Elevated Serum Gastrin Research Articles

The Effect of Endogenous Hypergastrinemia on Lower Esophageal Sphincter Pressure and Esophageal Motility

The effect of exogenous hypergastrinemia on esophageal motor function has been well documented. However, it is not known whether chronic endogenous hypergastrinemia influences esophageal motility and lower esophageal sphincter pressure. The purpose of this study was to investigate the effect of chronic hypergastrinemia on lower esophageal sphincter pressure and esophageal motility in patients with significantly elevated serum gastrin levels. 37 patients (28 women; mean age, 53.7 years) with autoimmune gastritis and 35 functional dyspepsia patients participated in this study. Esophageal motility testing was performed by using an eight-lumen water-perfused catheter. Ten wet swallows were given and each contraction was analysed for lower esophageal sphincter pressure, lower esophageal sphincter relaxation, contraction amplitude and peak velocity. Mean serum fasting gastrin level was 1382.8±731.9pg/mL in patients with autoimmune gastritis and 107±83.9pg/mL in the control group (p=0.000). Mean lower esophageal sphincter pressure (31.6±14.42mmHg vs. 20.5±8.05mmHg, p=0.000) and mean contraction amplitude (82.48±35.0mmHg vs. 58.11±21.75mmHg, p=0.001), in hypergastrinemic patients were significantly higher than in the control group. These results suggest that in patients with autoimmune gastritis, prolonged and significant elevation of serum gastrin levels, increases lower esophageal sphincter pressure and esophageal body contraction amplitude. However, this increase in lower esophageal sphincter pressure does not cause upper gastrointestinal symptoms in patients with autoimmune gastritis.

Pseudo-thrombotic thrombocytopenic purpura: A rare presentation of pernicious anemia

Schistocytes are fragmented red blood cells due to the flow of blood through damaged capillaries and indicate endothelial injury. They are typical of microangiopathic hemolytic anemia seen in life threatening conditions like disseminated intravascular coagulation or thrombotic thrombocytopenic purpura/hemolytic uremic syndrome .We report a rare sub-acute presentation of pernicious anemia with hemolysis, thrombocytopenia and numerous schistocytes that was initially diagnosed as a more serious thrombotic thrombocytopenic purpura.A 31-year-old Caucasian woman presented with fatigue and paresthesia of both feet for 1 week. Past medical history included hypertension and gastro-esophageal reflux disease. Examination revealed scleral icterus and pallor. Examination of the abdomen did not show hepatosplenomegaly. Initial laboratory tests showed severe anemia, and low platelets. Indirect bilirubin and serum Lactate De Hydrogenase were elevated. Prothrombin time, partial thromboplastin time, serum fibrinogen, and serum fibrin degradation product levels were normal. Peripheral smear revealed numerous schistocytes, anisocytosis and macro-ovalocytes. Thrombotic thrombocytopenic purpura (TTP) was suspected due to the constellation of sub-acute onset of fatigue and paresthesia along with thrombocytopenia, schistocytes and an elevated LDH. Plasmapheresis was initiated for possible TTP. However, platelet count worsened despite plasmapheresis for 4 days. On re-evaluation, vitamin B(12) was found to be low. Treatment with intra-muscular vitamin B(12) led to symptomatic and hematologic improvement. Pernicious anemia was confirmed by the presence of anti-intrinsic factor antibodies, elevated serum gastrin level and atrophic gastritis.Clinicians must be aware of unusual clinical presentation of vitamin B(12) deficiency with schistocytes as the management is simple and effective.

Malignant Range Elevation of Serum Chromogranin A due to Inadvertent Use of Proton Pump Inhibitor in a Subject with Pancreatic Incidentaloma

We present a case of highly elevated tenfold rise of serum chromogranin A in a young, morbidly obese, hypertensive female being investigated for pancreatic mass, weight loss, and elevated ESR. Following extensive noninvasive investigations, an ultrasound-guided pancreatic biopsy confirmed benign haemorrhagic cyst. A clue to the etiology of the hyperchromogranin A was the elevated serum gastrin level leading to suspicion of proton pump inhibitor administration confirmed by admittance to its use. Withdrawal of the medication led to dramatic resolution of the neuroendocrine tumor marker.

