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At least 19 recordsLinked to original sources

PubMed1978

Suppressor cell-mediated neutropenia in Felty's syndrome.

The mechanism of neutropenia in Felty's Syndrome (FS) was tested. The suppressor capacity of mononuclear cells from patients with FS on normal bone marrow granulopoiesis was tested by the in vitro colony forming unit in culture assay. Peripheral blood, bone marrow, and spleen cells from FS patients with marked neutropenia (less than 1,000 neutrophils/mm3) suppressed the colony forming unit in culture of normal bone marrow. Cells from rheumatoid arthritis patients without neutropenia, cells from patients with drug-induced neutropenia without rheumatoid arthritis, or plasma from FS patients failed to suppress the colony forming unit in culture. Though suppressor cells were predominantly thymus-derived (T) cells, monocytes were also effective in suppression. The suppressor efficiency of cells from the various compartments were spleen greater than bone marrow greater than peripheral blood. Splenectomy in FS transiently corrected the neutropenia and eliminated suppressor cell activity. Hyperactive suppressor cells may be responsible for the neutropenia in some patients with FS. Correction of neutropenia in these patients should be directed at modulating the suppressor cell subpopulation.

Adult↗

PubMed1979

Severe neutropenia in infectious mononucleosis.

Mild neutropenia is a well-known concomitant of infectious mononucleosis caused by the Epstein-Barr virus (EBV) occurring in the first weeks of illness. However, severe neutropenia (less than 200 polymorphonuclear leukocytes per mul) is not generally regarded as a complication of infectious mononucleosis. Three patients were seen with severe neutropenia and EBV infection, and an additional eight cases were found in the literature. In two of the latter cases the neutropenia was fatal. In the 11 cases the severe neutropenia began 14 to 40 days after illness and usually lasted for three to seven days. At the time of severe neutropenia, studies of marrow specimens showed increased proportions of promyelocytes and myelocytes. Our data suggest that EBV infection is the proximate cause of the severe neutropenia in some patients with infectious mononucleosis and that in such cases close observation and early treatment of suspected superinfections is necessary.

Adolescent↗

PubMed1978

Neutropenia associated with chrysotherapy for juvenile rheumatoid arthritis.

Severe neutropenia, in the absence of generalized bone marrow depression, is a rare complication in adults receiving chrysotherapy for rheumatoid arthritis and has not been described in children. Isolated, severe neutropenia developed in five children with systemic onset JRA while they were receiving gold injections. This potentially fatal complication occurred within eight weeks of beginning therapy in four patients, and after 24 weeks of well-tolerated therapy in the fifth. Leukopenia preceded neutropenia in two children. Localized infection was successfully treated in one child; septicemia was fatal to a second child. Neutropenia resolved within eight to 14 days of its onset in the four survivors; chelation with dimercaprol in one child did not appear to alter the recovery time. It is suggested that a systemic onset of JRA in children less than 6 years of age identifies a higher risk group developing severe neutropenia during chrysotherapy. Cessation of gold therapy upon recognition of a decreasing neutrophil count may prevent or ameliorate a developing neutropenia; careful observation for, and early treatment of, infection may alter its outcome.

Agranulocytosis↗

PubMed1979

A case of generalized amyloidosis associated with cyclic neutropenia.

A case of generalized amyloidosis associated with cyclic neutropenia is presented. A 24-yr-old female with cyclic neutropenia died from intestinal obstruction caused by necrosis and perforation of the small intestine. Post-mortem examination revealed generalized amyloidosis involving almost all organs. Amyloid deposits were prominent, especially in the alimentary tract, kidneys, spleen, and small blood vessels. As has been suggested in gray collie dogs with congenital cyclic neutropenia known to develop secondary amyloidosis in adulthood, an increase of antigenic stimulation during the intermittent bouts of acute infections may be one of the factors responsible for the development of secondary amyloidosis in this case. Although the association of amyloidosis and cyclic neutropenia in man has rarely been described, it is probable that amyloidosis is not a rare complication of human cyclic neutropenia, considering that patients with this hematologic disorder are chronically exposed to excessive antigenic stimulation.

Adult↗

PubMed1975

Cell production and cell function in human cyclic neutropenia.

