CASE REPORT Acute on Chronic Intestinal Pseudoobstruction Responds to Neostigmine MARK R. BORGAONKAR, MD, FRCPC and BARRY LUMB, MD, FRCPC KEY WORDS: colonic pseudoobstruction; Ogilvie’s disease; drug therapy; neostigmine; drug effects. Intestinal pseudoobstruction reflects a disruption of normal intestinal motor function (1) that may manifest as two distinct clinical syndromes—acute or chronic. Acute colonic pseudoobstruction (ACPO), or Ogilvie’s syndrome (2), usually occurs in the postoperative setting or following trauma (3). Medications such as opiates and those with anticholinergic effects may also precipi- tate ACPO. Chronic intestinal pseudoobstruction (CIP) has been described in a variety of conditions, including multiple endocrine neoplasia (MEN) type IIb as a result of a developmental visceral neuropathy (1). Therapy for both acute and chronic pseudoobstruc- tion is suboptimal. Effective management of acute cases is critical due to the significant risk of perforation and death (3). Current management consists of optimizing metabolic disturbances, treating associated medical con- ditions, and decompressing the colon (4). This approach may be ineffective and therefore other medications have been studied, including a number of prokinetic drugs. One such agent is neostigmine, an acetylcholinesterase inhibitor. Evidence of this drug’s efficacy had been lim- ited to several case series (5–7) until a recent clinical trial clearly showed that this compound is of benefit in ACPO (8). We report a case of a patient with MEN type IIb and chronic intestinal pseudoobstruction who pre- sented with two acute exacerbations, both of which were effectively treated with neostigmine. CASE REPORT A 23-year-old Native Canadian female presented to hos- pital with a two-week history of cough, fever, and progres- sive dyspnea. Four days prior to admission she developed painless abdominal distension initially associated with one to two loose stools per day. In the 24 hr prior to admission, her abdominal distension progressed and constipation and obstipation ensued. Cyclobenzaprine (Flexeril) had been started eight days prior to her presentation for back pain. The patient had taken 10 mg three times daily for one day and then 10 mg once daily for three more days. She had not had any infectious contacts or used antibiotics until four days prior when therapy with cefuroxime was initiated for a presumed respiratory tract infection. Past medical history was significant for multiple endocrine neoplasia (MEN) type IIb diagnosed at age 13. This presented with medullary carcinoma of the thyroid, which was treated with a total thyroidectomy and subsequently with radioactive iodine for metastases. She manifested mucosal neuromas but did not have hyperparathyroidism or pheochromocytoma. After this diagnosis the patient was evaluated for recur- rent abdominal distension, constipation, and diarrhea. Ab- dominal radiographs showed dilated large and small bowel, although contrast studies did not demonstrate mechanical obstruction. She was diagnosed with chronic intestinal pseudoobstruction secondary to MEN IIb. Therapy with cisapride was ineffective and she suffered a chronically distended abdomen with mild, intermittent discomfort. Esophageal motility studies were normal. The patient also had a history of recurrent peptic stricture of the esophagus requiring dilatation, bilateral slipped capitofemoral epiph- yses, and bilateral inguinal hernia repair. On admission, the patient was taking levothyroxine 0.175 mg daily and naproxen 250 mg three times daily in addition to flexeril and cefuroxime. She claimed no allergies, was a nonsmoker, and consumed alcohol occasionally. The family history was significant for systemic lupus erythematosus in her mother but no gastrointestinal disorders. Physical examination revealed a slender, unwell female with a pulse of 140 beats/min, temperature 39.9°C, and blood pressure 100/50 mm Hg. She had a Marfinoid body habitus and prognathism in keeping with the diagnosis of MEN IIb. The abdomen was markedly distended and tympanitic with high-pitched bowel sounds but without tenderness, masses, or organomegaly. Rectal examination was unremarkable. The white blood cell count was 6.7  10 9 /liter (normal: 4.0 –11.0  10 9 /liter) with toxic degranulation seen on the peripheral smear. Hemoglobin and platelets were normal. The sodium was 129 mmol/liter (135–145 mmol/liter), mag- Manuscript received December 2, 1999; revised manuscript re- ceived March 9, 2000; accepted March 23, 2000. From the Division of Gastroenterology, McMaster University, Hamilton, Ontario, Canada. Address for reprint requests: Dr. Mark R. Borgaonkar, Room 4W8, McMaster University Medical Centre, 1200 Main Street West, Hamilton, Ontario L8N 3Z5, Canada. Digestive Diseases and Sciences, Vol. 45, No. 8 (August 2000), pp. 1644 –1647 1644 Digestive Diseases and Sciences, Vol. 45, No. 8 (August 2000) 0163-2116/00/0800-1644$18.00/0 © 2000 Plenum Publishing Corporation