Elevated serum gastrin levels in Jervell and Lange-Nielsen syndrome: A marker of severe KCNQ1 dysfunction?

The potassium channel I(Ks), which is encoded by the KCNQ1 gene, is expressed in organ systems including the inner ear, kidneys, lungs, intestine, and stomach in addition to the heart. Increasing evidence indicates that I(Ks) in the stomach plays an essential role in enabling gastric acid production. It is not known whether gastric acid production is disordered in patients with long QT type 1. Serum gastrin levels become elevated in subjects with disordered gastric acid production. The purpose of this study was to evaluate serum gastrin levels, as a surrogate for impaired gastric acid secretion, in patients with KCNQ1 mutations, and to see if gastrin levels correlate with severity of cardiac disease. Fasting serum gastrin levels were measured using a standardized immunometric technique in an index case and 12 subjects with known KCNQ1 mutations. An adult female with Jervell and Lange-Nielsen syndrome (JLNS; with KCNQ1 nonsense mutations p.Arg518X and p.Arg190AlafsX95 ) presented with multiple gastric carcinoid tumors and grossly elevated serum gastrin levels (943-1,570 pmol/L; normal 6-55 pmol/L) and absent acid secretion. Gastrin levels in two girls with JLNS, unrelated to the index case (missense mutations p.Leu266Pro and Gly269Ser), also were high (305 and 229 pmol/L). Gastrin levels were normal in 10 KCNQ1 heterozygous single mutation carriers, even in those with severe long QT syndrome, including three heterozygous family members of the JLNS subjects. JLNS may be associated with elevated gastrin levels, impaired acid secretion, and risk of gastric carcinoid tumors. Among KCNQ1 single mutation carriers, gastrin levels were normal and did not appear to be linked to the severity of clinical expression of long QT syndrome.

Usefullness of Selective Arterial Secretagogue Injection Test by Calcium for Diagnosis of Pancreatic Gastrinoma

A 59-year-old man with the main symptom of chronic diarrhea was diagnosed as Zollinger-Ellison Syndrome because of an elevated serum gastrin level; however, no tumor was visualized by the first abdominal CT. Selective arterial secretagogue injection test by calcium was performed. The results indicated a duodenal or pancreatic head tumor. The patient was referred to us, and at that time the CT examination at our hospital showed a tumor in the dorsal site of the pancreatic head. The patient underwent enucleation of the tumor. Histopathological examination showed that the tumor was a gastrin-positive pancreatic neuroendocrine tumor. The serum gastrin level decreased to within the normal range on the first postoperative day, and the patient was discharged on the11th postoperative day. Selective arterial secretagogue injection test by calcium is useful for the localization of gastrinoma.

Erratum: Elevated Serum Gastrin Is Associated With a History of Advanced Neoplasia in Barrett's Esophagus

Wang, Judy S; Varro, Andrea; Lightdale, Charles J; Lertkowit, Nantaporn; Slack, Kristen N; Fingerhood, Michael L; Tsai, Wei Yann; Wang, Timothy C; Abrams, Julian A

Elevated Serum Gastrin Is Associated With a History of Advanced Neoplasia in Barrett's Esophagus

