posted July 20, 2000 04:42 PM            

E-ephedrine- is a broncial dialator - increases the amount of O2 the lungs absorb into the blood stream.

C- Caffeine- used to increase the heart reat and increase blood flow through the body.

A- Asprin- Is used to thin the blood allowing quicker absorbtion of O2, nutrients, and allowing the blood to flow more freely around the circulatory system.

This is my take on e/c/a....

posted July 23, 2000 02:50 PM         

Ephedrine is a non-selective beta agonist, which activates the beta receptors (in our case the beta-2 is what we are looking for) and also causes the release of norepinephrine from the nerve endings. Beta-2 activation on the fat cells causes the mobilization and release of fatty acids into the blood, where they can be taken up by the tissues for fuel.

Caffeine is an adenosine receptor antagonist. Caffeine binds these receptors and causes the release of norepinephrine from the nerve endings.

Aspirin inhibits the formation of prostaglandins. PGE has been shown to reduce the release of norepi from the nerve terminals, so inhibiting the formation of PGE should theoretically increase norepi release. The aspirin use has NOTHING to do with blood thinning, since there is no real change in blood viscosity with or without it.

So, from looking at what all these compounds do, we can see that the whole goal is to keep norepi levels high, which will bind the adrenergic receptors. The research has shown that ONLY the combination of ephedrine with caffeine in a 1:10 ratio shows synergism. The studies with the aspirin did NOT show any significant effect on fat loss, except in obese women. And since aspirin causes significant irritation to the GI tract, it is not a necessary compound in the formula.

posted July 23, 2000 09:33 PM         

Harefuah 1997 Jul;133(1-2):3-5, 80

[Therapeutic and toxic theophylline levels in asthma attacks--is there a need for additional theophylline]?

Zeidman A, Gardyn J, Fradin Z, Fink G, Mittelman M

Dept. of Medicine B, Rabin Medical Center, Petah Tikva.

Although first-line therapy for bronchial asthma has changed over the past decade to anti-inflammatory medication such as inhaled corticosteroids and cromolyn with possible addition of beta-agonists, theophylline is still useful and therefore widely used. However, several studies have raised serious questions regarding its efficacy in acute asthmatic exacerbations. These studies, the narrow therapeutic range of the drug, the frequency of side effects and interactions with common drugs, and individual variation in clearance and metabolism, have prompted its reevaluation in the management of asthma. Therapeutic serum levels of theophylline are between 10 to 20 mcg/ml. Most adults achieve these concentrations with daily slow-release oral theophylline preparations, 200-400 mg (approximately 10 mg/Kg) twice a day. However, when such a patient presents to the emergency room (ER) in an asthmatic attack, immediate intravenous theophylline is often given, regardless of maintenance treatment. Since the rationale for this common therapeutic approach has been challenged, the current study was undertaken. Serum theophylline levels were measured in 23 consecutive asthmatics presenting to the ER in an acute attack. 15 (68%) had therapeutic levels (above 10 mcg/ml) and 2 had toxic levels (above 20 mcg/ml), prior to receiving the standard intravenous theophylline dose given for an attack. These data indicate that most patients with bronchial asthma on oral maintenance theophylline do not require additional intravenous theophylline when in an attack. It probably will not benefit them and may even induce serious theophylline toxicity.

Schweiz Rundsch Med Prax 1996 Oct 29;85(44):1407-12

[Clinico-pharmacological case (4). Epileptic seizure as an unwanted drug effect on theophylline poisoning].

Schlienger RG, Wyser C, Ritz R, Haefeli WE

Abteilung Klinische Pharmakologie, Departement Innere Medizin, Kantonsspital Basel.

In spite of the better understanding of the pharmacokinetics and optimized galenics of oral theophylline formulations, therapy with this bronchodilator still bears risks because of its narrow therapeutic window combined with substantial inter- and intra-individual variability of theophylline metabolism. In particular, the comedication with a variety of drugs inhibiting theophylline metabolism requires consideration as a potential source of toxicity. Besides mild, self-limited adverse effects, potentially life-threatening toxic manifestations such as ventricular tachyarrhythmias, shock, and seizures can occur especially with high plasma concentrations. We report the case of a 72-year-old patient with chronic obstructive pulmonary disease who was admitted for surgical treatment of an ulcer of the foot. During combined therapy with theophylline and ciprofloxacin he developed signs of theophylline toxicity with a single episode of partial seizures. These symptoms rapidly improved with repetitive application of activated charcoal and sorbitol. Clinically relevant drug-drug interactions with theophylline and the role and mechanism of action of activated charcoal in intoxicated patients are discussed.