Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The safety of 738 high-risk patients treated with enalapril under various clinical programs was evaluated. High risk was defined as the presence of a collagen vascular disease; a renal disease, including renovascular hypertension; or either hypertension or refractory cardiac failure with serum creatinine greater than or equal to 1.7 mg/dl at baseline. Essential hypertension was the primary diagnosis in most of these patients. Treatment with enalapril in these patients usually continued without interruption for the length of the particular protocol. The incidence of adverse reactions resulting in discontinuation of treatment was comparable to that observed with other standard antihypertensive therapies in patients with milder forms of disease. No enalapril-related neutropenia, proteinuria, dysgeusia or ageusia were reported in these high-risk patients. The incidence of discontinuation due to rash was less than 0.5%. Resolution and/or improvement of captopril-related adverse effects was observed in many patients crossed over to treatment with enalapril. In patients with collagen vascular diseases and those with severe impairment of renal function (serum creatinine greater than or equal to 3.0 mg/dl), the incidence of discontinuation due to adverse experiences or death as well as the profile of reported adverse experiences was similar to those for the total group of high-risk patients. The data suggest that enalapril is efficacious and well tolerated by the high-risk patients.
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PMID:High-risk patients treated with enalapril maleate: safety considerations. 253 44

Neutrophil-associated IgG (NAIgG) and neutrophil-binding IgG in sara (NBIgG) of 77 patients with neutropenia suspected to be caused by autoimmune mechanisms (group A) and 31 patients with aplastic anemia or myelodysplastic syndrome (group B) were assayed by flow cytometry. Auto-NBIgG was elevated in 32% of the patients in group A, particularly in about 70% of those with collagen diseases or ITP, but the level was normal in group B. Elevated NAIgG with normal auto-NBIgG levels was found in 27% of the patients in group A and in 64% of the patients in group B. The assay of auto-NBIgG was useful for detection of anti-neutrophil autoantibodies and for the diagnosis of autoimmune neutropenia. In addition, the level of NAIgG may be non-specifically elevated in non-immune neutropenia.
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PMID:[Neutrophil-associated IgG and neutrophil-binding IgG in autoimmune neutropenia]. 258 44

Adverse effects of converting enzyme inhibitors are either substance-specific (neutropenia, proteinuria, skin rashes, taste disturbances) or due to the converting enzyme inhibition (hypotension, functional renal insufficiency, hyperkalemia, cough, angioedema). They are rare nowadays because of better knowledge of the pharmacokinetics and -dynamics of the converting enzyme inhibitors, resulting in lower dosage, and because of identifying patients at high risk. The dosage must be adjusted according to renal function, in order to prevent accumulation and toxicity. In addition to patients with renal insufficiency, patients at high risk are those with a stimulated renin-angiotensin-aldosterone system, i.e. patients with renovascular hypertension or heart failure. Patients with collagen vascular disease, for example, systemic lupus erythematosus or scleroderma, should not be considered for long-term therapy with converting enzyme inhibitors because of the increased risk of neutropenia. Life-threatening angioedema may develop, mainly during the first few hours after drug administration.
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PMID:[Angiotensin-converting enzyme inhibition: side effects and risks]. 285 Jun 87

When captopril was first introduced, it was used in high doses for severe hypertension, often in the presence of renal insufficiency, and side effects such as proteinuria, rash, neutropenia, and altered taste sensation were noted. Upon analysis, these effects were most commonly seen in patients with renal disease, autoimmune disease, or collagen vascular disease. These complications usually reversed rapidly upon discontinuation of treatment. In contrast, the growing use of the angiotensin converting enzyme inhibitors, captopril and enalapril, for treating mild to moderate hypertension and the trend toward the use of lower doses has shown these agents to be well tolerated with a low frequency of troublesome adverse effects. In fact, the original spectrum of adverse effects has virtually disappeared with the use of lower doses in patients with uncomplicated hypertension. In low doses, the converting enzyme inhibitors produce remarkably few incidences of symptomatic discomfort; the most common is skin rash, which often responds to dosage reduction. Cough and rare occurrences of angioedema have also been reported. Moreover, evidence is evolving that indicates that the converting enzyme inhibitors may sometimes decrease proteinuria and improve renal function; these effects may be especially important in diabetic hypertensive patients. Of note, these drugs can also attenuate the unwanted metabolic side effects of concurrent diuretic treatment.
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PMID:Safety issues during antihypertensive treatment with angiotensin converting enzyme inhibitors. 306 5

Detection of neutropenia depends on the white cell count and the differential count, both of which involve considerable error. Pathogenetically, neutropenia can be attributed one of the following mechanisms: insufficient (or inefficient) formation, enhanced destruction or utilization, or--rarely--shift to the marginal pool. Isolated neutropenia should be distinguished from neutropenia combined with anemia and/or thrombocytopenia. The latter is usually due to bone marrow failure, whereas the former depends on peripheral mechanisms. Drug induced neutropenia may appear either as unforeseen acute agranulocytosis (aminophenazone type), depending on preceding sensitization, or as a slowly developing, dose-dependent cytopenia. Gradually developing neutropenia is an early stage of a general disease (collagen diseases, leukemia and other neoplasias, infections).
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PMID:[Clarification of neutropenia]. 728 Jun 26

