Israel Medical Association Journal

Background: Heat shock proteins are highly conserved immunodominant antigens found in various species. Humoral immune responses to mycobacterial HSP65[1] and human HSP60 have been established in a number of human autoimmune diseases.

Objective: To assess the prevalence of antibodies to HSP60 kDa and HSP65 kDa in patients with Sjogren's syndrome as compared to normal subjects.

Methods: Thirty-seven patients with SS[2] were compared with normal controls. The antibodies against human HSP60 were measured by the Anti-Human (IgG/IgM) HSP60 ELISA kit. IgGs[3] and IgMs to mycobacterial HSP65 were determined using an enzyme-linked immunosorbent assay with mycobacterial recombinant HSP65 antigens.

Results: The levels of both anti-HSP60 and -HSP65 were lower among patients compared with controls. IgG autoantibodies to HSP60 were significantly different between groups: 162 ± 55.1 ng/ml in controls versus 112.3 ± 30.6 ng/ml in SS patients (P < 0.001). The levels among controls of anti-HSP65 IgM isotype were also significantly higher than among patients: 111.6 ± 33.4 U/ml versus 96.1 ± 8.9 U/ml (P = 0.01).

Conclusions: The results of the present study show that the levels of different isotypes of anti- HSP60 and HSP65 antibodies were lower in patients with SS than in normal subjects. Additional studies on larger patient populations are required to evaluate the prevalence of these autoantibodies in SS patients.

Objectives: To determine the effectiveness of a neuroreflexology-based screening test, specifically the Medex device (Medex Screen Ltd.), for diagnosing patients undergoing conventional internal organ assessment, in a hospital setting.

Methods: Patients admitted to an internal medicine department, who met the inclusion criteria and agreed to participate, underwent conventional medical evaluation that included past medical history and physical examination. Another examination was conducted by a second physician using the Medex device to determine internal organ pathologies. A third researcher compared the actual “conventional” diagnosis with the Medex device output using standard statistical analysis.   

Results: Overall, 150 patients participated in the study. Correlation was significant for all categories (P < 0.01) except for blood and lymphatic disease. A high sensitivity (>70%) was measured for cardiovascular, respiratory, gastrointestinal and genitourinary diseases. The highest measure of agreement, as represented by the Cohen-Kappa factor, was found for respiratory disease (0.57).

Conclusions: Although the exact mechanism is not entirely clear, measurement of electroskin impedance of dermal-visceral zones has the potential to serve as a screening tool for inner organ pathologies. Further research should be conducted to create more evidence to support or dispute the use of this technique as a reliable diagnostic tool.

Background: The appearance of pericarditis following insertion of a permanent pacemaker is not widely acknowledged in the literature.

Objectives: To describe our experience with pericarditis following 395 permanent pacemaker implantations over 2 years.

Methods: We retrospectively reviewed the medical records of 395 consecutive patients in whom new pacing systems or pacemaker leads had been implanted over a 2 year period. We searched the records for pericarditis that developed within 1 month after pacemaker implantation according to the ICD-9 code. The incidence, clinical picture, response to treatment and relationship to lead design and location were studied.

Results: Eight cases (2%) of pericarditis following implantation were detected. Clinical manifestations in all patients were similar to those of post-pericardiotomy syndrome and included chest pain (n=7), friction rub (n=1), fever (n=2), fatigue (n=2), pleural effusion (n=2), new atrial fibrillation (n=2), elevated erythrocyte sedimentation rate (n=4) and echcardiographic evidence of pericardial effusion (n=8). All affected patients had undergone active fixation (screw-in) lead implantation in the atrial position. The incidence of pericarditis with screw-in atrial leads was 3% compared to 0% in other cases (P < 0.05).

Conclusions: Pericarditis is not uncommon following pacemaker implantation with active fixation atrial leads. Special attention should be paid to identifying pericardial complications following pacemaker implantation, especially when anticoagulant therapy is resumed or initiated. The use of passive fixation leads is likely to reduce the incidence of pericarditis but this issue should be further investigated.