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• W2040721034 abstract "We describe a 39-year-old woman with an 8-month history of abdominal pain, diarrhea, and weight loss. Clinical and laboratory evaluation indicated the presence of a malabsorption syndrome. Endoscopy revealed multiple gastric ulcerations and an abnormal “picture” of the duodenal mucosa. At duodenal biopsy, necrosis confined to the distal parts of the enteric villi and a polymorphonuclear leukocyte response were found. Further evaluation revealed intestinal ischemia as a result of mesenteric atherosele- rosis. After a revascularization procedure was performed, the symptoms disappeared. The macroscopic and microscopic picture of the bowel normalized. In our search for risk factors of atherosclerosis, we found a substantially increased basal plasma homocysteine concentration. This case suggests that hyper homocysteinemia may have a causal role in the development of symptomatic, premature atherosclerosis of the mes enteric circulation. We describe a 39-year-old woman with an 8-month history of abdominal pain, diarrhea, and weight loss. Clinical and laboratory evaluation indicated the presence of a malabsorption syndrome. Endoscopy revealed multiple gastric ulcerations and an abnormal “picture” of the duodenal mucosa. At duodenal biopsy, necrosis confined to the distal parts of the enteric villi and a polymorphonuclear leukocyte response were found. Further evaluation revealed intestinal ischemia as a result of mesenteric atherosele- rosis. After a revascularization procedure was performed, the symptoms disappeared. The macroscopic and microscopic picture of the bowel normalized. In our search for risk factors of atherosclerosis, we found a substantially increased basal plasma homocysteine concentration. This case suggests that hyper homocysteinemia may have a causal role in the development of symptomatic, premature atherosclerosis of the mes enteric circulation. Chronic intestinal ischemia, a rare clinical disorder, accounts for an estimated 1 in 12,000 surgical admissions.1Caldwell JH Intestinal angina.in: Cooperman M Intestinal Ischemia. Futura, New York1983: 231-243Google Scholar The classic features are postprandial abdominal pain, aversion to food, and weight loss.2Mikkelsen WP Intestinal angina: its surgical significance.Am J Surg. 1957; 94: 262-267Abstract Full Text PDF PubMed Scopus (91) Google Scholar, 3Shaw RS Maynard III, EP Acute and chronic thrombosis of the mesenteric arteries associated with malabsorption: a report of two cases successfully treated by thromboendarter-ectomy.N Engl J Med. 1958; 258: 874-878Crossref PubMed Scopus (136) Google Scholar, 4Mikkelsen WP Zaro Jr, JA Intestinal angina: report of a case with preoperative diagnosis and surgical relief.N Engl J Med. 1959; 260: 912-914Crossref PubMed Scopus (23) Google Scholar, 5Webb WR Hardy JD Relief of abdominal angina by vascular graft.Ann Intern Med. 1962; 57: 289-295Crossref PubMed Google Scholar Other symptoms such as nausea, vomiting, constipation, or diarrhea may be found and occasionally dominate the clinical picture.6Marston A Chronic intestinal ischaemia.in: Marston A Vascular Disease of the Gastrointestinal Tract: Patho-physiology, Recognition and Management. Williams & Wilkins, Baltimore1986: 116-142Google Scholar, 7Hunter GC Guernsey JM Mesenteric ischemia.Med Clin North Am. 1988 Sep; 72: 1091-1115PubMed Google Scholar, 8Liberski SM Koch KL Atnip RG Stern RM Ischémie gastroparesis: resolution after revascularization.Gastroen-terology. 