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J W Donovan

Publications and source records attributed to J W Donovan.

At least 19 recordsLinked to original sources
PubMed1992

Whole-bowel irrigation as adjunctive treatment for sustained-release theophylline overdose.

STUDY OBJECTIVE: To determine a therapeutic benefit for whole-bowel irrigation (with polyethylene glycol-electrolyte lavage solution) as adjunctive treatment to multiple doses of activated charcoal following an overdose of sustained-release theophylline. DESIGN: Randomized crossover study. Three treatment arms were separated by one-week intervals. SETTING: Animal care facility housing. TYPE OF PARTICIPANTS: Eight female mongrel dogs. INTERVENTIONS: Unanesthetized dogs were given approximately 75 mg/kg of sustained-release theophylline. In treatment arm 1, 1 g/kg activated charcoal was administered by nasogastric tube at two hours after ingestion followed by 0.5-g/kg doses at five and eight hours. During treatment arm 2, beginning two hours after theophylline ingestion, 25 mL/kg whole-bowel irrigation solution was administered every 45 minutes for four doses followed by activated charcoal. In treatment arm 3, the first dose of activated charcoal was given ten minutes before beginning the whole-bowel irrigation protocol. MEASUREMENTS AND MAIN RESULTS: Serum theophylline levels were measured at zero, two, four, five, eight, 12, 16, and 24 hours after ingestion. Mean serum theophylline levels, area under the curve (P = .13), and terminal half-lives (P = .69) for each treatment group were not statistically different. This negative study had an 81% power to detect a 50% reduction in the area under the curve by whole-bowel irrigation treatment. CONCLUSION: In this model, whole-bowel irrigation did not add to the therapeutic benefits of activated charcoal.

Animals↗
PubMed1991

Inconsistencies in statistics of deaths from AIDS.

From 1983 to 1988 there were 396 registrations of death certified as caused by immunodeficiencies including the acquired immunodeficiency syndrome (AIDS). Detailed examination of other death registration data yields an estimate of 692 deaths in this period from AIDS and its sequelae. Over the same period, 617 notified AIDS patients are known to have died. The data sources can be reasonably closely reconciled for the years 1983 to 1987, but there is an unexplained shortfall in reporting of deaths of notified AIDS patients in 1988. A study which matches notifications and death registrations for the same individuals is needed to explain these findings, which have implications for statistics of survival times in AIDS and for estimates of the size of the epidemic.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Intravenous N-acetylcysteine, hepatotoxicity and plasma glutathione S-transferase in patients with paracetamol overdosage.

The concentration of glutathione S-transferase B1 (GST B1) subunits was measured in sequential plasma samples taken at frequent intervals for 48 h from ten patients with severe paracetamol poisoning who were treated with intravenous N-acetylcysteine. No significant increase in plasma GST B1 concentration was observed over the study period and with 4 h of starting treatment with N-acetylcysteine there were significant decreases in plasma GST B1 concentrations. None of the patients subsequently developed significant liver damage. At the dose used for the treatment of paracetamol poisoning, N-acetylcysteine has no hepatotoxic effects.

Acetaminophen↗
PubMed1989

The disposition and kinetics of intravenous N-acetylcysteine in patients with paracetamol overdosage.

Seventeen patients received standard treatment with intravenous N-acetylcysteine for 18 episodes of severe poisoning with paracetamol (acetaminophen). The dose of N-acetylcysteine was 150 mg/kg given in 15 min followed by 50 mg/kg in 4 h and 100 mg/kg over the next 16 h. Liver damage was absent or mild on 13 occasions (ALT greater than 500 mu/l) and severe on 5 (ALT less than 1000 mu/l). Total plasma N-acetylcysteine was estimated by HPLC. The mean maximum plasma concentration after the initial loading dose was 554 mg/l. Concentrations then fell rapidly and after 12 h a mean steady-state level of about 35 mg/l was maintained. When the infusion was discontinued N-acetylcysteine disappeared with a half-life of 5.7 h. The mean steady-state volume of distribution, AUC, mean residence time and total clearance were 536 ml/kg, 1748 mg.h.l-1, 2.91 h and 3.18 ml.min-1.kg-1. These values are generally consistent with those previously reported with much smaller doses and the disposition of N-acetylcysteine does not appear to be dose-dependent. The elimination of N-acetylcysteine was not impaired in the patients with severe liver damage, and the pharmacokinetic variables and plasma concentrations were similar in patients with and without hepatotoxicity. The dosage schedule for intravenous N-acetylcysteine should probably be modified since adverse reactions invariably occur early when plasma concentrations are at their highest, and liver damage was prevented just as effectively at the lowest as at the highest Cmax. High initial concentrations of N-acetylcysteine can be avoided with simple alternative regimens based on the kinetic data of this study.