In vitro studies have been done on haematopoietic cells from a patient with cyclic neutropenia characterized by severe depression of blood neutrophil levels every 21 days. Serial blood counts reveal periodic fluctuations in neutrophils, monocytes and reticulocytes. Agar culture of marrow cells shows normal concentration of colony forming cells. The percentage of colony forming cells in S phase is highly increased during profound neutropenia and normal during the recovery phase relating the granulocyte production to the peripheral neutrophil level. Studies of ingestion rate, bactericidal activity, lactate production and glucose oxidation during phagocytosis in isolated granulocytes show normal results. Also the ingestion rate in isolated monocytes is normal. Serial karyotype analyses of marrow cells during the neutrophil cycle display a normal pattern. Serum myeloperoxidase levels vary inversely with the peripheral neutrophil count indicating increased granulopoietic activity during profound neutropenia, which might be associated with non effective granulopoiesis during profound neutropenia, leading to a lack of granulocyte reserves in the marrow.

Adolescent↗

PubMed1977

Serum myeloperoxidase and lactoferrin in neutropenia.

Radioimmunosorbent assays for determination of serum content of the neutrophil proteins myeloperoxidase and lactoferrin are described. Serial studies were performed in patients with neutropenia. In 2 cases of cyclic neutropenia the myeloperoxidase level showed slight variations within the normal range during the cycle while lactoferrin displayed a clear correlation with neutrophil counts. In 1 case with persistent agranulocytosis myeloperoxidase was normal but lactoferrin was extremely low. During the regeneration phase of drug-induced neutropenia neutrophil counts and serum lactoferrin increased in a parallel fashion. Since serum myeloperoxidase was normal during profounded neutropenia it is suggested to derive primarily from myeloperoxidase-rich granulopoietic precursor cells of the marrow. Serum lactoferrin on the other hand seems to derive from leakage of more granulopoietic cells of blood and marrow. Studies of neutrophil proteins of serum may aid in evaluation of neutropenic patients.

Adolescent↗

PubMed1979

Neutropenia, inflammation, and the kinetics of transfused neutrophils in rabbits.

A rabbit model was used to study the effects of neutropenia and inflammation on the intravascular distribution, survival, and tissue accumulation of transfused neutrophils. Donor blood labeled with [(3)H]thymidine was infused into normal or neutropenic (vinblastine treated) animals. Inflammation was created by subcutaneous implantation of polyvinyl sponges, some with added endotoxin. Initial circulating neutrophil pool recovery, survival, and inflammatory site accumulation of labeled neutrophils were measured. Neutropenia was associated with a relative increase in the marginal pool size, manifested by a diminished initial circulating pool (CNP) recovery of transfused cells. The CNP recovery was directly proportional to recipient neutrophil count. Neutropenia had no effect on the intravascular survival of transfused cells and was accompanied by only a modest decrease in the inflammatory site recovery of the transfused neutrophils (10.4+/-5.4 vs. 14.4+/-4.0% in normals). Inflammation in the form of subcutaneous polyvinyl sponges was accompanied by an increase in margination with initial CNP recoveries of 24.3+/-4.7 and 27.6+/-8.8% at zero and 4 h after implantation respectively (normal, 38.2+/-9.9%). Transit through the CNP was hastened by inflammation with a t((1/2)) of 2.02+/-0.72 h (normal, 3.2+/-1.0 h). Addition of endotoxin to the sponges further perturbed cell kinetics. CNP recoveries were considerably lower and half-lifes were initially shorter and subsequently uninterpretable in studies done after endotoxin sponge insertion. Inflammatory site accumulation was markedly diminished to 7.4+/-1.9% of injected neutrophil label in the endotoxin sponge animals, suggesting that many of the transfused cells were functionally unavailable rather than marginated. These studies demonstrate that neutropenia and inflammation with or without endotoxin markedly alter the kinetics of transfused neutrophils and that CNP recovery of transfused cells is not necessarily predictive of their inflammatory site accumulation.

Agranulocytosis↗

PubMed1978

Drug-induced neutropenia in the Stockholm region 1973-75: frequency and causes.

The records of 133 patients, discharged with a diagnosis of "agranulocytosis" (i.e. blood neutrophil levels less than 1.0 x 109/1) during the years 1973-75 in the Stockholm county region, were reviewed. In 45 cases the neutropenia was probably caused by drugs other than cytostatics, giving an annual incidence of drug-induced neutropenia of 0.01%. The most common drugs were thenalidine, sulfonamides and thyreostatics. Only one of the 45 patients died during the neutropenic phase. It is concluded that the pattern of drugs causing neutropenia has changed in Sweden compared with studies from the latter half of the 1960's, and only about 40% of the cases have been reported to the authorities.

