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Biomedical subjects

K C Osterhoudt

Publications and source records attributed to K C Osterhoudt.

15 recordsLinked to original sources
PubMed2000

Central anticholinergic syndrome from orphenadrine in a 3 year old.

Orphenadrine (N,N-dimethyl-2(o-methyl-alpha-phenylbenzyloxy)ethylamine) is an analog of diphenhydramine with central and peripheral anticholinergic properties. It is commonly prescribed both as a muscle relaxant and as an adjunct to antipsychotic medications to prevent parkinsonism. We report a case of orphenadrine poisoning in a 3-year-old boy following ingestion of no more than two 100-mg tablets. Central anticholinergic toxicity was prominent, manifested by hallucinations and severe agitation. Orphenadrine can cause profound toxicity in children after ingestion of small doses, and should be considered as a potential cause for acute delirium in childhood.

Child, Preschool↗
PubMed2000

Brain abscess following delayed endoscopic removal of an initially asymptomatic esophageal coin.

Brain abscesses are rare occurrences in pediatric patients, and making their diagnosis can be difficult. The two most commonly cited risk factors are otorhinologic infections and cyanotic congenital heart disease (CCHD). We present a 13-month-old child with a brain abscess who, 2 weeks prior, underwent rigid endoscopy for the extraction of a coin from the esophagus. We believe this to be the first such report of a brain abscess after rigid endoscopy for removal of an esophageal foreign body. In this case the esophageal coin was initially asymptomatic and had been present for weeks prior to removal. The potential association between delayed coin extraction and development of an intracranial infection, suggested by this report, may warrant investigation.

Brain Abscess↗
PubMed2000

Prevention of childhood lead poisoning.

Although past national public health efforts have reduced lead exposure significantly, lead poisoning remains the most common environmental health problem affecting American children. Currently, lead exposure occurs predominantly through ingestion of lead-contaminated household dust and soil in older housing containing lead-based paint; exposure can be increased with housing deterioration or renovation. Environmental prevention efforts focus on improvement in risk assessment, development of housing-based standards for lead-based paint hazards, and safe and cost-effective lead hazard remediation techniques. Educational efforts address parental awareness of lead exposure pathways, hygiene, and housekeeping measures to prevent ingestion of dust and soil. Blood lead screening is recommended either universally at ages 1 and 2 years or in a targeted manner where local health departments can document a low prevalence of elevated blood lead levels. Nutritional interventions involve provision of regular meals containing adequate amounts of calcium and iron and supplementation for iron deficiency. Lead chelation should complement environmental, nutritional, and educational interventions, when indicated. Collaboration of multiple federal agencies in a new strategy to eliminate childhood lead poisoning should further prevention efforts.

Chelation Therapy↗
PubMed1997

Catnip and the alteration of human consciousness.

Uncertainty exists regarding the ability of catnip (Nepeta cataria) to affect human consciousness. We report a case of a toddler exhibiting central nervous system depression after consuming a large quantity of catnip. His obtundation was not attributable to another cause. We review the published literature describing the alleged psychoactive capabilities of catnip and present our case as further information for use in this ongoing controversy.

Consciousness↗
PubMed1996

Lessons from the late diagnosis of isovaleric acidemia in a five-year-old boy.

Chronic, intermittent isovaleric acidemia was undiagnosed in a boy with an increased anion gap metabolic acidosis until the boy was 5 years of age. This case emphasizes the importance of maintaining a high index of suspicion for inborn errors of metabolism in patients with metabolic acidosis, even in late childhood.

Acid-Base Equilibrium↗
PubMed1995

Rebound severe methemoglobinemia from ingestion of a nitroethane artificial-fingernail remover.

We describe life-threatening methemoglobinemia in a child who ingested a nitroethane artificial-fingernail remover initially mistaken to be an acetone-based polish remover. Nitroethane-induced methemoglobinemia may be delayed and recurrent; patients ingesting this substance may warrant close observation for at least 24 hours. Care givers are cautioned to determine the precise substance involved in ingestions of potentially toxic fingernail products.

