Pattern of shedding of the Norwalk particles in stools during experimentally induced gastroenteritis in volunteers as determined by immune electron microscopy gastritis eating late buy cheap nexium 20mg. Two outbreaks of foodborne gastroenteritis caused by a small round structured virus: evidence of prolonged infectivity in a food handler gastritis young living order 40mg nexium. Role of infected food handler in hotel outbreak of Norwalklike viral gastroenteritis: implications for control gastritis diet treatment ulcers order nexium 20 mg without prescription. Foodborne outbreak of Norwalk virus gastroenteritis: evidence for post-recovery transmission gastritis diet herbs discount 40mg nexium with mastercard. Outbreak of acute gastroenteritis in a geriatric long-term-care facility: combined application of epidemiological and molecular diagnostic methods. Outbreaks of gastroenteritis in elderly nursing homes and retirement facilities associated with human caliciviruses. Outbreak of Norwalk-like gastroenteritis associated with contaminated drinking water at a caravan park. Outbreak of viral gastroenteritis due to drinking water contaminated by Norwalk-like viruses. Community outbreak of food-borne small round-structured virus gastroenteritis caused by a contaminated water supply. Norwalk virus-associated gastroenteritis traced to ice consumption aboard a cruise ship in Hawaii: comparison and application of molecular method-based assays. Norwalk-like virus infection in military forces: epidemic potential, sporadic disease, and the future direction of prevention and control efforts. Viral agents of gastroenteritis: public health importance and outbreak management. To receive an electronic copy on Friday of each week, send an e-mail message to listserv@listserv. However, since the germicidal mechanism of alcohol is lipolysis, alcohol-based disinfectants appear to have a minimal effect on non-enveloped viruses, such as noroviruses. Because there is no cultivation method for human norovirus (HuNoV) in vitro, murine norovirus and feline calicivirus have been used as surrogates for HuNoV to analyze the efficacy of disinfectant regents. Therefore, whether these disinfectants and their conditions are effective against HuNoVs remain unknown. Additionally, pH adjustments and salting-out may contribute toward the virucidal effect of alcohol against other HuNoV genotypes and cancel the impediment of organic substance contamination, respectively. Therefore, similar to sodium hypochlorite, alcohol-based disinfectants containing electrolytes can be used for HuNoV inactivation. Alcohols are widely used as disinfectants for sanitization, especially for skin surfaces, cooking devices, tableware, and high-touch surfaces, such as doorknobs, balustrades, and elevator buttons in hospitals, other healthcare settings, and households. Among the several types of alcohol, ethanol and isopropanol are preferably used as disinfectants. Although the molecular mechanisms underlying the bactericidal effect of alcohol are not fully understood, high-percentage (around 70% [v/v]) ethanol shows a polymer-like structure with water through the formation of hydrogen bonds and hydrophobic bonds, generating a large hydrophobic cluster surface1. This hydrophobicity (or lipophilicity) subsequently damages the phospholipid membrane of bacteria by the delipidation and denaturation or coagulation of membrane proteins. Enveloped viruses, such as influenza viruses and coronaviruses, are also susceptible to alcohol-based disinfectants since their envelopes consist of a host lipid bilayer. HuNoVs are the leading cause of intestinal infectious gastroenteritis in people of all ages in developed and developing countries. HuNoV infections can lead to mortality in children, elderly, and immunocompromised patients. Although it is essential to completely decontaminate HuNoV-contained materials, effective inactivation methods remain to be identified. One of the reasons for this is that there were no in vitro cultivation systems for HuNoVs until 20163. Until then, the inactivation methods of HuNoVs were determined using feline calicivirus and/or murine norovirus as surrogates57. The virucidal efficacy of alcohol and alcohol-based disinfectants for HuNoVs are also considered based on the effects on feline calicivirus or murine norovirus. Inactivation of HuNoVs by ethanol, isopropanol, and sodium hypochlorite in suspension. Inoculation and sampling were performed as described in the Materials and Methods. However, the virucidal efficacy of alcohol for non-enveloped viruses varies in each virus. For example, murine norovirus is sensitive to alcohols, while feline calicivirus is resistant to them8. Therefore, even if viral genome reduction is observed, it is possible that HuNoVs are propagated. Therefore, the virucidal effects of HuNoV disinfectants should be determined by assessing their actual propagative availability. In addition, our results suggest that pH-adjusted alcohols, particularly low-pH alcohols, exhibit strong virucidal effects against HuNoVs. Thus, acid-alcohol disinfectants can be associated with good biological safety profiles and can be used for HuNoV