Proton pump inhibitors (PPIs) are frequently prescribed to patients with Barrett's esophagus (BE), but in a subset, they can induce significant hypergastrinemia. Elevated levels of gastrin have been associated with tumorigenic effects in a number of gastrointestinal cancers. We decided to investigate the association between serum gastrin levels and dysplasia in BE. We performed a cross-sectional study and enrolled patients with BE without dysplasia, low-grade dysplasia (LGD), high-grade dysplasia (HGD), or adenocarcinoma (AC), as well as gastroesophageal reflux disease controls, all chronically taking PPIs. Fasting serum gastrin was measured, and data were collected on patient characteristics, medication use, and the highest degree of BE neoplasia. A total of 95 patients were enrolled. The mean age was 64.7 (+/-10.0) years, and 70.5% were male. The median serum gastrin level was 40 pM. There was no significant difference in gastrin levels with increased degrees of BE neoplasia (overall P=0.68). In multivariable analysis, the highest quartile of gastrin was associated with significantly increased odds of advanced neoplasia (HGD or AC) (odds ratio (OR): 5.46, 95% confidence interval (CI): 1.20-24.8). In BE patients taking PPIs, an elevated serum gastrin is associated with a history of HGD or AC. Prospective studies are needed to determine whether patients with nondysplastic BE and elevated serum gastrin are at increased risk for neoplastic progression.

T1036 Clinical and Laboratory Features of Patients with Significantly Elevated Serum Gastrin Level

T1036 Clinical and Laboratory Features of Patients with Significantly Elevated Serum Gastrin Level

Review article: strategies to determine whether hypergastrinaemia is due to Zollinger–Ellison syndrome rather than a more common benign cause

As there is considerable overlap between the fasting serum gastrin concentrations found in Zollinger-Ellison syndrome and various common conditions such as Helicobacter pylori infection and acid suppressing medication use, establishing the cause of hypergastrinaemia in individual cases can sometimes be difficult. To review the causes of hypergastrinaemia and the role of additional non-invasive investigations in hypergastrinaemic patients. Review of articles following a Pubmed search. As gastrinomas may cause serious complications and be potentially life threatening, investigation of hypergastrinaemic patients should particularly focus on confirming or refuting the diagnosis of Zollinger-Ellison syndrome. Establishing the cause of hypergastrinaemia may be difficult when there is only a mild-to-moderate elevation of fasting serum gastrin concentration and concurrent treatment with proton pump inhibitor drugs and the presence of H. pylori infection can both confuse the clinical picture. A variety of provocative tests are therefore useful for establishing whether a hypergastrinaemic patient has a gastrinoma and current evidence suggests that the secretin test should be used first line. We suggest an algorithm for the investigation of patients found to have an elevated fasting serum gastrin concentration and address the roles of gastrin stimulation tests in current clinical practice.

Primary Lymph Node Gastrinoma or Occult Duodenal Microgastrinoma With Lymph Node Metastases in a MEN1 Patient

Gastrinoma tissue has been found frequently in lymph nodes located near the duodenum without a known primary tumor. Therefore, it has been suggested that a primary lymph node gastrinoma exists. We report on a 38-year-old woman suffering from multiple endocrine neoplasia type 1 (MEN1) confirmed by menin gene mutation analysis. MEN1 disease started with primary hyperparathyroidism followed by Cushing disease, the detection of tumors of the pituitary, adrenal cortex, and the pancreas and also an elevated serum gastrin level. An octreotide scan revealed 4 tumors in the upper abdomen. A selective arterial calcium stimulation test located the source of the hypergastrinemia to the area of the gastroduodenal and the superior mesenteric arteries. Total pancreatoduodenectomy was performed and conventional histopathologic examination revealed a well-differentiated cystic neuroendocrine tumor of the pancreas expressing glucagon and accompanied by several microadenomas. In addition, 3 suprapancreatic lymph nodes with gastrin-positive endocrine tissue were found. None of the pancreatic microadenomas expressed gastrin and no duodenal endocrine tumor was found despite careful macroscopic examination. Only after complete embedding of the duodenal and pancreatic tissue in 65 paraffin blocks, 2 microgastrinomas (0.45 and 0.8 mm in diameter) were identified in the duodenum. It is concluded that duodenal gastrinomas that give rise to lymph node metastases may be so tiny that they are easily overlooked in a routine examination and that systematic tissue monitoring is required to identify them.

