PubMed Health⌕ Search

Biomedical subjects

A Wehmeier

Publications and source records attributed to A Wehmeier.

At least 37 records · Page 2Linked to original sources
PubMed1995

Neutrophilic dermal infiltrates in granulocytopenic patients with acute leukemia.

Acute febrile neutrophilic dermatosis (AFND, Sweet's syndrome) is clinically characterized by fever, neutrophilic leukocytosis, and tender dermal plaques. Histological examination typically reveals infiltration of the dermis by neutrophils. In three patients (2 female, 1 male, 54-59 years) with acute leukemia (2 myelogenous, 1 lymphoblastic) dermal plaques developed during febrile episodes in chemotherapy-induced pancytopenia. The clinical appearance was compatible with AFND. The diagnosis was substantiated by skin biopsies which showed dense neutrophilic dermal infiltrates without leukemic cells. Leukocytoclastic vasculitis was considered as differential diagnosis. Plasma levels of soluble adhesion molecules ICAM-1, VCAM-1, and E-selectin regulating leukocyte transendothelial migration were in the normal range. Systemic glucocorticoids were avoided because of the high risk of infection during prolonged bone marrow aplasia. The lesions were treated with topical steroids and resolved without scarring within 1-5 weeks. AFND has been reported in association with acute leukemia at normal or elevated white blood cell counts. Although implausible from a pathophysiological point of view, similar neutrophilic dermal infiltrates were found in three patients during chemotherapy-induced pancytopenia with white blood cell counts distinctly below 1 x 10(9)/l.

Agranulocytosis↗
PubMed1995

Pulmonary toxicity during infusion of liposomal amphotericin B in two patients with acute leukemia.

Pulmonary toxicity with acute dyspnea occurred during infusion of a liposomal amphotericin B preparation (AmBisome) in two adult leukemic patients. The preparation was administered as a one hour infusion at a dose of 3 mg/kg body weight. Within 15 min after starting the infusion, both patients experienced sudden onset of dyspnea and chest tightness. Physical examination showed the patients to be anxious and restless with tachycardia and orthopnea but without other cardiopulmonary findings. No elevation of body temperature, rigors or chills were recorded. Symptoms disappeared within minutes after discontinuing the infusion. At present, the pathophysiologic mechanisms underlying these side effects are unknown.

Acute Disease↗
PubMed1993

[Immunoglobulin substitution in malignant lymphoma].

Substitution with intravenously administered immunoglobulin seems to be indicated in lymphoma patients with acquired immunoglobulin deficiency, i.e., primarily patients with chronic lymphocytic leukemia and multiple myeloma. Infectious complications, mainly of the upper airways, are a major cause of morbidity and mortality in these patients. The immunoglobulin levels are correlated with stage of the disease, frequency of infections, and patient survival. Besides immunoglobulin deficiency, there are less well characterized defects of cellular immunity. Three prospective studies evaluating the effectiveness of immunoglobulin substitution in patients with chronic lymphocytic leukemia and myeloma have been published. A dose of 400 mg/kg or 10 g of immunoglobulin was administered intravenously every 3 or 4 weeks. A reduction of bacterial infections, but not of deaths due to infectious complications, was observed. The treatment was usually well tolerated with few side effects. However, to date it has not been established which patient subgroups really benefit from immunoglobulin therapy in terms of improvement of quality of life. Thus a general recommendation of immunoglobulin therapy in chronic lymphocytic leukemia and multiple myeloma can at present not be made.

Humans↗
PubMed1992

[Prevalence of lupus anticoagulant, autoimmune hemolysis, thrombocytopenia and disorders of platelet function in unselected patients with SLE].

Prevalence of lupus anticoagulant (LA) in patients with systemic lupus erythematosus (SLE) and clinical manifestations vary widely between different clinical series. We investigated the relation between LA, autoimmune hemolytic anemia (AIHA), thrombocytopenia and platelet dysfunction in 80 unselected patients with SLE. AIHA was found in 6 patients (7.5%) and thrombocytopenia in 10 patients (12.5%), which was not related to platelet aggregation abnormalities. Compared to controls, patients with SLE showed significantly prolonged aPTT and kaolin clotting time (KCT), but platelet aggregation induced by both collagen and thrombin was not impaired. LA activity as defined by Rosner et al. (index for LA/ICA) was found in 15 patients (18.9%). Only 7 of these patients showed a positive platelet neutralization test (Triplett) and 9a positive tissue thromboplastin inhibition test (Schleider). In our SLE patients 23.7% have suffered from at least one thrombotic complication. In patients with LA activity thromboembolic complications were increased (p < 0.05). Thrombocytopenia was found in 6% of LA-negative but in 20% of LA-positive patients.

Abortion, Spontaneous↗
PubMed1991

Circulating activated platelets in myeloproliferative disorders.