Agranulocytosis↗

PubMed1979

Idiopathic neutropenia with normocellular bone marrow: an immune-complex disease.

The presence of circulating immune-complexes (IC) and their in vivo interaction with polymorphonuclear neutrophils (PMN) have been detected in two cases of idiopathic neutropenia with normocellular bone marrow. The injection of patients' sera into New Zealand White rabbits caused a striking neutropenia due to sequestration of PMN in the vascular bed of kidneys and lungs. The kinetics of PMN disappearance from peripheral blood and the pattern of sequestration overlapped that induced by the injection of pre-formed soluble IC. Treatment with plasmapheresis caused an early and lasting increase of PMN; rabbit PMN were almost unaffected by the injection of patient serum after the course of plasmapheresis. These data are consistent with the possibility that idiopathic neutropenia with normocellular bone marrow may be caused by persistent in vivo interaction between IC and circulating PMN.

Adult↗

PubMed1979

Chronic autoimmune neutropenia due to anti-NA1 antibody.

A 12-month-old child neutropenic since the age of 8 months, was referred to our institute for a sepsis from Candida albicans. On exploring the cause of neutropenia, an anti-NA1 antibody could be detected in the patient's serum. This antibody seemed to be responsible for the neutropenia because the child's PMN type was NA1+. The reactivity of the autoantibody with the patient's own granulocytes was confirmed by direct and indirect immunofluorescence studies performed on blood and marrow cells. A reduced number of T lymphocytes with poor PHA responsivity has been interpreted as the possible cause of the autoimmune disease. Steroid therapy did not cure the neutropenia but the child's general condition improved.

Agranulocytosis↗

PubMed1979

Effect of experimental neutropenia on initial gingivitis in dogs.

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.

Agranulocytosis↗

PubMed1979

Cimetidine-induced neutropenia: a possible dose-related phenomenon.

Neutropenia associated with high-dose cimetidine therapy developed in a patient in whom earlier therapy, as well as rechallenge with low-dose cimetidine, did not result in neutropenia. As other factors cannot be implicated, a dose-related toxicity of cimetidine appears likely. Although the mechanism of cimetidine-induced neutropenia is unknown, it may involve the previously demonstrated ability of histamine H2 receptor antagonists to block the histamine-induced initiation of DNA synthesis in bone marrow stem cells.

Adult↗

PubMed1979

[Neutropenia in epilepsy patients].

Blood neutrophils were studied in epileptic patients. Differentiation of neutropenia induced by epilepsy from neutropenia due to anticonvulsants enabled one to reveal that incidence of the latter amounts to 6%. Differentiation of drug-induced neutropenia (54 observations) depending on the pathogenetic mechanism or origin (tonic and allergic), features of the blood picture and the nature of the disease course (stable, recurrent, transitory) is of special importance for diagnosis and choice of therapeutic tactics.

Adolescent↗

PubMed1979

Neutrophil kinetics in chronic neutropenia.

Quantitative studies of bone marrow neutrophil pool sizes and production rates and of blood neutrophil kinetics were performed in 16 patients with chronic neutropenia without splenomegaly. Marrow netrophil cellularity was determined from a ferrokinetic estimate of marrow normoblasts and from neutrophil-erythroid ratios determined from marrow sections. Postmitotic pool turnover was derived from the postmitotic pool size and transit time, the latter determined from 3H-thymidine neutrophil emergence time. Blood neutrophil kinetics were studied with 32P-diisopropylfluoophosphate-labeled autologous neutrophils. Mitotic pool size was basal or below basal in 12 of the 16 patients. The turnover of the post-mitotic neutrophils was subbasal in 6, basal in 7, and above basal in 3 patients. Blood neutrophil turnover was within the normal range in 8 patients and decreased in 8. The degree of ineffective granulocytopoiesis was assessed by comparing the relative size of the mitotic pool, postmitotic pool turnover, and blood turnover. On this basis, 13 of the 16 patients showed appreciable degrees of ineffective granulocytopoiesis. Ineffective neutrophil production occurred both early and late in neutrophil development. These studies indicate that most patients with chronic neutropenia without splenomegaly lack a proliferative marrow response to the neutropenia and suggest that ineffective granulocytopoiesis is a common feature of this disorder.

