Infantile apnea is a rare disease that is characterized by cessation of breathing in an infant for at least 20 seconds or a shorter respiratory pause that is associated with a slow heart rate, bluish discolouration of the skin, extreme paleness, gagging, choking and/or decreased muscle tone. Infantile apnea occurs in children under the age of one and it is more common in premature infants. Symptoms of infantile apnea occur most frequently during the rapid eye movement (REM) stage of sleep. The nature and severity of breathing problems in patients can be detected in a sleep study called a polysomnography which measures the brain waves, heartbeat, body movements and breathing of a patient overnight. Infantile apnea can be caused by developmental problems that result in an immature brainstem or it can be caused other medical conditions. As children grow and develop, infantile apnea usually does not persist. Infantile apnea may be related to some cases of sudden infant death syndrome (SIDS) however, the relationship between infantile apnea and SIDS is not known. Cause
√ having a family history of sleep apnea. √ being overweight or obese. ✓ having certain medical conditions (cerebral palsy, Down syndrome, sickle cell disease, abnormalities in the skull or face)
✓ being born with a low birth weight. ✓ having a large tongue. Diagnosis
Classification
There are three major categories of apnea known as central, obstructive, and mixed apnea.
Race
Although pseudoporphyria has no predilection toward any one race, it has been shown that fair-skinned children who are highly prone to sunburn are more likely to develop naproxen-induced pseudoporphyria than those children with skin types III or higher. Wallace et al. demonstrated that even in the absence of a history of blistering, children with light skin and blue or green eyes are at an increased risk of developing shallow scars on the face while taking naproxen. Causes
Pseudoporphyria can be induced by a wide range of medications, excessive UV-A exposure, and hemodialysis. One frequently reported drug is naproxen. A frequent source of UV-A exposure is tanning booths. As recognition of pseudoporphyria increases and the number of new medications expands, the list of etiologic agents associated with pseudoporphyria will most likely continue to grow. Agents associated with pseudoporphyria are as follows:
Propionic acid derivatives (NSAIDs) - naproxen, diflunisal, ketoprofen, oxaprozin, mefenamic acid, rofecoxib
Ketone NSAID-nabumetone
Antibiotics - nalidixic acid, tetracycline, oxytetracycline, ampicillin-sulbactam, cefepime, fluoroquinolones (M Poh, personal communication, June 1999)
Antifungals - voriconazole
Diuretics - furosemide, chlorthalidone, butamide, triamterene/hydrochlorothiazide
Antiarrhythmics - amiodarone
Chemotherapy - 5-fluorouracil
Immunosuppressants - cyclosporine
Sulfones - dapsone
Vitamins - brewers yeast, pyridoxine
Vitamin A derivatives - etretinate, isotretinoin
Muscle relaxants - carisoprodol/aspirin
Nonsteroidal antiandrogens - flutamide
Other - hemodialysis, excessive UV-A, cola, oral contraceptive pills (levonorgestrel and ethinylestradiol), narrowband UV-B phototherapy (rarely)

Pathophysiology
The precise pathophysiologic mechanism of pseudoporphyria is not fully understood. Some drugs, especially non steroidal anti-inflammatory drugs, can trigger pseudoporphyria in the presence of ultraviolet light. The pathophysiology of pseudoporphyria associated with hemodialysis has not been fully explained. Aluminum hydroxide has been implicated in hemodialysis-associated pseudoporphyria.