Effect of toxoplasma co-inefected with intestinal helminthes on cell mediated immunity to tuberculosis patients

The effect of intestinal helminthes [IH] and Toxoplasma gondii [Tox] coinfection on anti-mycobacterium tuberculosis [MTB] immunity in patients with active pulmonary tuberculosis was studied in 96 patients of 4 groups. Thirteen patients had TB+IH+Tox [Gl], 15 had TB+IH [G2], 21 had TB+Tox [G3] and 47 had TB [G4]. The mean diameter of tuberculin and toxoplasmin tests was measured to assess cell mediated immunity. Anti-Toxoplasma IgG[1] and IgG[4] antibodies were sought in toxoplasmic patients by EL1SA for Thelper[1] [Th[1]] and Th[2] cytokine responses respectively. All patients were treated by 6 months anti-MTB therapy. Specific anti-IH therapies were given for patients with concomitant IH. Sputum examination for acid fast bacilli was done 2 weeks post-treatment and duration of sputum clearance was recorded. The results showed that IH co-infection had significant negative effect on mean diameter of tuberculin test compared to.G4 [5.87 +/- 0.08 vs 8.65 +/- 0.05mm; P < 0.01]. Concurrent Tox with TB significantly increased tuberculin test mean diameter [10.89 +/- 0.11 vs 8.65 +/- 0.05mm; P < 0.05]. Mean level of anti-Tox IgG[1] among G3 was significantly higher than in Gl [0.88 +/- 0.05vs0.55 +/- 0.02; P < 0.001], but vice versa was with IgG[4]. Mean tuberculin diameter increased significantly post-treatment in all Gs except G3. Anti-Tox IgG[1] showed significant increase [0.55 +/- 10.02 to 0.82 +/- 0.03; P < 0.001] but IgG[4] showed significant decrease [0.62 +/- 0.07 to 0.45 +/- 0.06, P < 0.01] post-treatment in Gl, but G3 was insignificantly affected. The duration of sputum clearance was significantly longer in patients with IH co-infection compared to G4 [29 +/- 1 vs 21.8 +/- 4.6, days p < 0.001]

Antineutrophil cytoplasmic antibodies types and titers inulcerative colitis patients. relationship with disease variables

Ulcerative colitis [UC] is a chronic, relapsing and tissue-destructive idiopathic inflammatory disease. Its etiology has not yet been fully elucidated. Autoimmune processes may play a role in the pathogenesis, since several types of autoantibodies, including antineutrophil cytoplasmic antibodies [ANCA] have been found in this disease. Although numerous studies have dealt with ANCA prevalence, antigenic specificities and clinical significance in UC, the relationship between ANCA types and titers with the disease variables remains controversial. This work aims to distinguish the fluorescence pattern of atypical ANCA [aANCA] from that of perinuclear ANCA [p-ANCA] in patients with UC. In addition, the study aims to elucidate the relation between ANCA type and titer in relation to disease variables [extent, activity, duration of the disease and response to treatment]. The study included 38 patients with UC, diagnosed by clinical, endoscopic and radiological examinations supported by histopathology. The patients were classified into 4 groups by using a clinical activity score during the study period, including group I [[active-quiescent] comprising 6 patients, group II [quiescent-active] including 10 patients, group ifi [active] comprising 4 patients and group IV [quiescent-] including 18 patients. Paired serum samples were collected from each patient for determination of ANCA type and titer by indirect immunofluorescence [HF]. In this work, 25 [65.8%] of 38 patients with UC had at least one sample included that was positive for ANCA by TIE. Twenty two [88%] of 25 positive ANCA samples were aANCA and 3 [12%] were p-ANCA. The presence of ANCA was not related to the clinical characteristics of patients in the four groups. Increasing ANCA titeos were detected in 6 patients. 2 in group I, I in group II and 3 in group IV, while decreasing ANCA titers were found in 10 patients: 2 in group 1, 3 in group 11 and 5 in group IV. No significant correlation was found between serum levels of ANCA or patterns of staining by [IF and different disease variables. In conclusion, a-ANCA were found at high prevalence in patients with UC. The a-ANCA represent a potentially valuable diagnostic seromarker for UC and should be differentiated from p-ANCA that are present primarily in patients with systemic vasculitides. Changes in ANCA titers in paired serum samples from UC patients were not correlated with the changes in disease variables. Further studies with antigen-specific tests are recommended to reveal whether UC activity or disease variablcs correlate with ANCA titers of any defined specificities