Long-Term Proton Pump Inhibitor Use in Children: A Retrospective Review of Safety

The objective of this work was to assess the efficacy of continuous proton pump inhibitor (PPI) therapy in children and to evaluate changes in biochemical, endoscopic, and histologic parameters during such treatment. A retrospective review of children receiving PPI therapy continuously for 1 year or more with baseline and follow-up esophageal and gastric biopsies on treatment was conducted to assess type, frequency, and duration of PPI dosing, symptom relief, gastrin levels, histologic findings, and adverse events. A total of 113 children (59 male, median age 4.5 years) were identified. Of these, 31% (35/113) were neurologically impaired. The median treatment duration was 35.2 months. Elevated serum gastrin levels occurred in 73% of children with no statistically significant differences in gastrin level by PPI type, dose, and dosing frequency or treatment duration. Adverse events were reported by 12% of children: diarrhea (5%) and constipation (4%) were the most frequent. Long-term PPI therapy appears to be effective, safe and well tolerated in children despite some biochemical, endoscopic, and histologic changes.

Coexistence of Megaloblastic Anemia and Iron Deficiency Anemia in a Young Woman with Chronic Lymphocytic Thyroiditis

Pernicious anemia is a megaloblastic anemia caused by vitamin B12 deficiency, and is the end-stage of autoimmune gastritis that typically affects persons older than 60 years. It is the most common cause of vitamin B12 deficiency. Pernicious anemia can also be diagnosed concurrently with other autoimmune diseases. We report the occurrence of megaloblastic anemia in a 22-year-old woman with chronic autoimmune thyroiditis for 10.5 years. Recently, she presented with microcytic anemia, and iron deficiency anemia was diagnosed initially. After administration of ferrous sulfate, macrocytic anemia was revealed and vitamin B12 deficiency was detected. Pernicious anemia was highly suspected because of the endoscopic finding of atrophic gastritis, and high titer of antigastric parietal cell antibody, as well as elevated serum gastrin level. After intramuscular injections of hydroxycobalamine 100 microg daily for 10 days, and monthly later, her blood counts returned to normal.

Elevated Serum Gastrin

Case 1: A 69 year old woman was referred for evaluation of suspected gastrinoma. She had experienced 10 years of intermittent hot flashes, loose stools, and near syncope. Outside workup included serum chromogranin A 54 (ULN 51), VIP normal, gastrin 1661 (ULN 114), and an EUS reportedly with a hypodense lesion in the pancreatic neck. Fine needle aspiration of this lesion for cytology was non-diagnostic. An octreotide scan was normal. CT of the abdomen with pancreatic protocol was normal. She then presented to our clinic, where EGD/EUS confirmed absence of a pancreatic lesion. The stomach showed a paucity of rugal folds, and gastric aspirate pH was 7. Biopsies from the gastric body showed active autoimmune gastritis with loss of parietal cells. Vitamin B12 level was 195 (LLN 224), and anti-parietal cell antibody was positive at 1:160. Case 2: A 70 year old man with a history of hypertension and Grave's disease status post thyroidectomy arrived to our clinic with the prevailing diagnosis of “a neuroendocrine pancreatic tumor.” Several months previously, he had an episode of acute gallstone pancreatitis (lipase 3220, ULN 63), underwent ERCP followed by cholecystectomy, and was discharged shortly thereafter. He was completely asymptomatic, but serum labs over the ensuing months showed a persistently elevated amylase (173–189, ULN 129) and lipase (297–508). To further investigate, he underwent a CT of the abdomen and an MRCP which were normal, followed by an EUS showing subtle changes of chronic pancreatitis. Because of continued elevated amylase and lipase levels and persistent concern for a pancreatic process, he underwent serum and urine workup for an islet cell tumor and pheochromocytoma, which was unrevealing. However, serum gastrin twice returned elevated (586, 849, ULN 100). A repeat CT scan of the abdomen and octreotide scan were both normal. After evaluation in our clinic, EGD was performed, showing gastric aspirate pH 8 with biopsies from the gastric body showing fundic gland dropout, a lymphocytic infiltrate, and ECL cell hyperplasia. Vitamin B12 was 139 (LLN 224), and anti-parietal cell antibody was positive at 1:160. Elevated serum gastrin levels can lead to exhaustive workups that are unnecessary, expensive, and potentially dangerous. The most common causes of an elevated serum gastrin are medication-induced (PPI) and atrophic gastritis. The first step in evaluating an otherwise unexplained elevated serum gastrin should be to check the gastric aspirate pH.

