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P Noel

Publications and source records attributed to P Noel.

At least 19 recordsLinked to original sources
PubMed1998

The erythroid leukemias: a comparative study of erythroleukemia (FAB M6) and Di Guglielmo disease.

Pure erythroid malignancies, such as Di Guglielmo disease (DG), in which the predominant immature elements are proerythroblasts, are excluded from the French-American-British (FAB) classification for acute leukemia and do not fit neatly into any of the categories of myelodysplasia. This retrospective review compares the clinical and laboratory features of DG and erythroleukemia (FAB M6) among 37 cases treated at a single institution over a 7-year period. DG was defined as >30% proerythroblasts and the absence of a myeloblastic component. Clinical and laboratory features were similar in both subtypes. High proportions of secondary leukemias and prior myelodysplastic syndromes (MDS) were noted (M6, 13 of 26 cases; DG, five of 11 cases; p = 0.85). Pancytopenia was common at presentation in both groups [median white blood cells (WBC), 2,600/mm3; HgB, 8.65 gm/dl; platelets, 38,000/microl]. Two-thirds of studied cases had chromosomal abnormalities typified by major karyotypic abnormalities (MAKA) involving three or more chromosomes. Abnormalities involving chromosome 5 and/or 7 occurred in 47% (48% M6 and 45% DG). Both erythroid malignancies carried a poor prognosis (M6, 6.0-month median survival; DG, 4-month survival; p = 0.74). Among those patients choosing aggressive rather than palliative therapy, higher remission rate (80 versus 25%) and survival advantage (11.5 versus 2.5 months) were seen in M6 compared to DG. However, only two long-term survivors exist. The similar clinical and laboratory features, cytogenetic patterns, and poor survival data suggest that the FAB classification schema should be modified to include DG.

Adolescent↗
PubMed1998

Treatment of acute myelogenous leukemia in the older patient with attenuated high-dose ara-C.

We have evaluated the activity and toxicity of cytosine arabinoside (ara-C; 750 mg/m2 intravenously given over 3 hours every 12 hours for 12 doses) to induce remission in older (median age, 73 years) newly diagnosed patients who had acute myelogenous leukemia (AML). A maximum of two cycles of induction were administered. Patients who achieved complete remission could receive three additional consolidation courses limited to 4 to 6 doses of ara-C every 12 hours, depending on marrow cellularity. Thirty patients were evaluable. Twenty-two patients had one or more unfavorable prognostic factors, including antecedent hematologic disorders (10), cytogenetic abnormalities (17), or hyperleucocytosis (5). Fourteen patients (47%) achieved complete remission. Four patients did not receive consolidation as planned because of medical contraindication or refusal, and three patients relapsed during consolidation. The median duration of complete remission was 326 days. Sixteen patients failed induction because of relative or absolute drug resistance in nine patients, or death in seven patients. Median survival for the entire group was 6 months. Toxicity was significant, with a median initial hospitalization of 29 days. These results are comparable to those reported in the literature and suggest that this regimen may be considered to be an alternative to an anthracycline-containing regimen.

Aged↗
PubMed1997

Chronic granulocytic leukemia: recent information on pathogenesis, diagnosis, and disease monitoring.

Current evidence strongly implicates the chromosome translocation t(9;22)(q34;q11.2) as the cause of chronic granulocytic leukemia. Therefore, identification of this genetic abnormality through either cytogenetic or molecular methods has become a requirement for diagnosis. Intense investigation of the mechanism by which t(9;22) transforms normal hematopoietic progenitors into malignant cells is ongoing. Recent advances in molecular diagnostic methods have allowed refined qualitative and quantitative methods of detecting t(9;22), which are useful for monitoring response status and detecting minimal residual disease. The current understanding of the pathogenesis of chronic granulocytic leukemia and the application of new diagnostic methods are discussed.

Blotting, Southern↗
PubMed1996

Motion sickness.

Motion sickness is a common phenomenon affecting most patients at some point in life. Car sickness, airsickness, seasickness, and space sickness all involve a neural mismatch or confusion between the vestibular, visual, and proprioceptive systems that produces the symptoms of motion sickness. Therapy is directed toward decreasing conflicting sensory input, controlling nausea, and speeding the process of adaptation.

Buspirone↗
PubMed1996

[A case of painful bilateral ophthalmoplegia].

The authors present a case of Tolosa-Hunt syndrome with the particularity of a simultaneous palsy of both oculomotor nerves. The evolution is followed during 16 years. The clinical description, the criteria of the syndrome and the differential diagnosis are discussed. The diagnosis is based on the clinical evolution, the transitory palsy of the oculomotor nerves and the involvement of the optic nerve. The response on steroid treatment was spectacular. Bilateral and fluctuant oculomotor palsy is possible in the TolosaHunt syndrome. General investigations are mandatory to exclude other pathologies.

