Clinical efficacy of inferior peripheral irido-capsulo-hyaloidotomy for pseudophakic malignant glaucoma.

PURPOSE: The present research aimed to investigate the effects of Inferior peripheral irido-capsulo-hyaloidotomy for the management of pseudophakic malignant glaucoma. METHOD: Ten pseudophakic eyes with aqueous misdirection were diagnosed between September 2017 and December 2018 (10 eyes of 8 patients), which were included in the prospective consecutive case series study. Seven eyes underwent Inferior laser peripheral irido-capsulo-hyaloidotomy, and three eyes underwent pars plana vitrectomy, zonulo-capsulo-hyaloidectomy, and inferior iridectomy. RESULTS: Eight eyes (80%) had angle-closure glaucoma. The mean duration of the follow-up was 12.25 ± 3.05 months (ranging from 10-18 months). The patients had a mean age of 69.25 ± 6 years. The IOP at the onset of malignant glaucoma was found to be 33.8 ± 5.5 mmHg, which was reduced to 13.9 ± 2.7 mmHg at the final visit (P value = 0.002). The reduction in the number ± SD of anti-glaucoma medications (3.3 ± 0.48 to 1.4 ± 0.51) and improvement in mean ± SD LogMAR visual acuity (1.2 ± 0.06 to 0.61 ± 0.26) between the onset and final visit were significant (p = 0.004 and P = 0.005, respectively). All the patients responded to Inferior peripheral irido-capsulo-hyaloidotomy (with YAG laser or with the surgical procedure), which led to a significant reduction in intraocular pressure (IOP) and deepening of the anterior chamber. CONCLUSION: The success rate of peripheral irido-capsulo-hyaloidotomy with laser or surgical procedure in the inferior quadrant was high regarding pseudophakic malignant glaucoma patients. The establishment of a patent inferior communication between the vitreous cavity and the anterior chamber was the main component in the treatment of pseudophakic malignant glaucoma patients.

Altered pattern of Naïve and memory B cells and B1 cells in patients with chronic granulomatous disease.

Chronic granulomatous disease (CGD) is a rare primary immunodeficiency disorder characterized by a greatly increased susceptibility to severe fungal and bacterial infections caused by defects in NADPH oxidase of phagocytic cells. We aimed to investigate immunophenotype alterations of naïve and memory B cells and B1a cells in peripheral whole blood from Iranian patients with CGD. Flow cytometric analysis was performed on peripheral blood samples from 31 CGD patients and 23 healthy controls (HC) to study naïve (IgD+/CD27-), memory (CD27+) B and B1a (CD5+) cells. Soluble CD27 (sCD27) and immunoglobulins were also measured by ELISA and the nephelometric method, respectively. We found significantly higher levels of naïve B cells and B1a cells but lower levels of memory B cells in CGD patients compared to HC.. There was no significant difference in soluble CD27 (sCD27) alteration between CGD patients and HC. Our findings suggested a role for NADPH oxidase in process of B cell differentiation and impairing conversion of naïve B cells to memory B cells and altered B1a cells in CGD patients. Increased susceptibility of CGD patients to opportunistic infections and autoimmune disorders could be partly explained by the altered phenotype of B lymphocytes in these patients.

Increased production of nitric oxide by neutrophils from patients with chronic granulomatous disease on interferon-gamma treatment.

Chronic granulomatous disease (CGD) is a rare immunodeficiency disorder in which phagocytic leukocytes fail to generate superoxide (O(2)(-)) and antimicrobial oxidants. The therapeutic validity of interferon-gamma (IFN-γ) has been well established in CGD patients but its underlying mechanisms remain poorly understood. One probable mechanism has been suggested to be modulation of nitric oxide (NO) release from phagocytic cells. Herein, we investigated NO production from neutrophil cells in CGD patients on treatment with IFN-γ in vivo and in vitro. We measured NO levels in sera from 19 CGD patients (group I: 7 patients treated with TMP-SMX, group II: 12 patients treated with TMP-SMX and IFN-γ simultaneously) and healthy control individuals (8 cases). We also measured NO production from neutrophils in both patients groups as well as in control group after adding 100 U IFN-γ in vitro. Our results showed that there was a significant difference between the groups in the NO levels of serum; patients who received IFN-γ had significantly higher amount of NO than the other groups. Besides, NO levels increased significantly after adding 100 U IFN-γ in vitro in three studied groups, considerably in the patients on treatment with IFN-γ. As a brief conclusion, the effect of IFN-γ in increasing NO production is obvious. This could be an explanation for the therapeutic effect of IFN-γ in patients with CGD as NO acts as a bactericidal agent and plays a role in host defense mechanism instead of O(2)(-).