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)

Two infants with lethargy, vomiting, convulsions, coma and marked metabolic acidosis were found to have very high concentrations of methylmalonic acid in their serum and urine. In vitro studies of fibroblasts demonstrated that the infants had different variants of methylmalonic acidemia.Vitamin B(12) was given in two different forms at 1 month of age and at 12 months of age. Each trial continued for 4 months but neither infant showed a clinical or biochemical response.In both infants hyperglycinemia, neutropenia and thrombocytopenia developed during acute metabolic crises only. Hypoglycemia was found in patient 2. Hyperammonemia was severe in patient 2 during acute crises but never appeared in patient 1. When clinically well, both infants continued to excrete abnormal amounts of methylmalonic acid in the urine and both had persistent compensated metabolic acidosis.Marked hyperuricemia developed in patient 1 at 18 months of age and led to progressive renal failure. Allopurinol therapy was necessary to keep the uric acid concentration within the normal range. Renal function returned to normal, as indicated by a marked increase in the renal clearance of creatinine and uric acid.Patient 1 is physically and mentally retarded, and has moderate hypotonia, hepatomegaly and persistent vomiting. Patient 2 has developed normally.The urine concentrations of methylmalonic acid in the four parents were normal.
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PMID:Methylmalonic acidemia: 6 years' clinical experience with two variants unresponsive to vitamin B12 therapy. 3 17

Plasmas from 31 patients with moderately severe to severe renal failure inhibited granulopoietic colony formation in human marrow in vitro. The inhibitory activity could not be removed by in-vitro dialysis but was present in an ultrafiltered fraction of molecular weight less than 25 000 daltons. It inhibited the production of colony-stimulating activity (C.S.A.) by leucocytes in the culture system but had little or no effect on preformed C.S.A. or on the granulopoietic colony-forming cell itself. The level of plasma inhibitory activity correlated with the degree of azotaemia but not with the neutrophil or monocyte counts. Despite the potency with which granulopoiesis was inhibited in vitro, none of the patients was severely neutropenic, and only 4 had mild neutropenia (neutrophil count 1.5--2.1 x 10(9)/1).
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PMID:Inhibitor of in-vitro granulopoiesis in plasma of patients with renal failure. 8 13

Regenerated cellulose membranes are widely used in the treatment of renal failure. The presence of hydroxyl (OH) groups on the membrane surface plays an important role in initiating complement activation and also influences thrombogenicity. The OH groups may be masked or reduced by alteration of the manufacturing process of the membrane. We have undertaken a clinical study of four cellulose-based membranes (Cuprophan, Hemophan, cellulose acetate, and cellulose triacetate) in which the hydroxyl groups of the membrane have been replaced and the magnitude of replacement has varied from less than 1% to greater than 80%, to assess the role that these modifications play in functional performance, biocompatibility (neutropenia, leukocyte activation, anaphylatoxin generation, and hypoxaemia). Our findings indicate that there does not appear to be a straightforward correlation between the numbers of hydroxyl groups replaced and modification of biocompatibility, suggesting that not all hydroxyl groups behave in a similar way.
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PMID:Cellulose-based haemodialysis membranes: biocompatibility and functional performance compared. 131 25

Dialysis efficiency, platelet and leukocyte counts, as well as malonyldialdehyde (MDA) level and lactate dehydrogenase (LDH) activity in serum were assessed in 10 patients (8 males, 2 females, aged 28-58 years) treated with repeated haemodialysis due to terminal renal failure. Patients were examined twice: during a 4-hour haemodialysis in the presence of heparin as the anticoagulant, and a week later in the course of another haemodialysis combined with infusion of heparin and prostacyclin. Statistically significant lower level of urea at the end of dialysis and significantly higher urea clearance were found during haemodialysis with prostacyclin-heparin infusion in comparison with infusion of heparin alone. As compared with the initial values obtained prior to dialysis, neutropenia and thrombocytopenia were observed during haemodialysis with heparin alone but the counts remained generally unaltered when both prostacyclin and heparin were administered. During and after haemodialysis with heparin and prostacyclin both MDA level and LDH activity were lower than in case of haemodialysis with heparin alone.
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PMID:Influence of prostacyclin infusion on haemodialysis efficiency and blood cells. 145 34

Autologous bone marrow transplantation (ABMT) is an increasingly effective treatment option for both hematologic malignancies and solid tumors. The dose-limiting toxicity of bone marrow suppression after intensive chemotherapy and/or radiation therapy can be minimized by reinfusing the patient's stored marrow. However, the ABMT procedure involves a period of profound neutropenia before the reinfused marrow engrafts and it also carries a significant risk of major organ toxicities. Common adverse effects of the procedure include mucositis, pneumonitis, renal failure, and veno-occlusive disease of the liver. In this article, Orem's Self-Care Model is used as a framework for assessing ABMT patients with the goal of recognizing developing complications early.
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PMID:Assessment of the autologous bone marrow transplant patient according to Orem's self care model. 147 87