Platelet activation in patients with myeloproliferative disorders is often suggested by increased platelet alpha-granule secretion and an acquired storage pool defect of dense granules. To determine whether activated platelets circulate in patients with chronic myeloproliferative disorders, we evaluated the binding of monoclonal antibodies against activation-dependent epitopes on resting platelets (P 12, CD 63, and CD 62) in 12 patients with prominent megakaryocytic proliferation (8 patients with essential thrombocythemia, 2 with chronic myeloid leukemia, and 2 patients with polycythemia rubra vera). In addition, platelet aggregation in response to collagen, adenosine diphosphate, platelet activating factor, and agglutination with ristocetin was investigated. In 3 patients there was an increased percentage of platelets binding at least 1 activation marker. In 2 other patients, a trend towards increased antibody binding was observed. Binding of the antibody to thrombospondin (P 12) was related to expression of the GMP 140 protein (CD 62, r = 0.76, p = 0.004). There was no correlation of platelet aggregation defects in vitro to increased expression of platelet activation markers or to thrombohaemorrhagic complications. However, circulating activated platelets were detected in three out of five patients with a history of bleeding or thrombotic complications. The results of this preliminary study suggest that some but not all patients with myeloproliferative disorders showed increased amounts of circulating activated platelets. The relation of bleeding and thrombotic complications to the expression of activation-dependent epitopes on platelets in myeloproliferative disorders requires further investigation.

Adult↗
PubMed1991

Incidence and clinical risk factors for bleeding and thrombotic complications in myeloproliferative disorders. A retrospective analysis of 260 patients.

Bleeding and thrombosis are frequent complications in myeloproliferative disorders (MPD) and are associated with severe organ damage and a high mortality. Elevated platelet count, elevated hematocrit, and patient age are regarded as risk factors for bleeding and thromboembolic events in MPD, although the significance of these parameters was not confirmed by clinical studies. We retrospectively analyzed vascular complications in 260 patients with MPD and tried to identify parameters predictive for bleeding and thrombembolic events. Our cohort consisted of 115 patients with chronic myeloid leukemia (CML), 84 patients with polycythemia vera (PV), 26 with essential thrombocythemia (ET), 25 with osteomyelofibrosis (OMF), and 10 patients with unclassifiable MPD. During a median follow-up period of 31 months, 126 patients with chronic MPD suffered bleeding or thrombotic events. Bleeding was observed in 57% of patients with OMF, 23% with PV, 20% with chronic phase CML, and 16% with ET. Thrombotic events were most common in patients with PV (36% of patients), followed by ET, OMF, and chronic phase CML (20%, 17%, and 6% of patients, respectively). Recurrent thrombotic episodes frequently occurred in patients with PV and ET, whereas patients with OMF often had more than one bleeding event. Thirty patients died of thrombohemorrhagic complications during follow-up. Multivariate analysis, including all patients with chronic MPD, revealed that elevated red blood cell count, higher hemoglobin level, and increased percentage of segmented neutrophils at the time of diagnosis were associated with thrombosis, whereas patients with bleeding complications were characterized by low red cell count, lower hemoglobin, and a lower percentage of segmented neutrophils. However, when analyzed by MPD subgroup, none of these parameters retained a predictive value for bleeding or thrombotic events. Moreover, elevated platelet count and patient age were not risk factors for bleeding complications. Thrombotic events were less frequent in patients below the age of 40, and were increased in patients aged 70 and above. However, this was primarily due to the high percentage of elderly patients in subgroups mainly affected by thrombosis (PV and ET). In most MPD subgroups, the rate of bleeding and thrombosis was highest just before and during the first months after diagnosis, and declined thereafter. Thrombohemorrhagic complications were less frequent after phlebotomy in PV and after therapy with alkylating agents in CML. The institution of cytoreductive therapy soon after the diagnosis was made may explain the reduced incidence of complications later in the disease. We conclude that morbidity and mortality from thrombohemorrhagic complications are high in myeloproliferative disorders.(ABSTRACT TRUNCATED AT 400 WORDS)

Bloodletting↗
PubMed1990

Influence of splenectomy on platelet morphometry and function.

Functional and morphometric platelet abnormalities may be influenced by splenectomy and thus contribute to postoperative thrombohaemorrhagic complications, especially in patients with splenomegaly and/or platelet defects. We investigated platelet function, platelet secretion, and platelet morphometry before and one week after splenectomy in seven patients with normal platelet production and normal spleen size (Hodgkin's disease) and five patients with splenomegaly and platelet abnormalities (4 with myeloproliferative disorders and 1 with chronic myelomonocytic leukemia). Severe postoperative thrombohaemorrhagic complications occurred only in patients with myeloproliferative disorders, although platelet count and mean platelet volume increased in almost all patients after splenectomy. Four patients with myeloproliferative disorders had impaired platelet aggregation before splenectomy that improved in only one patient after surgery. Platelet buoyant density in this patient group was decreased before splenectomy and normalised thereafter. Concomitantly, intraplatelet concentrations of alpha-granular proteins increased. Before splenectomy, there was a positive correlation between platelet density and platelet volume in patients with Hodgkin's disease (r = 0.59, p less than 0.001), but not in patients with myeloproliferative disorders. There was no correlation between platelet density and platelet volume after splenectomy in either patient group. In conclusion, morphometric platelet abnormalities were found in all patients after splenectomy. In patients with myeloproliferative/myelodysplastic disorders, decreased platelet buoyant density normalised and intraplatelet concentrations of alpha-granule proteins were elevated after splenectomy. However, platelet function defects in this patient group were not corrected and may have been a major cause of thrombohaemorrhagic complications in the postoperative period.