1990; 99: 252-257PubMed Google Scholar, 9Hoogenberg K Van Essen LH Van den Dungen JJ Limburg AJ Boeve WJ Kleibeuker JH Chronic mesenteric ischaemia: diagnostic challenges and treatment options.J Intern Med. 1995; 237: 293-299Crossref PubMed Scopus (10) Google Scholar The diagnosis is difficult inasmuch as no specific diagnostic tests are available. Angiography generally reveals obstruction of at least two of the three splanchnic arteries1Caldwell JH Intestinal angina.in: Cooperman M Intestinal Ischemia. Futura, New York1983: 231-243Google Scholar, 10Rogers DM Thompson JE Garrett WV Talkington CM Patman RD Mesenteric vascular problems: a 26-year experience.Ann Surg. 1982; 195: 554-565Crossref PubMed Scopus (164) Google Scholar, 11Marston A Clarke JM Garcia Garcia J Miller AL Intestinal function and intestinal blood supply: a 20 year surgical study.Gut. 1985; 26: 656-666Crossref PubMed Scopus (43) Google Scholar but is inconclusive because all splanchnic arteries can be occluded without syrnptoms.12Chiene J Complete obliteration of the coeliac and mesenteric arteries: the viscera receiving their blood-supply through the extra-peritoneal system vessels.J Anat Physiol. 1869; 3: 65-72Google Scholar, 13Matz EM Kahn PC Occlusion of celiac, superior mesenteric and inferior mesenteric arteries.Vase Dis. 1968; 5: 130-136PubMed Google Scholar Malabsorption syndrome resulting from chronic intestinal ischemia is a very rare clinical condition. II Herein we describe a woman who had malabsorption as a result of premature atherosclerosis of the mesenteric circulation, which was related to a substantial increase in the serum homocysteine level. A 39-year-old premenopausal woman was admitted to our hospital for assessment of diarrhea, weight loss, and abdomi- nal pain. Her previous medical history was unremarkable. She had a 25-pack-year history of smoking. The symptoms of nausea, vomiting, and frequent passage of watery stools had begun 8 months earlier while she was vacationing in Portugal. She also noticed a “nagging” pain in her upper abdominal area; a few days later, the diarrhea decreased, but the pain continued. Bowel movements stabilized at about 4 times a day, with formation of semisolid stools. Her appetite was poor. After 2 weeks of vacation, she returned to the Netherlands and was examined by her primary-care physician. Antacid medication containing aluminum oxide and magnesium hydroxide was prescribed but did not relieve the pain. The pain varied during the day and did not seem to be related to food intake. Four months before admission of the patient, the diarrhea worsened, and Campylobacter jejuni was isolated from a stool specimen. Initiation of antibiotic treatment decreased stool frequency to a maximum of 10 times a day without passage of blood or mucus. The abdominal pain worsened. Repeated stool cultures were negative, and findings on a roentgenogram of the upper gastrointestinal tract with use of barium were reported as normaL The patient had lost a total of 17 kg of body weight. On physical examination, the patient's blood pressure was 115/80 mm Hg, and her pulse was regular at a frequency of 94 beats/min. Her temperature was normal, She weighed 53 kg and was 168 em tall. A systolic bruit was detected in the abdomen, and on palpation of the upper abdominal area, tenderness was noted without severe rebound tenderness. Laboratory tests yielded an erythrocyte sedimentation rate of 43 mm in 1 hour, hemoglobin concentration of 13.5 g/dL, leukocyte count of 21 × 109/L, serum creatinine level of 0.66 mg/dL, and normal results for sodium, potassium, albumin, calcium, alkaline phosphatase, alanine aminotransferase, amylase, thiamine, folate, vitamin A, 25-hydroxycholecalciferol, and thyroid-stimulating hormone. The serum cholesterol level was 143 mg/dL. The D-xylose test results were abnormal. The mean stool fat content was 15 g in 24 hours (normal, less than 6), and the osmotic gap was increased at 248 mOsmol/L (normal, less than 100), indications of osmotic diarrhea and malabsorption. Fecal test