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E Nir

Publications and source records attributed to E Nir.

At least 19 recordsLinked to original sources
PubMed1998

[Abnormal liver function tests in the primary care setting].

Results of laboratory tests ordered during a primary care encounter may reveal findings of abnormal liver function tests, including elevated liver enzymes, hyperbilirubinemia, hypoalbuminemia or abnormal coagulation tests. The object of this study was to describe the spectrum of these liver function test (LFT) abnormalities in primary care. Results of all laboratory tests ordered during 10 months in an urban primary care clinic were retrospectively reviewed and the medical charts of patients with abnormal LFTs were studied. In 217/1088 (20%) of the tests at least 1 LFT abnormality was found in 156 patients. New diagnoses were made in 104 patients. The main diagnostic groups were: non-alcoholic fatty liver changes, Gilbert's disease, acute infectious hepatitis, alcoholic liver disease and cirrhosis and hepatotoxic drug injury. In 60 patients the physician classified the abnormality as negligible and not associated with significant disease. However, an abnormal test that had been ordered for evaluation of a specific complaint, was indeed likely to represent significant disease (X2 = 29.5, p < 0.001). We conclude that finding abnormalities in liver function tests is common in the primary care clinic but does not often indicate significant liver disease.

Adolescent↗
PubMed1997

[Oral anticoagulation therapy in the primary care setting].

The use of oral anticoagulant therapy (OAT) to prevent thromboembolism has been widespread in recent years. The concept of high- and low-intensity regimens has facilitated treatment for many, and has lowered the hazards of overly intense anticoagulation. However, a significant proportion of patients suited to the low intensity regimen are not being treated. It is not clear whether its wider use is limited by continued debate, lack of resources, lack of expertise, or other causes. We retrospectively reviewed the medical records of 32 patients treated with OAT administered in the primary care setting. The average age was 66 +/- 11 years (range 34-84). 9 were treated with high-intensity OAT: 8 due to artificial heart valves, and 1 due to a hypercoagulable syndrome with recurrent thromboembolism. 23 were treated with low-intensity OAT, 17 of whom had atrial fibrillation. 11 were also being treated continuously with other medication which interacted with OAT or interfered with other coagulation pathways. Such medication included: aspirin, dipyridamole, amiodarone, bezafibrate and allopurinol. Of 414 coagulation tests, 57% and 65% were in the therapeutic range in the high- and low-intensity OAT groups, respectively. There was no major bleeding event, but in 2 of 8 who bled, gastrointestinal bleeding led to hospitalization. Treatment was discontinued in 1 patient because of difficulties in achieving target INR, and in the 2 hospitalized for bleeding. The percentages of test results in, above and below the therapeutic range were similar to those in other large series, for both intensity regimens. We found that a significant proportion of patients were under chronic treatment with other medication which interacted with OAT. To estimate the rate of complications in primary care OAT, larger series are needed. We conclude that OAT can be given and monitored by the family physician, and that awareness of long and short term drug interactions with OAT is mandatory.

Administration, Oral↗
PubMed1994

Distinct intracellular lysozyme content in normal granulocytes and monocytes: a quantitative immunoperoxidase and ultrastructural immunogold study.

Using two different immunological methods, we performed a quantitative estimation of lysozyme (LZ) in normal mature granulocytes and monocytes. An immunoperoxidase reaction for LZ in granulocytes and monocytes of 10 healthy donors measured by a scanning microdensitometer as arbitrary units showed a significantly higher LZ content in granulocytes than in monocytes. An ultrastructural immunogold reaction (IGR) for LZ performed on post-embedded thin sections showed a higher number of total gold grains in neutrophilic granulocytes than in monocytes. In monocytic granules we found a high density of gold grains per micron 2, whereas in granulocytic granules lower values were obtained. In granulocytes, LZ was found in both primary myeloperoxidase (MPO)-positive and secondary MPO-negative granules, and in monocytes the granules showed weak MPO reactivity and high LZ content. Granulocytes previously subjected to phagocytosis of bacteria and latex particles showed release of LZ on degranulation inside the phagosome, whereas in monocytes the granules remained outside the phagosome and released LZ without degranulation. Our study demonstrated a significantly higher total LZ content in granulocytes, a higher granular LZ content in monocytes, and release of LZ from intact monocyte granules during phagocytosis.

Densitometry↗
PubMed1988

Gray platelet syndrome in the elderly.

A 68-year-old male who suffered from thrombocytopenia and mild splenomegaly for 18 years was found to present agranular gray platelets on peripheral blood smear. Bone biopsy revealed a mild, diffuse, reticular fibrosis with no collagen, and electron microscopy of the platelets showed an absence of almost all the alpha-granules. Platelet thrombospondin and fibronectin analysed by SDS-polyacrylamide gel electrophoresis and Rocket immunoelectrophoresis were absent. Follow-up of 4 years showed the same parameters with no evidence of active myeloproliferative or dysmyelopoietic disorders. Hemorrhagic diathesis was limited to ecchymoses and postprostatectomy bleeding, necessitating platelet transfusion. This led us to conclude that our patient probably had a constitutional primary alpha-granule deficiency or gray platelet syndrome. This extremely rare defect has been described in less than 10 patients, all of them very young. Our observation shows that these patients may have a long, uneventful survival.

