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Hypocellular acute leukemia
T-cell reactivity
Coxlella burnetli
Antlmlcrobial therapy
Q fever
Despite a worldwide distribution of Coxiella burnetii, only single cases of Q fever endocardltis have been reported outside Great Briiin and Australia. We pre@ 10 patll; fiie were female, onmental exposure, and the mitral valve was involved as commonly onlyfarhadahlloryofenvir as the au-tic valve. Dne patfent had congenital aortic stenosis, and three patientshada prosthetic valve. We confirm the importance of hepatic involvement, thrombocytopenia and hypergammaglobulinemia as diagnostic features. Diagnosis was established by finding an elevated complement-fixing antibody to Phase I C. bumetti antigen. Tetracycline, with or without lincomycin or cotrimoxazole, was used in nine patients, and one patient received cotrimoxazole as the sole antibiotic agent. Five patients died, and the mean survival is 36 months with a range of five to 66 months. We suggest that 0 fever endocardltis is frequently missed, and we recommend clinicians to consider the diagnosis in all cases of culture-negative endocarditis.
Tobin MI, Cahill N, Gearty G, et al.: Q fever endocardftis. Am J Med 1982; 72: 396400.
Cardiac dlsease
Infective endocardlils
The authors have studied the function of T cells in the peripheral blood obtained from longterm survivors with Hodgkin’s disease to determine the sensitivity of those T cells to normal suppressor cell immunoregulatory mechanisms. Concanavalin A-activated suppressor cells from normal dorxxs suppressed the proliferation of lymphocytes obtained from 11 patients (56.8 f 3.5 percent) and from 28 alfogeneic normal control subjects (39.8 .* 2.7 percent [p
Vanhaelen CPJ, Fisher RI: Increased sensitivity of T cells to regulation by normal suppressor cells persists in long-term survivors with Hodgkin’s disease. Am J Med 1982; 72: 385-390.
Hodgkin’s disease
Suppressor T ceils
Suppression sensitivity
Suppressor monocytes
Leukemia Granukxytopenia
Bone marrow Chemotherapy
Pulmonary hemorrhage Goodpasture’s syndrome
Glomerulonephritis
.--~
Nine patients with diffuse intrapulmonary hemorrhage and glomerulonephritis not due to antiglomerular basement membrane (anti-GBM) antibody are described and similar previously reported cases are reviewed. Eight patients were seen during a four-year interval and represented 47 percent of the cases of pulmonary hemcnhage and glomerulonephrffis seen duing this period. Oiagnoses included systemic vasculitis of unspecified type in two patients with seropositive fheumatoid arthritis, idiithic crescentic glomerulonephriiis with negative immunofluorescence in two, Wegener’s granulomatosis in two, and polyarteritis nodosa, Henoch-Schonlein purpura, and mixed connective tissue disease in one each. Differentiation from anti-GBM antibodymediated pulmonary hemorrhage and glomerulonephritis by clinical evaluation alone was frequently difficult, emphasizing the importance of both immunopathologic studies and evaluation of serum for anti-GBM antibody in all patients with pulmonary hemorrhage and glomerulonephritis.
Leatherman JW, Sibley RK, Davies SF: Diffuse intrapulmonary hemorrhage and glomerulonephritis unrelated to antr-glomerular basement membrane antibody. Am J h&d 1982; 72: 401-410.
VasculRis
Hemoptysis
--...
We examined the clinical features and therapeutic response of a group of patients with acute leukemia and hypocellular bone marrow. Therapists have generally avoided, delayedor modified therapy because of hypocellularity. We demonstrated not only that aggressive therapy is possible, but also that the remission rate is hi (complete remission = 73 percent) and survival prolonged (X > 40 months).
Howe RB, Bloomfield CD, McKenna RW: Hypocellular acute leukemia. Am J Med 1982; 72: 391-395.
Pancytopenia
Coxlella burnetli
Antlmlcrobial therapy
Q fever
Despite a worldwide distribution of Coxiella burnetii, only single cases of Q fever endocardltis have been reported outside Great Briiin and Australia. We pre@ 10 patll; fiie were female, onmental exposure, and the mitral valve was involved as commonly onlyfarhadahlloryofenvir as the au-tic valve. Dne patfent had congenital aortic stenosis, and three patientshada prosthetic valve. We confirm the importance of hepatic involvement, thrombocytopenia and hypergammaglobulinemia as diagnostic features. Diagnosis was established by finding an elevated complement-fixing antibody to Phase I C. bumetti antigen. Tetracycline, with or without lincomycin or cotrimoxazole, was used in nine patients, and one patient received cotrimoxazole as the sole antibiotic agent. Five patients died, and the mean survival is 36 months with a range of five to 66 months. We suggest that 0 fever endocardltis is frequently missed, and we recommend clinicians to consider the diagnosis in all cases of culture-negative endocarditis.
Tobin MI, Cahill N, Gearty G, et al.: Q fever endocardftis. Am J Med 1982; 72: 396400.
Cardiac dlsease
Infective endocardlils
The authors have studied the function of T cells in the peripheral blood obtained from longterm survivors with Hodgkin’s disease to determine the sensitivity of those T cells to normal suppressor cell immunoregulatory mechanisms. Concanavalin A-activated suppressor cells from normal dorxxs suppressed the proliferation of lymphocytes obtained from 11 patients (56.8 f 3.5 percent) and from 28 alfogeneic normal control subjects (39.8 .* 2.7 percent [p
Vanhaelen CPJ, Fisher RI: Increased sensitivity of T cells to regulation by normal suppressor cells persists in long-term survivors with Hodgkin’s disease. Am J Med 1982; 72: 385-390.
Hodgkin’s disease
Suppressor T ceils
Suppression sensitivity
Suppressor monocytes
Leukemia Granukxytopenia
Bone marrow Chemotherapy
Pulmonary hemorrhage Goodpasture’s syndrome
Glomerulonephritis
.--~
Nine patients with diffuse intrapulmonary hemorrhage and glomerulonephritis not due to antiglomerular basement membrane (anti-GBM) antibody are described and similar previously reported cases are reviewed. Eight patients were seen during a four-year interval and represented 47 percent of the cases of pulmonary hemcnhage and glomerulonephrffis seen duing this period. Oiagnoses included systemic vasculitis of unspecified type in two patients with seropositive fheumatoid arthritis, idiithic crescentic glomerulonephriiis with negative immunofluorescence in two, Wegener’s granulomatosis in two, and polyarteritis nodosa, Henoch-Schonlein purpura, and mixed connective tissue disease in one each. Differentiation from anti-GBM antibodymediated pulmonary hemorrhage and glomerulonephritis by clinical evaluation alone was frequently difficult, emphasizing the importance of both immunopathologic studies and evaluation of serum for anti-GBM antibody in all patients with pulmonary hemorrhage and glomerulonephritis.
Leatherman JW, Sibley RK, Davies SF: Diffuse intrapulmonary hemorrhage and glomerulonephritis unrelated to antr-glomerular basement membrane antibody. Am J h&d 1982; 72: 401-410.
VasculRis
Hemoptysis
--...
We examined the clinical features and therapeutic response of a group of patients with acute leukemia and hypocellular bone marrow. Therapists have generally avoided, delayedor modified therapy because of hypocellularity. We demonstrated not only that aggressive therapy is possible, but also that the remission rate is hi (complete remission = 73 percent) and survival prolonged (X > 40 months).
Howe RB, Bloomfield CD, McKenna RW: Hypocellular acute leukemia. Am J Med 1982; 72: 391-395.
Pancytopenia