results for occult blood were positive. Findings on the parasitologic examination were normal. Esophagogastroduodenoscopy disclosed multiple shallow ulcerations in the body and antrum of the stomach. The bulbar and postbulbar duodenal mucosa was unevenly covered with white adherent material, and multiple erosions were noted at both sites. Omeprazole (a proton pump inhibitor), 40 mg/day, was initiated. Examination of gastric biopsy specimens showed a chronic inflammatory response with few Helicobacter pylori organisms and nonspecific acute ulceration. Numerous fibrin thrombi were evident in the small vessels of the mucosa and submucosa. Postbulbar duodenal biopsy specimen showed necrosis of the distal parts of the villi and a cellular infiltration of polymorphonuclear leukocytes (Fig. 1 A). Endoscopic reexamination after 2 weeks of treatment with omeprazole showed no resolution of either the gastric or duodenal lesions. A small bowel enema examination disclosed an abnormally smooth outline of the jejunum for a considerable length (Fig. 2). A computed tomographic scan of the abdomen revealed extensive calcification of the ab- dominal aorta. Lateral aortography showed severe stenosis of the celiac trunk and superior mesenteric artery (Fig. 3). The inferior mesenteric artery was patent. Uncomplicated aortomesenteric and aortoceliac bypass was performed, and the symptoms disappeared.Fig. 2Small bowel enema examination, showing abnormal smooth outline of proximaljejunum (arrows).View Large Image Figure ViewerDownload (PPT)Fig. 3Lateral aortogram, showing severe stenosis at origins of celiac trunk and superior mesenteric arteries (arrows).View Large Image Figure ViewerDownload (PPT) Two months postoperatively, endoscopic findings were normal. A repeated biopsy of the stomach showed minimal chronic inflammatory changes, and the duodenal biopsy specimen was normal (Fig. 1 B). The patient gained 10 kg of body weight. Because the patient was young, possible occult risk factors for premature atherosclerosis were evaluated. The family history revealed that a brother had development of symptomatic peripheral atherosclerosis at age 34 years and had died at age 43 of a myocardial infarction. Examination of the lipid spectrum showed normal findings; however, the fasting total plasma homocysteine level was increased substantially-107 μmol/L (normal, 1.5 to 16.5). No concomitant deficiency of folic acid, pyridoxine, or cobalamin was detected, an indication of a hereditary variant of hyperhomocysteinemia. Our patient had ischemic gastroenteritis with ulceration of the stomach, duodenum, and small bowel that resulted in malabsorption. Although H. pylori infection was detected, ischemia was the more likely cause of gastric and duodenal ulceration. This was supported by the absence of healing of the gastric and duodenal bulb lesions after 2 weeks of omeprazole treatment and the abundant presence of fibrin thrombi in the small vessels of gastric mucosa and submucosa, suggestive of vascular stasis. Moreover, duodenal erosions were located both bulbar and postbulbar, the latter site of which is unrelated to H. pylori infection. The diagnosis was delayed because symptoms were initially ascribed to episodes of bacterial enteritis. Intestinal ischemia was suspected after computed tomographic scanning revealed calci fications of the abdominal aorta. Angiography disclosed severe stenosis at the origins of the celiac and superior mesenteric arteries. A bypass operation resulted in rapid disappearance of symptoms and healing of stomach and small bowel lesions. Ulceration of the stomach and small intestine due to chronic intestinal ischemia has been previously reported.8Liberski SM Koch KL Atnip RG Stern RM Ischémie gastroparesis: resolution after revascularization.Gastroen-terology. 