Aged↗
PubMed1987

Chediak-Higashi syndrome.

The use of cytochemical, electron microscopic, immunofluorescent, and tissue culture techniques has led to important advances in our understanding of the mechanisms underlying the pathogenesis of the Chediak-Higashi syndrome (CHS). This rare and fatal autosomal recessive disorder is clinically characterized by partial albinism, frequent pyogenic infections, and an accelerated lymphohistiocytic phase. The pathological hallmark of CHS is the presence in all white blood cells of massive lysosomal inclusions, which are formed through a combined process of fusion, cytoplasmic injury, and phagocytosis. The abnormal inclusions exhibit both azurophilic and specific granular markers, and are probably responsible for most of the impaired leukocyte and other cell functions in CHS patients. In addition, a selective profound natural killer (NK) cell function and platelet storage pool deficiencies have been described in these patients. Impaired microtubule assembly and functions, mediated by abnormal intracellular cyclic nucleotide levels, which could be corrected by treatment with ascorbic acid, were suggested to be the pathophysiological basis for CHS abnormalities. However, some recent studies have questioned this cytoskeletal model, which is suggested to be rather a secondary manifestation of CHS.

Antineoplastic Agents↗
PubMed1986

In vitro hepatitis B virus infection of human bone marrow cells.

Infection of humans with hepatitis B virus (HBV) frequently results in suppression of hematopoiesis; in some cases this may lead to severe bone marrow failure. The mechanism whereby HBV infection affects hematopoiesis is unknown. In vitro exposure of human bone marrow to HBV results in a dose-dependent inhibition of erythroid (erythroid burst forming units, BFU-E; erythroid colony-forming units CFU-E), myeloid (colony-forming units-granulocyte macrophage CFU-GM), and lymphoid (CFU-[T-lymphocytic]-TL) hematopoietic stem cells. Inactivation or immunoabsorption of HBV from sera resulted in loss of HBV-induced inhibition of hematopoietic stem cells. De novo gamma interferon was not detectable in the supernatants of cultures of bone marrow cells with HBV. Antibodies to gamma interferon did not affect the suppression of hematopoietic stem cells by HBV. Hepatitis B surface antigen (HBsAg) was detected by immune electron microscopy in nuclei of greater than 70% of immature hematopoietic cells including myeloblasts, normoblasts, and lymphoblasts; granulocytes had mostly cytoplasmic HBsAg. Hepatitis B virus core antigen (HBcAg) was also detected in about 5% of HBV infected bone marrow cells by immunoperoxidase staining. These data indicate that HBV can infect hematopoietic cells and their progenitors, thus suggesting a wider range of tropism for HBV than previously reported. These results may provide a basis to study HBV infection in vitro, and the effects of HBV on hematopoiesis.

Antilymphocyte Serum↗
PubMed1986

Chediak-Higashi syndrome. Expression of the cytoplasmic defect by in vitro cultures of bone marrow progenitors.

Studies on proliferation and differentiation of granulocyte-monocyte progenitor cells in Chediak-Higashi syndrome (CHS) were done on a 1-month-old patient, using the soft-agar bone marrow culture technique. The number of granulocyte-macrophage colony-forming cells (GM-CFC) was markedly increased, but with a normal distribution into granulocyte, macrophage, or mixed colonies. Morphologic, cytochemical, and ultrastructural studies showed that 70% of the colonies consisted of cells with giant lysosomes typical of CHS, and in the remaining 30% abnormal cells were not detected. The supply of granulocyte-macrophage colony-stimulating factor (GM-CSF) by the patient's peripheral blood leukocytes was markedly decreased. Inhibition of normal in vitro granulopoiesis by the patient's lymphocytes or serum was not demonstrated. It appears that granulocyte progenitors in CHS proliferate normally, or even in excess, probably in response to intramedullary destruction of granulocytes. The majority of the progenitors are intrinsically defective and give rise to colonies that contain the abnormality. In others the defects are unidentifiable, probably due to the immaturity of the specific fusion process of the cytoplasmic granules. The abnormal leukocytes in CHS are also defective in their capacity to provide GM-CSF, and this may account in part to the overt neutropenia. These studies demonstrate that the basic cytoplasmic abnormalities of the granulocytes and monocytes in CHS are embedded in the granulocytic-monocytic committed stem cell.

Bone Marrow↗
PubMed1985

A subpopulation of suppressor cells in Richter's syndrome with both monocytic and T-lymphocytic characteristics.

