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עמוד בית
Fri, 19.07.24

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October 2007
F. Sperber, U. Metser, A. Gat, A. Shalmon and N. Yaal-Hahoshen

Background: The imaging parameters that mandate further diagnostic workup in focal asymmetric breast densities are not clearly defined.

Objectives: To identify indications for further workup in FABD[1] by comparing mammographic and ultrasonographic findings with the pathology results of women with FABD.

Methods: Ninety-four women (97 FABD) were referred for core needle biopsy after incidental discovery of FABD on routine mammograms (n=83) or on diagnostic mammograms performed for palpable masses (n=11). Clinical data included patient’s age, use of hormone replacement therapy, family history of breast cancer, and the presence of a palpable mass. Mammograms and sonograms were evaluated for lesion size and location, associated calcifications, architectural distortion, and change from previous examinations when available. Two patient groups emerged according to the pathological findings and the data were compared.

Results: The average age, size and location of the lesions in the malignant (n=5) and benign (n=92) groups were similar. There was a significant difference (P < 0.05) for the presence of a clinically palpable mass (60% vs. 9%, respectively), a cluster of calcifications (60% vs. 12%), associated architectural distortion (exclusively in the malignant group) and a solid mass on sonography (50% vs. 9%). The malignant group had a higher rate of family history of breast cancer and HRT[2] use.

Conclusions: FABD usually present a benign etiology and can safely be managed by follow‑up. The presence of an architectural distortion, a cluster of malignant‑appearing or indeterminate calcifications, a sonographic mass with features of possible malignancy, or a clinically palpable mass mandates tissue diagnosis.






[1] FABD = focal asymmetric breast densities



[2] HRT = hormone replacement therapy


A. Lipey, A. Kogan, T. Ben-Gal, E. Mor, A. Stamler, B. Medalion, B.A. Vidne, E. Porat and G. Sahar
D.I. Nassie, A. Volkov, J. Kronenberg and Y.P. Talmi
September 2007
O. Tamir, R. Peleg, J. Dreiher, T. Abu-Hammad, Y. Abu Rabia, M. Abu Rashid, A. Eisenberg, D. Sibersky, A. Kazanovich, E. Khalil, D. Vardy and P. Shvartzman

Background: Until three decades ago coronary heart disease and stroke were considered rare in the Israeli Bedouin population. Today, this population shows increasing high prevalence compared to the Jewish population.

Objectives: To evaluate the prevalence of diagnosed cardiovascular risk factors among the Bedouin (hypertension, diabetes mellitus, dyslipidemia), and to assess compliance with follow-up tests and drug treatment.

Methods: The study included all listed patients aged 20 years and older in eight clinics in major Bedouin towns, and in two large teaching clinics in Beer Sheva (Jewish population). Risk factor data were extracted from the clinics' computerized databases. For those diagnosed with hypertension, diabetes or dyslipidemia, drug purchasing data were collected from the pharmacy database to determine compliance with treatment, and from the central laboratory mainframe (HbA1c and low density lipoprotein-cholesterol) to evaluate follow-up and control.

Results: A significantly higher prevalence of diabetes in all age groups was found in the Bedouin population compared to the Jewish population; age-adjusted results show a prevalence of 12% vs. 8% respectively (P < 0.001). The prevalence of dyslipidemia and age-adjusted hypertension was lower among Bedouins (5.8% vs. 18.2%, P < 0.01 and 17% vs. 21%, P < 0.001 respectively). Two-thirds of hypertensive Bedouin patients and 72.9% of diabetic Bedouin patients were not compliant with treatment. For dyslipidemia only 10.4% of the Bedouins were compliant compared with 28.2% in the Jewish population (P < 0.001).

Conclusions: Compliance with drug therapy and follow-up tests was found to be a major problem in the Bedouin population.
 

J. Baron, D. Greenberg, Z. Shorer, E. Herskhovitz, R. Melamed and M. Lifshitz
A. Chernikovski, N. Loberant, I. Cohen, F. Nassar, J. Lerner and E. Altman
August 2007
M. Wolf, A. Primov-Fever, Y.P. Talmi and J. Kronenberg

Background: Posterior glottic stenosis is a complication of prolonged intubation, manifesting as airway stenosis that may mimic bilateral vocal cord paralysis. It presents a variety of features that mandate specific surgical interventions.

Objectives: To summarize our experience with PSG[1] and its working diagnosis.

Methods: We conducted a retrospective review of a cohort of adult patients with PGS operated at the Sheba Medical Center between 1994 and 2006.

Results: Ten patients were diagnosed with PGS, 6 of whom also had stenosis at other sites of the larynx and trachea. Since 2000, all patients underwent laryngeal electromyographic studies and direct laryngoscopy prior to surgery. Surgical interventions included endoscopic laser procedures (in 2 patients), laryngofissure and scar incision (in 1), laryngofissure with buccal mucosa grafting (in 3) or with costal cartilage grafting (in 1), laryngofissure with posterior cricoid split and stenting (in 1); one patient was not suitable for surgery. Postoperative follow-up included periodical fiberoptic endoscopies. Voice analysis was evaluated by the GRBAS grading. Seven patients were successfully decannulated within one to three procedures. Voice quality was defined as good in 7 patients, serviceable in 2 and aphonic in 1.

Conclusions: Posterior glottic stenosis may be isolated or part of complex laryngotracheal pathologies. Electromyographic studies and direct laryngoscopy must be included in the diagnostic workup. Costal cartilage or buccal mucosa grafts are reliable, safe and successful with respect to graft incorporation and subglottic remodeling.

 






[1] PSG = posterior glottic stenosis


July 2007
S.Atar, K.Tolstrup, B.Cercek, and R.J. Siegel.

Background: Chlamydia pneumoniae has previously been associated with higher prevalence of valvular and cardiac calcifications.

Objectives: To investigate a possible association of seropositivity for C. pneumoniae and the presence of cardiac calcifications (mitral annular or aortic root calcification, and aortic valve sclerosis).

Methods: We retrospectively analyzed serological data (immunoglobulin G TWAR antibodies) from the AZACS trial (Azithromycin in Acute Coronary Syndromes), and correlated the serological findings according to titer levels with the presence of cardiac calcifications as detected by transthoracic echocardiography.

Results: In 271 patients, age 69 ± 13 years, who underwent both serological and echocardiographic evaluation, we found no significant association between the "calcification sum score" (on a scale of 0–3) in seropositive compared to seronegative patients (1.56 ± 1.15 vs.1.35 ± 1.15, respectively, P = 0.26). The median "calcification sum score" was 1 (interquartile range 0–3) for the seronegative group, and 2 (interquartile range 0–3) for the seropositive group (P = 0.2757). In addition, we did not find a significant correlation of any of the individual sites of cardiac calcification and Chlamydia pneumoniae seropositivity.

Conclusion: Our findings suggest that past C. pneumoniae infection may not be associated with the pathogenesis of valvular and cardiac calcifications.
 

O.Scheuerman, L.de Beaucoudrey, V.Hoffer, J.Feinberg, J.L.Casanova, and B.Z.Garty
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