Khalil Al Farsi

Aetiological profile of women presenting with premature ovarian failure to a single tertiary care center in Oman

Background Premature ovarian failure is estimated to affect at least 1%–3% of adult women. There are several aetio-pathogenic factors that may cause premature ovarian failure including iatrogenic causes, genetic, autoimmune, infectious and idiopathic. The aim of this study was to identify the aetiological profile of women with premature ovarian failure presenting to Sultan Qaboos University hospital. Method A retrospective medical record review was conducted from June 2006 to October 2012. All women diagnosed with symptoms and/or laboratory evidence of premature ovarian failure (follicle stimulating hormone ≥40 UI/L and less than 40 years of age) were enrolled in this study. Possible causes of premature ovarian failure were obtained and classified into main aetiological factors. Results There were 90 patients during the study period, of which, 39 (43%) were following chemotherapy and bone marrow transplant. The second most common reason was idiopathic (n = 29; 31%) followed by autoimmune diseases (n = 8; 9%) and genetic disorders (n = 7; 8%). Most chemotherapy cases (69%) were among the young age group, while in the older age group idiopathic was the commonest (48%). Conclusion Compared to the world literature, the most common cause of premature ovarian failure in this study was chemotherapy induced, especially in young girls undergoing bone marrow transplantation. This is due to high prevalence of transplantable hereditary haematological disorders like thalassemia and sickle-cell disease in this part of the world. Current standard of care recommends cryopreservation of ovarian tissue to preserve ovarian function in young girls undergoing bone marrow transplantation for such disorders.

Levels of regulatory T cells and invariant natural killer cells and their associations with regulatory B cells in patients with non-Hodgkin lymphoma

Due to their immunoregulatory properties, several specialized cell subsets, including regulatory T (Treg), invariant natural killer T (iNKT) and regulatory B (Breg) cells, are involved in the pathogenesis of non-Hodgkin lymphoma (NHL). However, the interaction between various cells remains to be elucidated. The aim of the present study was to evaluate the levels of Treg, iNKT and Breg cell subsets and their interrelationships in the peripheral blood (PB) and bone marrow (BM) of patients with B-cell NHL who received rituximab-based regimens and achieved a complete remission. A total of 20 patients and 20 healthy age- and sex-matched controls were prospectively enrolled for investigation of Treg, iNKT and Breg cell subsets in PB and BM by flow cytometry and cell culture. Prior to administration of combination chemotherapy with rituximab, the patients had lower levels of Breg cells and, to a lesser degree, Treg cells, but not iNKT cells, in PB compared with controls. Compartmental differences in the levels of Treg and Breg cell subsets, but not iNKT cells, were observed between PB and BM, suggesting an increase in trafficking through the blood of these regulatory cell subsets to the marrow. Following complete remission, the levels of circulating Treg, iNKT and Breg cell subsets increased. The levels of Treg cells were not significantly associated with iNKT and Breg cell subsets, although negative correlations were observed. Taken together, these results may provide new insights into the potential role of regulatory cell subsets in patients with B-cell NHL. However, whether the observed differences between PB and BM may affect clinical outcomes requires further investigation.