We evaluated T-lymphocyte functions in the peripheral blood of a patient with B-cell chronic lymphocytic leukemia after transformation to large cell lymphoma (Richter's syndrome). A subpopulation of E-rosette adherent cells were found with T-lymphocytic surface markers (OKT3+/8+/4+), monocytic characteristics (latex ingestion, nonspecific esterase staining), and suppressor activity. In contrast to the patient's nonadherent T-cells, this subpopulation suppressed PHA proliferation of autologous lymphocytes, pokeweed mitogen (PWM)-induced proliferation of normal non-T cells, and a mixed lymphocyte reaction. Further studies are warranted in patients with Richter's syndrome, in order to determine the frequency and significance of our findings.

Cell Adhesion↗
PubMed1985

Cellular immune functions in patients with primary hyperparathyroidism: effects of histamine and cimetidine.

The possibility of a link between parathyroid hyperfunction and cellular immune functions was studied in primary hyperparathyroid (1 degree HP) patients. The effect of cimetidine on lymphocyte functions in 1 degree HP patients and control subjects was also investigated. Histamine-induced suppressor activity of lymphocytes from 1 degree HP patients was significantly greater than that of controls. Cimetidine addition to both normal and 1 degree HP lymphocyte cultures abolished histamine-induced suppression. In vivo administration of cimetidine, while ineffective towards normal lymphocytes, depressed phytohemagglutinin stimulation of 1 degree HP lymphocytes, indicating possible immunological damage caused by this drug, which is frequently used in the treatment of patients with 1 degree HP.

Cimetidine↗
PubMed1985

Effect of N-methylisatin-beta-4':4'-diethylthiosemicarbazone on intracellular Moloney leukemia virus constituents.

N-Methylisatin-beta-4':4'-diethylthiosemicarbazone (M-IBDET) inhibits intracellular production of viral constituents in a mouse cell line, 3T3/MLV, chronically infected with Moloney leukemia virus. Electron microscopic observations confirmed that inhibition of virus production by the drug was not associated with any structural changes in the cell morphology or any damage to the plasma membrane, the site of viral assembly and 'budding'. Treatment of the cells with 17 microM M-IBDET for 6 h inhibited extracellular virus production by 80% but did not affect the level of viral RNA in the cytoplasm or in the plasma membrane. Intracellular reverse transcriptase activity and levels of viral structural proteins were significantly inhibited. Thus, although the drug did not affect viral RNA, it reduced viral protein synthesis.

Animals↗
PubMed1985

Effect of theophylline on the proportion and function of T-suppressor cells in asthmatic children.

T-cell subpopulations and their function were studied in asthmatic children with or without theophylline therapy. A decreased proportion and function of theophylline-sensitive T-suppressor cells was found in fresh peripheral blood of asthmatic children. Following peripheral blood mononuclear cells (PBMC) incubation in theophylline-free medium, the proportion of theophylline-sensitive T-cells in asthmatic children treated with theophylline was elevated to normal values. However, their suppressive effect on control lymphocyte proliferation was unchanged.

Adolescent↗
PubMed1985

Chronic T cell lymphocytosis with large granular lymphocytes of helper (OKT4) phenotype.

A 54-year-old asymptomatic male patient was followed for more than 7 y and presented a constant T cell lymphocytosis without skin involvement or bone marrow depression. No clinical or haematological aggravation was noted during this follow-up. Morphologically, the cells were large granular lymphocytes strongly positive for beta-D-glucuronidase, negative for acid phosphatase and with features of T cells on transmission and scanning electron microscopy. The immunological studies of the lymphocytes showed the following parameters: E rosettes+, mouse rosettes-, SmIg-, OKT3+, OKT4+, OKT8-, OKT6-, Ia-, TdT-, NK-, HTLV-, decreased PHA and PWM stimulation, no interleukin 2 production and failure to enhance Ig synthesis in a PWM driven system. The karyotype was normal. This case of chronic T cell lymphocytosis with large granular lymphocytes helper profile and defect of helper function, not reported in the literature, may correspond to a distinct entity in the heterogeneous group of chronic T cell disorders.

Antibodies, Monoclonal↗
PubMed1985

Behçet's disease: clinical and immunological response to immunosuppressive therapy. A case report.

A patient with Behçet's disease had recurrent bilateral uveitis with retinal exudates and visual deterioration while under intermittent corticosteroid treatment. His peripheral blood lymphocytes showed the following abnormalities: low percentage of T cells; low T cell suppressor activity; high spontaneous B cell proliferation; and high response to phytohemagglutinin. Prostaglandin-producing adherent cells were found to have suppressive activity. Chlorambucil induced a clinical and immunological remission.

Adult↗
PubMed1984

Platelet aggregation defect in megakaryoblastic leukemia.

Platelet aggregation induced in vitro with ADP, adrenalin and ristocetin was tested in 7 patients with megakaryoblastic leukemia (MKL). All patients had normal or high platelet counts and presented with hemorrhagic diathesis including purpura ecchymosis and epistaxis. Platelet morphology was grossly abnormal and electron microscopy revealed few, or absence of, alpha-granules. Platelet aggregation was reduced in all the cases with at least one aggregating agent. Our studies confirm that MKL is often accompanied by a thrombocytopathy which should be taken into account in the management of these patients.

Aged↗