inactivation. Although the efficacy of alcohol-based disinfectants against non-enveloped viruses is controversial, whether these disinfectants show virucidal effects on HuNoVs remains to be elucidated. It has been reported that low-pH ethanol enhances the virucidal effect on non-enveloped viruses6. Therefore, we next tested whether acidethanol has potential as a disinfectant for the inactivation of HuNoVs. In addition, isopropanol could be substituted for ethanol for the acid-alcohol sanitization of HuNoVs. We examined the virucidal effect of 70% ethanol-15% lemon juice, which contains 1% citric acid, against HuNoV. Considering the use of acidethanol as a hand sanitizer for HuNoVs, a short incubation time is likely required for inactivation. Therefore, we next examined how much time is needed for the inactivation of HuNoVs with acidethanol. Next, we investigated whether alkaline-alcohol also shows a virucidal effect on HuNoVs. To adjust the pH and generate a weak alkaline (pH ~ 11), we used sodium bicarbonate buffer because both sodium hydrogen carbonate and sodium carbonate are recognized as food additives, and thus its safety has been confirmed similar to citric acid. Although alkaline-ethanol (carbonate buffer plus Scientific RepoRtS (2020) 10:15878 doi. These data indicate that ethanol, and probably isopropanol, have an actual virucidal effect on HuNoVs that is dependent on the pH. Impact of organic substances on the virucidal activity of acid-alcohol against HuNoVs. As mentioned above, NaClO has a powerful virucidal effect, even on non-enveloped viruses. However, NaClO also strongly reacts with other organic substances contained in feces and vomit. Therefore, we next investigated the virucidal effect of acidethanol on HuNoVs under conditions containing beef extract as an extra-organic substance12. As electrolyte solutions, some mineral salts are used to precipitate proteins and low molecular organic compounds, which is a process termed coagulation or salting-out. It is speculated that if organic substances are removed from virus particles, acidethanol may Scientific RepoRtS Vol. The solutions of the indicated HuNoV genotypes containing 3% or 5% beef extracts were suspended with threefold (A) or ninefold (B) volumes of the indicated disinfectants for 5 min. Therefore, we used an increased volume of these disinfectants, similar to the experiments shown in. Many reports have investigated the effects of alcohol-based disinfectants against murine norovirus and feline calicivirus as surrogates for HuNoV6,8,13. We further examined the morphological change in virus particles after the incubation with disinfectants. Virucidal activity of commercially available alcohol-based disinfectants against HuNoVs.
Mononuclear Leucocytes Lymphocytes There are two varieties: Small Lymphocytes Their size ranges from 7-10µm in diameter gastritis bile reflux diet generic 20 mg nexium free shipping. Small lymphocytes have round gastritis ginger proven 20mg nexium, deep-purple staining nucleus which occupies most of the cell gastritis diet mercola purchase nexium 20 mg online. They have more plentiful cytoplasm that stains pale blue and may contain a few reddish granules gastritis diet in spanish buy cheap nexium 40 mg online. Platelets these are small, non nucleated, round/oval cells/cell fragments that stain pale blue and contain many pink granules. When blood vessels are injured, platelets rapidly adhere to the damaged vessel and with one another to form a platelet plug. During this process, the soluble blood coagulation factors are activated to produce a mesh of insoluble fibrin around the clumped platelets. This assists and strengthens the platelet plug and produces a blood clot which prevents further blood loss. Transportation Blood transport oxygen form the lungs to the cells of the body and carbon dioxide from the cells to the lungs. It also carries nutrients from the gastrointestinal tract to the cells, heat and waste products away from cells and hormones form endocrine glands to other body cells. It also adjusts body temperature through the heat-absorbing and coolant properties of its water content and its variable rate of flow through the skin, where excess heat can be lost to the environment. Blood osmotic pressure also influences the water content of cells, principally through dissolved ions and proteins. Protection the clotting mechanism protects against blood loss, and certain phagocytic white blood cells or specialized plasma proteins such as antibodies, interferon, and complement protect against foreign microbes and toxins. In postnatal life in humans, erythrocytes, granulocytes, monocytes, and platelets are normally produced only in the bone marrow. Lymphocytes are produced in the secondary lymphoid organs, as well as in the bone marrow and thymus gland. Although many questions 10 Hematology remain unanswered, a hypothetical scheme of hemopoiesis based on a monophyletic theory is accepted by many hematologists. According to this theory, the main blood cell groups including the red blood cells, white blood cells and platelets are derived from a pluripotent stem cell. This stem cell is the first in a sequence