tissue were compared.

Results: Forty-four NSCLCs from 35 smokers and 9 non-smokers were analyzed, with 26 of the 44 (59%) at stage I disease. Using five microsatellite markers (D17S250, D5S346, D2S123, BAT-25, BAT-26) (known as Bethesda markers) for MSI determination, 6 of the 44 tumors (13.6%) exhibited MSI in at least one marker. Similarly, genotyping for LOH at chromosome 3p was performed using two markers (D3S4103, D3S1234) located at 3p14.2 l. With D3S4103, 33 of the 44 patients successfully analyzed were homozygous and therefore non-informative with respect to LOH. Using D3S1234, 33 of 36 patients (91.7%) were heterozygous, and 23 of these individuals' tumors (69.7%) displayed LOH. Unexpectedly, 4 of 33 tumors (12.1%) genotyped by D3S4103, and 16 of 36 tumors (44.5%) genotyped by D3S1234 showed a pattern of MSI, even though only one of these tumors showed a similar pattern when genotyped with the five consensus markers. Overall, 23 of 44 tumors (52.3%) demonstrated MSI on at least one marker, and 5 of these 23 tumors (21.7%) had MSI on two or more markers.

Conclusions: MSI using 3p markers and not the Bethesda markers occurs at a high rate and in early stages in Jewish NSCLC patients.






[1] NSCLC = non-small cell lung cancer

[2] DNA-MMR = DNA mismatch repair

[3] MSI = microsatellite instability

[4] LOH = loss of heterozygosity


November 2005
A. Yellin, S.T. Zwas, J. Rozenman, D.A. Simansky and E. Goshen
Background: Somatostatin receptor scintigraphy has been used widely for the evaluation of neuroendocrine tumors in the gastrointestinal tract. Its use for detecting and staging thoracic carcinoids is only sporadically reported.
Objectives: To evaluate the possible roles of SRS[1] in the management of proven or suspected pulmonary carcinoids. 

Methods: We conducted a retrospective study of all patients undergoing SRS for known or suspected pulmonary carcinoids in a tertiary referral center during a 10 year period. During this period 89 patients underwent resection of pulmonary carcinoids and SRS was used for detection, staging or localization purposes in 8 of them (9%). Scans were labeled true positive, true negative, false positive, or false negative in comparison with histologic or follow-up results. 

Results: SRS was true positive in 6/6 lung locations; true positive in 2/8, true negative in 4/8 and false positive in 2/8 lymph node locations; and true positive in 1/8, true negative in 6/8 and false negative in 1/8 distant locations. The sensitivity, specificity, positive and negative predictive values and accuracy were 90%, 83%, 83%, 91% and 87% respectively. The scans were strongly positive in the tumors and involved lymph nodes. SRS correctly localized an occult secreting pulmonary carcinoid. Granulomatous and reactive lymph nodes showed increased uptake. SRS was accurate in ruling out distant metastases. 

Conclusions: SRS is effective for visualizing and localizing pulmonary carcinoids. It assists in the staging of these tumors by detecting lymph node involvement and confirming or ruling out distant metastases. Inflamatory areas in the lung or lymph nodes may be falsely positive.


[1] SRS = somatostatin receptor scintigraphy

 
Legal Disclaimer: The information contained in this website is provided for informational purposes only, and should not be construed as legal or medical advice on any matter.
The IMA is not responsible for and expressly disclaims liability for damages of any kind arising from the use of or reliance on information contained within the site.
© All rights to information on this site are reserved and are the property of the Israeli Medical Association. Privacy policy

2 Twin Towers, 35 Jabotinsky, POB 4292, Ramat Gan 5251108 Israel