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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 19 patients with Felty's syndrome, marrow production of neutrophils and neutrophil distribution were studied. Despite accelerated marrow release and disappearance of mature blood neutrophils, there was little or no increase in the marrow mitotic pool or in vitro progenitor cells. Only two patients had an increase in marrow neutrophils and precursors. Antineutrophil antibody was detected in seven of nine patients studied. Neither abnormal margination of blood neutrophils nor impaired marrow release of cells was detected. Skin exudate cellularity tended to correspond to prior history of infections, asymptomatic patients having more cellular exudates. Sustained neutrophil increments were observed in six of 10 patients following splenectomy, but in no patient did neutrophil kinetics return completely to normal. Three of four patients who failed to respond to splenectomy with sustained increments in blood neutrophils had a reduced mass of marrow neutrophils and neutrophil precursors when studied prior to splenectomy. No diminution in neutropenia was observed in any of five patients treated with lithium carbonate. This study indicates that multiple factors are involved in the pathogenesis of neutropenia in Felty's syndrome. In particular, neutropenia was associated with inadequate marrow granulocytopoiesis. The severity of the impairment, as determined by the mass of marrow neutrophils and precursor cells, may be useful in predicting response to splenectomy.
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PMID:Neutrophil kinetics in Felty's syndrome. 743 11

A variety of mechanisms have been demonstrated or suggested to explain the neutropenia that accompanies Felty's syndrome. This case report presents with Felty's syndrome with recurrent infections with initially had a clinical response to splenectomy. Eleven years later profound neutropenia recurred. In-vitro evidence for cell mediated autosensitisation of peripheral blood lymphocytes to autologous bone marrow cells was found. The cellular abnormalities improved after high-dose corticosteroids but not lithium. However, there did not appear to be a reduction in the incidence of clinical infections. The finding suggests that granulocytopenia in some patients with Felty's syndrome may be an autoimmune phenomenon.
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PMID:Cell mediated autoimmune granulocytopenia in a case of Felty's syndrome. 743 67

A 73-year-old woman was diagnosed with seropositive destructive rheumatoid arthritis in 1981. She was treated with cortisone, chloroquine, and cyclophosphamide (Sendoxan) in 1982 and 1984 and contracted severe neutropenia. After that she only received cortisone. During 1991, again low neutrophilic counts were registered, especially granulocytopenia. At first, B-cell lymphoma was suspected, but later Felty's syndrome was established. The patient was treated with high-dose cortisone with some success and had a few minor septic episodes. In May 1992 she contracted a traumatic wound on the back of the lower leg. Conservative treatment resulted in a worsening of the condition and an increased wound area, most likely related to the neutropenic condition. In mid July the patient was hospitalized. Bacterial isolates yielded mixed gram-negative enteric bacteria from the wound. Parenteral antibiotic treatment was started, followed by oral drugs, rhG-CSF (filgrastim) was given subcutaneously once a day, starting 3 days after admission. This resulted in increased numbers of peripheral granulocytes. The ulcer started to heal and by mid August the patient received a transplant with autologous skin grafting. In mid September the wound was completely healed. It is concluded that the combination of antibiotics, skin transplantation, and G-CSF was necessary for the successful result. Actually, the bacterial growth did not call for antibiotics, but it was considered necessary to cover for staphylococci. No worsening of the underlying arthritis was observed.
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PMID:Successful treatment of chronic wound infection in neutropenia and rheumatoid arthritis with filgrastim (rhG-GSF) 752 58

A patient with Felty's syndrome and rheumatoid arthritis was treated with recombinant granulocyte stimulating factor rhG-CSF (Neupogen) in view of severe neutropenia. He had a prompt rise in his neutrophil count and associated with this a severe flare of his arthritis and a skin rash. rhG-CSF was stopped, his neutrophil count fell rapidly and his symptoms resolved. rhG-CSF and the resulting rise in neutrophil count may be associated with flare of autoimmune disease in susceptible individuals.
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PMID:Felty's syndrome treated with rhG-CSF associated with flare of arthritis and skin rash. 754 May 27

