A controlled, household-randomized, open-label trial of the effect that treatment of Helicobacter pylori infection has on iron deficiency in children in rural Alaska

BACKGROUND: Helicobacter pylori infection and iron deficiency are prevalent in disadvantaged populations worldwide. Previous small or uncontrolled studies have reported that successful treatment of H. pylori infection may resolve iron deficiency or anemia. METHODS: We screened 68% of children 7-11 years old living in 10 western Alaska villages. The 219 children with iron deficiency (serum ferritin level, <22.5 pmol/L [<10 microg/L]) and H. pylori infection (diagnosed on the basis of (13)C-labeled urea breath tests) were enrolled in a household-randomized, unblinded trial. All children received iron supplementation for 6 weeks; children in the intervention group also received a 2-week course of treatment for H. pylori infection plus another 2-week course of treatment if the infection had not resolved at 2 months after treatment initiation. RESULTS: At 2 months after treatment initiation, 32% of children in the intervention group and 39% of children in the control group had iron deficiency. At 14 months after treatment initiation, 65% of children in the intervention group and 72% of children in the control group had iron deficiency (adjusted relative risk [ARR], 0.90 [95% confidence interval [CI], 0.74-1.1]); in addition, 22% of children in the intervention group and 14% of children in the control group had anemia (ARR, 1.6 [95% CI, 0.86-2.9]). Results were similar when children were compared by H. pylori infection status. CONCLUSIONS: In a high-prevalence population, treatment and resolution of H. pylori infection did not improve isolated iron deficiency or mild anemia up to 14 months after treatment initiation.     

A hematologist's view of unexplained iron deficiency anemia in males: impact of Helicobacter pylori eradication

BACKGROUND AND OBJECTIVES: Helicobacter pylori infection with, or without coexisting autoimmune gastritis has been implicated in several recent studies as an important cause of IDA in patients with unexplained iron deficiency anemia (IDA). However, the role of H. pylori in the causation of IDA is still unsettled as the vast majority of reported patients were premenopausal women in whom menstrual blood loss was likely the dominant factor determining IDA. DESIGN AND METHODS: Prospective study of 44 consecutive male IDA patients referred for hematologic evaluation. Following standard endoscopic studies, all patients were screened for non-bleeding GI conditions including celiac disease, autoimmune gastritis and H. pylori gastritis. All subject with H. pylori infection were offered triple therapy for H. pylori eradication. RESULTS: Only 15 patients had a likely source of blood loss identified. The 29 males with "unexplained" IDA were distinguished by their younger age (36+/-20 vs. 57+/-17 years p<0.001), poor initial response to oral iron treatment, and high prevalence of H. pylori infection (25 of 29 vs. 5 of 15 p<0.0001) with (10) or without (15) coexistent autoimmune gastritis. Three had celiac disease. Following H. pylori eradication, all patients achieved normal hemoglobin levels with follow-up periods ranging from 4 to 69 months (38+/-15 months mean+/-1SD). This was accompanied by a significant decrease in H. pylori IgG antibodies and serum gastrin. Sixteen patients discontinued iron treatment, maintaining normal hemoglobin and ferritin and may be considered cured. Remarkably, 4 of the 16 achieved normal hemoglobin without ever having received oral iron after H. pylori eradication. INTERPRETATION AND CONCLUSIONS: The favorable long-term clinical results of H. pylori eradication offer strong evidence for a cause-and-effect relation between H. pylori and IDA. Recognition of the respective roles of H. pylori and autoimmune gastritis in the pathogenesis of iron deficiency may have a strong impact on the clinical management of unexplained and refractory iron deficiency anemia.     