Nine patients with progressive, metastatic disease from primary carcinoma of the colon were entered into a phase I/II study using continuous intravenous infusions of granulocyte-macrophage colony-stimulating factor (GM-CSF) and high dose melphalan (120 mg m-2). GM-CSF was given alone to six patients during the first part of the study to determine a dose that would produce a peripheral leucocyte count (WCC) greater than or equal to 50 X 10(9) 1(-1) and was initially given at 3 micrograms kg-1 day-1 and escalated to 10 micrograms kg-1 day-1 after 10 days. The infusion was discontinued when the WCC exceeded 50 X 10(9) 1(-1) and after a gap of one week, melphalan was given over 30 min. GM-CSF was recommenced 8 h later and was continued until the neutrophil count had exceeded 0.5 X 10(9) 1(-1) for greater than 1 week. One patient achieved a WCC greater than 50 X 10(9) 1(-1) with GM-CSF 3 micrograms kg-1 day-1, but the other five who entered this phase of the study required dose escalation to 10 micrograms kg-1. No toxicity attributed to GM-CSF was seen. After melphalan, the median times to severe neutropenia (less than 0.5 X 10(9) 1(-1] and thrombocytopenia (greater than 20 X 10(9) 1(-1] were 6 and 9 days respectively. The median durations of neutropenia and thrombocytopenia were 14 and 10 days respectively. All patients required intensive support with a median duration of inpatient stay of 24 days. There was one treatment related death due to renal failure. One complete and two partial remissions (33% response rate) were seen but these were of short duration (median of 10 weeks). This study demonstrates that GM-CSF given by continuous intravenous infusion produces significant increments of peripheral granulocyte counts at 3 and 10 micrograms kg-1 day-1 and is not associated with any toxicity. The duration of neutropenia and thrombocytopenia induced by high-dose melphalan appears to be reduced by the subsequent administration of GM-CSF to times which are at least as short as have been reported in historical series which have used autologous bone marrow rescue.
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PMID:Granulocyte-macrophage colony stimulating factor (GM-CSF) after high-dose melphalan in patients with advanced colon cancer. 169 72

Cuprophane membranes elict intense blood-surface interactions during clinical hemodialysis. The goal of the present studies was to determine whether calcium channel blockade may alter hemodialysis-related leukotriene B4 (LTB4) generation and neutropenia in 12 patients with end-stage renal failure. The patients were randomized to receive either placebo or nitrendipine for six weeks. Compared with untreated patients, the calcium channel blocker treatment group had significantly lower predialysis plasma LTB4 levels, Nitrendipine reduced both the magnitude of LTB4 generation and of neutropenia during the early phase of hemodialysis, but did not alter the close temporal relation of LTB4 accumulation and neutrophil activation. Therefore, the generation and release of LTB4 by neutrophils may be a calcium-dependent event. Furthermore, these results suggest that activation of neutrophil 5-lipoxygenase may contribute to the alterations in neutrophils of hemodialysis patients.
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PMID:Hemodialysis-related leukotriene B4 generation and neutropenia during calcium channel blockade. 172 50

Data from clinical trials with benazepril suggest that the safety profile of benazepril is similar to that of other angiotensin-converting enzyme (ACE) inhibitors. Treatment-related side effects occurred in 20% of benazepril-treated patients and in 18% of patients receiving placebo. The most commonly reported side effects with benazepril were headache, dizziness, and fatigue. The incidence of side effects was not affected by the degree of hypertension, age, gender, race, dosage, or the degree of renal impairment. Side effects believed to be related to the pharmacologic action of ACE inhibitors as a class include symptomatic hypotension, which occurred at a relatively low rate with benazepril, and hyperkalemia and elevation of serum creatinine, which occurred to the same extent with benazepril as has been noted with other ACE inhibitors. The mechanism of cough as an ACE inhibitor side effect is unknown; the incidence was similar to that with other ACE inhibitors. Rash and taste disturbance have occurred rarely with benazepril. The incidence of neutropenia and of proteinuria was the same in both the benazepril and placebo groups. Renal failure in hypertensive patients treated with benazepril has not been reported. Overall, benazepril is generally well tolerated by hypertensive patients. The incidence of most side effects is comparable to that with other ACE inhibitors and placebo.
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PMID:Safety profile of benazepril in essential hypertension. 189 40

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

Six cases of drug-induced toxic epidermal necrolysis treated in a burns unit are presented. The mean skin loss was 67.3 per cent of the total body surface area. Two patients developed renal failure and two had ocular symptoms. The mortality rate was 50 per cent, with two patients dying from septicaemia and one from respiratory and renal failure. The diagnosis of toxic epidermal necrolysis can be confirmed by skin biopsy. We recommend that this disease is treated in a burns unit so that both adequate wound care and essential intensive supportive treatment can be given. Antibiotics are indicated only for specific infections such as septicaemia or pneumonia. Steroids have been shown to increase greatly the mortality from septic complications and are not recommended. The mortality ranges from 10 per cent to 70 per cent and bad prognostic factors include increasing age, greater than 50 per cent of body surface skin loss and neutropenia.
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PMID:Treatment of toxic epidermal necrolysis and a review of six cases. 214 Sep 40


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