Evolution of nonspecific duodenal lymphocytosis over 2 years of follow-up

AIM: To assess the evolution of duodenal lymphocytosis(DL), a condition characterized by increased intraepithelial lymphocytes(IELs), over 2 years of follow-up.METHODS: Consecutive patients undergoing upper endoscopy/histology for abdominal pain, diarrhea, weight loss, weakness or other extraintestinal features compatible with celiac disease(CD) were included. Evaluation of IELs infiltrate in duodenal biopsy sampleswas carried out by CD3-immunohistochemistry and expressed as number of positive cells/100 enterocytes. Diagnostic agreement on the IELs count was tested by calculating the weighted k coefficient. All patients underwent serological detection of autoantibodies associated with CD: Ig G and Ig A anti-tissue transglutaminase and endomysium. Each patient underwent further investigations to clarify the origin of DL at baseline and/or in the course of 2 years of follow-up every six months. Autoimmune thyroiditis, intestinal infections, parasitic diseases, bacterial intestinal overgrowth, hypolactasia and wheat allergy were detected. Colonoscopy and enteric magnetic resonance i m a g i n g w e r e p e r f o r m e d w h e n n e c e s s a r y. R i s k factors affecting the final diagnosis were detected by multinomial logistic regression and expressed as OR.RESULTS: Eighty-five patients(16 males, 69 females, aged 34.1 ± 12.5 years) were followed up for a mean period of 21.7 ± 11.7 mo. At baseline, endoscopy/duodenal biopsy, CD3 immunohistochemistry revealed: > 25 IELs/100 enterocytes in 22 subjects, 15-25 IELs in 37 and < 15 IELs in 26. They all had negative serum anti-transglutaminase and anti-endomysium, whilst 5 showed Ig G anti-gliadin positivity. In the course of follow-up, 23 developed CD seropositivity and gluten sensitivity(GS) was identified in 19. Other diagnoses were: 5 Helicobacter pylori infections, 4 jejunal Crohn's disease, 1 lymphocytic colitis and 1 systemic sclerosis. The disease in the remaining 32 patients was classified as irritable bowel syndrome because of the lack of diagnostic evidence. At multivariate analysis, the evolution towards CD was associated with an IELs infiltrate > 25(OR = 1640.4) or 15-25(OR = 16.95), human leukocyte antigen(HLA) DQ2/8(OR = 140.85) or DQA1*0501(OR = 15.36), diarrhea(OR = 5.56) and weakness(OR = 11.57). GS was associated with IELs 15-25(OR = 28.59), autoimmune thyroiditis(OR = 87.63), folate deficiency(OR = 48.53) and diarrhea(OR = 54.87).CONCLUSION: DL may have a multifactorial origin but the IELs infiltrate and HLA are strong predictive factors for CD development and a clinical diagnosis of GS.

Lymphocytosis in Idiopathic Thrombocytopenic Purpura Patients Infected by <i>Helicobacter pylori</i>

Background and Objectives: Several recent reports have demonstrated a close linkage between idiopathic thrombocytopenic purpura (ITP) and Helicobacter pylori (H. pylori) infection in some patient’s populations. However, the pathogenetic mechanisms of H. pylori-induced thrombocytopenia remain obscure. Therefore, we investigated the prevalence of H. pylori infection pylori and performed a comparative analysis of a subset of H. pylori-infected patients (group A) with non-infected patients (group B) using the standard statistical methods. Design and Methods: From December 2001 to October 2002, we investigated the presence of gastric H. pylori infection in 30 adult ITP patients and 19 patients were treated with standard antibiotic therapy for H. pylori eradication (amoxicillin and clarithromycin plus lansoprazole combination). We used the standard statisticsto analyze the difference between group A and group B. Results: H. pylori eradication was achieved in 17/19 (89.4%) H.pylori-infected patients. An improvement of platelet count was observed in 14/19 patients (73.6%) who achieved the eradication. Five of these patients achieved CR (two patients were with the acute ITP) and nine patients reached PR. The difference between the mean platelet count ± S.D. before and after H. pylori therapy was statistically significant in patients with successful decontamination (65 ± 48 × 109/L vs. 200 ± 140 × 109/L;p = 0.018). Lymphocyte counts at the diagnosis of H. pylori infected cases were significant higher than those of non-infected cases (1.58 ± 0.13 ×

Monoclonal B-cell Lymphocytosis in a Patient with Wegener Granulomatosis： A Case Report and Update on 2016 World Health Organization Classification

The association between autoimmune disease and risk of monoclonal malignancy is well studied. Howeven monoclonal B-cell lymphocytosis （MBL） in patients with autoimmune diseases has rarely been reported. The newly published 2016 revision of the World Health Organization （WHO） classification of lymphoid neoplasms has officially accepted MBL as an independent disease entity Herein, we present a case of Wegener granulomatosis （WG） with MBL.

Papular mycosis fungoides: Six new cases and association with chronic lymphocytic leukemia

Papular mycosis fungoides(MF) is a rare presentation of MF. Six illustrative cases of papular MF were retrospectively reviewed. Five of the cases studied by immunohistochemistry had variable numbers(range: 1%-20%) of CD30+ cells in the dermal infiltrate, a finding that is characteristic of lymphomatoid papulosis but may occasionally occur in typical early MF. Although none of our papular MF patients had progressive disease, lesions with relatively high numbers of CD30+ cells in 3 patients did not respond well to skin-directed treatments used for MF. Interestingly, these patients had evidence of coexisting clonal B cell populations in the blood(one with clonal B cell lymphocytosis and two with B-cell chronic lymphocytic leukemia). We conclude that:(1) papular MF may contain CD30+ cells, thereby causing confusion with lymphomatoid papulosis; and(2) papular MF, like more typical MF, may be associated with clonal B-cell proliferations including chronic lymphocytic leukemia.

Assessment of Antiretroviral Efficacy of the Medicinal Synthetic Aluminum-Magnesium Silicate {Al4(SiO4)3 + 3Mg2SiO4 → 2Al2Mg3(SiO4)3}

HIV/AIDS patients were treated, daily, with MSAMS (50 mg/kg), MSAMS-stabilized Ampicillin trihydrate (7.5 mg/kg) and immunace extra-protectionM? (1 tablet), for one month and then, with only MSAMS and the immune stimulants. They were tested, monthly, for viral loads and CD4- lymphocytes counts. Those whose viral loads became undetectable were tested for HIV confirmation (antigens/antibody). Their mean-viral load increased (P = 0.020) from 1820.30 ± 868.75 to 2855.90 ± 960.98 after first month, before reducing (P = 0.0.030) to: 1565.20 ± 743.17;759.20 ± 473.65;345.50 ± 115.01;192.80 ± 97.40;95.00 ± 55.80;37.40 ± 26.46;17.50 ± 16.88 (undetectable). Their mean-CD4 count was 496.80 ± 194.39 (lymphopenia). It reduced (P = 0.008) to 263.90 ± 149.26 after first month, before increasing (P = 0.001) to: 507.90 ± 133.19;692.70 ± 113.34;840.20 ± 139.41;1007.30 ± 163.50;1537.10 ± 302.10;1924.60 ± 247.45;2707.00 ± 837.87 (lymphocytosis). Patients whose viral loads became undetectable tested HIV-negative, one month after. CD4-lymphocytes count, approximating to zero-viral load, calculated from equation (Y = 2297.80 - 1.4731X) of line of best fit of graph of their viral loads onCD4-lymphocytes counts, was 1559.84/ml.