Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phenothiazine-induced bone marrow depression (BMD) was evaluated in three separate but complementary data bases: (1) Among 1,048 patients admitted to psychiatric hospitals, there was no evidence of subclinical depression of the white blood cell (WBC) count attributable to phenothiazines used before admission. (2) Among 18,587 medical inpatients, there were 34 patients admitted for BMD in the absence of neoplasia or prior cytotoxic drug therapy; one of the latter reported using chlorpromazine hydrochloride, but it is doubtful whether this drug was the cause of the BMD. (3) Among 24,795 medical, surgical, and gynecological patients surveyed over a ten-month period in 1972, there were four who were admitted for BMD; one of the latter had a reversible leukopenia attributed to trifluoperazine hydrochloride.
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PMID:Outpatient phenothiazine use and bone marrow depression. A report from the drug epidemiology unit and the Boston collaborative drug surveillance program. 0 Sep 78

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.
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PMID:Neutropenia associated with chrysotherapy for juvenile rheumatoid arthritis. 10 49

In the first phase of treatment of acute lymphatic leukemia in children (ALL) with aggresive cytostatic protocols, the doctor is, in some patients, forced to modify the antitumor therapy over a certain period of time because of bone marrow depression. The authors attempted to pull patients with ALL through this critical phase of the disease - by administering "profilactically" Lithium Carbonate (Li2CO3) ( in order to stimulate granulopoiesis) or, if anaemia, leukopenia and thrombocytopenia had already occurred, by administering concentrates of erythrocytes, leukocytes and platelets - without discontinuing the administration of cytostatics. The results of these attempts are reported.
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PMID:[Treatment of bone marrow aplasia in phase I of acute lymphatic leukemia treatment in children]. 12 57

Chlorozotocin was given to 37 patients with advanced malignant tumors in a daily X 5 schedule at 6-week intervals. Total iv doses for each course ranged from 75 to 200 mg/m2. Myelosuppression was dose-limiting, with a platelet count depression regularly observed at doses of greater or equal to 150 mg/m2; leukopenia occurred only at the highest dose level. Nausea and vomiting were mild and uncommon. No hyperglycemia or adverse drug-related effects on renal or hepatic function were observed. No major antitumor activity occurred; however, three patients with renal cell carcinoma and one patient each with lung cancer, ovarian carcinoma, and Hodgkin's disease had minor objective decreases in tumor size. A dose range of 150--200 mg/m2 iv for each 5-day course is recommended for phase II studies.
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PMID:Phase I trial of chlorozotocin. 15 63

An ongoing prospective study of the role of viruses in renal transplant recipients has provided identification of two patterns of cytomegalovirus (CMV) infection. In both patterns, fever and leukopenia occur within 6 months after transplant. In addition, the benign form is characterized by renal biopsy evidence of rejection and brisk Antibody responses to CMV. The lethal syndrome runs a typical 4 week course, beginning with prostration, orthostatic hypotension, mild hypoxemia and progressing to severe pulmonary and hepatic dysfunction, muscle wasting, central nervous system depression, and death. antibody responses to CMV are minimal, and renal biopsy does not show rejection despite elevation of serum creatinine. At autopsy, CMV is found in lung, liver, kidney, gastrointestinal tract, and brain. Successful management of the potentially lethal kidney, gastrointestinal tract, and brain. Successful management of the potentially lethal CMV syndrome requires rapid clinical recognition and immediate reduction of immunosuppressive therapy. future prospects for control include development of a CMV vaccine and specific antiviral chemotherapy.
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PMID:Clinical characteristics of the lethal cytomegalovirus infection following renal transplantation. 19 56

