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At least 721 records · Page 40Linked to original sources
PubMed1988

Immunologically mediated disease of the airways after pulmonary transplantation.

Obliterative bronchiolitis has occurred in eleven of 30 recipients of cardiopulmonary allografts who survived at least 4 months after transplantation, has caused significant morbidity, and has been associated with four of eleven late deaths in this series. Although some improvement, or at least stability, of pulmonary function has followed augmented immune suppression, it appears that once the process is recognized clinically, much of the damage to the airways is irreversible. The histopathology, response to therapy, and, most important, the response of donor specific alloreactivity in the lymphocytes from the lung (bronchoalveolar lavage and peripheral blood) suggest immune- mediated basis for bronchiolitis obliterans. The presence of donor specific alloreactivity detected by primed lymphocyte testing predicted obliterative bronchiolitis in five of six recipients (83% sensitivity, 91% specificity) was absent in ten of eleven recipients who have not as yet developed the process (negative predicted value of 91%). Currently, the presence of a positive primed lymphocyte test in the bronchoalveolar lavage of the cardiopulmonary recipient is an indication for early treatment by augmented immune suppression.

Bronchiolitis Obliterans↗
PubMed2001

BAL modulates glutamate transport in synaptosomes and synaptic vesicles from rat brain.

The therapeutic use of BAL (2,3-dimercaptopropanol) as treatment for poisoning has been halted by data suggesting serious neurotoxicity. This article is a report on the effects of BAL and other dithiols, DMSA (meso-2,3-dimercaptosuccinic acid) and DMPS (2,3-dimercaptopropane-1-sulfonic acid), on [3H]glutamate release and uptake by rat brain synaptosomes and [3H]glutamate uptake by synaptic vesicles. BAL (100 microM) inhibited glutamate uptake (30%) and stimulated its basal release (30%) in synaptosomes, without affecting K+-stimulated release. BAL also inhibited glutamate uptake by synaptic vesicles (up to 60%). DMPS and DMSA (100 microM) had no significant effects on these parameters. The data reported here provide some evidence of glutamate involvement in BAL-induced neurotoxicity by demonstrating direct effects of BAL on glutamatergic system modulation.

Animals↗
PubMed1990

Oral antimony intoxications in man.

Four cases of acute oral antimony intoxication are reported. Three patients survived without sequelae. One patient, a 93-yr-old male, died from multiple organ failure. Toxicological analysis of blood, urine, and tissues revealed a severe intoxication.

Adult↗
PubMed1986

Gold-induced ileitis.

We describe a patient with rheumatoid arthritis who developed severe ileitis after being treated with gold salts; the patient responded to elimination of the gold therapy and to BAL.

Arthritis, Rheumatoid↗
PubMed1990

Polyneuropathy due to acute arsenic intoxication: biopsy studies.

A 41-year-old vintner attempting suicide ingested 8-9 g of arsenic and developed a symmetric polyneuropathy with acute Wallerian degeneration of myelinated fibers. Under treatment with modified British Anti-Lewisite (BAL; "Dimaval") his polyneuropathy slowly, but incompletely, subsided over three years at which time another sural nerve biopsy specimen showed regenerative proliferation of myelinated and unmyelinated axons but no signs of Wallerian degeneration. By laser microprobe mass analysis (LAMMA) arsenic was located in the first biopsied sural nerve specimen but not in the second specimen. These findings demonstrated: 1) arsenic induced serial morphometric and electron microscopic findings of nerve fiber degeneration and regeneration, 2) documentation of arsenic within myelinated nerve fibers, and 3) the usefulness of the LAMMA technique as a diagnostic procedure in this context.

Acute Disease↗
PubMed1993

Combined ibuprofen and monoclonal antibody to tumor necrosis factor-alpha attenuate hemodynamic dysfunction and sepsis-induced acute lung injury.

A number of key mediators are implicated in the pathophysiology of sepsis. In previous studies of a septic porcine model, ibuprofen pretreatment prevented the early but not the late rise in pulmonary vascular resistance index (PVRI) and the early but not the late fall in arterial PO2 (PaO2), whereas monoclonal antibody to tumor necrosis factor alpha (anti-TNF alpha) prevented the late but not the early rise in PVRI and the late but not the early fall in PaO2. This study examined the impact of pretreatment with combined ibuprofen and anti-TNF-alpha on the course of sepsis and acute lung injury (ALI) in pigs. Three groups were studied for 5 hours. Groups I (n = 9) and II (n = 5) received a 1-hour infusion of Pseudomonas aeruginosa. Group II received ibuprofen (12.5 mg/kg) and anti-TNF-alpha (5 mg/kg) before P. aeruginosa, and a further bolus of ibuprofen at 120 minutes. Group III (n = 11) received sterile saline. Group I demonstrated a significant (p < 0.05) rise in plasma TNF-alpha that was abolished in group II. The SVRI in group II did not change significantly from baseline through the study and the SVRI rose sharply in group I following onset of the infusion of P. aeruginosa, as did PVRI. There was no significant change in PVRI from baseline in group II, except for the final 60 minutes; PVRI in group II was significantly less than in group I throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Correlation of the local and systemic cytokine response with clinical outcome following thermal injury.