of regular and orderly steps of cell growth and maturation. The pluripotent stem cells may mature along morphologically and functionally diverse lines depending on the conditioning stimuli and mediators (colony-stimulating factors, erythropoietin, interleukin, etc. During fetal life, hemopoiesis is first established in the yolk sac mesenchyme and later transfers to the liver and spleen. The splenic and hepatic contribution is gradually 11 Hematology taken over by the bone marrow which begins at four months and replaces the liver at term. From infancy to adulthood there is progressive change of productive marrow to occupy the central skeleton, especially the sternum, the ribs, vertebrae, sacrum, pelvic bones and the proximal portions of the long bones (humeri and femurs). Hemopoiesis occurs in a microenvironment in the bone marrow in the presence of fat cells, fibroblasts and macrophages on a bed of endothelial cells. An extracellular matrix of fibronectin, collagen and laminin combine with these cells to provide a setting in which stem cells can grow and divide. In the bone marrow, hemopoiesis occurs in the extravascular part of the red marrow which consists of a fine supporting reticulin framework interspersed with vascular channels and developing marrow cells. A single layer of endothelial cells separates the extravascular marrow compartment from the intravascular compartment. When the hemopoietic marrow cells are mature and ready to circulate in the peripheral blood, the cells leave the marrow parenchyma by passing through fine "windows" in the endothelial cells and emerge into the venous sinuses joining the peripheral circulation. Increased demands for cells as a consequence of disease or physiologic 14 Hematology change are met by increased cell production. Several hematopoietic growth factors stimulate differentiation along particular paths and proliferation of certain progenitor cells. In addition, there are several different cytokines that regulate hematopoiesis of different blood cell types. Cytokines are small They act glycoproteins produce by red bone marrow cells, leucocytes, macrophages, and fibroblasts. The classes of hematopoietic growth factors and their functions are described in Table 1. Also fatty marrow that starts to replace red marrow during childhood and which consists of 50% of fatty space of marrow of the central skeleton and proximal ends of the long bones in adults can revert to hemopoiesis as the need arises. Formation of apparently normal blood cells outside the confines of the bone marrow mainly in the liver and spleen in post fetal life is known as Extramedullary Hemopoiesis. Formation of Red blood cells (Erythropoiesis) 17 Hematology Erythropoiesis is the formation of erythrocytes from committed progenitor cells through a process of mitotic growth and maturation. The first recognizable erythyroid cell in the bone marrow is the proerythroblast or pronormoblast, which on Wright or Giemsa stain is a large cell with basophilic cytoplasm and an immature nuclear chromatin pattern. Subsequent cell divisions give rise to basophilic, polychromatophilic, and finally orthochromatophilic normoblasts, which are no longer capable of mitosis. At the same time the nuclear chromatin pattern becomes more compact tan clumped until, at the level of the orthochromatophilic normoblast, there remains only a small dense nucleus, which is finally ejected from the cell. Under normal conditions the transit time from the pronormoblast to the reticulocyte entering the peripheral blood is about 5 days. Pronormoblast (Rubriblast) Pronormoblast is the earliest morphologically recognizable red cell precursor. The chromatin forms delicate clumps so that its pattern appears to be denser and coarser than that seen in the pronormoblast. Cytoplasm: slightly wider ring of deep blue cytoplasm than in the pronormoblast and there is a perinuclear halo. Polychromatophilic Normoblast Size: 12-14µm in diameter Nucleus: smaller than in the previous cell, has a thick membrane, and contains coarse chromatin masses. Nucleus: small and central or eccentric with condensed homogeneous structure less chromatin. Reticulocyte After the expulsion of the nucleus a large somewhat basophilic anuclear cell remains which when stained with new methylene blue, is seen to contain a network of bluish granules. This network is responsible for the name of the cell and consists of precipitated ribosomes. As the bone marrow reticulocyte matures the network becomes smaller, finer, thinner, and finally within 3 days disappears. Mature erythrocyte Size: 7-8µm in diameter 21 Hematology Cytoplasm: biconcave, orange-pink with a pale staining center occupying one-third of the cell area. Regulation of Erythropoiesis Erythropoietic activity is regulated by the hormone erythropoietin which in turn is regulated by the level of tissue oxygen. Erythropoietin is a heavily glycosylated hormone (40% carbohydrate) with a polypeptide of 165 aminoacids. Normally, 90% of the hormone is produced in the peritubular (juxtaglomerular) complex of the kidneys and 10% in the liver and elsewhere. There are no preformed stores of erythropoietin and the stimulus to the