Diplopia↗
PubMed1995

Continuous infusion etoposide/carboplatin for treatment of refractory acute leukemia.

Etoposide (125 mg/m2/d) and carboplatin (200 mg/m2/d) were administered by continuous 5-day intravenous infusion to 10 patients with relapsed or refractory acute leukemia (7 ANLL, 1 ALL, 2 blast crisis of CGL). No complete or partial response was observed despite dose-limiting toxicity characterized by severe diarrhea in four patients and neutropenic colitis in two additional cases. We cannot recommend the present schedule of drug administration for the treatment of acute leukemia.

Adolescent↗
PubMed1994

Electroencephalographic mapping and 99mTc HMPAO single-photon emission computed tomography in carbon monoxide poisoning.

STUDY OBJECTIVE: To investigate whether topographic analysis of EEG mapping and technetium-99m (99mTc) hexamethylpropylenamine oxide (HMPAO) brain single-photon emission computed tomography (SPECT) can detect cerebral anomalies in the acute phase of carbon monoxide poisoning. DESIGN: Twelve patients aged 18 to 55 years with severe carbon monoxide poisoning and no history of neurologic disorder were evaluated. Either nasal (5 patients) or hyperbaric (7 patients) oxygen therapy was administered. Criteria for hyperbaric oxygen therapy were blood CO of more than 20%, loss of consciousness, pregnancy, or signs of cardiac injury. After oxygen treatment, all patients had a blood CO value of 0% and no patient had persistent acute signs of toxicity. Patients then were investigated by confentional EEG, EEG mapping, and 99mTc HMPAO brain SPECT. These procedures were performed on the day of admission. PARTICIPANTS: After nasal (5 patients) or hyperbaric (7 patients) oxygen therapy was administered, 12 adults with severe carbon monoxide poisoning were evaluated. All studies were performed on the day of admission. MEASUREMENTS: Conventional EEG, EEG mapping, and 99mTc HMPAO brain SPECT. RESULTS: While classic EEG was normal in 9 of 12 patients and showed diffuse anomalies in 3, EEG mapping and 99mTc HMPAO brain SPECT demonstrated unilateral or bilateral regional anomalies in 8 of 12 patients. Anomalies were localized in temporo-parieto-occipital areas, the watershed areas of the major cerebral arteries, or in temporal cortex. CONCLUSION: These preliminary results suggest that EEG mapping and 99mTc HMPAO brain SPECT can be complementary tools to diagnose early regional cerebral anomalies in carbon monoxide-poisoned patients.

Acute Disease↗
PubMed1993

The 5q- syndrome: a single-institution study of 43 consecutive patients.

A favorable prognosis and a low rate of leukemic transformation has been attributed to the 5q- syndrome, a myelodysplastic syndrome (MDS) characterized by macrocytic anemia, hypolobulated micromegakaryocytic hyperplasia, and an interstitial deletion of chromosome 5. We examined the characteristics and outcome of 43 consecutive patients in our institution strictly defined by morphologic criteria and a solitary 5q- cytogenetic defect. The median age at diagnosis was 68 years, with a clear female predominance (7:3). Eighty percent of the patients were red blood cell transfusion-dependent at diagnosis and all untransfused patients had macrocytic indexes. In contrast, significant neutropenia or thrombocytopenia was rare. The French-American-British (FAB) class distributions were RA (72%), RARS (7%), RAEB (16%), and RAEB-IT (5%). At a median follow-up of 31 months, 56% of the patients survive, with a projected median survival of 63 months. The incidence of acute leukemia was 16% and was uniformly fatal. Clinical hemosiderosis occurred in 28% of the patients, resulting in two deaths. Neither survival nor the risk of leukemic transformation was predictable from initial clinical parameters, including FAB classification, Bournemouth score, and degree of aneuploidy. The lack of significant neutropenia and thrombocytopenia seemed to account for a very low incidence of infection and bleeding resulting in a prognosis equal or superior to historical patients with MDS. Therapeutic endeavors, including the use of corticosteroids, androgens, cis-retinoic acid, pyridoxine, and danazol, were largely unsuccessful.

Acute Disease↗
PubMed1993

Primary systemic amyloidosis: a rare complication of immunoglobulin M monoclonal gammopathies and Waldenström's macroglobulinemia.

