Biomedical subjects

S al-Ismail

Publications and source records attributed to S al-Ismail.

5 recordsLinked to original sources

PubMed1998

Clinical use of FFP: results of a retrospective process and outcome audit.

An audit has been carried out on the usage of 216 units of fresh frozen plasma (FFP) issued to 41 patients. This involved the systems of FFP issue, the appropriateness of prescription as well as the recorded benefits. Sixty-six per cent of the initial requests for FFP appeared to satisfy criteria for appropriate use. Review of the case notes resulted in some changes to earlier decisions and a slight increase to 73% of those accepted as valid. Only 94% of the FFP issued could be proved to have been given to identified patients and only 88% of case notes showed the reason for treatment. Pre- and post-treatment coagulation results were available for all patients. In 15% of cases, pretreatment results were not significantly abnormal, and consequently no post-treatment improvement found. Coagulation improvement was documented in 78% of cases, and clinical statements on patient progress noted in 40%. In 80% of cases, the patient received other blood products carrying a potential virus risk. Six of the remaining eight patients were treated to stabilize oral anticoagulation. For these patients, virus-inactivated prothrombin concentrates could have been used, resulting in almost the same reduction in virus transmission risk for the group of 41 patients as could be obtained by using virus-inactivated FFP.

Blood Coagulation Disorders↗

PubMed1995

New glucose-6-phosphate dehydrogenase mutations associated with chronic anemia.

We have identified the glucose-6-phosphate dehydrogenase mutations responsible for enzyme deficiency in nine individuals with chronic nonspherocytic hemolytic anemia. We found the variants Tokyo, Iowa, Shinshu, and Guadalajara in British subjects and Kobe in an Italian. In addition we have determined the variant Corum has the mutation 820 G-->A and have found in British subjects the mis-sense mutations 224 T-->C, 488 G-->A and 833 C-->T which have not been described before. Some, but not all, of the mutations involve amino acids located near putative substrate binding sites.

Anemia, Hemolytic↗

PubMed1994

Immunophenotyping of normal lymphocytes.

We report the data of direct and indirect immunofluorescence labelling of peripheral blood mononuclear cells obtained from 40 normal controls and nine patients having blood tests for non-haematological disorders (PNHD controls) using flow cytometric analysis. Polyclonal and monoclonal antibodies were used to define the expression of cell surface antigen of T cells, their subsets, B cells, natural killer cells (NK) and myeloid cells. Normal values of absolute number and percentages of each of the populations of mononuclear cells were established and were sufficiently reproducible to be of clinical use. The percentages of positive values of T cells, T-cell subsets, and B cells in ten normal controls when mononuclear cells were used, were comparable to those using whole blood lysis, APAAP immuno-alkaline phosphatase, and E and M rosettes. The results obtained were similar in both the normal and PNHD controls. In most instances the percentage recovery of identified T, B and NK cells was complete. Currently we are using the results as reference values for lymphoid sub-populations in normal controls.

Adult↗

PubMed1994

Leukemia-associated changes identified by quantitative flow cytometry. III. B-cell gating in CD37/kappa/lambda clonality test.

Normal and malignant B-lymphoid cells were studied for CD37 antigen expression with three-color immunofluorescence (IF) in combination with kappa/lambda light chain staining, and by quantitative immunofluorescence utilizing the QIFI test. Peripheral B cells brightly expressed CD37 antigen (median 80-114 x 10(3) molecules/cell). Moderate to high levels (> 20 x 10(3)/cell) of CD37 expression were detected in 364 in 366 cases of peripheral B-cell disorders including all cases of B-ALL, B-cell lymphomas and B-CLL as well as eight of ten cases of PLL. By contrast, slg- B-cell precursors and other cell types in normal bone marrow (BM) were CD37-/CD37dull (< 10 x 10(3) molecules/cell). The negativity for CD37 or only CD37dull expression was confirmed in 180 of 182 cases of precursor B-ALL and 196 cases of non-B malignancies. Among the CD37 cluster, the RFB7 antibody of IgM class showed the weakest binding to non-B cells. In 64 normal samples of blood and BM the CD37+ gated cells showed normal kappa/lambda ratios as expected, while in 100 cases of B malignancy striking changes such as kappa/lambda monoclonality (79%) and aberrant slg- or sigdull expression (21%) were seen among the gated CD37+ B cells. The CD37/kappa/lambda test identified as few as 0.5% kappa+ or lambda- monoclonal B cells admixed to normal BM: circulating B-lymphoma cells were seen in nine patients with morphologically normal blood count. The discrimination of the Kolmogorov-Smirnov (KS) test for kappa/lambda excess was also improved by CD37+ B gating. Thus CD37+ B-cell gating and kappa/lambda analysis is a simple and sensitive routine test, e.g. when combined with autogating on a Cytoron-Absolute cytometer, for identifying malignant B cells in minimally involved BM and blood.

Antibodies, Monoclonal↗

PubMedDate not supplied

Postinfection purpura fulminans in a patient heterozygous for prothrombin G20210A and acquired protein S resistance.

Purpura fulminans usually consists of large, often symmetrical, spreading ecchymosis, which may later develop into extensive areas of skin necrosis and peripheral gangrene. Postinfectious purpura fulminans associated with an autoantibody directed against protein S has been described. The interaction and the contribution of recently described mutations such as factor V Leiden and prothrombin G20210A to the development and progression of postinfectious purpura fulminans and venous thrombosis is not known. The authors describe a patient heterozygous for prothrombin G20210A who developed purpura fulminans and extensive venous thrombosis secondary to acquired protein S deficiency.

Autoantibodies↗