production of the hormone is the oxygen tension in the tissues (including the kidneys). Ineffective erythropoiesis/Intramedullary hemolysis Erythropoiesis is not entirely efficient since 10-15% of eryhtropoiesis in a normal bone marrow is ineffective, i. In megaloblastic erythropoiesis, the nucleus and cytoplasm do not mature at the same rate so that nuclear maturation lags behind cytoplasmic hemoglobinization. The end stage of megaloblastic maturation is the megalocyte which is abnormally large in size (9-12µm in diameter). Formation of white blood cells (Leucopoiesis) Granulopoiesis and Monocytopoiesis Neutrophils and monocytes, which evolve into macrophages when they enter the tissues, are arise form a common committed progenitor. The myeloblast is the earliest recognizable precursor in the granulocytic series that is found in the bone marrow. On division the myeloblast gives rise to promyelocyte which contain 24 Hematology abundant dark "azurophilic" primary granules that overlie both nucleus and cytoplasm. With subsequent cell divisions these primary granules become progressively diluted by the secondary, less conspicuous "neutrophilic" granules that are characteristic of the mature cells. This concomitant cell division and maturation sequence continues form promyelocytes to early myelocytes, late myelocytes, and they metamyelocytes, which are no longer capable of cell division. As the metamyelocyte matures the nucleus becomes more attenuated and the cell is then called a "band" or "stab" form. Subsequent segmentation of the nucleus gives rise to the mature neutrophil or polymorphonuclear leucocyte.
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If a blood request form is not yet used in your hospital gastritis duodenitis symptoms generic 20 mg nexium free shipping, it can be adapted to meet local needs gastritis problems symptoms nexium 40mg. Any failure to follow correct procedures can lead to incompatible transfusions gastritis dietz order 20mg nexium with mastercard, which may be fatal gastritis korean cheap 40 mg nexium visa. If a blood request form is not yet used in your hospital, talk to senior clinical and blood bank staff about the importance of introducing one, what it should contain and procedures for using it. Any national rules or regulations governing the taking and labelling of blood samples must be followed at all times. All staff responsible for taking blood samples should be specifically trained for this task. Is the procedure for taking blood samples correctly followed by all relevant staff? If there is no formal procedure in your hospital or you think that it could be improved, talk to senior colleagues about the importance of ensuring that blood samples are taken correctly and, in particular, labelled accurately. Organize a training session to ensure that all relevant staff understand the critical importance of accurate labelling of the sample tube. This is particularly important if the patient has had a recent red cell transfusion that was completed more than 24 hours earlier. Antibodies to red cells may appear very rapidly as a result of the immunological stimulus given by the transfused donor red cells. A fresh blood sample is essential to ensure that the patient does not receive blood which is now incompatible. In particular, if a blood ordering schedule is not yet used in your hospital for obstetric and surgical procedures, talk to senior clinical and blood bank staff about the importance of developing one as a guide to blood requirements. The blood bank plays a central part in ensuring that patients receive compatible blood. Typically, the blood bank will reserve these units for a maximum of 48 hours after the time for which they were requested. If uncrossmatched blood is issued in an emergency, this should be clearly indicated on the compatibility label. Individuals who (genetically) lack antigen A or antigen B have antibodies (IgM class) against the red cell type(s) that they have not inherited. However, Rhesus antibodies (anti-Rh D) only appear after a Rhesus negative individual is sensitized by Rh D positive red cells. Anti-A or anti-B recipient antibodies are almost always capable of causing rapid destruction (haemolysis) of incompatible transfused red cells as soon as they enter the circulation. A red cell transfusion that is not crossmatched carries a high risk of causing an acute haemolytic reaction. Note: Red cell concentrates, from which the plasma has been removed, are preferable when non-group specific blood is being transfused. They most often result from errors made in identifying the patient when blood samples are being taken or when blood is being administered. For the treatment of transfusion reactions, see Section 7: Adverse Effects of Transfusion. Even a single transfusion of Rh D positive red cells to a Rh D negative person will usually provoke production of anti-Rh D antibody. This can cause: Haemolytic disease of the newborn in a subsequent pregnancy Rapid destruction of a later transfusion of Rh D positive red cells. These antibodies, which can also cause severe reactions to transfusion, include: Rhesus: C, c, E, e Kell Duffy Lewis. Whatever