PURPOSE: To determine the natural history of amyloidosis associated with Waldenström's macroglobulinemia and immunoglobulin M (IgM) monoclonal gammopathy. PATIENTS AND METHODS: From January 1968 to September 1990, 50 patients with a serum IgM monoclonal protein and biopsy-proven amyloidosis were evaluated at the Mayo Clinic. There were 32 men and 18 women (age range, 43 to 93 years). RESULTS: Percentages of patients presenting with cardiac, renal, hepatic, and pulmonary amyloid were 44%, 32%, 14%, and 10%, respectively. Forty-two percent of the patients had an M protein value greater than 1.5 g/dL, and 12% had an M component greater than 3 g/dL. Subcutaneous fat, rectum, and bone marrow showed amyloid in 84%, 72%, and 50%, respectively, providing a simple technique for diagnosing amyloidosis. The bone marrow biopsy was consistent with Waldenström's macroglobulinemia in 10, a plasma-cell proliferative disorder in 10, and lymphoma or a lymphoproliferative disorder in 11; results were normal, nondiagnostic, or hypercellular in 17. Forty-three of 50 patients died. The median survival of the entire group was 24.6 months. Fifty-three percent of deaths were due to cardiac amyloid, 12% to respiratory failure, 7% to macroglobulinemia, 7% to liver failure, and 7% to kidney failure. CONCLUSION: The presence of amyloid cardiomyopathy and an increased creatinine concentration at diagnosis had an adverse impact on survival. Of the 22 patients who presented with cardiomyopathy, the median survival was 11.1 months, with only two surviving longer than 5 years. The median survival of the 28 patients without cardiomyopathy at diagnosis was 27 months, with eight 5-year survivors (P = .013). All eight amyloid deposits studied stained for Ig light chain, indicating that this amyloidosis is of the primary (AL) type.

Adult↗
PubMed1992

Refractory thrombocytopenia. A myelodysplastic syndrome that may mimic immune thrombocytopenic purpura.

The French-American-British classification scheme of myelodysplastic syndromes includes a category of refractory cytopenia that includes refractory thrombocytopenia (RTC). Because dysmegakaryopoiesis manifesting as an isolated cytopenia can be difficult to identify morphologically and because it may be accompanied by megakaryocytic hyperplasia, RTC may be confused with idiopathic thrombocytopenic purpura. A review of 1,220 cases of myelodysplastic syndromes at Mayo Clinic Jacksonville and Mayo Clinic Rochester from 1979 to 1990 yielded 9 cases (0.7%) of isolated thrombocytopenia (RTC) associated with clonal chromosome abnormalities. Review of 319 marrow chromosome analyses performed at the cytogenetics laboratory at Mayo Clinic Rochester from 1979 to 1990 for patients with low platelet count yielded two additional cases of RTC (0.6%). Of the 11 RTC cases, 3 previously had been misdiagnosed as idiopathic thrombocytopenic purpura. All patients had oval macrocytes in peripheral blood smears and abnormal megakaryocyte morphology in bone marrow aspirates, lacked antiplatelet antibodies, and did not have splenomegaly on clinical examination. The most common clonal chromosome abnormalities involved chromosomes 3, 5, 8, or 20. Steroid therapy was ineffective. Clinical and laboratory findings can establish the diagnosis of RTC and allow the physician to avoid recommending inappropriate therapy (steroids or splenectomy) for these patients.

Aged↗
PubMed1991

Differential expression of isopeptide bonds N epsilon (gamma-glutamyl) lysine in benign and malignant human breast lesions: an immunohistochemical study.

N epsilon (gamma-glutamyl) lysine isopeptide bonds were detected in situ in histological sections from benign and malignant human breast tissue using the monoclonal antibody (MAb) 81D1c2. On cryostat sections of fresh-frozen mammary tissue post-fixed in acetone, or on paraffin sections also from mammary tissue fixed in Bouin's solution, the MAb reacted preferentially with glandular epithelial cells and staining was restricted to the nuclei. In 41 out of 44 benign lesions examined, staining was strong or moderate, while in 25 out of 33 malignant lesions no staining was observed. In the 8 remaining lesions of this group, staining was positive but weak. The difference in reactivity of this MAb with the 2 types of lesions is highly significant (p less than 0.0005) according to the chi 2 test.

Adult↗
PubMed1991

Atrial fibrillation as a risk factor for deep venous thrombosis and pulmonary emboli in stroke patients.

In 539 consecutive stroke patients admitted to a rehabilitation department, we studied the possible role of atrial fibrillation as a risk factor for deep venous thrombosis and pulmonary embolism by analyzing a series of relevant clinical data in patients with and without atrial fibrillation and in patients with and without venous thromboembolic complications. Deep venous thrombosis as well as advanced age and cardiac disease were significantly (p less than 0.001) more frequent in patients with atrial fibrillation. However, in a model of simultaneous logistic regression carried out on the presence of absence of venous thromboembolic complications, atrial fibrillation was the only significant risk factor. In view of the morbidity and mortality linked to deep venous thrombosis, our findings argue for preventive anticoagulation therapy in stroke patients suffering from atrial fibrillation and merit further study.

Aged↗