Oxycodone/aspirin (trade name Percodan) is a combination drug marketed by Endo Pharmaceuticals. It is a tablet containing a mixture of 325 mg  (5 grains) of aspirin and 4.8355 mg of oxycodone HCl (equivalent to 4.3346 mg of oxycodone as the free base); it is an opioid/non-opioid combination used to treat moderate to moderately severe pain. The safety of the combination during pregnancy has not been established, although aspirin is generally contraindicated during pregnancy, and the drug has been placed in pregnancy category D. Inactive ingredients include D&C Yellow 10, FD&C Yellow 6, microcrystalline cellulose, and corn starch. Percodan was first marketed by DuPont Pharmaceuticals and prescribed in the United States in 1950. Once a widely prescribed painkiller, it has largely been replaced by alternative oxycodone compounds containing paracetamol (acetaminophen) instead of aspirin, such as Percocet. Adverse effects
Pharmacology
The oxycodone component in the combination is technically 14-hydroxy-7,8-dihydrocodein-6-one, a white odorless, crystalline powder which is synthesized from the opium alkaloid thebaine. Thebaine by itself has no therapeutic value. Oxycodone is metabolized into oxymorphone. Unlike morphine and like codeine, oxycodone has a good oral potency. Prior to the introduction of paracetamol, Percodan was the mainstay in post-operative oral pain treatment due to the potency and long half-life of oxycodone. It originally contained a small amount of caffeine. Reformulation
Percodan was reformulated in 2005; prior to 2005, it contained two oxycodone salts—4.62 mg of oxycodone hydrochloride and 0.38 mg of oxycodone terephthalate.
Aase syndrome or Aase–Smith syndrome is a rare inherited disorder characterized by anemia with some joint and skeletal deformities. Aase syndrome is thought to be an autosomal dominant inherited disorder. The genetic basis of the disease is not known. The anemia is caused by underdevelopment of the bone marrow, which is where blood cells are formed. It is named after the American paediatricians Jon Morton Aase and David Weyhe Smith, who characterized it in 1968. Signs and symptoms
Among the presentation are:
Mildly slowed growth
Pale skin
Delayed closure of fontanelles (soft spots)
Narrow shoulders
Triple jointed thumbs, absent or small knuckles, decreased skin creases at finger joints
Inability to fully extend the joints from birth (congenital contractures)
Cleft palate
Deformed ears
Droopy eyelids

Complications
Complications related to anemia include weakness, fatigue, and decreased oxygenation of the blood. Decreased white blood cells alter the bodys ability to fight infection. If a heart defect exists, it may cause multiple complications (depending on the specific defect). Severe cases have been associated with still birth or early death. Cause
Some cases of Aase syndrome (45%) have been shown to be inherited, and are due to a change in one gene which makes ribosomal proteins. However, many cases are not inherited and occur without a known cause. Diagnosis
A CBC (complete blood count) will show anemia and a decrease in the white blood cell count. An echocardiogram may reveal heart defects (ventricular septal defect is most common). X-rays will show skeletal abnormalities as described above. A bone marrow biopsy may be performed.