Variable hematologic presentation of autoimmune gastritis: age-related progression from iron deficiency to cobalamin depletion

Iron deficiency is a known complication of achlorhydria and may precede the development of pernicious anemia. Among 160 patients with autoimmune gastritis identified by hypergastrinemia and strongly positive antiparietal antibodies, we explored the overlap between 83 subjects presenting with iron deficiency anemia (IDA), 48 with normocytic indices, and 29 with macrocytic anemia. Compared with macrocytic patients, patients with IDA were 21 years younger (41 +/- 15 years versus 62 +/- 15 years) and mostly women. All groups had a high prevalence of thyroid disease (20%) and diabetes (8%) suggestive of the autoimmune polyendocrine syndrome. Stratification by age cohorts from younger than 20 years to older than 60 years showed a regular and progressive increase in mean corpuscular volume (MCV) from 68 +/- 9 to 95 +/- 16 fl, serum ferritin levels from 4 +/- 2 to 37 +/- 41 microg/L, gastrin level from 166 +/- 118 to 382 +/- 299 pM/L (349 +/- 247 to 800 +/- 627 pg/mL), and a decrease in cobalamin level from 392 +/- 179 to 108 +/- 65 pg/mL. The prevalence of Helicobacter pylori infection was 87.5% at age younger than 20 years, 47% at age 20 to 40 years, 37.5% at 41 to 60 years, and 12.5% at age older than 60 years. These findings challenge the common notion that pernicious anemia is a disease of the elderly and imply a disease starting many years before the establishment of clinical cobalamin deficiency, by an autoimmune process likely triggered by H pylori.     

Iron deficiency due to excessive therapeutic phlebotomy in hemochromatosis

Thirteen adults (eight men, five women) with hemochromatosis had undergone routine iron depletion therapy but while on maintenance phlebotomies developed iron deficiency which persisted for 25 +/- 13 (mean +/- 1 SD) months before diagnosis. All had symptoms and signs of iron deficiency. Levels of transferrin saturation were 10% +/- 5% (1 SD), and serum ferritin concentrations were 8 +/- 3 ng/mL. Eleven had anemia; eight had hypochromia and microcytosis. Bone marrow specimens obtained in five patients revealed no stainable iron. Medical records indicated that parameters of body iron status were infrequently or incorrectly used for adjusting the frequency of phlebotomies. Two patients developed iron deficiency due to additional blood loss from esophageal varices and bilateral hip replacement, respectively. Ten of the patients were treated with ferrous sulfate, 325 mg daily, for 2-6 weeks when anemia was corrected. In patients who were not given iron, anemia and microcytosis recovered in 8-24 months. We conclude that (i) sustained iron deficiency in hemochromatosis patients should be prevented by monitoring hemoglobin levels and serum ferritin; and (ii) hemoglobin concentrations and values of mean corpuscular hemoglobin may be higher in iron-deficient persons with hemochromatosis than in individuals without hemochromatosis. Symptomatic iron deficiency in hemochromatosis patients may be treated safely with a brief course of ferrous sulfate. Recovery is slower when iron is not given. However, iron supplementation is unnecessary and not recommended for the mild, self-limited anemia and decreased serum iron and ferritin concentrations encountered after initial iron depletion therapy for hemochromatosis.     

Safety and efficacy of subcutaneous bolus injection of deferoxamine in adult patients with iron overload

We compared 48-hour urinary iron excretion after a twice-daily subcutaneous bolus injection of deferoxamine and after 12 hours of subcutaneous continuous infusion of the drug in 27 patients with iron overload (mean age, 55.7 years). In most patients, the iron overload was due to multiple transfusions administered during chemotherapy or as part of supportive care for a hematologic or oncologic disorder. One patient had sickle cell anemia and 1 had hereditary hemochromatosis and spherocytosis. Similar urinary iron excretion was observed with the 2 methods of administration; mean +/- SD values were 6935.3 +/- 3832.3 microg/48 hours with subcutaneous bolus injection and 6630.4 +/- 3606.9 microg/48 hours with subcutaneous continuous infusion (P =.3). Twenty-six patients (96.3%) chose to continue therapy with bolus injection. The long-term efficacy of bolus injection was evaluated by measuring the serum ferritin concentration at regular intervals for a follow-up time of 20.1 +/- 4.5 months. Ferritin concentration decreased to below 1000 microg/L in 73% of the patients and to below 500 microg/L in 42% and became normal in 26%. Best results were obtained in patients who were no longer receiving blood transfusions when chelation therapy was initiated. Three of 26 patients (11.5%) had mild, transient side effects after bolus injection. Larger prospective, randomized studies must be conducted before deferoxamine bolus injection can be routinely recommended for patients with iron overload. (Blood. 2000;95:2776-2779)     