1990; 99: 252-257PubMed Google Scholar, 9Hoogenberg K Van Essen LH Van den Dungen JJ Limburg AJ Boeve WJ Kleibeuker JH Chronic mesenteric ischaemia: diagnostic challenges and treatment options.J Intern Med. 1995; 237: 293-299Crossref PubMed Scopus (10) Google Scholar, 14Garisch JA Marks IN Mesenteric ischemia-a diagnostic triad?.SAfrMedJ. 1980; 57: 91-92Google Scholar, 15Force T MacDonald D Eade OE Doane C Krawitt EL Ischémie gastritis and duodenitis.Dig Dis Sei. 1980; 25: 307-310Crossref PubMed Scopus (28) Google Scholar, 16Allende HD Ona FV Celiac artery and superior mesenteric artery insufficiency: unusual cause of erosive gastroduo-denitis.Gastroenterology. 1982; 82: 763-766PubMed Scopus (26) Google Scholar, 17Talansky AL Katz S Naidich J Aphthous ulcers in ischémie gastroenterocolitis: a case report.Am J Gastroenterol. 1985; 80: 257-259PubMed Google Scholar, 18Cherry RD Jabbari M Goresky CA Herba M Reich D Blundell PE Chronic mesenteric vascular insufficiency with gastric ulcération.Gastroenterology. 1986; 91: 1548-1552PubMed Google Scholar, 19Hojgaard L Krag E Chronic ischémie gastritis reversed after revascularization operation.Gastroenterology. 1987; 92: 226-228PubMed Google Scholar In addition, abnormalities in motility8Liberski SM Koch KL Atnip RG Stern RM Ischémie gastroparesis: resolution after revascularization.Gastroen-terology. 1990; 99: 252-257PubMed Google Scholar and absorption3Shaw RS Maynard III, EP Acute and chronic thrombosis of the mesenteric arteries associated with malabsorption: a report of two cases successfully treated by thromboendarter-ectomy.N Engl J Med. 1958; 258: 874-878Crossref PubMed Scopus (136) Google Scholar, 5Webb WR Hardy JD Relief of abdominal angina by vascular graft.Ann Intern Med. 1962; 57: 289-295Crossref PubMed Google Scholar, 9Hoogenberg K Van Essen LH Van den Dungen JJ Limburg AJ Boeve WJ Kleibeuker JH Chronic mesenteric ischaemia: diagnostic challenges and treatment options.J Intern Med. 1995; 237: 293-299Crossref PubMed Scopus (10) Google Scholar, 11Marston A Clarke JM Garcia Garcia J Miller AL Intestinal function and intestinal blood supply: a 20 year surgical study.Gut. 1985; 26: 656-666Crossref PubMed Scopus (43) Google Scholar, 20Dardik H Seidenberg B Parker JG Hurwitt ES Intestinal angina with malabsorption treated by elective revascularization.JAMA. 1965; 194: 1206-1210Crossref PubMed Scopus (15) Google Scholar, 21Watt JK Watson WC Haase S Chronic intestinal ischaemia.BMJ. 1967; 3: 199-202Crossref PubMed Scopus (7) Google Scholar, 22Nerstrom B Worning H Chronic intestinal ischemia with severe steatorrhea treated by reconstruction of the superior mesenteric artery.NordMed. 1970; 83: 591-594Google Scholar, 23Tilson MD Stansel HC Abdominal angina: intestinal absorption eight years after successful mesenteric revascularization.AmJSurg. 1976; 131: 366-368Scopus (5) Google Scholar have been noted. In patients with abnormal angina, disturbance of absorption, however, is rare.11Marston A Clarke JM Garcia Garcia J Miller AL Intestinal function and intestinal blood supply: a 20 year surgical study.Gut. 1985; 26: 656-666Crossref PubMed Scopus (43) Google Scholar The malabsorption in our patient was explained by the morphologic changes in the small bowel. Abnormalities detected on small bowel biopsy due to chronic ischemia have been previously described, including nonspecific inflammatory changes and villous atrophy.15Force T MacDonald D Eade OE Doane C Krawitt EL Ischémie gastritis and duodenitis.Dig Dis Sei. 1980; 25: 307-310Crossref PubMed Scopus (28) Google Scholar, 21Watt JK Watson WC Haase S Chronic intestinal ischaemia.BMJ. 1967; 3: 199-202Crossref PubMed Scopus (7) Google Scholar, 22Nerstrom B Worning H Chronic intestinal ischemia with severe steatorrhea treated by reconstruction of the superior mesenteric artery.NordMed. 