Patients who took 10 mg/kg of hydroxyurea every day for a year had significantly higher hemoglobin levels, and it was a well-tolerated treatment for patients who did not respond well to blood transfusions. Another hemoglobin-inducer includes thalidomide, although it has not been tested in a clinical setting. The combination of thalidomide and hydroxyurea resulted in hemoglobin levels increasing significantly in transfusion-dependent and non-transfusion dependent patients As of 2015, thalassemia occurs in about 280 million people, with about 439,000 having severe disease. It is most common among people of Greek, Italian, Middle Eastern, South Asian, and African descent. Males and females have similar rates of disease. It resulted in 16,800 deaths in 2015, down from 36,000 deaths in 1990. Those who have minor degrees of thalassemia, similar to those with sickle-cell trait, have some protection against malaria, explaining why they are more common in regions of the world where malaria exists. Signs and symptoms
Iron overload: People with thalassemia can get an overload of iron in their bodies, either from the disease itself or from frequent blood transfusions. Too much iron can result in damage to the heart, liver, and endocrine system, which includes glands that produce hormones that regulate processes throughout the body. The damage is characterized by excessive deposits of iron. Without adequate iron chelation therapy, almost all patients with beta-thalassemia accumulate potentially fatal iron levels. Infection: People with thalassemia have an increased risk of infection. This is especially true if the spleen has been removed.
Side effects
Dry mouth, urinary retention, headaches, vomiting, diarrhea, constipation, blurry vision are possible side effects of the medication. Since glycopyrronium reduces the bodys sweating ability, it can even cause hyperthermia and heat stroke in hot environments. The medication also induces drowsiness, an effect exacerbated by the consumption of alcohol. Pharmacology
Mechanism of action
Glycopyrronium competitively blocks muscarinic receptors, thus inhibiting cholinergic transmission. Pharmacokinetics
Glycopyrronium bromide affects the gastrointestinal tracts, liver and kidney but has a very limited effect on the brain and the central nervous system. In horse studies, after a single intravenous infusion, the observed tendencies of glycopyrronium followed a tri-exponential equation, by rapid disappearance from the blood followed by a prolonged terminal phase. Excretion was mainly in urine and in the form of an unchanged drug. Glycopyrronium has a relatively slow diffusion rate, and in a standard comparison to atropine, is more resistant to penetration through the blood-brain barrier and placenta. Research
It has been studied in asthma. References
External links
"Glycopyrronium bromide". Drug Information Portal. U.S. National Library of Medicine. "Glycopyrronium". Drug Information Portal. U.S. National Library of Medicine.