The discovery that women with PMS have low serotonin levels in the brain has led doctors to try drugs which raise serotonin. These drugs are known collectively as antidepressants. The best known is Prozac (chemical name fluoxetine).
One of the first studies of Prozac in PMS looked at 21 women with premenstrual depression. They took Prozac or a dummy pill for three months. After that they swapped treatments. None of the women, or the doctors treating them, knew which drugs each woman was taking until after the study had finished.
There was a striking reduction in symptoms in the women taking Prozac compared with those on placebo. Symptoms quickly returned in the majority of women once the Prozac therapy had ended.
The New Zealand researchers who conducted the study said that the work had supported the theory that PMS was in part caused by low serotonin in the brain as well as showing that this drug could be effective in treating severe PMS.
The current recommended dose of Prozac is 20mg a day by mouth and most doctors would restrict it to women who had severe psychological symptoms, such as depression/ as part of their PMS.
Tranquillizers – drugs that treat anxiety – are rarely used for PMS nowadays as it is recognized that they can be addictive. One of the best known examples is Valium. They often cause more problems than they solve and would only be prescribed for a very short time – days rather than weeks.
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Dextropropoxyphene is a synthetic opioid agonist structurally related to methadone. Dextropropoxyphene is indicated for mild to moderate pain. It should be used with caution in patients with significant hepatic or renal impairment and in the elderly, in whom accumulation of the drug or its metabolite, norpropoxyphene, may predispose to toxicity. The side effects are similar to other opioid drugs. A small proportion of patients develop light-headedness, dysphoria and confusion at standard doses, necessitating changing to a different drug. Dextropropoxyphene is commercially available as napsylate alone or as hydrochloride with paracetamol.
Fentanyl-Fentanyl is a synthetic opioid agonist used for perioperative pain. It can be given by the IV, IM, SC, ED or transdermal routes. It has a short duration of action (0.5-lh) and can be used for painful procedures or to prevent incident pain. Fentanyl 0.1 mg is equivalent to morphine 10 mg IM. Patients intolerant of morphine and requiring parenteral therapy can be treated by continuous IV or SC infusion, although the latter is limited to lower doses because of the volumes required.
Fentanyl is the first opioid drug to be marketed for transdermal use. Fentanyl is absorbed from a Transdermal Therapeutic System’, each patch providing analgesia for 72 hours. After application of the first patch the plasma concentration of fentanyl rises slowly and does not peak for 12-24 hours; other analgesia will be required during this time. The amount of fentanyl absorbed varies between patients. There will be continued release of drug from the ‘reservoir’ in the subcutaneous tissues for about 24 hours after the patch is removed. The starting dose, as described in the product information and package insert, is calculated from the previous 24 hour requirement of oral morphine or equivalent. Transdermal fentanyl is effective in patients intolerant of oral morphine or unable to take it because of dysphagia or drowsiness. It is particularly useful in renal failure.
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CONSIDER DENGUE

Posted by: admin in Categories: HIV.
The dengue virus is continually slipping across the Texas border from Mexico, but it does not spread within the United States, probably because people on the Texas side spend most of their time in mosquito-proof houses, cars, and workplaces. By keeping people inside mosquito-proof structures, computers and televisions may help curb the spread—the virus becomes stranded like a traveler in an airport in which all flights have been canceled.
Similar evidence comes from a different disease at the other end of the border between the United States and Mexico. Bloody diarrhea killed thousands of people from Mexico south through Guatemala during the late 1960s and early 1970s. But besides a few tourists who brought home a life-threatening infection, the epidemic hardly affected U.S. residents. Some people were infected by those who brought the lethal bacteria north of the Mexican border, but as with dengue, the chain of infection petered out on its own, this time probably because even the poorest U.S. citizens tend to have good access to drinking water that is free from fecal contamination.
The medical history lesson of the twentieth century is that people in rich countries are protected against many of the worst infectious diseases because of infrastructure.
Mosquito-proof housing, sewage disposal, basic hygiene, and clean water protect us better than any surveillance system. Countries without such protective infrastructure are vulnerable. But would an early warning system reduce their vulnerability?
The recent Latin American experience with cholera provides some insight. Remembering the nineteenth-century experience—”en los tiempos del colera,” as Gabriel Garcia Marquez put
it—Latin America braced for cholera’s return during the 1970s. The threat seemed imminent as a new cholera pandemic flowed northward from Indonesia in the 1960s, to India in the west and to China and the Philippines in the east. By the early 1970s it had spread through the Middle East and into Africa. The front spread wherever food and water were poorly protected from fecal contamination. By the mid-1970s it had reached the western countries of sub-Saharan Africa. Latin America now seemed particularly vulnerable because the infrastructure that could protect the richer countries was absent from most of Latin America. The Atlantic Ocean lay between South America and cholera-ridden West Africa, but the Atlantic was an insufficient barrier in the nineteenth century; it could not be trusted to provide a barrier in the twentieth century, when it could be traversed by jumbo jets in a few hours. Yet the pandemic did not spread into Latin America in the 1970s, nor in the 1980s.
It did in the 1990s. It entered Latin America by the back door, arriving in Lima, Peru, in January 1991. Within a year it had spread throughout South and Central America, and it shows no sign of leaving. Its toll during the 1990s was over a million cases and tens of thousands of deaths.
The poor countries did not need an early warning system for cholera. They had decades of lead time. Rather, they needed the infrastructure of the rich countries—but not the entire infrastructure. They needed then, and most still need, the two keys to protection: clean water and adequate waste disposal. No country with these two assets has suffered much from cholera. Even in Latin America this generalization holds. Chile, for example, ranks relatively high in water quality and waste disposal. Within two months after the first cholera cases showed up in Lima, the disease entered Santiago, Chile. Then again about a year later, it entered Chile’s northern provinces. During the first few years of cholera’s visitation, Peru reported over a hundred thousand cases. Chile, Peru’s next-door neighbor, reported under a hundred. In 1994, when Peru reported about 25,000 cases, Chile reported one.
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