1970; 83: 591-594Google Scholar Remarkably, most major textbooks of gastroenterology and internal medicine still do not mention chronic ischemia as a possible cause of abnormal findings on small bowel biopsy.24Powell OW Approach to the patient with diarrhea.in: Yamada T 2nd ed. Textbook of Gastroenterology. Vol 1. Lippincott, Philadelphia1995: 845Google Scholar, 25Surawicz CM Morphology of the small intestine in health and disease.in: Gitnick G Principles and Practice of Gastroenterology and Hepatology. 2nd ed. Appleton & Lange, Norwalk (CT)1994: 241-250Google Scholar, 26Greenberger NJ Isselbacher KJ Disorders of absorption.in: Isselbacher KJ Braunwald E Wilson JD Martin JB Fauci AS Kasper DL 13th ed. Harrison's Principles of Internal Medicine. Vol 2. McGraw-Hill, New York1994: 1386-1403Google Scholar, 27Toskes PP Malabsorption.in: Wyngaarden JB Smith Jr, LH Bennett JC Cecil Textbook of Medicine. 19th ed. Saunders, Philadelphia1992: 687-699Google Scholar Thus, this sequela of chronic intestinal ischemia is not recognized universally. The cause of chronic intestinal ischemia is generally narrowing of the proximal part of the splanchnic arteries due to atherosclerosis.11Marston A Clarke JM Garcia Garcia J Miller AL Intestinal function and intestinal blood supply: a 20 year surgical study.Gut. 1985; 26: 656-666Crossref PubMed Scopus (43) Google Scholar Uncommon causes are vasculitis, radiation-induced vasculopathy, fibromuscular dysplasia, fibri- noid necrosis of the vascular wall after aortic surgical treatment of coarctation, and a controversial syndrome termed the “celiac band syndrome.”7Hunter GC Guernsey JM Mesenteric ischemia.Med Clin North Am. 1988 Sep; 72: 1091-1115PubMed Google Scholar, 11Marston A Clarke JM Garcia Garcia J Miller AL Intestinal function and intestinal blood supply: a 20 year surgical study.Gut. 1985; 26: 656-666Crossref PubMed Scopus (43) Google Scholar, 28Ripley HR Levin SM Abdominal angina associated with fibromuscular hyperplasia of the celiac and superior mesenteric arteries.Angiology. 1966; 17: 297-310Crossref PubMed Scopus (31) Google Scholar In our patient, atherosclerosis was diagnosed as the cause of mesenteric vascular insufficiency. The basal plasma homocysteine concentration was substantially increased. In recent years, hyperhomocysteinemia has been recognized as a major risk factor for the development of symptomatic, premature atherosclerosis.29Ueland PM Refsum H Brattström L Plasma homocysteine and cardiovascular disease.in: Francis Jr, RB Atherosclerotic Cardiovascular Disease, Hemostasis, and Endo-thelial Function. Marcel Dekker, New York1992: 183-236Google Scholar, 30Boers GH Hyperhomocysteinaemia: a newly recognized risk factor for vascular disease.Neth J Med. 1994; 45: 34-41PubMed Google Scholar, 31Stampfer MJ Malinow MR Willett WC Newcomer LM Upson B Ullmann D et al.A prospective study of plasma homocyst(e)ine and risk of myocardial infarction in US physicians.JAMA. 1992; 268: 877-881Crossref PubMed Scopus (1579) Google Scholar, 32Boers GH Smals AG Trijbels FJ Fowler B Bakkeren JA Schoonderwaldt HC et al.Heterozygosity for homocystin-uria in premature peripheral and cerebral occlusive arterial disease.N Engl J Med. 1985; 313: 709-715Crossref PubMed Scopus (669) Google Scholar, 33Clarke R Daly L Robinson K Naughten E Cahalane S Fowler B et al.Hyperhomocysteinemia: an independent risk factor for vascular disease.N Engl J Med. 1991; 324: 1149-1155Crossref PubMed Scopus (2045) Google Scholar Mutations in the genes of cystathionine synthase and 5,10-methylenetetrahydrofolate reductase (Fig. 4) that lead to a deficiency of these enzymes have been shown to be responsible.33Clarke R Daly L Robinson K Naughten E Cahalane S Fowler B et al.Hyperhomocysteinemia: an independent risk factor for vascular disease.N Engl J Med. 1991; 324: 1149-1155Crossref PubMed Scopus (2045) Google Scholar, 34Kang SS Wong PW Bock HG Horwitz A Grix A Intermediate hyperhomocysteinemia resulting from compound heterozygosity of methylenetetrahydrofolate reducíase mutations.Am J Hum Genet. 