scholarly journals Cameron lesion: An unusual cause of anemia

2010 ◽  
Vol 63 (5-6) ◽  
pp. 423-426 ◽  
Author(s):  
Ivan Jovanovic ◽  
Tamara Alempijevic ◽  
Dragan Popovic ◽  
Nada Kovacevic ◽  
Miodrag Krstic
Keyword(s):  
Iron Deficiency ◽  
Proton Pump ◽  
Signs And Symptoms ◽  
Proton Pump Inhibitor Therapy ◽  
Microcytic Anemia ◽  
Gastric Ulcers ◽  
Surgical Reconstruction ◽  
Deficiency Anemia ◽  
Current Therapy ◽  
Cameron Lesions

Introduction. Cameron lesions are linear gastric ulcers or erosions positioned on the crests of mucosal folds at the diaphragmatic impression, in patients with large hiatal hernia, and can cause iron deficiency anaemia. Case report. We present a case of a 56-year-old woman who was referred to our institution for further investigation after she was examined in gastroenterology emergency room (GER) for signs and symptoms of severe hypochromic microcytic anemia without signs of acute gastrointestinal bleeding and with no obvious cause of chronic blood loss. Endoscopy showed linear ulceration at the level of diaphragm-Cameron lesions with large hiated hernia. She was treated with proton pump inhibitors and iron supplements. The laparoscopic fundoplication was done. Six months later she was asymptomatic. Conclusion. Large hiatus hernia may cause iron deficiency anemia due to occult bleeding from Cameron erosions. The current therapy concept includes the surgical reconstruction of the hiatus together with gastric fundoplication in combination with the proton pump inhibitor therapy.

Case report of severe iron deficiency anemia caused by proton pump inhibitor in an elderly patient

2017 ◽  
Vol 17 (4) ◽  
pp. 662-663 ◽  
Author(s):  
Suguru Mabuchi ◽  
Risa Suzuki ◽  
Mari Sasaki ◽  
Marie Nakamura ◽  
Norihiko Izumimoto ◽  
...  
Keyword(s):  
Elderly Patient ◽  
Case Report ◽  
Iron Deficiency ◽  
Proton Pump Inhibitor ◽  
Iron Deficiency Anemia ◽  
Proton Pump ◽  
Deficiency Anemia

scholarly journals Kandidias Oral pada Penderita Anemia Defisiensi Besi (Fe) dan Penetalaksanaannya

2012 ◽  
Vol 19 (1) ◽  
pp. 77
Author(s):  
Sri Budiarti Wongsohardjono
Keyword(s):  
Body Weight ◽  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Oral Candidiasis ◽  
Dorsal Surface ◽  
Body Weight Loss ◽  
Microcytic Anemia ◽  
The Body ◽  
Deficiency Anemia ◽  
Normal Limits

Background: Iron deficiency anemia is a microcytic anemia caused by chronic blood loss dueto such problems as excessive menstrual flow, gastrointestinal bleeding, gasterektomi or malabsorption that reduces the absorption of Fe. Predisposing factors that lead to the disruption of the ecology of oral candidiasis or oral microbiological changes can be due to malnutrition (iron deficiency, folic acid, vitamin B12) and the very old age. Objective: To report a case of iron deficiency anemia with oral candidiasis and its management. Case Report: A 69-year man in the reference by peer demonstrated swollen gums, mouth pain and difficulty in swallowing. A moth ago he was hospitalized and boarded for a week but no change, his body weight loss was 25kg. paleconjunctiva and face, droliing, looked weak. The body temperature was 370 C; the BP measurement was: 125/80mmHg; with body weight was 50kg; right and left submandibular  lymph nodes become enlarging and soreness palpatiom. Symmetrical face. Right and left lip corners are angular kheilitis, cheek mucosa, palate hyperemia, gingival stipling was disappeared, hyperemia, dorsal surface smooth tongue, hyperemia, depapilasi, OHI: bad; thick saliva, hypersalivation. A lot of dental caries and the remaining roots. Management: Examination of the saliva with KOH solution looked a hyphe. Routine blood tests and profile of fe all within normal limits except RBC was 3,37.106 / uL; HGB: 11.0 g / dl; HCT: 32.2%, Fe 29.00 u g / dl (below normal). Treatment with 3% perhidrol mouthwash, Nyistatin solution 3 x daily. Zegase tablet 2x daily. Paracetamol tablets if necessary. Conclusion sixteen days later the patient recovered.