Multiple endocrine neoplasia type 1 (MEN 1) is associated with an increased prevalence of diabetes mellitus and impaired fasting glucose

Multiple endocrine neoplasia type 1 (MEN 1) is an autosomal dominant syndrome characterized by primary hyperparathyroidism, pituitary neoplasia and foregut lineage neuroendocrine tumours. It has also been associated with premature cardiovascular death. As diabetes is a risk factor for increased cardiovascular mortality we investigated the prevalence and clinical correlates of glycaemic abnormalities in a large MEN 1 kindred. The glycaemic status of 72 MEN 1 affected and 133 unaffected members of a single large MEN 1 pedigree was assessed. Fasting glucose results were categorized and compared using WHO criteria. Associations between glycaemic status and MEN 1 phenotype were assessed. Thirteen (18.1%) patients with MEN 1 compared to 5 (3.8%) control patients were diabetic (P < 0.001). Six (8.3%) MEN 1 patients had impaired fasting glucose compared to 4 (3%) of controls (P < 0.05). Of patients with MEN 1, uncontrolled hypercalcaemia (P < 0.05) and elevated serum gastrin (P < 0.05) were more common amongst patients diagnosed with abnormal glycaemia than those with normoglycaemia. There was a nonsignificant trend for elevated chromogranin A, pancreatic polypeptide, gastric inhibitory polypeptide (but not glucagon) and history of bronchopulmonary carcinoid in MEN 1 patients with elevated glycaemia. Diabetes and impaired fasting glucose occur significantly more frequently amongst MEN 1 patients than controls and is associated with uncontrolled hyperparathyroidism and evidence of enteropancreatic hyperstimulation.

Effects of 5 years of treatment with rabeprazole or omeprazole on the gastric mucosa

Prolonged gastric acid suppression leads to hypergastrinaemia, which promotes hyperplasia of the enterochromaffin-like (ECL) cells of the oxyntic mucosa. The objective was to determine the effects of 5 years of treatment with rabeprazole or omeprazole on the gastric mucosa. Two hundred and forty-three patients received rabeprazole (20 mg or 10 mg) or omeprazole (20 mg) once daily for up to 5 years, for gastro-oesophageal reflux disease and 51% completed the whole 5 year period. Gastric biopsy specimens were taken and examined for gastritis, Helicobacter pylori infection, and ECL cell status. H. pylori infection in the gastric corpus was more common than in the antrum, and remained constant, whereas antral H. pylori infection became less common as the study progressed. H. pylori infection was a highly significant predictor of higher gastritis scores, which were similar among the three treatment groups. ECL cell hyperplasia occurred in a minority of patients, and was associated with serum gastrin concentrations. No ECL cell dysplasia or tumours were observed. There were no significant differences among the treatment groups in gastritis or ECL cell hyperplasia grades. This study has confirmed the link between ECL cell hyperplasia and elevated serum gastrin concentrations, but has found no evidence that this progresses to high grades of hyperplasia during 5 years of treatment with rabeprazole or omeprazole.

