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 role of neutrophilic granulocytes in the loss of gingival collagen has been studied by inducing experimental neutropenia during initial gingivitis in beagle dogs. Neutropenia was induced for 4 d in three animals with normal gingiva by repeated injections of rabbit anti-neutrophil serum. During neutropenia microbial plaque was allowed to form on the teeth. Samples of junctional (crevicular) leukocytes and gingival fluid were taken on days 0 and 4. Block biopsies of buccal gingiva were obtained on day 4. Stained semi- and ultrathin sections were used for histometric and stereologic tissue analysis. Gingival fluid flow increased from day 0 to day 4 in all dogs while junctional leukocytes increased in one dog only. Subgingival plaque had formed in most biopsies, and in the junctional epithelium very few neutrophilic granulocytes were present. In the coronal connective tissue subjacent to the junctional epithelium lymphoid cells, structurally abnormal neutrophilic granulocytes and monocytes/macrophages were diffusely scattered. The gingival collagen appeared mainly displaced by the inflammatory cells rather than dissolved. The data suggest that neutrophilic granulocytes may contribute to the loss of gingival collagen during initial gingivitis in dogs. The neutrophils also seem to be of importance for the limitation of subgingival plaque growth along the tooth surface.
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PMID:Effect of experimental neutropenia on initial gingivitis in dogs. 37 Sep 65

Multiple infections and severe neutropenia were found in a previously healthy 29 year old man with no history of similar syndromes in the family, drug ingestion or exposure to environmental toxins. There was no evidence at the time of presentation of diseases previously associated with agranulocytosis (e.g., neoplasia, thyrotoxicosis, chronic infection, collagen-vascular disease or leukoagglutinating antibody). His serum contained a nonagglutinating, complement-dependent, cytotoxic antibody, however, reactive with peripheral blood granulocytes from 35 per cent of normal donors. The neutropenia was not affected by steroids but resolved promptly after splenectomy. Microscopic examination of the spleen revealed ingestion of polymorphonuclear leukocytes by splenic macrophages. Family studies indicated that the target antigen was non-HLA and that the antibody was not absorbed by lymphocytes or platelets. We conclude that the agranulocytosis was autoimmune in origin and suggest that similar myeloid-specific immune responses could influence granulocyte tranfusion and bone marrow transplantation by alloimmune "rejection" that would not be avoided by matching only for HLA specificities.
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PMID:Acquired agranulocytosis with granulocyte specific cytotoxic autoantibody. 44 60

Sera from two patients with granulocytopenia associated with collagen vascular disease caused the destruction of normal human granulocytes by autologous lymphocytes in vitro. Granulocyte cytotoxicity was measured by the release of 51Cr during incubation with test sera and lymphocytes in microtiter plates. Between 8% and 46% granulocytoxicity was produced in granulocytes from 8 normal donors by the sera from these two patients. Less than 6% granulocytotoxicity was seen with the sera from 14 normal subjects and 29 patient controls. Treatment of lymphocyte preparations with carbonyl iron and magnetic separation to remove phagocytic cells or treatment with complement-coated red cells followed by repeated gradient centrifugation to remove complement receptor-bearing lymphocytes did not reduce the granulocytotoxicity. There was a dose-response relationship between the concentration of positive sera and granulocytotoxicity. When these sera were fractionated by Sephadex G-200 gel filtration and by ion-exchange chromatography with DEAE-cellulose, the active component appeared in the IgG-containing fractions. Thus, IgG antibody-dependent, lymphocyte-mediated granulocyte cytotoxicity represents a means of detecting human granulocyte antibodies and is a possible mechanism of autoimmune neutropenia in these two patients.
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PMID:Antibody-dependent lymphocyte-mediated granulocyte cytotoxicity in man. 61 59

Eighteen immuno-compromised children (malignancies, hematological diseases, collagen diseases) with neutropenia and infections were treated with imipenem/cilastatin sodium (IPM/CS), and the efficacy and the safety of the drug were evaluated. 1. Responses to IPM/CS were excellent in 13 patients, good in 1, and fair in 4. None of the patients displayed a poor response to the treatment thus the efficacy rate was 77.8%. 2. Of 5 patients with sepsis, 4 had excellent or good responses. IPM/CS was effective against sepsis caused by Enterococcus faecalis and Pseudomonas aeruginosa. 3. In patients with severe neutropenia (WBC less than 100/mm3), the efficacy rate was 70%. 4. As for side effects, elevations of GOT and GPT were observed in 1 patient with liver cirrhosis. These results indicate that IPM/CS is safe and effective in immuno-compromised children with neutropenia and infections.
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PMID:[Clinical evaluation of imipenem/cilastatin sodium against infections in compromised children (malignancy, hematological disease, collagen disease)]. 143 90