scholarly journals Mutation of the gastric hydrogen-potassium ATPase alpha subunit causes iron-deficiency anemia in mice

Blood ◽  
2011 ◽  
Vol 118 (24) ◽  
pp. 6418-6425 ◽  
Author(s):  
Lara Krieg ◽  
Oren Milstein ◽  
Philippe Krebs ◽  
Yu Xia ◽  
Bruce Beutler ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Iron Absorption ◽  
Osmotic Fragility ◽  
Microcytic Anemia ◽  
Deficiency Anemia ◽  
Α Subunit ◽  
Hypochromic Microcytic Anemia ◽  
Gastric Proton Pump ◽  
Potassium Atpase

Abstract Iron is an essential component of heme and hemoglobin, and therefore restriction of iron availability directly limits erythropoiesis. In the present study, we report a defect in iron absorption that results in iron-deficiency anemia, as revealed by an N-ethyl-N-nitrosourea–induced mouse phenotype called sublytic. Homozygous sublytic mice develop hypochromic microcytic anemia with reduced osmotic fragility of RBCs. The sublytic phenotype stems from impaired gastrointestinal iron absorption caused by a point mutation of the gastric hydrogen-potassium ATPase α subunit encoded by Atp4a, which results in achlorhydria. The anemia of sublytic homozygotes can be corrected by feeding with a high-iron diet or by parenteral injection of iron dextran; rescue can also be achieved by providing acidified drinking water to sublytic homozygotes. These findings establish the necessity of the gastric proton pump for iron absorption and effective erythropoiesis.

Severe Iron-Deficiency Anemia Still an Issue in Toddlers

2014 ◽  
Vol 53 (14) ◽  
pp. 1352-1358 ◽  
Author(s):  
Gabrielle Paoletti ◽  
Debra L. Bogen ◽  
A. Kim Ritchey
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Motor Development ◽  
Retrospective Chart Review ◽  
Microcytic Anemia ◽  
Deficiency Anemia ◽  
Cow’S Milk ◽  
Milk Consumption ◽  
Cow's Milk ◽  
The Mean

Background and Objectives. Chronic, severe iron-deficiency anemia (IDA) in the first years of life increases the risk of irreversibly compromised cognitive, affective, and motor development. While IDA in infants has decreased because of dietary changes (iron-fortified formula and delaying cow’s milk), toddlers (13-36 months) are equally vulnerable to the adverse effects of IDA. We aimed to show that despite public health efforts, severe IDA remains a problem in toddlers and is associated with excess milk consumption. Methods. Retrospective chart review of children 6 to 36 months admitted to or evaluated by hematology at a children’s hospital from January 1, 2005 to December 31, 2010 with a severe microcytic anemia (hemoglobin [Hb] <9 g/dL and mean corpuscular volume (MCV) <75 fL). Results. We identified 68 infants and toddlers with severe IDA; most (84%) were 13 to 36 months old. The mean Hb and MCV were 6.0 g/dL (range = 2.2-8.9 g/dL) and 54.0 fL (range = 45.5-69.8 fL), respectively. Fatigue, poor appetite, and pica were the most common symptoms, found in 43%, 29%, and 22% of patients, respectively. Only 41% of parents reported pale skin while 77% of physicians recorded it on physical exam. Daily cow’s milk consumption surpassed 24 ounces for 47 of 48 children with reported intake; 11 consumed more than 64 ounces per day. Conclusions. Despite current screening recommendations, severe IDA continues to be a problem in toddlers and strongly correlates with excess cow’s milk consumption. This reiterates the importance of screening for IDA into routine toddler care.