Patients receiving cytotoxic drugs are at an increased risk of bacterial infection. Drug-induced leukopenia may be responsible for depression of host defenses; however, there is little information concerning the qualitative effects, if any, of cytotoxic agents on granulocyte antibacterial activity. Since methotrexate is now being used in massive doses in vivo, we investigated the effects of this drug on antibacterial and metabolic functions of normal polymorphonuclear leukocytes in vitro. Phagocytosis, quantitative protein iodination, and staphylococcal killing of normal polymorphonuclear leukocytes were found to decrease with exposure to increasing concentrations of methotrexate. The effects of methotrexate on these cell functions were rapid in onset and readily reversed by washing the cells, suggesting a locus of action on the cell membrane rather than at the level of nucleic acid synthesis. Exposure of cells to similar concentrations of folic acid or folinic acid produced no impairment of bacterial phagocytosis, suggesting that the observed effects are specific for methotrexate. The concentrations of methotrexate that produced these impairments are readily achieved in vivo and may alter antibacterial defenses in patients receiving this therapy.
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PMID:Inhibition of human granulocyte function by methotrexate. 30 60

Preoperative folate levels were initially normal in 30 patients with gastrointestinal tract disease but fell within 48 h by 60-95% in 20 patients who received intravenous nutrition for 6-12 d with aminoacid-sorbitol-ethanol (ASE). This depression persisted in patients not given folate supplements. Folate levels in 10 control patients not given ASE showed only minimal decline. Haematological changes were reduced to a minimum in 10 patients given 0.5 mg i.v. folic acid daily whilst eight unsupplemented patients showed evidence of megaloblastic haemopoiesis. Three of these eight patients developed thrombocytopenia and/or leukopenia which was fatal in one patient.
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PMID:Acute folate deficiency associated with intravenous nutrition with aminoacid-sorbitol-ethanol: prophylaxis with intravenous folic acid. 41 77

Significant peripheral white blood cell depression was noted in 75% of postmastectomy patients receiving chest wall and nodal irradiation and in 50% of patients receiving only peripheral nodal irradiation. Leukopenia was documented for as long as 36 months following therapy. With the current trend to earlier institution of chemotherapy, the routine use of postoperative irradiation must be reevaluated.
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PMID:Leukopenia after postmastectomy irradiation. 94 94

Eighteen volunteers in tow study groups were inoculated with influenza A (H3N2) and their peripheral blood T, B and null cells enumerated at subsequent intervals. Infection with wild-type virus or with a live, attenuated virus vaccine markedly reduced the proportion and absolute number of T-cell rosettes 24 hours after inoculation. T-Cell depression preceded the onset of clinical illness in symptomatic subjects, continued during illness, and returned to normal with recovery. T-cell lymphopenia was most pronounced in volunteers infected with wild-type virus and was accompanied by an increase in null cells. Lymphocytes from six wild-virus recipients with T-cell leukopenia were incubated in vitro with a calfthymus extract (thymosin), significantly increasing the percentage of T rosettes in all six subjects (P less than 0.0001). These data indicate that influenza is accompanied by pronounced quantitative and functional changes in T cells.
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PMID:Influenza: response of T-cell lymphopenia to thymosin. 108 84

An initial clinical phase I trial of inosine dialdehyde has been carried out in 40 patients at dose levels of 30-4000 mg/m2 for 5 days given intravenously (iv) monthly. At 1.5 g/m2, noncumulative dose-related toxicity occurred in all patients which consisted of nausea and vomiting, local pain, alterations in coagulation mechanism, elevated partial thromboplastin time, and positive Coombs' test. No dose-limiting leukopenia, thrombocytopenia, anemia, or bleeding occurred; however, depression of the leukocyte and platelet counts, and decreased hemoglobin value were observed. The dose-limiting toxic effect was renal tubular damage with reversible acute renal failure in one of four patients who received 3000 mg/m2 iv for 5 days. Refractory hypercalcemia was controlled in three of three patients without tumor effect. Responses occurred in patients with seminoma, oat cell carcinoma, and melanoma. A starting dose of 2 g/m2 for 3 days monthly is recommended for phase II trials and a trial in lung carcinoma is now being conducted.
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PMID:Clinical phase I trial of inosine dialdehyde (NSC-118994). 110 41


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