A 58-year-old white male with Felty's syndrome was successfully treated with granulocyte colony stimulating factor (GCSF). GCSF can correct the granulocytopenia of Felty's syndrome and may be a beneficial therapeutic adjunct in patients who have serious infections associated with neutropenia. The patient developed a flare of arthritis concomitant with increased circulating neutrophils following GCSF therapy.
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PMID:Flare of arthritis with successful treatment of Felty's syndrome with granulocyte colony stimulating factor (GCSF). 754 May 28

Recombinant myeloid growth factors have been increasingly used in recent years to combat induced and disease associated neutropenia. Their application in the management of Felty's syndrome with intercurrent infection has raised concern that resultant neutrophilia and activation of a diverse array of polymorphonuclear cell functions may have an adverse effect on the rheumatoid disease process. We describe a patient with Felty's syndrome receiving short term treatment with recombinant human granulocyte colony stimulating factor (GCSF), who then developed acute renal failure in conjunction with leukocytoclastic vasculitis and presumptive gout. We address the issue of "adding fuel to the fire" and review reported implications of GCSF in induction of vasculitis.
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PMID:Vasculitis complicating granulocyte colony stimulating factor treatment of leukopenia and infection in Felty's syndrome. 754 56

Felty's syndrome (FS), the association of rheumatoid arthritis (RA) and idiopathic neutropenia, remains an unexplained phenomenon. HLA-DR4 is found in over 90% of cases. Patients with FS may have a T cell lymphocytosis of CD3+CD8+CD57+ large granular lymphocytes (LGL syndrome). In this study of 47 patients with FS, 19% had clear evidence for LGL expansions, while in total 42% had variable evidence for the LGL syndrome using currently available techniques. Of these T cell expansions, 76% were clonal, as demonstrated by Southern blotting and analysis with T cell receptor (TCR) beta chain constant region probes. This technique may fail to detect clonal populations in some patients. Cytofluorographic analysis using antibodies specific for TCR V beta chains identified patients with clonal LGL expansions with results comparable to those obtained with Southern blotting. No evidence for shared V beta usage among expansions from different patients was seen. The role of LGL in RA and FS is currently unclear, but this technique offers a practical and accessible means of identifying patients with LGL expansions, as a starting point for further investigation.
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PMID:Large granular lymphocyte expansions in patients with Felty's syndrome: analysis using anti-T cell receptor V beta-specific monoclonal antibodies. 762 87

The risk of infection is increased in patients with Felty's syndrome, neutropenia being one of the main reasons for the susceptibility to infection. We report the case of a 56-year-old patient with Felty's syndrome in whom successive therapy with GM-CSF, splenectomy, and G-CSF was tried because of recurrent severe infections. Therapy with GM-CSF and G-CSF resulted in improvement of neutropenia and in successful treatment of cutaneous and pulmonary infections.
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PMID:GM-CSF and G-CSF in Felty's syndrome. 768 11

Neutropenia in Felty's Syndrome predisposes patients to recurrent bacterial infections. We have treated a patient for more than one year with G-CSF and ascertained that this growth factor can safely correct neutropenia over a long period of time. G-CSF may constitute a new agent for the treatment and prophylaxis of infection in Felty's syndrome.
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PMID:Long-term correction of neutropenia in Felty's syndrome with granulocyte colony-stimulating factor. 768 94

A patient with Felty's syndrome (FS) and persistent profound neutropenia developed recurrent infections and sepsis syndrome. No impairment of granulocyte-macrophage colony development was observed in vitro. Marrow morphology revealed an absence of mature neutrophil forms despite administration of granulocyte-colony stimulating factor (G-CSF). However, pretreatment with bolus cyclophosphamide (CY) permitted the growth factor to relieve this impairment of late myeloid maturation and resulted in a brisk, albeit short, burst of neutrophilia. This suggests that immune interference in myelopoiesis can be overcome by growth factor administration if immune activity is adequately dampened by immunosuppressive therapy.
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PMID:Sequential administration of cyclophosphamide and granulocyte-colony stimulating factor relieves impaired myeloid maturation in Felty's syndrome. 769 May 20


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