Muscle spasm associated with therapeutic use of Cang Er Zi Wan.

INTRODUCTION: Cang Er Zi Wan (CEZW) is a herbal medication derived from Xanthium sibiricum that is used to treat allergies and upper respiratory problems. Its toxicity has been described in grazing animals, in experimental studies, and in human overdoses. We describe a case of muscular spasm that was associated with the therapeutic use of CEZW. CASE REPORT: A 17-year-old female was prescribed CEZW for chronic allergies. Shortly after her second dose of 10 pills BID, she developed intermittent muscular spasms. She was seen in an Emergency Department and had normal vital signs and no significant laboratory abnormalities. Her physical exam was significant only for intermittent spasm of the muscles of the face, neck, and upper extremities. No tremor, fasciculation, dystonia, akisthisia, chorea, bradykinesia, or clonus was noted. She discontinued the CEZW and the symptoms slowly decreased over 4 days. Testing of the product did not detect any other medications or drugs. DISCUSSION: CEZW is a herbal medication that contains X. sibiricum. X. sibiricum is a widespread weed that has caused muscular spasm, seizures, and death in animals that graze on it as well as animals experimentally exposed to it. Eleven cases of accidental human ingestion of Xanthium leading to spasm, somnolence, hypoglycemia, renal, and liver toxicity have been described. We describe a unique case of isolated muscular spasms because of the therapeutic use of a CEZW product.

Poison hemlock-induced respiratory failure in a toddler.

The ingestion of poison hemlock, or Conium maculatum, is described in a 2-year-old boy. He had the onset of abdominal pain and weakness after being fed C. maculatum picked by his sister from the roadside 2 hours earlier. He had a rapidly progressive muscular weakness and was intubated for respiratory failure. His symptoms completely resolved within 24 hours of the ingestion. Conium maculatum is a common weed that causes toxicity by its primary toxin, coniine, which stimulates nicotinic receptors and causes a syndrome of rapidly progressive muscle weakness and paralysis. We describe the course of a benign-appearing plant ingestion resulting in respiratory failure.

Interactions of flavones and other phytochemicals with adenosine receptors.

Dietary flavonoids have varied effects on animal cells, such as inhibition of platelet binding and aggregation, inhibition of inflammation, and anticancer properties, but the mechanisms of these effects remain largely unexplained. Adenosine receptors are involved in the homeostasis of the immune, cardiovascular, and central nervous systems, and adenosine agonists/antagonists exert many similar effects. The affinity of flavonoids and other phytochemicals to adenosine receptors suggests that a wide range of natural substances in the diet may potentially block the effects of endogenous adenosine. We used competitive radioligand binding assays to screen flavonoid libraries for affinity and a computational CoMFA analysis of flavonoids to compare steric and electrostatic requirements for ligand recognition at three subtypes of adenosine receptors. Flavone derivatives, such as galangin, were found to bind to three subtypes of adenosine receptors in the microM range. Pentamethylmorin (Ki 2.65 microM) was 14- to 17-fold selective for human A3 receptors than for A1 and A2A receptors. An isoflavone, genistein, was found to bind to A1 receptors. Aurones, such as hispidol (Ki 350 nM) are selective A1 receptor antagonists, and, like genistein, are present in soy. The flavones, chemically optimized for receptor binding, have led to the antagonist, MRS 1067 (3,6-dichloro-2'-(isopropoxy)4'-methylflavone), which is 200-fold more selective for human A3 than A1 receptors. Adenosine receptor antagonism, therefore, may be important in the spectrum of biological activities reported for the flavonoids.