Helicobacter pylori infection and serum ferritin: A population-based study among 1806 adults in Germany

OBJECTIVE: Helicobacter pylori may possibly affect the iron metabolism by occult bleeding, impaired absorption of non-hem iron, and by scavenging hem iron or ferritin, as some studies have suggested. The aim of this study was to analyze the association between H. pylori infection and serum ferritin, a marker of the body iron stores. In this analysis, we paid particular attention to the role of dietary iron intake and CagA, an established virulence factor of the agent. METHODS: The analysis is based on a cross-sectional national health and nutrition survey among healthy people in Germany conducted in 1987/1988. The examination included a detailed questionnaire on medical history and lifestyle factors, a 7-day food record, and blood samples. Infection with H. pylori was measured serologically by ELISA and Westernblot. RESULTS: In total, 39.2% of 1806 persons aged 18 to 89 yr included in the study were H. pylori positive, of whom 57.6% had an infection with a CagA-positive H. pylori strain. Age- and sex-adjusted geometric mean of ferritin was 54.5 microg/dl among H. pylori-infected compared with 63.8 microg/dl among uninfected persons. A multiple linear regression model with log-transformed serum ferritin concentration as dependent variable and H. pylori infection and several potential confounding factors as independent variable was fitted. In this model, H. pylori infection was associated with a 17.0% decrease of the serum ferritin concentration (95% CI = 9.8-23.6). The association between H. pylori infection and serum ferritin levels did not vary by gender, age, and iron intake, and it was similar for CagA-positive and CagA-negative H. pylori infections. CONCLUSIONS: The decreased serum ferritin concentration among subjects infected with H. pylori might be induced by the uptake of ferritin in the stomach by H. pylori. Possible health implications of H. pylori-induced low ferritin levels warrant further investigation.     

Is there any relationship between pernicious anemia and iron deficiency ?

INTRODUCTION: Previous studies have suggested that iron deficiency could be due to atrophic gastritis of the body/fundus. The aim of this study was to determine the prevalence of iron deficiency among patients with pernicious anemia and associated factors. PATIENTS AND METHODS: All patients with pernicious anemia diagnosed at our institution between January 1990 and February 2005 were included. Inclusion criteria were: 1- histological diagnosis of atrophic fundic gastritis and 2- criteria of gastric autoimmune involvement. Histology of gastric biopsies was performed in a blinded manner. Iron deficiency was defined as serum ferritin level<15 microg/L in women and<40 microg/L in men. RESULTS: Ninety-five patients (69 women), mean age 60 years (range: 23-90) were included. Twenty patients (21.1%) had normal blood cell counts; 12 patients (12.6%) had microcytosis with or without anemia and 53 patients (55.8%) macrocytosis with or without anemia. Serum ferritin levels were measured in 58 patients, 16 (27.6%) of whom, all women, had iron deficiency. They were significantly younger (39.2 years) than patients without iron deficiency (61.6 years, P<0.0001). Serum gastrin levels did not differ between the groups with and without iron deficiency. A significantly more severe inflammatory infiltrate of the fundus and endocrine cell hyperplasia was observed in iron deficiency patients. Multivariate analysis showed that iron deficiency was linked to female gender and age<50 years. CONCLUSION: Iron deficiency and microcytic anemia are not rare in patients with pernicious anemia and should not rule out the diagnosis. Iron deficiency does not appear to be related to the degree of atrophic fundic gastritis but is linked to female gender and young age, suggesting menstrual blood loss could play a role. Whether decreased iron absorption due to reduced acid secretion favors the expression of gynecological iron loss cannot be ascertained.     

