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Biomedical subjects

S Dunkley

Publications and source records attributed to S Dunkley.

14 recordsLinked to original sources
PubMed2006

Rituximab treatment of mild haemophilia A with inhibitors: a proposed treatment protocol.

Inhibitors are an uncommon complication of mild haemophilia A but represent a severe disease, typically with high titre inhibitors and an associated high rate of bleeding. We present data from three patients with MHAI who were successfully treated with Rituximab alone and unequivocally prove that such inhibitors respond to this agent. A treatment protocol is suggested.

Adult↗
PubMed2002

Cranial venous outflow obstruction in the pseudotumour syndrome: incidence, nature and relevance.

This study reports a retrospective analysis of the evidence of cranial venous outflow pathology in 188 patients with pseudotumour syndrome (PTS) investigated over the period 1968-1999. Standard methods of investigation appropriate to the period were used, i.e. cerebral angiography, CT and MR scanning. Recently, some patients had specific venous studies including intraluminal cranial venous sinus pressure measurements. A sub-group (25 patients) was investigated for haematological abnormalities. The overall incidence of cranial venous outflow abnormality was 19.7% (37 cases). In decades, related to the predominant investigative method, the figures were: to 1979, 4.2% (2 cases); to 1989, 15.0% (8 cases); to 1999, 31.0% (27 cases). A cause of the venous abnormality was identified in 20 cases, most commonly haematological and iatrogenic. In 17 patients (all females) no cause was identified. Fifteen of the 25 patients (60%) tested specifically were found to have a haematological abnormality, although no correlation was shown between this and a demonstrable venous outflow abnormality. The conclusion was drawn that there is a high incidence (close to one-third) of venous outflow abnormalities in PTS with detailed investigation. Issues of mechanism and therapy are discussed.

Adolescent↗
PubMed1999

Thrombosis and bleeding in myeloproliferative disorders: identification of at-risk patients with whole blood platelet aggregation studies.

Seventy-five patients with chronic myeloproliferative disorders were studied to investigate platelet function by simultaneous measurement of platelet aggregation by the impedance method and ATP dense granule release using a whole blood platelet lumi-aggregometer, in an attempt to identify patients at risk for thrombosis and bleeding. Thirty-nine patients had at least one abnormal result indicating platelet hyperactivity (i.e. impedance or release with one agonist being above the reference range); 16 patients had platelet hypoactivity (i.e. at least one result was below the reference range), whilst 14 had co-existence of hyper- and hypoactivity. Six patients had normal results. 20/53 patients with platelet hyperactivity (alone or mixed) had a positive history of venous and/or arterial thrombosis; in comparison, only two of the other 22 patients had a positive history. During a median follow-up of 33 months, nine patients with and one patient without platelet hyperactivity respectively developed new thrombotic events before the addition of specific therapy. A total of 50 patients with and eight patients without platelet hyperactivity respectively received specific treatment including aspirin and/or cytotoxic therapy. All but one elderly patient with platelet hyperactivity have remained free of new thrombotic events on specific therapy. Two of the 17 patients with platelet hypoactivity had major clinical bleeding. These observations highlight the need to test platelets for hyper- as well as hypo-function and suggest a useful role for routine whole blood platelet aggregation studies to identify the patients at risk for thrombosis or bleeding.

Aged↗
PubMed1999

Acute promyelocytic leukaemia complicating multiple myeloma: evidence of different cell lineages.

The association of leukemia and multiple myeloma is well described usually as a complication of chemotherapy but also in the absence of chemotherapy or at diagnosis. Such leukemias are typically acute myeloid leukemia (AML), particularly myelomonocytic subtype, and cases of acute promyelocytic leuke (APL) are rarely reported. Controversy exists as to whether myeloma and AML originate from a single haematopoietic progenitor or arise from different cell lineages. We report a case of a 58 year old female who developed APL 10 months following diagnosis of nonsecretory light chain (kappa) myeloma which had been treated with local spinal irradiation and low dose oral melphalan and prednisone. Clonality had originally been demonstrated by light chain restriction (kappa) of her bone marrow plasma cells whilst immunoglobulin heavy chain and T cell receptor genes were germ line. At development of APL cytogenetics revealed t(15;17) and PML-RAR fusion gene was detected by RT-PCR. The patient was treated with all-trans retinoic acid (ATRA) and received 2 cycles of consolidation chemotherapy with Idarubicin. Following this therapy the t(15;17) and PML-RAR were both undetectable whilst the clonal population of kappa staining plasma cells persisted. This particular patient represents a rare case of APL complicating multiple myeloma with persistence of the myeloma clone but disappearance of PML-RAR alpha RNA following therapy. This case study appears to support the argument that the APL and myeloma originated from distinct cell lineages.

Antibiotics, Antineoplastic↗
PubMed1998

Aggressive natural killer cell leukemia/lymphoma.

A 32 year old Caucasian male presented with fever, massive hepatosplenomegaly and lymphadenopathy. Peripheral blood and bone marrow findings were consistent, both morphologically and immunophenotypically, with a natural killer cell leukemia/lymphoma. The disease was rapidly progressive and was fatal within five days after presentation.

Adult↗
PubMedDate not supplied

Facial paralysis with an inflammatory parotid mass.

Facial paralysis in association with a parotid mass is usually associated with a diagnosis of malignancy. Benign parotid neoplasms and inflammatory processes resulting in facial paralysis are extremely rare. This report describes such a case and highlights some of the difficulties surrounding the diagnosis and management of these cases.

Biopsy, Needle↗