Adult↗

PubMed1977

Infections in patients with neutropenia.

We review published reports and our experience in regard to the causative organisms of infections in patients with neutropenia. The organisms isolated from infected patients were almost exclusively pyogenic and enteric bacteria, and our patients had no history of serious viral or fungal infections, documenting the importance of the neutrophil in normal host defense against extracellular but not intracellular pathogens. Staphylococcus aureus was the single most commonly cultured organism; however, Pseudomonas and Escherichia coli were almost as commonly isolated. Positive cultures were obtained primarily from the blood or cutaneous, subcutaneous, or deep tissue abscesses. In patients with congenital neutropenia, pneumonia, otitis media, and abscesses were the most frequent infections diagnosed clinically. There is a suggestion that recent antibiotic therapy shifted the spectrum of infecting organisms toward enteric bacteria.

Adolescent↗

PubMed1979

Marrow granulocyte reserves in black Americans. Hydrocortisone-induced granulocytosis in the "benign" neutropenia of the black.

The bone marrow granulocyte reserves of nine black patients with "benign" neutropenia were estimated by measuring the maximum neutrophil increment after the administration of hydrocortisone. Thirty control subjects, including 16 black and 14 white adults, were also studied. The mean neutrophil increment in the black patients with neutropenia was significantly less than that in the control subjects. The mean increment in the black control was also significantly less than that in the white control subjects. Four of the 16 black control subjects had neutrophil counts below 2,000/microliter; if these four are excluded from the analysis, the difference between the black and white control subjects is no longer significant. These data suggest that there is a subpopulation of healthy black adults with neutrophil counts below 2,000/microliter with reduced marrow granulocyte reserves as tested by corticosteroids. Bone marrow aspirates in four of the neutropenic patients showed normal cellularity and myeloid maturation suggesting that the lower increments are due to a difference in granulocyte release rather than to a difference in granulocyte production.

Adolescent↗

PubMed1979

Drug-induced neutropenias in the Stockholm region 1976-1977.

Previously we reviewed the incidence and causes of drug-induced neutropenia in the Stockholm region during the years 1973-75. We here present an equivalent study for the years 1976-77. The yearly incidence of drug-induced neutropenia, cytostatics excluded, remained around 0.01%. About one half of the cases were caused by sulphonamides. Among the other causes, antithyroid drugs and phenothiazines were most frequent. The mortality rate was 27%, in contrast to only 2% in our previous study. Of the seven patiets who died, 5 had taken sulphonamides.

Adolescent↗

PubMed1979

Neutrophil marrow profiles in patients with rheumatoid arthritis and neutropenia.

Neutrophil marrow cellularity was determined in 14 neutropenic patients with rheumatoid arthritis (RA) from measurements of neutrophil-normoblast ratios in marrow biopsies and ferrokinetic estimates of marrow normoblasts. A marrow profile was developed for each patient comprising the numbers of promyelocytes and myelocytes, of metamyelocytes and bands, and of segmented neutrophils in whole marrow. In each case a maturation ratio was calculated by dividing the number of metamyelocytes and bands by the number of promyelocytes and myelocytes. The physiologic marrow response to loss of neutrophils from circulation was assumed to be an increase in promyelocytes and myelocytes due to proliferation and influx, a reduction in segmented cells due to early release, and a normal maturation ratio. The results were interpreted in the light of the 95% confidence limits for data previously obtained from 13 normal subjects: in patients with neutropenia reduced or basal numbers of promyelocytes and myelocytes were interpreted as absence of the anticipated proliferative response; increased numbers of marrow segmented cells were attributed to failure of release; a low maturation ratio was assessed to reflect intramedullary cell loss. The pattern in two patients with Felty's syndrome was consistent with a physiological response to neutrophil destruction. The other 12 patients had neutrophil marrow abnormalities. Seven patients with Felty's syndrome and four patients without splenomegaly had absolute or relative hypoplasia of neutrophil marrow or low maturation ratios. One patient with a normal spleen size had an increased number of marrow segmented cells yet failed to mobilize cells normally in response to dialysis coil-activation of C3. Abnormalities of neutrophil marrow may contribute to neutropenia in RA irrespective of the presence of splenomegaly. Recognition of neutrophil marrow abnormalities in these patients may be of value in prognosis and management.

Adult↗