Acute intermittent porphyria, with or without askin eruptions, is the most common form of porphyria clinically seen (1). It is probably a genetic abnormality but its mechanism of action in producing clinical signs and symptoms is not known. Attacks have been precipitated by Sulfanol, Trianol, barbiturates, and possibly alcohol. In the cutaneous form of the disease, the earliest sign is often the appearance of bullae or vesicles on the skin over the face, hands, or legs after exposure to sunlight. Pigmentation and hirsutism may also be present. Examination of organ tissues shows inconstant and nonspecific changes in the central nervous system and within sympathetic ganglia. It is speculated that the nonspecific degeneration in the sympathetic ganglia may be the causative factor in the severe abdominal pain during an attack. Various nervous system abnormalities observed before and during these attacks include nervousness, mild hysteria, cranial nerve deficits, paresthesias, muscular weakness, seizures, and psychosis. Severe abdominal pain which is usually colicky may be diffuse or localized. Abdominal distension is frequent, but generally there is no real muscle spasm or rebound tenderness. The pain may mimic a host of intraabdominal disorders. The diagnosis is frequently missed, and multiple laparotomies are common. The diagnosis is effected by examining the urine for the presence of porphyrins. Acute intermittent porphyria will produce large amounts of porphobilinogen and coproporphyrin during the clinical attack. These compounds then diminish or disappear with remission of the clinical signs and symptoms. The changes reported by x-ray examination of the abdomen include segmental spasm or distension of the colon. In several cases there has been volvulus of the cecum associated with small bowel strangulation. Small bowel studies have shown clumping of barium and disordered motility. There are no references to gastric changes. This communication presents a case of acute intermittent porphyria which was followed during and after an attack. The upper gastrointestinal studies showed changes felt to be related to the disease process. A 12-year-old white female was admitted to the hospital with a two-day history of nausea, vomiting, and generalized abdominal pain. No muscle spasm or localized tenderness was demonstrated. A bullous, purpuric eruption was observed on the skin of the lower legs, feet, and one forearm. The patient had suffered several similar skin eruptions in the six years previous to the present illness. The previous episodes were not accompanied by abdominal pain, and the eruptions cleared spontaneously. At the age of six years, the patient had undergone a splenectomy for thrombocytopenia at another hospital. There is no history of any further blood dyscrasia, and the spleen was reported normal. Laboratory studies on admission to our hospital showed a white blood cell count of 27,000 with 87 per cent segments and 5 per cent bands.