Helicobacter pylori infection in childhood: results of management with ranitidine bismuth citrate plus amoxicillin and tinidazole

BACKGROUND AND AIMS: To verify whether a triple therapy bismuth citrate plus amoxicillin and tinidazole eradicates H. pylori infection in pediatric patients. METHODS: Fifty children (30 females; mean age 12.4 +/- 1.1 years, range 10-15 years) suffering from upper abdominal complaints and Helicobacter pylori (H. pylori)-associated gastroduodenal disease were treated with a 4 week course of ranitidine bismuth citrate (400 mg, twice daily) plus oral tinidazole (20 mg/kg) and amoxicillin (50 mg/kg) for the first 2 weeks. RESULTS: The endoscopic diagnoses were: esophagitis (seven cases), gastritis (six cases), gastroduodenitis (43 cases), duodenitis (one case), gastric ulcer (two cases) and duodenal ulcer (13 cases). Helicobacter pylori was eradicated in 40 (80%) patients and clinical improvement was noticed in 39 (78%) of symptomatic subjects. Duodenal ulcers were healed in all the children, but lymphoid nodular hyperplasia was persistent in all patients, independent of the H. pylori status. The potentially drug-related adverse events (blackening of the tongue, six patients; diarrhea, one patient; disturbance of taste, two patients) were registered in seven (14%) patients and dark stools were observed in 48 (96%) patients. No children withdrew from the study because of either side-effects or clinical laboratory changes. No patient had toxic levels of blood bismuth (values ranged between 2.1 and 5.4 microg/L, mean value 3.4 +/- 1.04 microg/L). CONCLUSIONS: Findings suggest that the present treatment regimen is effective enough in the resolution of H. pylori-associated peptic ulcer disease of childhood.     

Serum ferritin and Helicobacter pylori infection in children: a sero-epidemiologic study in Korea

BACKGROUND: Helicobacter pylori infection is known to affect iron metabolism and serum ferritin levels, which are reduced in adults with H. pylori infection. The aim of the present study was to investigate the association between H. pylori infection and iron status in healthy Korean children. METHODS: The H. pylori seropositivity in 753 schoolchildren aged 6-12 years was screened for using an ELISA and confirmed by western blot analyses. Serum ferritin levels were measured using an immunoradiometric assay in 36 H. pylori-seropositive children and in 72 age- and gender-matched seronegative controls. RESULTS: The median serum ferritin levels were significantly lower in H. pylori-seropositive children than in seronegative controls (24 vs 39 ng/mL; P < 0.001). The prevalence of iron deficiency (ferritin < 15 ng/mL) in H. pylori-seropositive children was significantly higher (13.9%) than in seronegative children (2.8%). This association persisted after adjusting for age and their socioeconomic status (odds ratio, 5.6; 95% confidence interval, 1.0-30.6). CONCLUSION: Serum ferritin levels are reduced in children with H. pylori infection. The H. pylori infection may lead to iron deficiency in children.     

Lactoferrin sequestration and its contribution to iron-deficiency anemia in Helicobacter pylori-infected gastric mucosa

BACKGROUND AND AIM: It is known that lactoferrin serves as a source of iron for Helicobacter pylori in gastric mucosa. The present study was undertaken to investigate the relationship between lactoferrin and H. pylori infection coexistent with iron-deficiency anemia by determining the lactoferrin levels in gastric biopsy specimens, and by locating the major sites of lactoferrin expression, according to the presence or absence of iron-deficiency anemia. METHODS: One hundred and one adolescents who underwent gastroduodenoscopy were divided into four groups: controls without H. pylori infection (NL; n =43); patients with H. pylori infection (HP; n = 26); patients with iron-deficiency anemia (IDA; n = 6); and patients with H. pylori gastritis and coexisting iron-deficiency anemia (HPIDA; n = 26). The gastric mucosal levels of lactoferrin were measured by immunoassay. Immunohistochemical technique was used to allow identification of the location and quantification of the lactoferrin expression. RESULTS: The mucosal level of lactoferrin was highest (3.93 +/- 2.73 ng/microg protein) in HPIDA, followed by 2.67 +/- 1.79 ng/microg protein in HP, 0.59 +/- 0.57 ng/microg protein in NL and 0.14 +/- 0.10 ng/microg protein in IDA. Their multiple comparisons were statistically significant at the 0.05 level. After the eradication of H. pylori in 12 HPIDA patients who underwent follow-up endoscopy, the mean mucosal level of lactoferrin decreased significantly, while the blood hemoglobin level correspondingly increased. The major sites of lactoferrin expression by immunohistochemistry were in glands and neutrophils within epithelium. Lactoferrin was stained weakly in NL and IDA, and strongly in HP and HPIDA. CONCLUSION: The lactoferrin sequestration in the gastric mucosa of HPIDA was remarkable, and this finding seems to give a clue that leads to the clarification of the mechanism by which H. pylori infection contributes to iron-deficiency anemia.     