1991; 48: 546-551PubMed Google Scholar, 35Ueland PM Refsum H Plasma homocysteine, a risk factor for vascular disease: plasma levels in health, disease, and drug therapy.J Lab Clin Med. 1989; 114: 473-501PubMed Google Scholar Deficiencies of other enzymes that function in homocysteine metabolism (Fig. 4) may be involved but have not yet been established. Plasma homocysteine concentration is also determined by external factors. Folic acid, vitamin B12 or vitamin B6 deficiency, and chronic renal failure increase the concentration.35Ueland PM Refsum H Plasma homocysteine, a risk factor for vascular disease: plasma levels in health, disease, and drug therapy.J Lab Clin Med. 1989; 114: 473-501PubMed Google Scholar In addition, gender, premenopausal or postmenopausal state, and age are known influential factors. The pathogenesis of premature atherosclerosis in hyperhomocysteinemia is unknown; various hypotheses have been proposed.29Ueland PM Refsum H Brattström L Plasma homocysteine and cardiovascular disease.in: Francis Jr, RB Atherosclerotic Cardiovascular Disease, Hemostasis, and Endo-thelial Function. Marcel Dekker, New York1992: 183-236Google Scholar Currently, data are limited on hyperhomocysteinemia and symptomatic, premature atherosclerosis of the mesenteric circulation. Boers and associates32Boers GH Smals AG Trijbels FJ Fowler B Bakkeren JA Schoonderwaldt HC et al.Heterozygosity for homocystin-uria in premature peripheral and cerebral occlusive arterial disease.N Engl J Med. 1985; 313: 709-715Crossref PubMed Scopus (669) Google Scholar described a 48-year-old woman who had abdominal angina and hyperhomocysteinemia, defined as a pathologic increase of the serum homocysteine level after methionine loading. Postmortem studies have shown a correlation between the severity of atherosclerosis in the coronary and cerebral vascular beds and the severity of atherosclerosis in the mesenteric arteries.36Reiner L Jimenez FA Rodriguez FL Atherosclerosis in the mesenteric circulation: observations and correlations with aortic and coronary atherosclerosis.Am Heart J. 1963; 66: 200-209Abstract Full Text PDF PubMed Scopus (52) Google Scholar Therefore, hyperhomocysteinemia is likely to be a risk factor for symptomatic, premature atherosclerosis of the mesenteric circulation. Our patient's history strongly suggests that this is indeed true. Because the plasma homocysteine level can often be decreased by administration of pyridoxine, folic acid, and betaine,37Brattström L Israelsson B Norrving B Bergqvist D Thörne J Hultberg B et al.Impaired homocysteine metabolism in early-onset cerebral and peripheral occlusive arterial disease: effects of pyridoxine and folie acid treatment.Atherosclerosis. 1990; 81: 51-60Abstract Full Text PDF PubMed Scopus (372) Google Scholar, 38Franken DG Boers GH Blom HJ Trijbels FJ Kloppenborg PW Treatment of mild hyperhomocysteinemia in vascular disease patients.Arterioscler Thromb. 1994; 14: 465-470Crossref PubMed Google Scholar screening for hyperhomocysteinemia in young patients with abdominal angina seems appropriate. Whether a reduction in the plasma homocysteine level will decrease future ischemic vascular events remains to be proved." @default.
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• W2040721034 title "Malabsorption Syndrome Associated With Ulceration of the Stomach and Small Bowel Caused by Chronic Intestinal Ischemia in a Patient With Hyperhomocysteinemia" @default.
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