The clinical presentation of ADP includes a wide range of neurologic and gastrointestinal symptoms. The severity of symptoms is dependent on how functional the ALAD enzyme is in each person. The higher the enzyme activity, the fewer symptoms a person will exhibit and the later they will present. The less functional a persons ALAD enzyme is, the earlier they will present and the more severe their symptoms will be. The disease can present during early childhood (as well as in adulthood) with acute neurologic symptoms that resemble those encountered in acute intermittent porphyria. Patients can also have gastrointestinal symptoms during acute attacks, including abdominal cramping, vomiting, and constipation. Gastrointestinal symptoms can result in failure to thrive and poor weight gain in children. Other symptoms that can occur during an acute attack include a rapid heart beat, high blood pressure, and respiratory difficulties. Acute attacks can last for weeks and are also called "neurovisceral" attacks due to the neurological complications associated. Patients have reported numbness and tingling in the extremities, seizures, burning pain, poor coordination, inability to move muscles voluntarily, and psychological disturbances. Psychosis, though rare, has occurred in severe instances. Many triggers have been identified for acute ADP attacks including fasting, a low carb diet, dehydration, alcohol intake, the use of estrogen or progesterone, certain drugs, and other mental and physical stressors.
Aminolevulinic acid dehydratase deficiency porphyria
Harderoporphyria
Pseudoporphyria
Hepatoerythropoietic porphyria
Donath–Landsteiner hemolytic anemia
Erythropoietic porphyria
Hepatic porphyria
Erythropoietic protoporphyria