Hematogenous spinal infection in central Greece.

STUDY DESIGN: We retrospectively analyzed spinal infection (SpI), in a teaching Hospital, in Central Greece. OBJECTIVE: To study presentation, etiology, and outcome of SpI in Central Greece. SUMMARY OF BACKGROUND DATA: SpI most frequently involves the intervertebral disc and adjacent vertebral bodies and can cause neurologic impairment. METHODS: Thirty three patients (23 men; age [mean +/- standard deviation], 60.6 +/- 11.3 years; disease duration, 44.5 [+/-54.7] days) hospitalized with SpI between January 2000 and December 2007 were included in the study. All patients had magnetic resonance imaging of the spine. RESULTS: Nineteen patients had pyogenic SpI (57.6%) and 14 patients had granulomatous SpI, 11 due to Brucella spp (34.4%), 3 due to Mycobacterium tuberculosis (9.4%). Staphylococcus aureus was the most frequent cause of pyogenic SpI, and spondylodiscitis (SpD) was the most frequent localization. Epidural entension was found in 8 of 17 pyogenic SpD and in 2 of 11 brucellar SpD patients. Subdural extension was detected in 3 patients with pyogenic SpD. Blood cultures were positive in 17 of 19 patients with pyogenic SpI. Two patients had concomitant endocarditis (staphylococcal 1, enterococcal 1). The most common associated disease was diabetes mellitus. All but 2 patients received medical treatment alone. Two patients died of uncontrollable sepsis. CONCLUSION: Back pain in presence of fever, constitutional symptoms, and/or high inflammation markers should alert physicians for spinal infection. In endemic areas, Brucella is a frequent cause of SpI.

Diabetes mellitus and lung function.

OBJECTIVES: To assess the nature of pulmonary dysfunction in type 1 diabetes and the relationship of pulmonary function tests to diabetic factors and complication. SUBJECTS AND METHODS: Sixteen type 1 diabetic patients and 26 control subjects matched for age and sex were studied. We performed spirometry measurements and measured pulmonary diffusing capacity (DL(CO)) in sitting and supine position by the single-breath method corrected by alveolar volume (VA). Glycosylated hemoglobin (HbA(Ic)), retinopathy and microalbuminuria were included as parameters of metabolic control and diabetic complications. RESULTS: Diabetic patients showed a significant reduction of the following pulmonary function tests (% predicted value) as compared with control subjects: total lung capacity (TLC, 92.6 +/- 14.5 vs. 113.9 +/- 17.5, p < 0.001), lung diffusing capacity in sitting position (DL(CO), 90.4 +/- 21.1 vs. 107.7 +/- 15.6, p = 0.004), lung diffusing capacity in supine position (DL(CO), 88.3 +/- 19.3 vs. 111.9 +/- 19.9, p = 0.001). The differences in diffusing capacity corrected by alveolar volume in sitting and supine position (DL(CO)/VA) were not significant. By changing the posture from sitting to supine position both diabetic patients and control subjects significantly increased DL(CO)/VA (103.4 +/- 17.7 vs. 112.7 +/- 22.3, p = 0.046 and 99.5 +/- 13.4 vs. 114.4 +/- 13, p < 0.001, respectively). There was no correlation between pulmonary function tests and diabetic complications. CONCLUSION: These data indicate that type 1 diabetic patients showed reduced TLC and DL(CO), features of pulmonary restrictive dysfunction. There was no correlation between abnormal pulmonary function and the presence of other diabetic complications.

Increased incidence of anti-LKM autoantibodies in a consecutive cohort of hepatitis C patients from central Greece.

OBJECTIVES: In Greece, there are insufficient data regarding the presence of non-organ and liver-related autoantibodies in hepatitis C patients. This study in a consecutive cohort of 39 such patients from central Greece investigates (1) the prevalence of non-organ and liver-related autoantibodies, and (2) the reactivity of anti-liver-kidney microsomal type 1 antibodies (in the case of positivity with at least one of the methods used) against their molecularly defined antigens. DESIGN: All serum samples were tested by standard and molecular assays for the presence of anti-nuclear antibodies, smooth muscle antibodies, anti-liver-kidney microsomal type 1 antibodies, antibodies against parietal cells, anti-CYP2A6, anti-CYP1A2 and anti-CYP2D6 autoantibodies. METHODS: Indirect immunofluorescence, competitive enzyme-linked immunosorbent assays, immunoblotting and novel radioligand assays based on immunoprecipitation of [35S]-methionine labelled recombinant CYP2A6, CYP1A2 and CYP2D6 His-taq fusion proteins produced by in vitro transcription/translation were used. RESULTS: Seven out of 39 patients (17.9%) tested positive for smooth muscle antibodies, 2/39 (5.1%) tested positive for anti-nuclear antibodies, 1/39 (2.5%) tested positive for parietal cell antibodies, and 4/39 (10.3%) were found to be anti-liver-kidney microsomal positive (with at least one of the methods used). All sera were negative for anti-CYP2A6 and anti-CYP1A2 autoantibodies. Three out of four anti-liver-kidney microsomal positive samples had the typical liver-kidney microsomal staining pattern shown by indirect immunofluorescence. However, none tested positive for anti-CYP2D6 autoantibodies using the competitive CYP2D6 enzyme-linked immunosorbent assay, the specific CYP2D6 radioligand assay, and western blot using either human microsomes or recombinant CYP2D6. The fourth patient tested negative for anti-liver-kidney autoantibodies by either indirect immunofluorescence or the competitive enzyme-linked immunosorbent assay, but was repeatedly positive for anti-CYP2D6 autoantibodies by the sensitive and specific radioligand assay. Western blot experiments using human microsomes in this patient serum revealed two bands of 50 kDa and 55 kDa that documented as anti-CYP2D6 and anti-uridine triphosphate glucuronosyltransferase autoantibodies when recombinant CYP2D6 and recombinant uridine triphosphate glucuronosyltransferase autoantigens were used for immunoblot, respectively. CONCLUSIONS: A relatively high incidence of anti-liver-kidney microsomal autoantibodies (10.3%) was found in a consecutive sample of Greek patients with hepatitis C. The expanded panel of assays, however, failed to document CYP2D6 as the target autoantigen of anti-liver-kidney microsomal autoantibodies in most patients. We report for the first time the detection of parietal cell antibodies and both anti-CYP2D6 (anti-liver-kidney microsomal type 1) and anti-uridine triphosphate glucuronosyltransferase (anti-liver-kidney microsomal type 3) autoantibodies in patients who were hepatitis C positive/hepatitis D negative. Further studies are needed to confirm our findings and to determine whether these preliminary results have a clinical importance or not.