system is used, the principles for ensuring safe transfusion remain the same. There must be clear, agreed procedures, staff should be trained to follow them and all the basic elements of a quality system need to be in place. These tests may be complicated and can cause considerable delay in providing red cells. When this occurs, non-urgent transfusions and surgery that is likely to require transfusion should be delayed until suitable blood is found in order to avoid risks to the patient. However, when a patient needs transfusion urgently and it is difficult to find compatible red cell units, the doctor responsible for the blood bank should be asked to advise on the risk of a life-threatening reaction if blood is given that is not fully compatible. If blood is required within this period, the sample is thawed and used to perform an urgent compatibility test. Using this method, the blood bank will usually need only 1530 minutes to have blood ready for issue for the patient, provided that blood of a suitable group is available in the blood bank. As a result, the blood bank can make better use of the red cells that it has available. This is often due to mistakes when collecting blood from the blood bank It is therefore essential that every hospital has a standard operating procedure for the collection of blood from the blood bank and its storage in the clinical area prior to transfusion. When blood is issued from the blood bank, the time of issue must always be recorded. The person responsible for the blood bank should make sure that blood does not leave the refrigerator until it is issued for transfusion. It only takes about 30 minutes for a unit of blood to reach 10°C and it is rarely necessary to warm blood before transfusing it. In this event, usually due to shortage of a particular group, the blood bank should inform the clinician responsible and also record the fact on the documentation that accompanies the blood units. Any breaks in the blood cold chain increase the dangers for the recipients of blood products and are wasteful of a scarce, valuable resource. Clinical staff are responsible for ensuring that blood products issued by the blood bank for transfusion are kept at the correct temperature until their infusion into the patient. The upper limit of 6°C is essential to minimize the growth of any bacterial contamination in the unit of blood. The lower limit of 2°C is essential because red cells that are allowed to freeze become haemolysed. If they are transfused, the presence of cell membrane fragments and free haemoglobin can cause fatal bleeding problems or renal failure. Storage at a temperature between 2°C and 6°C is essential to make sure the dextrose is not used too quickly. Whole blood and red cells should be issued from the blood bank in a blood transport box or insulated carrier that will keep the temperature under 10°C if the ambient (room) temperature is greater than 25°C or there is a possibility that the blood will not be transfused within 30 minutes. Unless required for immediate transfusion, the packs should be stored in the ward or operating theatre blood refrigerator at a temperature between 2°C and 6°C (see p. Red cells and whole blood should be infused within 30 minutes of removal from refrigeration. Red cells and whole blood that have been out of the correct storage conditions for more than 30 minutes should never be returned to the refrigerator for later use because of the potential for bacterial contamination and the loss of cell function. Platelet concentrates Platelet concentrates must be kept at a temperature of 20°C to 24°C on a platelet agitator to maintain platelet function. Since there is a risk of bacterial proliferation, the storage life is restricted to 3 or 5 days, depending on the type of blood bag used. Platelets that are held at lower temperatures lose their blood clotting capability. Platelet concentrates should be issued from the blood bank in a blood transport box or insulated carrier that will keep the temperature at about 20°C to 24°C. As with whole blood or red cells, bacteria can proliferate in plasma that is held at ambient (room) temperature. Fresh frozen plasma should be thawed in the blood bank in a waterbath between +30°C and +37°C and issued in a blood transport box in which the temperature is maintained between +2°C and +6°C. If not required for immediate use, it should be stored in a refrigerator at a temperature of 2°C to 6°C and transfused within 24 hours. If the transfusion cannot be started within this period, they must be stored in a refrigerator at a temperature of 2°C to 6°C. The temperature inside every refrigerator used for blood storage in wards, operating rooms and other clinical areas should be monitored and recorded every four hours to ensure that the temperature remains within this range. If the ward does not have a refrigerator that is appropriate for storing blood, the blood should not be released from the blood bank until immediately before transfusion. The units of blood should be kept in baskets in an upright position or laid flat on the shelf. All unused blood products should be returned to the blood bank so that their return and reissue or destruction can be recorded. If it is not, identify any changes needed in the storage and transportation system, including procedures for monitoring and recording the temperature every four hours in all refrigerators used for blood storage.