Clinical features of hematological disorders caused by copper deficiency during long-term enteral nutrition

OBJECTIVE: Copper deficiency has been reported to cause hematological disorders. However, its clinical and hematological characteristics are not fully understood. Therefore, we investigated bedridden patients suffering from copper deficiency and tried to clarify the clinical features of hematological disorders caused by this condition. PATIENTS AND METHODS: Five patients with typical copper deficiency who had been dependent upon enteral nutrition for a long period of time due to various diseases were investigated. We measured hematological parameters and observed the response to copper supplementation therapy and the recovery process of hematological disorders. RESULTS: Their mean age was 82.6+/-10.4 years and the mean duration of enteral nutrition was 16.4+/-5.2 months. Their serum copper concentration was extremely decreased (range, 3 to 8 microg/dl). All five patients had anemia and neutropenia. On the other hand, platelet count remained within the normal range. After copper supplementation therapy, hemoglobin concentration increased from 6.8+/-0.7 g/dl to 9.9+/-0.7 g/dl within a few months (p<0.01). Neutrophil count also increased from 750+/-370/microl to 3,690+/-1,210/microl in a few weeks (p<0.01). Mean corpuscular volume (MCV) decreased from 94.3+/-7.3 fl to 86.0+/-4.8 fl (p<0.05). Elevated serum ferritin and erythropoietin (EPO) levels were normalized after the improvement of anemia. CONCLUSION: Bicytopenia (anemia and neutropenia) with normal platelet count is a feature of hematological disorders caused by copper deficiency. MCV tends to indicate macrocytic anemia. Serum ferritin and EPO levels are elevated. These hematological abnormalities are improved within a few months after copper supplementation therapy.     

Clinical usefulness of serum pepsinogen II in the management of Helicobacter pylori infection

BACKGROUND: Serum pepsinogen II (sPGII) levels are known to increase during Helicobacter pylori infection. AIM: To assess H. pylori infection and success of H. pylori therapy by means of sPGII levels. METHODS: sPGII levels were determined in 156 H. pylori-positive and 157 H. pylori-negative consecutive patients with dyspeptic symptoms. Additionally, sPGII determination was performed in 70 H. pylori-positive patients 2 months after H. pylori eradication therapy. In 29 of these 70 patients, gastroscopy was performed to evaluate the effect of H. pylori therapy on gastric activity. RESULTS: H. pylori-positive subjects demonstrated a significantly higher mean of sPGII levels than H. pylori-negative subjects (16.8 +/- 7.4 vs. 8.6 +/- 3.7 microg/l; p < 0.001). The best sPGII cut-off for predicting H. pylori infection was 9.93 microg/l (sensitivity 83%, specificity 73%). The best cut-off values to evaluate success of therapy were: sPGII of 9.47 microg/l, a sPGII variation level (difference between baseline and after therapy) of 4.54 microg/l, and a sPGII Deltavalue (sPGII variation divided by sPGII before therapy) of 25% (sensitivity 93%, specificity 91%). CONCLUSIONS: sPGII levels may be used as a reliable marker of H. pylori infection in the initial diagnosis as well as to evaluate H. pylori eradication and subsequent changes in gastric inflammation.     

Effect of Helicobacter pylori infection and low-dose aspirin use on iron stores in the elderly