Cosmetics↗
PubMed1987

Cadmium uptake and toxicity via voltage-sensitive calcium channels.

The mechanism of cellular uptake of cadmium, a highly toxic metal ion, is not known. We have studied cadmium uptake and toxicity in an established secretory cell line, GH4C1, which has well characterized calcium channels. Nimodipine, an antagonist of voltage-sensitive calcium channels, protected cells against cadmium toxicity by increasing the LD50 for CdCl2 from 15 to 45 microM, whereas the calcium channel agonist BAY K8644 decreased the LD50. Organic calcium channel blockers of three classes protected cells from cadmium toxicity at concentrations previously shown to block high K+-induced 45Ca2+ influx and secretion. Half-maximal protective effects were obtained at 20 nM nifedipine, 4 microM verapamil, and 7 microM diltiazem. Increasing the extracellular calcium concentration from 20 microM to 10 mM also protected cells from cadmium by causing a 5-fold increase in the LD50 for CdCl2. Neither the calcium channel antagonist nimodipine nor the agonist BAY K8644 altered intracellular metallothionein concentrations, while cadmium caused a 9-20-fold increase in metallothionein over 18 h. Cadmium was a potent blocker of depolarization-stimulated 45Ca2+ uptake (IC50 = 4 microM), and the net uptake of cadmium measured with 109Cd2+ was less than 0.3% that of calcium. Although the rate of cadmium uptake was low relative to that of calcium, entry via voltage-sensitive calcium channels appeared to account for a significant portion of cadmium uptake; 109Cd2+ uptake at 30 min was increased 57% by high K+/BAY K8644, which facilitates entry through channels. Furthermore, calcium channel blockade with 100 nM nimodipine decreased total cell 109Cd2+ accumulation after 24 h by 63%. These data indicate that flux of cadmium through dihydropyridine-sensitive, voltage-sensitive calcium channels is a major mechanism for cadmium uptake by GH4C1 cells, and that pharmacologic blockade of calcium channels can afford dramatic protection against cadmium toxicity.

Animals↗
PubMed1984

Effect of cytochalasins on surfactant release from alveolar type II cells.

Cytochalasins enhanced surfactant secretion from primary cultures of [3H]choline-labeled type II epithelial cells from the rat. Cytochalasins A, B, C, D and dihydrocytochalasin B enhanced secretion of phosphatidyl-[3H]choline [(3H]PC) in a dose-dependent manner with EC50 values of 1, 2, 0.5, 0.1 and 1 microM for cytochalasins A, B, C, D and dihydrocytochalasin B, respectively. Only cytochalasin A caused significant cytotoxicity as determined by release of the intracellular enzyme lactate dehydrogenase (EC 1.1.1.17). Dose responses of surfactant release induced by cytochalasins B, C and D were biphasic; maximal release was observed between 0.1-1.0 microM for cytochalasins C and D between 1 and 10 microM for cytochalasin B. Secretion decreased toward control levels at concentrations of cytochalasin above these maximal concentrations. Increased rates of [3H]PC release were noted between 1 and 3 h after exposure to cytochalasin D. Increased rates of surfactant release induced by cytochalasin D were additive to release induced by the beta-adrenergic agonist, terbutaline, or forskolin, although cytochalasin D had no direct effect on cytosolic cyclic AMP levels. Changes in cell shape and microfilament organization were observed by phase-contrast microscopy and fluorescence microscopy using rhodamine-conjugated phalloidin after exposure of the isolated type II cells to cytochalasin D. Disruption of microfilaments associated with lamellar bodies of the purified type II cells occurred after treatment with cytochalasin D. Cytochalasin D augmented surfactant release from purified type II cells and disrupted the microfilament structure of those cells, supporting the hypothesis that alterations in microfilaments are associated with surfactant release.

Animals↗