Eighty-eight patients with acute thermal injury were evaluated. Forty-eight hours after injury, TNF, IL-6, and IL-8 were significantly present in the systemic circulation, lung, normal skin, and thermally injured skin. The presence of TNF, IL-6, and IL-8 proteins in the lung, normal skin, and thermally injured skin were associated with TNF, IL-6, and IL-8 mRNA upregulation. Logistic regression analysis controlling for the Abbreviated Burn Severity Index demonstrated that the presence of IL-8 in the lung was associated with early pulmonary physiologic dysfunction (p = 0.006) and nosocomial pulmonary infection (p = 0.040). We conclude that acute thermal injury initiates an early systemic, lung, and skin response involving TNF, IL-6, and IL-8. The TNF, IL-6, and IL-8 protein present in the lung and skin in response to acute thermal injury are generated locally and do not originate from the systemic cytokine pool. The lung cytokine response to acute thermal injury may initiate local organ failure.

Adult↗
PubMed1975

Chelation therapy in lead nephropathy.

Although treatment has been well defined for childhood lead poisoning and for industrial lead exposure, the treatment of lead nephropathy has been poorly studied. The available chelating agents are reviewed and the results of treatment in 17 cases of lead nephropathy are shown. It is concluded that lead nephropathy should be recognized early and treated energetically, as this may stabilize or improve renal function. Since EDTA is excreted much like creatinine, the dosage must be reduced proportionately in response to elevated serum creatinine levels in the patient with renal failure.

Acute Kidney Injury↗
PubMed1989

Fatal cardiac arrhythmia in a patient with interstitial myocarditis related to chronic arsenic poisoning.

We have reported the case of a 42-year-old man exposed to arsenic at least three times over a ten-month period from an agricultural source. He showed classical symptoms and signs of arsenic poisoning. During chelation therapy and apparent recovery from the poisoning, he suddenly and unexpectedly died; postmortem examination revealed a myocarditis similar to that reported previously. The case demonstrates the need for electrocardiographic monitoring of all patients with arsenic poisoning, during both the initial phase of the illness and convalescence.

Adult↗
PubMed1991

Massive acute arsenic poisoning.

A 28-year-old male ingested 75 g of arsenic trioxide in a successful suicide attempt. The presentation, management and postmortem findings are presented and discussed.

Acute Disease↗
PubMed1994

Platelet shape change and Ca2+ mobilization induced by collagen, but not thrombin or ADP, are inhibited by phenylarsine oxide.

In this report we have examined the effects of the protein tyrosine phosphatase inhibitor phenylarsine oxide (PAO) on receptor-mediated platelet shape change, secretion and aggregation. PAO was found to inhibit platelet aggregation induced by collagen, thrombin, ADP and epinephrine at IC50 values of 0.35 mumol/l, 2.5 mumol/l, 0.2 mumol/l and 0.3 mumol/l, respectively. Agonist-induced secretion of ATP was inhibited at similar or lower concentrations of PAO. The specificity of the interaction of PAO with platelet proteins was demonstrated by the ability of the disulfhydryl compound 2,3-dimercaptopropanol, which abstracts PAO from proteins to form a stable cyclic adduct, to reverse PAO inhibition of both agonist-induced platelet secretion and aggregation. Dimercaptopropanesulphonic acid, a membrane-impermeable analogue of dimercaptopropanol, did not reverse inhibition of collagen-induced shape change or aggregation by PAO, thereby demonstrating that PAO acted intracellularly. PAO inhibited collagen-induced shape change and internal Ca2+ mobilization but had no effect on these two phenomena when induced by thrombin or ADP. PAO was also unable to prevent arachidonic acid-induced shape change, indicating that PAO acts at a site prior to the phospholipase A2-mediated release of arachidonic acid to inhibit collagen-induced shape change. PAO induced the accumulation of a number of phosphotyrosine-containing proteins and inhibited the collagen-induced phosphorylation of a 40 kD protein. The potency and agonist-specific effects of PAO on platelet activation suggest that this inhibitor will be of value in elucidation of signal transduction pathways involved in receptor-mediated platelet function.

Adenosine Diphosphate↗