BACKGROUND AND AIMS: Helicobacter pylori infection has been associated with lower ferritin levels in some adult populations, but subsets of potentially higher risk subjects, such as the elderly have not been examined. The aim of the present study was to determine the impact of H. pylori infection and low-dose aspirin use on iron stores in a well elderly population. METHODS: Consecutive subjects aged 65 years or older attending day care facilities were studied. Each subject was assisted in completing a medical questionnaire. Serum ferritin, hemoglobin, mean corpuscular volumes (MCV) and IgG antibodies (ELISA) against H. pylori were measured. RESULTS: In 220 subjects (age 75 +/- 8 years), 42% were H. pylori seropositive (male 41%, female 44%). The median (IQR) ferritin level (ug/L) was higher in men 149 (89-280) than women 94 (54-161), p < 0.002. The ferritin levels were not different in H. pylori positive males 151 (105-283) compared with H. pylori negative males 145 (72-249), or H. pylori positive females 93 (60-142) compared with H. pylori negative females 97 (45-149). This relationship was not altered when controlled for non-steroidal anti-inflammatory agents (NSAID) use (9% of subjects), alcohol or dietary iron intake. Low-dose aspirin use was common (28%), but did not have an independent impact on iron stores: male users 181 (95-248), non-users 145 (86-284); female users 92 (43-162), non-users 95 (62-163). However, in female aspirin users, H. pylori infection was associated with significantly lower ferritin levels: 65 (43-112) compared with uninfected subjects 103 (41-180), p < 0.04. CONCLUSIONS: In this well elderly population, the combination of H. pylori infection and low-dose aspirin use was associated with significantly lower serum ferritin concentrations in females. This difference supports the observation that H. pylori, even in asymptomatic subjects, may be a stressor of iron stores.     

Increased plasma malondialdehyde and fructosamine in anemic Hpylori infected patients： Effect of treatment

AIM： TO unravel the possible association of malondialdehyde （MDA） and fructosamine in anemic H pylori infected patients and to observe the alteration in MDA and fructosamine levels in these patients after treatment for one month. METHODS： Fructosamine, MDA and glucose were estimated in 22 anemic H pylori infected patients and 16 healthy controls. Hematological parameters were also evaluated in both the groups using Sysmex-K-100 automated cell counter. The H pylori infected patients were randomly divided into two groups. Hpylori infected patients in Group Ⅰ received both iron supplementation and anti-H pylori therapy, while patients in Group Ⅱ received only iron supplementation. All the biochemical and hematological parameters were estimated after one month of treatment. RESULTS： In anemic H pylori infected patients, while MDA （5.41 ± 2.16 vs 2.26 ± 0.50; P 〈 0.05） and fructosamine （2.64 ± 0.93 vs 1.60 ± 0.35; P 〈 0.05） were significantly increased, iron （32.72 ± 14.93 vs 110.25 ± 26.58; P 〈 0.05）, hemoglobin （6.9 ± 2.6 vs 12.66 ± 0.74; P 〈 0.05） and ferritin （28.82 ± 16.27 vs 140.43 ± 30.72; P 〈 0.05） levels were significantly decreased compared with the controls. With partial correlation analysis, fructosamine was found to have a significant positive correlation with MDA. In Group I, while MDA level decreased significantly （3.11 ± 1.73 vs 5.50 ± 2.46; P 〈 0.05）, there was a significant increase in iron （84.09 ± 29.51 vs 36.09 ± 17.81; P 〈 0.05）, hemoglobin （10.40 ± 1.11 vs 7.42 ± 1.90; P 〈 0.05） and ferritin （116.91 ± 63.34 vs 30.46 ± 17.81; P 〈 0.05） levels after one month. There was no significant change in the levels of fructosamine in group Ⅰ after treatment. Similarly, no significant alterations were noted in the levels of IDA, fructosamine, hemoglobin or ferritin in Group Ⅱ patients after one month of treatment. CONCLUSION： An increased level of fructosamine and MDA was found in anemic H pylori infected patients. Pr     

