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)

A 4 7/12-year-old Caucasian female with a history of "croup-like symptoms" and persistent airway obstruction, was found to have a primary lymphosarcoma by biopsy at the time of laryngoscopy and bronchoscopy. No metastatic disease was found. After an induction course of vincristine, prednisone and local irradiation, she received CNS prophylaxis with intrathecal methotrexate and cranial irradiation. Maintenance therapy, administered over a 2 3/4 year period, consisted of cyclophosphamide, methotrexate, and 6-mercaptopurine. Excluding the diagnostic evaluation, she was hospitalized only once for the management of suspected sepsis, gastrointestinal ulceration and severe bone marrow depression. Since discontinuing treatment 27 months ago, she has remained free of disease.
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PMID:Primary lymphosarcoma of the larynx in a child. 10 77

Five patients received overdoses of vincristine ranging from 3.5 to 32 mg. Neurotoxicity accounted for most of the complications observed. Peripheral neuropathies, cranial nerve palsies, paralytic ileus, atony of the bladder, hypertension, hypotension, seizures, inappropriate ADH secretion, and severe bone marrow depression were all encountered. Two patients died within 72 hours of the overdose. Another patient died of sepsis 22 days after the overdose. Two patients recovered and were discharged. The three patients who survived longer than a few days showed improvement in the vincristine-induced neuropathy, and the two long-term survivors had essentially complete recovery. It appears that if a patient can be supported through the critical period following an overdose, he can be expected to recover normal neurologic function.
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PMID:Overdosage with vincristine. 18 48

Peritonitis in rats was produced by cecal ligation and puncture. Sixteen hours following cecal ligation and puncture, the gangrenous cecum was removed and the animals received either 4 ml saline (nontreated), 0.75 ATP-MgCl2 (100 mumoles ATP plus 50 mumoles MgCl2), and 2.0 ml of 50% glucose or 2.0 ml of 50% mannitol and 1.25 ml saline. Two hours after the removal of the cecum, RES function was evaluated by measuring the intravascular clearance of a 131 I triolein-labeled gelatinized test lipid emulsion. The intravascular half-time (t1/2) in the nontreated animals was double that of sham-operated animals, suggesting that significant depression in RES function occurred during sepsis. Administration of ATP-MgCl2 plus glucose following sepsis resulted in t1/2 values similar to those of sham-operated animals, indicating that the impairment of pagocytic activity of the RES was reversed with treatment. The beneficial effect of treatment following sepsis does not appear to be due to hypertonicity, since administration of 50% mannitol failed to decrease the t1/2. The precise mechanism of the beneficial effect of ATP-MgCl2 + glucose on restoration of RES function is not known.
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PMID:Impairment of reticuloendothelial system function with sepsis and its improvement with ATP-MgCl2 plus glucose administration. 26

Reticuloendothelial system (RES) depression has been correlated with diminished resistance to trauma, shock, and sepsis in man and animals. Previous studies have related the depression of RES hepatic Kupffer cell phagocytic function after trauma to diminished bioassayable opsonic activity. The present study determined if the loss of biological activity and RES alteration correlated with immunoreactive serum opsonic alpha 2 SB glycoprotein levels after trauma. Serum opsonic activity was measured by liver slice bioassay, and immunoreactive opsonic protein was measured by rocket electroimmunoassay. RE function was determined by colloid clearance over a 24-hour post-trauma period. Anesthetized rats (250-300 gm) subjected to sublethal or severe (greater than LD50) whole-body NCD trauma were the shock models investigated. Immunoreactive levels in 63 rats prior to injury were 518 +/- 24 microgram/ml. Neither biological nor immunoreactive levels were altered over 24 hours in anesthetized sham-traumatized controls. Temporal alteration in the initial decrease and recovery pattern of biologically active and immunoreactive opsonic protein levels significantly correlated following both sublethal and severe injury. Moreover, the patterns of immunoreactive levels of the opsonic protein correlated with the functional phagocytic activity of the RES as determined by vascular clearance of a test dose of blood-borne radiolabeled particulates. This glycoprotein falls after trauma, and the magnitude and duration of the decline increases with severity of injury. Immunoreactive opsonic alpha 2 SB glycoprotein appears to be an accurate measurement of circulating opsonic activity and RE Kupffer cell function after trauma, especially with respect to clearance. Thus, immunoreactive opsonic protein warrants clinical consideration as a noninvasive measure of reticuloendothelial systemic defense in patients after trauma and burn.
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PMID:Immunoreactive serum opsonic alpha 2 sb glycoprotein as a noninvasive index of RES systemic defense after trauma. 26 6

