There is, however, not yet any conclusive evidence that AHC is fatal or that it shortens life expectancy, but the relatively recent discovery of the disorder makes large data for this type of information unavailable. Treatment for AHC has not been extremely successful, and there is no cure. There are several drugs available for treatment, as well as management strategies for preventing and dealing with hemiplegic attacks. Management strategies
Hemiplegic attacks can be brought on by particular triggers, and management of AHC often centers around avoiding common or known triggers. While triggers vary greatly from person to person, there are also some common ones which are prevalent in many patients. Common triggers include temperature changes, water exposure, bright lights, certain foods, emotional stress, and physical activity. While avoiding triggers may help, it cannot prevent all hemiplegic episodes because many occur without being triggered. Because attacks and other associated symptoms end with sleep, various sedatives can be used to help patients sleep. Flunarizine
The most common drug used to treat AHC is flunarizine. Flunarizine functions by acting as a calcium channel blocker. Other drugs, in order of frequency of use are benzodiazepines, carbamazapine, barbiturates, and valproic acid. Flunarizine is prescribed for the purpose of reducing the severity of AHC attacks and the number of episodes, though it rarely stops attacks altogether. Minimizing the attacks may help reduce damage to the body from hemiplegic attacks and improve long-term outcomes as far as mental and physical disabilities are concerned.Experts differ in their confidence in flunarizines effectiveness.
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.