Helicobacter pylori impairs iron absorption in infected individuals

BACKGROUND: Infection with Helicobacter pylori is recognised as a major risk factor for chronic gastritis, peptic ulcer disease and gastric cancer. The association between H. pylori infection and iron deficiency anaemia has been established. Multiple mechanisms have been advocated to explain the relationship between H. pylori and iron status and their association might reduce iron deposit. AIM: Aim of this study was to investigate whether H. pylori infection affects iron absorption. METHODS: The study was designed on a prospective basis. Fifty-five subjects underwent upper gastrointestinal endoscopy and biopsy to investigate the presence of H. pylori and, when this was positive, also search of serum anti-CagA was performed. Tests included an oral iron absorption test with the administration of 1 mg/kg of Fe2+. Iron levels were measured before and 2 h after iron administration (delta iron). H. pylori-positive subjects were administered antibiotic therapy for 1 week and, 2 months later, the oral iron absorption test was repeated and urea-breath test was first performed. RESULTS: H. pylori-positive subjects had lower serum level of ferritin and lower delta iron compared to H. pylori-negative subjects. That difference is significant in anaemic women and is independent of the presence of serum anti-CagA antibodies. After H. pylori eradication iron absorption test was similar to those of non-infected subjects. CONCLUSION: H. pylori infection impairs iron uptake. That mechanism, together with others, may contribute to the depletion of iron in infected patients.     

Effect of anti-Helicobacter pylori therapy on outcome of iron-deficiency anemia: a randomized, controlled study.

BACKGROUND: Helicobacter pylori infection may play a role in iron-deficiency anemia. METHODS: In 52 patients with iron-deficiency anemia, H. pylori status was determined using rapid urease test and histology. H. pylori -positive patients were randomly assigned to receive anti- H. pylori treatment either immediately (Group I) or after a delay of one month (Group II); in addition, all patients received oral ferrous sulfate for three months. Patients testing negative for H. pylori (Group III) received only oral ferrous sulfate. Hematological parameters were tested every month. RESULTS: Of 52 patients, 32 (61.5%) had H. pylori infection. At the end of one month, median increase in hemoglobin level was lower in Group II than in Groups I and III (1.1 g/dL vs. 3.6 g/dL and 1.9 g/dL, respectively; p=0.025), as were that in serum iron (19 mcg/dL vs. 55.5 mcg/dL and 41 mcg/dL; p=0.019). During the second month, after H. pylori infection in Group II had been treated, median increase in hemoglobin in this group was comparable to those in Groups I and III (3.7 g/dL vs. 2.5 g/dL and 2.5 g/dL. CONCLUSION: In patients with iron-deficiency anemia, presence of H. pylori infection is associated with a poorer response to oral iron therapy, which improves with treatment for H. pylori infection.     

H63D mutation in the HFE gene increases iron overload in beta-thalassemia carriers

BACKGROUND AND OBJECTIVES. Hereditary hemochromatosis (HH) is an autosomal recessive disorder of iron metabolism. The HFE gene implicated in this disorder has been identified on chromosome 6 (6p21.3). The most prevalent mutation in HH patients changes the 282 cysteine residue to tyrosine (C282Y). The role of a second mutation which changes the 63 histidine to aspartic acid (H63D) in iron overload has been controversial. The aim of this study was to evaluate the effect of the H63D mutation on the ferritin levels of beta-thalassemia carriers. DESIGN AND METHODS. beta-thalassemia carriers have a tendency to increase iron absorption because of mild anemia and slightly increased erythropoiesis. Differences in ferritin levels between homozygotes for H63D and wild type may indicate a modulator effect of the HFE mutation on iron absorption. We studied 152 healthy males, heterozygous for beta-thalassemia. Serum ferritin was measured by chemiluminescence. H63D genotypes were determined by digestion of polymerase chain reaction (PCR) products with MboI restriction enzyme. RESULTS. Forty-five subjects were H63D heterozygotes and four subjects were H63D homozygotes. Ferritin levels were (mean +/- SD): 250 +/- 138 microg/L in homozygotes for the wild type H/H; 295 +/- 186 microg/L in H/D heterozygotes; and 389 +/- 75 microg/L in homozygotes for the mutation D/D. The difference in ferritin values between H/H and D/D is statistically significant (p=0.022). INTERPRETATION AND CONCLUSIONS. beta-thalassemia carriers who are homozygotes for the H63D mutation have higher ferritin levels than beta-thalassemia carriers with the H/H genotype, suggesting that the H63D mutation may have a modulating effect on iron absorption.     