The angiotensin converting enzyme (ACE) inhibitors are a group of effective drugs with a unique mechanism of action. These drugs have proven to be useful for hypertension and congestive heart failure. Early clinical trials of captopril used doses that are now known to be inappropriately high, and dose-related adverse effects were observed frequently. The recognition that lower doses are effective has reduced the incidence of adverse reactions and resulted in improved patient tolerance. When patients are properly selected and correctable risk factors are removed, serious side effects are uncommon. Unfortunately, the early reputation of nephrotoxicity persists, as does the belief that significant blood dyscrasias, endocrine effects and rash are serious risks for the average patient. After wide use of captopril, enalapril and lisinopril, and investigational trials of nearly a dozen newer agents, a sufficiency of clinical observation, experimental evidence and accurate postmarketing recording of events is accumulating to allow insight into the major toxicities with regard to more intelligent patient selection, more rational dosing and proper identification of risk factors. The most common adverse reactions are cough and skin rash. It appears that the agents are generally not cross-reactive with regard to skin rash, although it is not clear whether this effect is drug-specific or class-specific with regard to cough. Statistically but not clinically significant lowering of haemoglobin and hematocrit is common; these effects are inconsequential in most patients. Neutropenia, once thought to be prevalent, now appears to be so only in patients with autoimmune or collagen-vascular disease; the majority of patients outside these groups are at low risk. Hyperkalaemia is a frequent occurrence. This should not be surprising in view of the effect of the ACE inhibitors on plasma aldosterone. When dietary potassium intake is regulated and sources of altered potassium excretion are identified, hyperkalaemia is seldom a serious problem. Identification of sodium and water deficits allows correction before the drugs are started, and the frequency of hypotension and hyperkalaemia caused by the drugs is quite low if these factors are properly managed. An unexpected finding emerging in recent years is the dry cough associated with ACE inhibitor therapy. Its mechanism is not definitely known. Nonsteroidal anti-inflammatory drugs may control this symptom in some patients. The frequent observation of proteinuria in patients taking ACE inhibitors has gained notice and sometimes caused undue alarm. It is difficult to separate disease effects in diabetes and hypertension from true drug effects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adverse effects of angiotensin converting enzyme (ACE) inhibitors. An update. 153 95

We evaluated the effect of neutropenia or administration of a serine proteinase inhibitor on the early suture-holding capacity of intestinal anastomoses in rats. One group of rats was treated with antineutrophil serum, and another group received the soybean trypsin inhibitor. Controls received inactivated serum or saline. Anastomotic suture-holding capacity (breaking strength), myeloperoxidase activity, and collagen were measured 0 and 72 hours after surgery. Suture-holding capacity decreased by 70% in controls and 35% in soybean trypsin inhibitor-treated rats, but remained on level with immediate postoperative strength in neutropenic rats, where low myeloperoxidase levels reflected effective wound margin neutropenia. Collagen content and solubility were similar in all groups. These findings indicate that reduction in early wound margin strength is neutrophil dependent, and that neutrophil serine proteinases are important mediators in that process.
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PMID:Neutrophil-dependent decrease in early wound margin strength. 159 78