Antineutrophil antibodies may be found in the sera of patients with chronic neutropenia as well as in the sera of a variety of patients with neutropenia and associated autoimmune or infectious disorders. We evaluated an immunofluorescent flow cytometric technique for the measurement of antineutrophil antibodies in serum. Sera from patients with suspected immune neutropenia were studied and compared with a group of sera from normal healthy individuals, as well as with sera from patients with rheumatoid arthritis and systemic lupus erythematosus. Of 159 patients with suspected immune neutropenia and a variety of associated clinical disorders, 59 (37%) were found to have evidence for enhanced binding of IgG to normal target neutrophils, interpreted as positive for antineutrophil antibodies. Whereas 0/37 non-neutropenic patients with typical RA had positive results, 51/244 (21%) of sera from nonneutropenic patients with SLE or other collagen vascular disorders showed enhanced IgG binding to neutrophils. Living neutrophils were used to study the effects of cellular activation, and increased antibody binding was observed with certain sera that contained IgG directed against activation-dependent antigens. We found that, under controlled conditions, flow cytometry can be reliably used to detect antineutrophil autoantibodies, with unfixed, living neutrophils as antigenic targets.
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PMID:Detection of antineutrophil autoantibodies by flow cytometry: use of unfixed neutrophils as antigenic targets. 827 57

The minimal acute inflammatory response to tissue injury is one of the most dramatic differences between fetal and adult wound healing. Considering the prominent role of inflammation in adult tissue repair, this study tested the hypothesis that the minimal fetal inflammatory response to tissue injury plays a central role in the "scarless" fetal repair process. Sponge implants were treated with lethally irradiated or live bacteria and placed subcutaneously in fetal rabbits to test the ability of the fetus to mount an acute inflammatory response to bacterial antigens present at the wound site and to analyze the effects of this inflammatory response on fetal fibroplasia and neovascularization. After harvest, these implants were examined histologically for inflammation, fibroblast infiltration, collagen deposition, and neovascularization, and collagen deposition was measured using hydroxyproline quantitation by high-performance liquid chromatography. Bacteria-treated implants showed dose-dependent acute inflammatory responses and significant increases in collagen deposition compared with control sponges. Implants containing live bacteria demonstrated maximal fibroplasia and neovascularization. These findings suggest that, despite neutropenia and immaturity of the fetal immune system, the fetus is capable of mounting an acute inflammatory response to avirulent bacteria present at the wound site. Fetal inflammatory cells which respond to this bacterial stimulus appear capable of initiating an adult-like healing response. Thus, by failing to provide a bacterial stimulus for leukocyte recruitment at the site of tissue injury, the sterile fetal environment appears to play a role in effecting "scarless" fetal wound healing.
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PMID:Biology of fetal repair: the presence of bacteria in fetal wounds induces an adult-like healing response. 846 58

Factors that predispose to infection in general, of course, may predispose to infection with anaerobes. Included in this category are diabetes mellitus, neutropenia, hypogammaglobulinaemia, malignancy, splenectomy, collagen vascular disease, cytotoxic drug therapy, corticosteroid therapy and other immunosuppression. However, even with these situations there may be certain, more specific, associations: anaerobic cholecystitis and anaerobic osteomyelitis in diabetics, neutropenic colitis, and the increased incidence of local anaerobic infections associated with carcinoma of the lung, colon and uterus. Conditions that lead to decreased redox potential more specifically predispose to infection with anaerobes. Included in this category are obstruction and stasis, tissue anoxia, tissue destruction, vascular insufficiency, prior aerobic infection, burns, foreign body implantation, and calcium salts in a wound (in association with fractures). Other specific clinical situations that predispose to anaerobic infections include leukaemia; oral, gastrointestinal, and female pelvic surgery; trauma at other sites; childbirth; aspiration pneumonia; human and animal bites; and therapy with agents with poor activity against anaerobes (e.g. aminoglycosides, quinolones). AIDS patients appear to be predisposed to severe periodontal disease and its complications.
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PMID:Host factors predisposing to anaerobic infections. 851 53

Chronic neutropenia associated with collagen vascular disease is seen principally with Felty's syndrome complicating rheumatoid arthritis. Multiple recent reports document the efficacy of both granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) in reversing the neutropenia and decreasing the risk of infections in Felty's syndrome. Long-term use of G-CSF appears well tolerated and effective in Felty's syndrome. Of concern, however, have been flares of arthritis and development of leukocytoclastic vasculitis in several patients following the use of colony-stimulating factors (CSFs) in Felty's syndrome. The incidence of these complications of CSF therapy appears to be greater in Felty's syndrome than in other disorders. Future studies will need to address the incidence of these side effects, evaluate strategies to reduce risks, and clarify the optimum use of CFSs in Felty's syndrome.
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PMID:Use of colony-stimulating factors in the treatment of neutropenia associated with collagen vascular disease. 920 36

Granulocyte colony-stimulating factor (G-CSF) is a hematopoietic growth factor (HGF) with many applications in cancer therapy. The most important applications are reduction in the incidence of febrile neutropenia, acceleration of neutrophil recovery after chemotherapy or bone marrow transplantation, and mobilization of progenitor cells. Many cutaneous adverse reactions associated with HGF have been reported in recent years, including injection site reactions, pyoderma gangrenosum, Sweet's syndrome, cutaneous leucocytoclastic vasculitis, and widespread folliculitis. The presence of large histiocytes on the dermis between collagen bundles has been proposed as a characteristic histopathologic finding in cutaneous eruptions secondary to granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor. We report on a patient with a high-risk ductal infiltrating carcinoma of the breast who received high-dose chemotherapy (HDC) with peripheral blood progenitor cell (PBPC) rescue. The patient received G-CSF after PBPC for a faster granulocyte recovery. She developed a cutaneous eruption located on back, buttocks, axillae, groin and sites where electrocardiography electrodes had been placed. From the histopathological point of view, the eruption was characterized by the presence of numerous large, atypical histiocytes in the dermis with several mitotic figures, mimicking involvement of the dermis by a malignant process.
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PMID:Histopathology of cutaneous reaction to granulocyte colony-stimulating factor: another pseudomalignancy. 987 Jun 76


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