However gastritis diet 100 buy nexium 20 mg with mastercard, by virtue of its own physicochemical characteristics and biological interactions gastritis medication discount 20mg nexium, iron presents a series of challenges to its safe application gastritis diet oatmeal best nexium 40mg. Even intestinal side effects are usually not seen after oral intake of 3060 mg iron gastritis diet uk cheap nexium 20 mg. However, the subsequent sections are useful to understand the toxic potential of iron. Thus, very high oral iron exposures are needed to produce shock in humans (19, 20), and are relevant to ther- Safety of interventions to reduce nutritional anemias 289 apy and prophylaxis only in the context of accidental overdose. Young children are especially at risk (20) as they may accidentally ingest high iron doses in relation to body weight. They are 40 mg/day for the younger age groups down to infancy and 45 mg/day for adults. The criterion was gastrointestinal irritation, which has been criticized as an erroneous basis for reference to the chronic dietary setting (23). Similar investigations were performed to rank emetic impact and gastrointestinal damage from oral iron in cats and rabbits (15). Such ranking shows that the toxic impact varies among different iron species, in parallel to their relative bioavailability. The implication of animal studies for humans is problematic, however, as considerable differences in the quantitative aspect of iron kinetics have been found among humans, rats, and mice (and even between different stains of mice), with no qualitative differences noted (1618). Acute iron toxicity in humans Ingestion of acute overdoses of oral iron preparations causes mucosal erosion in the stomach and intestine. Blood-containing vomit and diarrhea are the first symptoms, followed by a "silent interval" of up to 24 hours. Gastrointestinal strictures are the long-term sequelae of intestinal damage, and may require surgical intervention. In the course of acute iron intoxication, large amounts of absorbed iron may produce shock symptoms by arteriolar dilatation, capillary leakage, and heart failure, leading to symptoms of shock. These effects are due to mucosal irritation and to altered gastrointestinal motility and depend on the free iron concentration in the lumen (29). More recent data suggest that even 80 mg iron does not increase intestinal side effects in pregnant women beyond the usual discomfort associated with pregnancy (31). Due to the impact of inflammation on ferritin expression and to contradictory findings among different trials, a dose-response relationship for these effects has not been firmly established (21, 23, 32). Moreover, the acute phase protein, antichymotrypsin, was increased in the serum after daily supplementation of 20 mg iron/day for 8 weeks in Guatemalan children (41). To select those oxidative and inflammatory responses that respond to oral iron supplementation in a systematic manner, we investigated the kinetics of changes in 23 biomarkers over time after intake of 120 mg iron/day for 7 days in three volunteers. These responses were not of the magnitude seen in pathological conditions; they were, however, considerably elevated over the baseline state (42), showing that iron intake causes responses in oxidative biomarkers in healthy adult humans. Iron-induced oxidative stress participated in the pathophysiology of inflammatory bowel disease (43) and rheumatoid arthritis (44) in animal experiments. Moreover, systemic inflammation induces catabolic responses in intermediary metabolism (45), which have been suggested as a cause of early growth retardation (46) observed in iron-replete infants supplemented with iron (47, 48). Thus, in iron-deficient children with reduced growth, oral iron supplementation reduced infection prevalence (56, 57) in line with the early observations of McKay. In a number of studies, iron administration improved iron status without negative impact on the prevalence of infection (5860). In line with these observations, a systematic review on iron supplementation and infection found no evidence for increased prevalences in non-malaria areas, with the exception of diarrhea (61). This underscores the nonabsorbed fraction of supplemented oral iron having a negative impact in the gut lumen and increasing prevalence of diarrhea, whereas parenteral iron administration to neonates seems to increase the risk of E. Therapeutic interventions Treatment of iron deficiency anemia Therapeutic iron supplementation employs what might be considered high oral doses, such as of 50400 mg iron/day or cumulative parenteral administration of 250 mg iron/week. The effects on preexisting disease symptoms such as iron deficiency anemia and its consequences (62) can be individually monitored and iron doses should be continuously geared to a changing demand. Iron and bacterial infections in humans the effect of iron on human