Canine cyclic hematopoiesis (CH) is an autosomal recessive disease of gray collie dogs that is characterized by 14-day cycles of neutropenia, monocytosis, thrombocytosis, and reticulocytosis. Platelets from CH dogs have decreased dense-granule serotonin pools and decreased aggregation responses to collagen, platelet-activating factor (PAF), and thrombin. Recombinant granulocyte colony-stimulating factor (rG-CSF) was administered (5 micrograms/kg, b.i.d.) to four CH and six normal dogs to determine if G-CSF therapy corrected qualitative platelet defects in CH dogs. Neutrophil counts increase to greater than 25,000 cells/microliters within 24 h after starting treatment in all dogs. Treatment with G-CSF blocked neutropenic episodes in the CH dogs. Platelet aggregation, and serotonin content and secretion were significantly (p less than 0.05) decreased in the CH dogs both before and during recombinant human (rh) G-CSF treatment compared to normal dogs. Neutrophil myeloperoxidase, a primary granule enzyme, was significantly (p less than 0.05) decreased in CH dogs and was not corrected by rhG-CSF treatment. Administration of rG-CSF to CH dogs eliminated cell cycles but apparently did not correct cellular defects in CH dogs. Identification of primary biochemical defects in cells from CH dogs may be crucial to investigating the biochemical basis for cyclic hematopoiesis.
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PMID:Effects of recombinant granulocyte colony-stimulating factor treatment on hematopoietic cycles and cellular defects associated with canine cyclic hematopoiesis. 169 76

The case survey of drug-induced hematologic disorders in Shikoku District (Ehime Prefecture) disclosed 21 patients. Cases were 12 rheumatoid arthritis patients, 2 brain tumor, one epilepsy, 2 liver cirrhosis, one neuralgia, one arthralgia, one hyperthyroidism, and one IBL-like T-lymphoma. Causative drugs for aplastic anemia were Metalcaptase, Shiosol, Voltaren and Emeside. Drug-induced aplastic anemia was so severe that 4 out of 5 patients had died of bone marrow dysfunction. Neutropenia was caused by drugs as Rimatil, Cefobit, Sepatren, Mercazole, Sulpyrin, Aleviatin, Cefamedin and Metalcaptase. The real causes of these drug-induced hematologic disorders have not been clear. Remarkably high incidence among rheumatoid arthritis patients is suggestive several reasons as unique reactivity associated with HLA, suppression on hematologic stem cells by abnormal metabolites, and immunologic dysfunction commonly seen in collagen diseases. Further studies of more accurate incidence of drug-induced hematologic disorders are needed in investigating real causes of unhappy side-effects.
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PMID:[Drug-induced hematologic disorders in Shikoku district]. 192 Aug 31

Three cases of captopril-associated neutropenia are described, which illustrate the clinical presentation, variable predisposing factors and outcome of this rare but potentially serious adverse event. Particular risk factors of renal failure and collagen vascular disease were present in only 1 patient, while a second patient had reversible mild renal impairment. The doses of captopril used ranged from 25 mg to 50 mg 3 times a day. Two patients recovered after withdrawal of the drug but the third died of septicaemia. Captopril-associated agranulocytosis is reviewed.
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PMID:Captopril-associated agranulocytosis. A report of 3 cases. 201 67

Hematologic abnormalities are common in association with collagen diseases, specially Systemic Lupus Erythematosus and include anemia, neutropenia, thrombocytopenia with alterations in lymphocyte subpopulations. On the other hand, patients with unexplained fibrosis of the bone marrow (the syndrome of idiopathic myelofibrosis or primary myelofibrosis) have clinical and laboratory evidence of immunologic dysfunction. Clinical findings include the presence of arthritis, vasculitis and erythema nodosum. Laboratory abnormalities include the presence of circulating immune complexes, antinuclear antibodies, positive direct Coombs test, elevated latex fixation and a circulating lupus type anticoagulant. Total hemolytic complement markedly depressed has also been reported. These data suggest that immunologic mechanisms associated with activation of the complement system play an important role in the disease process of some patients with agnogenic myeloid metaplasia with myelofibrosis. A review of the literature revealed that myelofibrosis occurring in the setting of collagen diseases is rare. However, a role for immunologic factors in the pathogenesis of myelofibrosis is also supported by the patients with coincident well defined collagen disease and myelofibrosis. In this report, we present two patients with such an association. Case 1 was a 58-year-old male with a two year duration history of rheumatic arthritis. He had bone erosions on hands, splenomegaly and myelofibrosis. Rheumatoid factor (latex) was positive: 1:2560. He had positive LE cells and hypocomplementemia: 37 CH50/ml (NV 70-150). The patient did not meet criteria for SLE. Case 2 was a 36-year-old female admitted because of dyspnea and fever. Diagnosis of myeloid metaplasia with myelofibrosis and progressive systemic sclerosis had been made four years before hand.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Coexistence of myelofibrosis and collagen diseases]. 213 Feb 12


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