It was reported in a published article, that an 8 year old white female, previously in excellent health without any gastrointestinal complaints, in approximately 1993, was vaccinated with the first and second doses of hep B vaccine recombinant, 'as a part of routine childhood vaccinations." Shortly after the first dose, the pt developed a rash on her arms and legs. One month later, following the second dose, she developed diffuse skeletal muscle weakness and difficulty walking. This was followed by persistent nausea, vomiting, and abdominal pain. Subsequently, she experienced a 25lb weight loss. It was reported that the symptoms persisted for several years. During that time, she was treated with cisapride, sucralfate, omeprazole, metoclopramide, ranitidine, and dicyclomine. She did not experience "significant relief" and it was reported that the metoclopramide caused a dystonic reaction. Diagnostic testing was performed. A solid-phase gastric emptying scan revealed a mild to moderate delay at 2 H. The pt developed symptoms of pyrosis and regurgitation. An upper endoscopy was performed and revealed esophagitis. A 24 hr pH probe, performed while the pt was taking omeprazole, revealed abnormal reflux into the distal esophagus. NIssen fundoplication was performed, but the symptoms of acid-reflex persisted. Additional pH monitoring and esophageal manometry confirmed persistent acid reflux and ineffective esophageal motility. An troduodenal manometry revealed antral hypomotility with normal small bowel motility. The pt was treated with domperidone and was placed on a liquid/low residue diet. Following treatment, the symptoms improved and the pt experienced persistent weight gain. The pt was still "mildly" symptomatic 8 years after diagnosis. She remained dependent on prokinetic therapy for symptom management and maintenance of nutritional status. It was reported that this case displays some of the clinical characteristics of gastroparesis that develops following viral illness. However, the pt had no history of viral illness prior to onset of the symptoms of gastroparesis. In addition, no known cause of gastroparesis was found following a thorough evaluation. The authors emphasize that there was a "temporal association between the suspected inciting event and the onset of symptoms." The authors also felt that there was good evidence of support the development of an inflammatory neuropathy after vaccination, which could lead to gastroparesis. They believe that this pt's gastroparesis occurred as a result of neuropathic injury to either the enteric nervous system or the autonomic nervous system. It was further noted that this may have been a result of immune activation leading to chronic and prolonged inflammation and then permanent nerve damage. It was noted  that this pt was not rechallenged with another vaccine of the same type that produced symptoms. This is one of five cases presented by the authors, who felt that the five cases present "strong evidence that gastroparesis can develop in response to an inflammatory condition such as Lyme disease or a vaccination." All five patients were "young," white females. The authors hypothesize that perhaps this population is predisposed to immunopathologic injury of the ENS or AHS, related to specific HLA types or hormone levels. Of the five patients, this pt is the only patient reported to have received hep B vaccine recombinant. Upon internal review, difficulty walking, skeletal muscle weakness, neuropathic injury, esophagitis, and gastroparesis were considered to be other important medical events (OMIC). Additional info has been requested.