ZOLLINGER-ELLISON SYNDROME WITH NORMAL SERUM GASTRIN LEVEL

Introduction: Zollinger-Ellison syndrome is characterized by gastric acid hypersecretion leading to refractory/recurrent peptic ulceration due to non-beta islet cell tumor. Diagnosis of Zollinger-Ellison syndrome is made by elevated serum gastrin levels or secretin stimulation test in appropriate clinical setting. We describe a case of Zollinger-Ellison that had near normal serum gastrin levels. Diagnosis was made with endoscopic ultrasound and confirmed by octreotide receptor scintigraphy and histopathology. Case Report: 53-year-old white male with history of 40 lbs weight loss over four months and peptic stricture was referred for evaluation of abdominal pain, diarrhea and symptoms of gastroesophageal reflux despite being on omeprazole 40 mg twice daily. Abdominal exam did not show any evidence of fluid or masses. The patient underwent an esophageal gastroduodenoscopy, which showed diffuse ulceration of esophagus, erosions in the stomach, ulceration in the duodenal bulb and second part of the duodenum. Liver enzymes were elevated and a trans abdominal ultrasound showed dilated pancreatic duct. A CT scan obtained at the same time did not reveal any abnormalities. Serum gastrin level initially was 37 pg/ml and later rose to 161 pg/ml; normal (40–200 pg/ml). Patient refused secretin stimulation test because of fear of symptoms off proton pump inhibitors. An endoscopic ultrasound (EUS) was performed which showed a 25 mm × 30 mm mass in the head of the pancreas. Fine needle aspirate of that mass suggested endocrine tumor. Octerotide scan showed high uptake in the mid epigastric area consistent with gastrinoma. The patient underwent a Whipple procedure and resection of low grade neuroendocrine tumor of the pancreas which stained positive for chromogranin, synaptophysin and pancytokeratin consistent with gastrinoma. The patient was discharged home after one week stay in the hospital. Currently patient is doing well without any complaints of gastroesophageal reflux, one-month post surgery. Discussion: Our case illustrates the fact that normal serum gastrin levels do not rule out the diagnosis of Zollinger-Ellison syndrome. When clinical suspicion of Zollinger- Ellison syndrome is high additional testing i.e. secretin stimulation test (which shows a paradoxical rise in the gastrin levels) or EUS should be done to confirm or refute the diagnosis. A EUS can be very helpful in such situations by not only establishing the diagnosis but also localizing the tumor for surgery.

Rebound hypersecretion after inhibition of gastric acid secretion.

Drugs inhibiting gastric acid secretion are widely used because of the high prevalence of acid-related disorders. However, from clinical experience it seems that symptom relapse is common after withdrawal of these drugs. Experimental as well as clinical studies have demonstrated an increased acid secretion after a period of treatment with either histamine 2 receptor antagonists or proton pump inhibitors. Rebound hypersecretion is likely to reflect the following sequence of events: Long-term inhibition of acid output is accompanied by elevated serum gastrin levels, leading to enterochromaffin-like cell activation and proliferation, resulting in increased amounts of histamine being mobilized from these cells to stimulate the parietal cells. The clinical consequences of rebound hypersecretion have not been settled.

Clinical significance of serum gastrin levels in patients with colorectal cancer

An association between elevated serum gastrin levels and the presence of human colorectal cancer has been reported, and gastrin has been shown to stimulate the growth of experimentally induced colon neoplasia. The aim of this study was to determine the preoperative and postoperative concentrations of serum gastrin in 53 patients with colorectal cancer and to assess the correlation between gastrin levels and tumor characteristics and prognosis. A prospective study was performed over a six-year period during which 53 patients received potentially curative surgery for colorectal cancer. The prognostic variables used for the analysis included age, sex, tumor site, stage and degree of differentiation, preoperative and postoperative serum values of carcinoembryonic antigen (CEA) and gastrin, cancer-related mortality, and survival. CEA and gastrin serum values were determined using radioimmunological methods. Follow-up was carried out with clinical and radiological tests. The mean preoperative gastrin concentration was 51.2+/-27.4 pg/mL (range 12-146). Significantly increased serum gastrin concentrations, which returned to normal after surgery, were detected only in patients with well-differentiated cancer (74.2+/-28.3 pg/mL; moderately differentiated, 52.1+/-23.8; poorly differentiated, 29.9+/-12.3, p=0.02). The prognosis was unrelated to serum gastrin level; instead, tumor stage, preoperative CEA value, and degree of differentiation affected patient survival. This study showed that the serum gastrin concentration is not an appropriate clinical oncogenic factor. Although occurring only in well-differentiated tumors, serum gastrin is unrelated to the prognosis of patients with colorectal cancer.