infections reflects the ambiguity of a nutrient that is needed by the pathogen as well as for host-defence mechanisms. In 1928, McKay (49) reported that iron supplementation reduced respiratory and gastrointestinal infections in London infants by 50%. Hyperferremia after intravenous iron dextran administration seems to last 23 days (53). Thus, parenteral iron administration in the neonatal period is contraindicated (55). Treatment of geohelminth infections As geohelminths do more harm than iron deficiency anemia alone, the net health impact of anthelmintic treatment is likely to go beyond that of iron supplementation. Solomons tation improved iron status and reduced severe anemia but did not alleviate growth retardation or mild anemia. Anthelmintic treatment in the same study, by contrast, also reduced mild anemia in children under 24 months of age, reduced wasting in children under 30 months of age, and increased appetite (65). Thus, effective treatment of iron deficiency in the course of helminth infection requires anthelmintic treatment and iron supplementation simultaneously, and also has additive effects in the control of maternal anemia during pregnancy without signs of malformation. Mebendazole and albendazole are approved for use in children over 12 months of age (67). High-dose therapy may lead to abdominal pain, headache, fever, fatigue, leukopenia, and thrombocytopenia. In hookworm infections use of albendazole seems superior to use of mebendazole (66). Soil-transmitted helminth infections should be treated with albendazole, leomisole, mebendazole, or pyrantel, the latter costing less than $0. Treatment of a child with schistosomiasis with praziquantel is effective in 85% of cases, reducing fecal and urinary egg excretion by 90% (68). This has led to international consensus recommendations for supplementation programs at the population level, notably for two subgroups: pregnant women; and infants and toddlers 624 months of age (70). Gestational supplementation the most venerable nutrient supplementation program in public health has been the prenatal distribution of the hematinic combination of iron and folic acid, generally as a combined tablet. The traditional dosage was a daily dose of 120 mg of iron and 200 µg of folic acid, and this practice remains widespread in developing countries today. This is despite the revision of recommendations in 1998 (70) to a formulation of 60 mg of iron and 200 µg folic acid and a later further adjustment to 400 µg. Concerns for cost, compliance, and safety motivated some professionals to explore intermittent, as opposed to daily, dosing of prenatal hematinics (71). Prophylactic interventions Prophylactic supplementation with iron In contrast to therapeutic situations, large scale public health oral iron supplementation aims primarily to prevent iron deficiency in high risk populations, such as infants 624 months of age or women of childbearing age. At any given point in A Mexico City experience A recent prospective randomized trial among pregnant women in Mexico City addressed the relative safety of two gestational supplementation regimens in terms of hemoconcentration, low birth weight, and premature delivery (39). Sixty pregnant women received a daily supplement tablet of 60 mg of iron, 200 µg of folic acid, and 1 µg of vitamin B12 from their twentieth gestational week onwards, whereas 60 women consumed two tablets (with twice the nutrients) only on one day per week over the same interval. Efficacy for preventing low hemoglobin at delivery was equivalent for both hematinic regimens. Side effects of nausea, heartburn, and constipation were higher in the daily supplement group. Treatment assignment per se was not associated with Safety of interventions to reduce nutritional anemias 293 the adverse pregnancy outcomes. Daily supplementation, however, was associated with a greater number of women with excessively elevated hemoglobin, of >145 g/L (adjusted for altitude) after 816 weeks of supplementation; within this sub-group (n=25 after 16 weeks of supplementation), moreover, the relative risk of low birth weight and prematurity was over 6 times greater than in women with lower hemoglobin (P<0. The safety concern derives from the observation that an altered process in the physiology of red cell circulation mediating poor neonatal outcomes is associated with the recommended prenatal regimen, at least in this high altitude location (2240 m above sea level). For these anemic children such intervention has a "therapeutic" character as they try to "cure" a preexisting deficiency. However, these interventions lack monitoring of the therapeutic success and there is no dose adaptation to changes in demand. The other fraction without iron deficiency obviously has had a sufficient iron supply so far. For them the intervention is prophylactic and aims to prevent future deficiency with the same doses used for the iron-deficient fraction. These children receive iron until they become too old to belong to the high risk group. These iron adequate children run an increased risk of imbalances caused by excess iron, such as impaired growth (47, 48) or dying from malaria (4,73).