Numerous studies have demonstrated that reticuloendothelial system (RES) depression induced by colloid blockade increases susceptibility to circulatory shock following trauma and sepsis. Recent data have suggested that this may relate to the failure of the RES to clear potentially embolic material derived from activation of the hemostatic system. The present study thus compared the hypotensive response precipitated by trauma or sepsis with that resulting from induction of intravascular coagulation. Mean arterial blood pressure (MABP) was monitored for 120 minutes after sublethal NCD trauma and after intra-aortic injection of live E coli (approximately 10(10) organisms per rat), E coli endotoxin (0.1 mg/100 gm), or bovine thrombin (10 units/100 gm) in 400-500 gm rats 30 minutes after RE blockade (50 mg/100 gm gelatinized lipid colloid) or saline injection. All rats were anesthetized with sodium pentobarbital. No hypotension was observed in blockaded control rats. After trauma, MABP decreased by 20 minutes after injury and recovered to normal levels by 1 hour post-trauma. MABP decreased in blockaded rats after trauma and remained diminished through 2 hours. After live E coli endotoxin or thrombin, both the normal and the blockaded groups underwent an initial hypotension of similar magnitude. A second period of hypotension was much more pronounced in the RE-blockaded animals. Reduced MABP persisted in these animals through 2 hours. These data indicate that RE blockade enhances the hypotensive response to intravascular coagulation and that resulting from trauma or sepsis. This effect was especially apparent during the second phase of hypotension during sepsis and intravascular coagulation. It was suggested that the RES manifests some protective effect against the agents inducing this secondary hypotensive response.
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PMID:Effect of reticuloendothelial blockade on the development of hypotension after trauma, sepsis, and intravascular coagulation. 26 5

One of the more intriguing aspects of the spleen is the protection against certain bacterial infections afforded by its unique vascular and immune function. There have been extensive clinical surveys which indicate an incidence of overwhelming postsplenectomy infection (OPSI) above that of the disease for which the splenectomy was done. In the absence of the spleen, either congenital or subsequent to surgical removal, this overwhelming sepsis has a 50% case fatality rate. The most common infective organism has been Diplococcus (tstreptococcus) pneumoniae (D. pneumoniae). Intensive investigations indicated loss of phagocytic function of the spleen, depression of serum IgM levels, a possible suppression of the lymphocyte responsiveness, and changes in opsonin-alternative complement system as potential causes of OPSI. Preventive measures against OPSI include trials of prophylactic Phenoxymethyl Penicillin (penicillin) and pneumococcal vaccine.
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PMID:Overwhelming postsplenectomy infection. 32 70

Serial measurements of CH50, C3, C4, and factor B were performed on three newborn infants with group B streptococcal sepsis. Two of the septic infants had a colonized but noninfected identical twin. All three infants with group B streptococcal sepsis had hypotension, prolonged coagulation times, neutropenia, and respiratory failure. During the course of the sepsis, factor B was depressed 30% to 35%, C3 was depressed 40% to 60%, and CH50 was depressed by 100% when compared to their cord blood levels. Two of the infants also had a 50% to 70% depression of C4. In contrast, no significant decrease in complement levels occurred in the siblings of the twins or in two additional control infants. These data are characteristic of older patients with Gram-negative sepsis and strongly suggest that the group B Streptococcus has endotoxin-like properties.
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PMID:Complement activation and group B streptococcal infection in the newborn: similarities to endotoxin shock. 34 Oct 69

Myocardial failure is uniformly fatal when associated with post-traumatic sepsis and multisystem failure. Controversy exists as to whether endotoxin has a direct effect on the myocardium. A nonanoxic isolated arterially perfused rabbit interventricular septum was used in this study to evaluate the effects of endotoxin, live E. coli, and endotoxin/septic shock plasma on myocardial function and ultrastructure. Purified E. coli endotoxin and live E. coli bacteria did not have a significant direct effect on rabbit cardiac muscle function or ultrastructure. Perfusion of the rabbit septum with plasma from rabbits exsanguinated following a 2-hour septic or endotoxin shock insult, however, caused significant (p less than 0.02) myocardial depression when compared with control septa perfused with normal rabbit plasma. Septa perfused with shock plasma demonstrated ultrastructural alterations of mitochondria that were not noted in control preparations.
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PMID:Myocardial depression in sepsis. 36 63

Severe injury, whether the result of a major accident, a large burn, or a complicated surgical operation, often results in sepsis. Under such conditions both specific and nonspecific host defense systems are affected. The individual facets of major concern are chemotaxis, phagocytosis, intracellular killing, complement depletion, and depression of humoral and cellular mediated immunity. The most profound changes occur in cell-mediated immunity. Within a few hours o injury, the number of circulating T cells becomes depleted, concomitantly thoracic duct lymphocytes are markedly reduced. This change is not only quantitative but functional. The clinical impact of these deficient host defense mechanisms lies in the fact that low virulent organisms may become a lethal threat to the injured patient. Currently, investigators are attempting to reverse thse deficiencies through the use of immunotherapy.
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PMID:Natural host defense mechanisms. 39 70

Sera from 103 fasting individuals 3 to 76 years of age and free of clinical infectious disease and sera from 183 patients with infectious disease were assayed for serum total non-esterfied fatty acids (tNEFA) and compared. Data were also separated into five groups according to age of donor: 3--7, 8--19, 20--35, 36--60, and 61--76 years. The mean group serum levels of tNEFA increased with age. Among patients with infectious diseases sixty-five were diagnosed as having hepatitis, 41 with infectious mononucleosis, 18 with cellulitis, 12 with pulmonary tuberculosis, 11 with non-pneumococcal pneumonia, 9 with pneumococcal pneumonia, 8 with pharyngitis, 6 with pyelonephritis, 6 with aseptic meningitis, 4 with Gram-negative sepsis, and 3 with encephalitis. The sera from 23 non-fasting patients with gonorrhea were also tested. The serum tNEFA levels were found to be altered, in fact depressed from normal group values, only in patients with pneumonia or tuberculosis. This depression may be related to aberrant pulmonary metabolism during pneumonia.
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PMID:Reduced level of non-esterified fatty acids in sera from patients with infectious respiratory disease. 69 41


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