Adult↗
PubMed1990

A prospective study of haemostatic parameters in relation to the clinical course of myeloproliferative disorders.

Platelet function and the clinical course of the disease were prospectively investigated in 29 patients with myeloproliferative disorders. Serial determinations (median: 5 investigations per patient within 17 months) of platelet aggregation, plasma and intraplatelet concentrations of beta-thromboglobulin (beta TG) and platelet factor 4 (PF4), and of fibrinopeptide A (FPA) plasma levels were carried out. In the chronic phase of polycythaemia vera, patients with thrombohaemorrhagic complications during the study period had higher platelet count, more severe platelet aggregation defects, and increased plasma levels of beta TG and FPA compared to patients without complications. However, thrombohaemorrhagic complications were not predicted by changes in these parameters in the individual patient during the chronic disease phase. When patients with chronic myelogenous leukaemia entered blast crisis, bleeding complications were related to thrombocytopenia, impaired platelet function and low intraplatelet concentrations of beta TG and PF4. Cytoreduction by chemotherapy in the chronic phase of CML did not alter beta TG and PF4 plasma levels, whereas treatment of polycythaemia rubra vera by venesection favourably influenced platelet alpha-granule secretion and increased intraplatelet concentrations of beta TG and PF4.

Adult↗
PubMed1989

Platelet volume parameters as a diagnostic tool: the influence of anticoagulation and storage conditions on platelet impedance volume.

Rapid progress has been made in the design of aperture impedance cell counters, and parameters such as mean platelet volume and platelet distribution width have become routinely available to most physicians. Platelet volume is influenced by both platelet production in the bone marrow and platelet activation or sequestration in the circulation. In thrombocytopenic patients, it is often possible to differentiate between megakaryocytic and amegakaryocytic disease states on the basis of platelet volume analysis. In patients with thrombocytosis, a myeloproliferative disorder may be suspected if the platelet distribution width is high. However, the conditions of sample preparation and storage still give rise to considerable inaccuracy in the determination of platelet volume parameters. In this study, platelet impedance volume was strongly influenced by anticoagulation, storage time, and incubation temperature. Changes in platelet volume were more pronounced in whole blood than in platelet rich plasma. However, mainly large platelets were lost during the preparation of platelet rich plasma. Collecting blood directly into a mixture of citrate and low dose glutaraldehyde stabilized platelet volume for up to 2 h after venipuncture at room temperature. This method reduces platelet volume changes in vitro and is in this respect superior to the usual EDTA blood count or the use of platelet-inhibitory agents.

Anticoagulants↗
PubMed1989

[Fever of unknown origin and colchicine-sensitive amyloidosis: familial Mediterranean fever?].

A 39-year-old man who had for 20 years suffered from recurrent fever, abdominal pain and joint pains was diagnosed to have generalized amyloidosis type AA. Suspected of having familial mediterranean fever (FMF) he was treated with colchicine, 2 mg daily. Within four years the fever bouts became milder and the amyloidosis no longer progressed. Since the patient was a foundling it was impossible to prove FMF, despite the typical signs and the successful treatment.

Adult↗
PubMed1989

Bleeding and thrombosis in chronic myeloproliferative disorders: relation of platelet disorders to clinical aspects of the disease.

Bleeding and thrombosis are a major cause of morbidity and mortality in myeloproliferative disorders (MPD). This study evaluates the relation between thrombohemorrhagic complications and platelet abnormalities in different subgroups of MPD. In 57 MPD patients thrombohemorrhagic complications occurred in 71% of patients with polycythemia rubra vera and 50% of patients with osteomyelofibrosis and primary thrombocythemia but in only 29% of patients with chronic myelogenous leukemia. Increased beta-thromboglobulin and platelet factor 4 plasma levels, platelet aggregation defects, and increased dispersion of the platelet volume distribution curve were most frequent in those subgroups where most serious thrombohemorrhagic complications were observed, and multiple platelet-related abnormalities were often found simultaneously. Fibrinopeptide A plasma levels were rarely elevated, however. Our results indicate that platelet abnormalities associated with bleeding and thrombosis are primarily determined by the clinical subgroup of myeloproliferative disease.

Adult↗