Clinical significance of serum gastrin levels in patients with colorectal cancer.

An association between elevated serum gastrin levels and the presence of human colorectal cancer has been reported, and gastrin has been shown to stimulate the growth of experimentally induced colon neoplasia. The aim of this study was to determine the preoperative and postoperative concentrations of serum gastrin in 53 patients with colorectal cancer and to assess the correlation between gastrin levels and tumor characteristics and prognosis. A prospective study was performed over a six-year period during which 53 patients received potentially curative surgery for colorectal cancer. The prognostic variables used for the analysis included age, sex, tumor site, stage and degree of differentiation, preoperative and postoperative serum values of carcinoembryonic antigen (CEA) and gastrin, cancer-related mortality, and survival. CEA and gastrin serum values were determined using radioimmunological methods. Follow-up was carried out with clinical and radiological tests. The mean preoperative gastrin concentration was 51.2+/-27.4 pg/mL (range 12-146). Significantly increased serum gastrin concentrations, which returned to normal after surgery, were detected only in patients with well-differentiated cancer (74.2+/-28.3 pg/mL; moderately differentiated, 52.1+/-23.8; poorly differentiated, 29.9+/-12.3, p=0.02). The prognosis was unrelated to serum gastrin level; instead, tumor stage, preoperative CEA value, and degree of differentiation affected patient survival. This study showed that the serum gastrin concentration is not an appropriate clinical oncogenic factor. Although occurring only in well-differentiated tumors, serum gastrin is unrelated to the prognosis of patients with colorectal cancer.

Plasma Vitamin B-12 Concentrations in an Elderly Latino Population Are Predicted by Serum Gastrin Concentrations and Crystalline Vitamin B-12 Intake

The prevalence of vitamin B-12 deficiency increases with age, probably resulting from malabsorption of food-bound B-12 secondary to gastric atrophy. On the basis of this assumption, the Institute of Medicine (IOM) recommends those aged >50 y consume crystalline vitamin B-12. There is limited information on the prevalence of gastric atrophy in the elderly and whether the IOM recommendation would be effective. The objective of this study was to assess predictors of vitamin B-12 status and their interactions in free-living elderly. Individuals (n = 57) with deficient plasma vitamin B-12 (p-B12 < 148 pmol/L) were compared with 68 individuals with marginal p-B12 (148-221 pmol/L) and 52 with normal p-B12 (>221 pmol/L) in a cross-sectional sample (n = 1546) of elderly (>60 y) Latinos in California. Associations were examined among p-B12 and serum gastrin, vitamin B-12 intake from food and crystalline sources, and medications that putatively affect vitamin B-12 absorption. Serum gastrin was elevated, indicating gastric atrophy, in 48% of participants with deficient p-B12, 23% with marginal p-B12 and 21% of normal p-B12 participants, and was a significant predictor of deficient p-B12 and high plasma homocysteine (p-tHcy). Median total vitamin B-12 intake exceeded recommendations and was similar among status groups. Crystalline vitamin B-12 intake in the normal p-B12 group was higher than in the deficient p-B12 group (P < 0.01), and tended to be higher than the marginal group (P = 0.07). When serum gastrin was elevated, p-B12 was predicted by crystalline vitamin B-12, but not by intake of vitamin B-12 from food. Elevated serum gastrin was highly prevalent and predicted vitamin B-12 depletion. Crystalline vitamin B-12 intake predicted p-B12 in individuals with elevated serum gastrin, supporting IOM recommendations to increase consumption of crystalline vitamin B-12.