scholarly journals Inherited microcytic anemias

Hematology ◽  
2020 ◽  
Vol 2020 (1) ◽  
pp. 465-470
Author(s):  
Maria Domenica Cappellini ◽  
Roberta Russo ◽  
Immacolata Andolfo ◽  
Achille Iolascon
Keyword(s):  
Iron Deficiency ◽  
Blood Cell ◽  
Iron Metabolism ◽  
Red Blood Cell ◽  
Iron Status ◽  
Transferrin Saturation ◽  
Microcytic Anemia ◽  
Deficiency Anemia ◽  
Mean Corpuscular Hemoglobin ◽  
Distribution Width

Abstract Inherited microcytic anemias can be broadly classified into 3 subgroups: (1) defects in globin chains (hemoglobinopathies or thalassemias), (2) defects in heme synthesis, and (3) defects in iron availability or iron acquisition by the erythroid precursors. These conditions are characterized by a decreased availability of hemoglobin (Hb) components (globins, iron, and heme) that in turn causes a reduced Hb content in red cell precursors with subsequent delayed erythroid differentiation. Iron metabolism alterations remain central to the diagnosis of microcytic anemia, and, in general, the iron status has to be evaluated in cases of microcytosis. Besides the very common microcytic anemia due to acquired iron deficiency, a range of hereditary abnormalities that result in actual or functional iron deficiency are now being recognized. Atransferrinemia, DMT1 deficiency, ferroportin disease, and iron-refractory iron deficiency anemia are hereditary disorders due to iron metabolism abnormalities, some of which are associated with iron overload. Because causes of microcytosis other than iron deficiency should be considered, it is important to evaluate several other red blood cell and iron parameters in patients with a reduced mean corpuscular volume (MCV), including mean corpuscular hemoglobin, red blood cell distribution width, reticulocyte hemoglobin content, serum iron and serum ferritin levels, total iron-binding capacity, transferrin saturation, hemoglobin electrophoresis, and sometimes reticulocyte count. From the epidemiological perspective, hemoglobinopathies/thalassemias are the most common forms of hereditary microcytic anemia, ranging from inconsequential changes in MCV to severe anemia syndromes.

Two nonsense mutations in the TMPRSS6 gene in a patient with microcytic anemia and iron deficiency

Blood ◽  
2008 ◽  
Vol 112 (5) ◽  
pp. 2089-2091 ◽  
Author(s):  
Flavia Guillem ◽  
Sarah Lawson ◽  
Caroline Kannengiesser ◽  
Mark Westerman ◽  
Carole Beaumont ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Microcytic Anemia ◽  
Deficiency Anemia ◽  
Nonsense Mutations ◽  
Hepcidin Expression ◽  
Hypochromic Microcytic Anemia ◽  
Iv Iron ◽  
Membrane Bound ◽  
Inherited Mutations ◽  
Iron Utilization

Abstract Genetic causes of hypochromic microcytic anemia include thalassemias and some rare inherited diseases such as DMT1 deficiency. Here, we show that iron deficiency anemia with poor intestinal absorption and defective iron utilization of IV iron is caused by inherited mutations in TMPRSS6, a liver-expressed gene that encodes a membrane-bound serine protease of previously unknown role that was recently reported to be a regulator of hepcidin expression.

scholarly journals Dietary Composition Influences Incidence of Helicobacter pylori-Induced Iron Deficiency Anemia and Gastric Ulceration

2016 ◽  
Vol 84 (12) ◽  
pp. 3338-3349 ◽  
Author(s):  
Amber C. Beckett ◽  
M. Blanca Piazuelo ◽  
Jennifer M. Noto ◽  
Richard M. Peek ◽  
M. Kay Washington ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Gastric Ulceration ◽  
High Salt ◽  
Gastric Ulcers ◽  
Deficiency Anemia ◽  
Content Type ◽  
H Pylori