Improvement of complete blood count in patients with iron deficiency anemia and Helicobacter pylori infection after the eradication of Helicobacter pylori

BACKGROUND/AIMS: Recent reports support the possible association between Hp infection and iron deficiency anemia. In the present study, the effects of the eradication therapy on iron deficiency anemia were investigated. METHODOLOGY: Fourteen women with iron deficiency anemia were enrolled (mean age: 36.4 years; range: 20-52 years old). None of the patients received iron supplementation. Several examinations including upper and lower gastrointestinal endoscopy were performed to reveal any gastrointestinal bleeding sites in all patients. Gastric biopsies during endoscopy were taken from the subjects except one whose serum anti-Hp IgG was positive. After diagnosing the Hp infection by means of microbiology, histology and Gram stain, a combination therapy consisting of lansoprosol, clarithromycin and amoxicillin was administered to each patient. Hematologic examinations and the body iron status were evaluated periodically, following the eradication therapy. RESULTS: Endoscopic findings were as follows: Seven patients with antral gastritis, two patients with pangastritis, whereas five patients were found to be endoscopically normal. None of the subjects were found to have gastrointestinal bleeding of any type. Serum hemoglobin, iron and transferrin saturations of the patients were found to be increased at 20-24 weeks of follow-up after the eradication therapy. Serum ferritin levels were not found to be increased. CONCLUSIONS: Hp infection may be involved in cases of iron deficiency anemia of unknown origin, and the eradication of the infection may improve blood parameters other than serum ferritin levels.     

Comparison between deferoxamine and deferiprone (L1) in iron-loaded thalassemia patients

INTRODUCTION: Iron-chelating therapy with deferoxamine in patients with thalassemia major has dramatically improved the prognosis of this disease. However, the limitations of this treatment have stimulated the design of alternative orally active iron chelators. OBJECTIVE: To compare the effectiveness and safety of, and compliance with, oral deferiprone (L1), and deferoxamine, in thalassemia major patients. METHODS: All patients were followed up in one center in Lebanon. Sixteen patients were on L1 (75 mg/kg/d), and 40 patients on subcutaneous deferoxamine (20-50 mg/kg/d). Serum ferritin level, urinary iron excretion (UIE) and side effects were monitored over a two year period. Results: Patients on L1 had an initial serum ferritin concentration of 3663+/-566 microg/l (mean+/-SEM), that dropped to 2599+/-314 at 6 months (p<0.02; paired t-test), and stabilised at that level over the 24 months follow up. Patients on deferoxamine had an initial mean serum ferritin concentration of 3480+/-417 (NS compared to the L1 group), which dropped gradually to 3143+/-417 (p<0.05) and 2819+/-292 (p<0.02) at 6 and 24 months, respectively. The most common adverse reactions associated with L1 were arthralgia and nausea, but they did not necessitate stopping the drug. CONCLUSION: L1 had comparable efficacy as deferoxamine with minimal side effects and better compliance. Provided long term side effects are not encountered, L1 seems to be a valuable alternative iron chelator for patients unable or unwilling to use deferoxamine effectively.     

The impact of B(12) treatment on gastric emptying time in patients with Helicobacter pylori infection

GOALS: The role that vitamin B12 deficiency plays in upper gastrointestinal motor dysfunction is not clear. The aim of this study was to determine whether B12 replacement therapy improves prolonged gastric emptying time in dyspeptic patients with Helicobacter pylori infection. MATERIALS AND METHODS: The study included 34 H. pylori-positive patients who had low serum levels of B12 but had no other factors associated with altered gastric motility. Each patient underwent a radionuclide gastric emptying study before and after 3 months of B12 replacement therapy. Dyspepsia scores were calculated pretherapy and posttherapy using a semiquantitative scale. A vitamin B12 preparation (1000 microg/d) was given intramuscularly for the first 10 days and then orally for 80 days. H. pylori eradication therapy was delayed for 3 months until the posttreatment radionuclide study was completed. RESULTS: The mean gastric emptying time before B12 treatment was significantly longer than that after treatment (230 +/- 190 minutes vs. 98 +/- 29 minutes, respectively; P < 0.0001). The mean dyspepsia score was also significantly improved by treatment (5.4 +/- 1.0 vs. 1.2 +/- 1.0, respectively; P < 0.0001). CONCLUSION: Vitamin B12 deficiency appears to play an important role in the development of gastric dysmotility and its clinical consequences. Replacement therapy will improve gastric emptying in some patients with dyspepsia.