Acetaminophen↗
PubMed1989

Plasma glutathione S-transferase and F protein are more sensitive than alanine aminotransferase as markers of paracetamol (acetaminophen)-induced liver damage.

Concentrations of glutathione S-transferase (GST; glutathione transferase; EC 2.5.1.18) B1 subunits, F protein, and the activity of alanine aminotransferase (ALT; EC 2.6.1.2) were measured in sequential plasma samples taken from nine patients with self-administered paracetamol (acetaminophen) poisoning. GST exceeded the reference interval in all patients at the time of admission, and F protein was increased in seven. In contrast, abnormal activities of ALT in plasma were found in only one of the nine on admission, a patient admitted 12 h after poisoning. Subsequent to admission nine, eight, and five patients, respectively, had abnormal concentrations of GST, F protein, and ALT. When expressed as multiples of the upper reference limit, the highest values for GST measured in each patient always far exceeded the greatest abnormalities in ALT; this was true for F protein in only five patients. Patients in whom the concentration of GST exceeded 10 micrograms/L on admission subsequently went on to develop moderate or severe liver damage, despite treatment with N-acetylcysteine. F protein and ALT measurements on admission were not as efficient as GST at predicting the clinical outcome of the patients. We conclude that GST and F protein offer clear advantages over ALT for detecting minor degrees of acute liver dysfunction, particularly when only centrilobular damage may be involved.

Acetaminophen↗
PubMed1986

Attending coverage.

Explore the source record for details and available documents.

Emergency Medicine↗
PubMed1986

Significant envenomation from a preserved rattlesnake head (in a patient with a history of immediate hypersensitivity to antivenin).

We present a case of significant envenomation from a severed, preserved rattlesnake head in a 22-year-old man. The patient was treated successfully with 15 vials of Crotalidae polyvalent antivenin despite a history of severe immediate hypersensitivity reaction to antivenin. The patient developed a mild case of serum sickness five days after antivenin infusion that was treated successfully with a course of steroids. The patient experienced complete recovery. This case demonstrates the hazard of even preserved snake heads and fangs.

Administration, Oral↗
PubMed1985

Clotting of fibrinogen. 1. Scanning calorimetric study of the effect of calcium.

The denaturation temperature Td and the enthalpy of thermal denaturation delta Hd of the D nodules of fibrinogen increase 12-13 degrees C and 40%, respectively, when fibrinogen is clotted by thrombin in the presence of 10(-3) M calcium ion. The rate of change of Td and delta Hd is first order in thrombin concentration. In the absence of calcium, little change in Td is observed, but the increase in delta Hd still occurs. The shift in Td as a function of logarithm of calcium concentration is sigmoid, with a half-point at 2.5 X 10(-5) M calcium for human and 6.0 X 10(-5) M calcium for bovine fibrinogens, suggesting that the shift is due to binding of calcium at the high-affinity binding sites of fibrin. The Td of the D nodule of native fibrinogen also increases, but not as much, on addition of calcium. This increase in Td is also sigmoid with log calcium, with a half-point of 1.6 X 10(-3) M calcium for human and 3.2 X 10(-3) M calcium for bovine fibrinogens, and appears to be due to binding of calcium to the low-affinity binding sites of fibrinogen. At calcium concentrations greater than 10(-4) M, traces of factor XIII in the bovine fibrinogen preparation become activated and cause cross-linking of the fibrin gel. But the changes in Td and delta Hd still occur when factor XIIIa is inactivated by iodoacetamide, and the rate of the changes is not altered by addition of large amounts of factor XIIIa.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Clotting of fibrinogen. 2. Calorimetry of the reversal of the effect of calcium on clotting with thrombin and with ancrod.

When clotting is effected by thrombin in the presence of calcium, the endotherm for the D nodules of fibrinogen broadens significantly and then becomes narrow again, while increasing in size. Clotting effected by the snake venom enzyme Ancrod, which releases only the A fibrinopeptides from the E nodule, shows only the broadening of the D endotherm. Accordingly, significant interactions of the D nodules of fibrinogen become possible only when the B fibrinopeptides of the E nodule are released on clotting. When calcium present during clotting is removed from the fibrin clot with ethylenediaminetetraacetic acid, the endotherm for the D nodules of fibrin shows nearly complete reversal if clotting was effected with Ancrod but appears to be divided into two endotherms if clotting was effected with thrombin. At neutral pH, new endotherms were observed for fibrinogen in the temperature range 105-140 degrees C.

Ancrod↗