Epidemiologic studies have provided conflicting data regarding an association betweenHelicobacter pyloriinfection and iron deficiency anemia (IDA) in humans. Here, a Mongolian gerbil model was used to investigate a potential role ofH. pyloriinfection, as well as a possible role of diet, inH. pylori-associated IDA. Mongolian gerbils (eitherH. pyloriinfected or uninfected) received a normal diet or one of three diets associated with increasedH. pylorivirulence: high-salt, low-iron, or a combination of a high-salt and low-iron diet. In an analysis of all infected animals compared to uninfected animals (independent of diet),H. pylori-infected gerbils had significantly lower hemoglobin values than their uninfected counterparts at 16 weeks postinfection (P< 0.0001). The mean corpuscular volume (MCV) and serum ferritin values were significantly lower inH. pylori-infected gerbils than in uninfected gerbils, consistent with IDA. Leukocytosis and thrombocytosis were also detected in infected gerbils, indicating the presence of a systemic inflammatory response. In comparison to uninfected gerbils,H. pylori-infected gerbils had a higher gastric pH, a higher incidence of gastric ulcers, and a higher incidence of fecal occult blood loss. Anemia was associated with the presence of gastric ulceration but not gastric cancer. Infected gerbils consuming diets with a high salt content developed gastric ulcers significantly more frequently than gerbils consuming a normal-salt diet, and the lowest hemoglobin levels were in infected gerbils consuming a high-salt/low-iron diet. These data indicate thatH. pyloriinfection can cause IDA and that the composition of the diet influences the incidence and severity ofH. pylori-induced IDA.

scholarly journals Prevalence and Determinants of Iron Deficiency Anemia in Adolescents Girls of Low Income Communities in Lahore

2017 ◽  
Vol 23 (2) ◽  
Author(s):  
Fatima Hassan ◽  
Shafya Salim ◽  
Ayesha Humayun
Keyword(s):  
Iron Deficiency ◽  
Urban Communities ◽  
Iron Deficiency Anemia ◽  
Adolescent Girls ◽  
Low Income ◽  
Signs And Symptoms ◽  
Heme Iron ◽  
Deficiency Anemia ◽  
Dietary Iron ◽  
Low Income Families

AbstractBackground:  Iron deficiency anemia (IDA) in adolescent girls has strong health implications during re-productive years. Current research aimed to assess prevalence and determinants of iron deficiency anemia in adolescent girls of low income families residing in semi urban communities of Lahore, Pakistan.Method:  This cross sectional analytical study selected 116 unmarried adolescent girls between the ages of 13 – 19 years from low income families through convenience sampling from semi-urban communities. Dietary data was collected using 3 – day recall, whereas a self-constructed, structured questionnaire was used to collect data on socio-demographic factors. Hemoglobin and serum Ferritin levels were assessed along with an assessment of clinical signs and symptoms of folate and iron deficiency. Data was enteredand analyzed using SPSS version 21.Results:  IDA was present in 68.8% of adolescent girls, of which 40.2% were moderately (8 – 10 gm/dl) and 28.8% were mildly (10.9 – 11.9 gm/dl) anemic. Working status (p < 0.041), source of dietary iron (p < 0.001), frequency of heme iron consumption (p < 0.001), protein consumption/day (p < 0.001) and HEI score (p < 0.001) showed statistically significant association with IDA. Binary regression analysis showed frequency of heme iron consumption [AOR = 29.13, 95% CI (9.627 to 88.203)] and HEI score [AOR = 6.877, 95% CI (.065 to 44.405]) to be the most significantly associated determinant of IDA. Mean Hb level was also significantly different between working and nonworking adolescents (p = 0.001, 95% CI = -1.124 to -0.322). Significant mean difference in serum Ferritin levels between working and nonworking adolescents (p = 0.04 [95% CI = -21.89 to -0.50]) was also observed. 94% and 91% girls showed signs and symptoms of iron and folate deficiency respectively. How-ever BMI, age, educational status of the girls and their parents were not found to be associated with IDA.Conclusion:  Prevalence of IDA was alarmingly high in adolescent girls of low socioeconomic class. Working status, source of dietary iron, frequency of heme iron consumption, protein consumption/day and HEI score were found to be determining anemia. Nutrition education targeting IDA is the need of the day to control and prevent this public health epidemic.

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