We report here four cases of genital ulcers that developed after the administration of all-trans retinoic acid (ATRA) for the treatment of acute promyelocytic leukemia (APL). Between October 2007 and March 2010, three males and one female (age range 19-35 years) were identified to have genital ulcers after being prescribed all-trans retinoic acid (ATRA) as a part of chemotherapy for APL. This is the first series of cases describing genital ulcers, as a unique and rare complication of ATRA used for treatment of APL in these patients, with no other cause identified. Following temporary cessation of ATRA for a few days in these three cases, improvement of the ulcers was noted

BackgroundWe explored the potential relationship between steady state serum bilirubin levels and the incidence of cholelithiasis in the context of UGT1A1 gene A(TA)nTAA promoter polymorphism in Omani sickle cell anemia (SCA) patients, homozygotes for African (Benin and Bantu) and Arab-Indian βS haplotypes, but sharing the same microgeographical environment and comparable life style factors.Methods136 SCA patients were retrospectively studied in whom imaging data including abdominal CT scan, MRI or Ultrasonography were routinely available. Available data on the mean steady state hematological/biochemical parameters (n=136), βs haplotypes(n=136), α globin gene status (n=105) and UGT1A1 genotypes (n=133) were reviewed from the respective medical records.ResultsThe mean serum total bilirubin level was significantly higher in the homozygous UGT1A1(AT)7 group as compared to UGT1A1(AT)6 group. Thus, not cholelithiasis but total serum bilirubin was influenced by UGT1A1 polymorphism in this SCA cohort.ConclusionAs observed in other population groups, the UGT1A1 (AT)7 homozygosity was significantly associated with raised serum total bilirubin level, but the prevalence of gallstones in the Omani SCA patients was not associated with α thalassaemia, UGT1A1 polymorphism, or βs haplotypes.

<span style="font-size:10pt;font-family:'Tahoma','sans-serif';">Excepting host genetic factors, other influences on the pharmacokinetic and pharmacodynamic behavior of warfarin are subject to variations during the treatment despite attempts to stabilize the INR. In 214 Omani patients on warfarin therapy, we evaluated the extent of influence of known genetic predictors of warfarin dose variability, namely <i>CYP</i>2<i>C</i>9, <i>CYP</i>4<i>F</i>2 and <i>VKORC</i>1 gene polymorphisms in a genetically heterogeneous patient population. When patients were stratified according to their daily warfarin maintenance dose (to maintain INR between 2 and 3) into “low dose” (sensitive), “medium dose” (intermediate) and “high dose” (resistance) groups, overall, seven patients with three or four mutant alleles fell in the sensitive group and consequently 25% (7 out of 28) of at risk patients for over anticoagulation can be recognized by prospective pharmacogenetic testing in this patient population. Pre-prescription genotyping of these loci prior to therapy initiation will therefore benefit a small fraction of this population.</span><span style="font-size:9pt;font-family:'Tahoma','sans-serif';"> </span>

Objective: To evaluate immunological response to Covid-19 vaccines in immunocompromised haematology patients and compare with immunocompetent healthy controls Design: We compared total Anti SARS CoV 2 spike antibody and T cell response in 45 immunocompromised haematology patients with 30 healthy adults following 2 doses of Covid 19 vaccine for 3 to 5 months at 30 day intervals Setting: University Hospital, United Kingdom, Single Centre, March 2021 to December 2021 Main Outcome measures: Peak quantitative spike-specific antibody and cellular responses Results: We found 1. Non significant difference in T cell and total Anti SARS CoV 2 S antibody response between study and control group patients 2. Six (13%) study group participants did not have detectable Total Anti SARS Cov 2 S antibodies at any time point throughout the study monitoring period. 3. Three (7%) of the study group participants had no response, even after additional booster doses of Covid-19 vaccine. 4. All (100%) of the control group had detectable Anti SARS Cov 2 S antibodies after 2 doses of Covid 19 vaccine. 5. No participant died or was hospitalised due to severe Covid-19 infection during the study period. This included study group participants who had no antibody response at any time point. Conclusions: Though there was a non significant difference in T cell and total Anti SARS CoV 2 S antibody response between immunocompromised patients and healthy controls this did not result in any severe infection or Covid 19 related mortality in our study cohort. We did not identify any patient-specific factor (age, gender), specific haematological condition or treatment as determinant of response. Covid-19 vaccination was well tolerated without major side effects in both groups. What was already known about this topic: prior to starting this study there were no studies to confirm immunological response following Covid 19 vaccination in immunocompromised haematology patients. During the conduct of our study there have been publications from researchers confirming blunted serological response in 62-66% of immunocompromised haematology patients compared to 74 to 95% in healthy controls. What this study adds: Our study did not identify a significant difference in serological or T cell response between immunocompromised and healthy groups. Though 13% of immunocompromised patients had no response to Covid-19 vaccination none of them suffered from severe Covid-19 infection. We believe T cell response to Covid-19 vaccination has an important role in providing protective efficacy against Covid 19.