Распространенность и клинические признаки латентного железодефицита и ЖД анемии.

[Dr.Vad]

Некоторые факты распространения железодефицита и ЖДА (в том числе на территории России), а также клинические проявления (цитируется выборочно из "Фармакотерапия железнодефицитной анемии")

Железодефицитные состояния

Железодефицитные состояния (ЖДС) — одна из распространенных форм алиментарной недостаточности, а железодефицитная анемия является наиболее частой в структуре малокровия. По данным ВОЗ, 700 млн человек страдает железодефицитным анемиями (ЖДА). В отдельных регионах их частота среди детей достигает 30-70%, среди женщин — 11-40%, а среди девочек-подростков — 9%. Как показало наше исследование, частота железодефицитных анемий различалась значительно в разных группах: среди студенток-медиков — 12,4%, среди беременных — 10,1%, среди лиц старшей возрастной группы (61-95 лет) — только 3,04%.

Важно знать, что среди населения широко распространен латентный (скрытый) дефицит железа (ЛДЖ), когда показатели гемоглобина еще в норме, но транспортные и органные запасы железа уже истощены. Он колеблется от 19,5 до 30%. Кроме того, от 50 до 86% женщин в различных популяциях имеют факторы риска развития анемии. Четырехлетнее динамическое наблюдение О.В. Сазоновой (1991) показало, что естественное развитие дефицита железа у женщин трудоспособного возраста характеризуется возникновением явного и скрытого малокровия даже среди практически здоровых лиц — в 6,3% и 25% случаев, а среди угрожаемых в отношении ЖДС — в 12,3% и 46,2% случаев соответственно.

В то же время спонтанное (без соответствующей терапии) купирование ЛДЖ в течение двух лет происходит лишь у 13,4% женщин, в 60,0% случаев он сохраняется, а в 26,6% — трансформируется в манифестную форму дефицита железа — анемию.
...............................

Проявления дефицита железа

Недостаток железа, развивающаяся в последующем тканевая и гемическая гипоксия приводят к значительным трофическим изменениям волос (истончение, усиленное их выпадение, раннее поседение). Наряду с этим появляется ломкость ногтей, поперечная их исчерченность, зазубренность ногтевого края, искривление ногтевой пластинки, уплощение, вогнутость ногтей вплоть до ложкообразных (койлонихия), нередко наблюдается недержание мочи. У больных с дефицитом железа возникает извращение вкуса в виде пристрастия к сырому мясу, тесту, к мелу, зубному порошку и т.д. Больных привлекают запахи плесени, бензина, керосина, ацетона и т.д. Сидеропения приводит к атрофии слизистой оболочки языка, ангулярному стоматиту, к глосситу, к кариесу зубов.

При исследовании слизистой оболочки пищевода у таких больных могут выявляться участки ороговения, атрофического изменения в слизистой и в мышечной оболочке пищевода, что может проявиться сидеропенической дисфагией (симптом Пламмера—Винсона). Кроме того, больные ЖДС жалуются на слабость, утомляемость, хроническую усталость, разбитость, снижение работоспособности, головные боли, головокружение, мелькание мушек перед глазами, шум в голове, у них отмечается бледность кожных покровов и слизистых оболочек. Выраженность и сочетания этих проявлений сидеропении зависят от степени тяжести и от длительности дефицита железа. При ЛДЖ эти симптомы отмечаются в 70-80% случаев, а при ЖДА — в 100% и обусловлены снижением железозависимых и железосодержащих ферментов в мышцах и развитием внутриклеточной гипоксии.

У больных с ЖДА отмечаются различные расстройства со стороны сердечно-сосудистой системы в виде вегетативной дисфункции, миокардиодистрофии, в том числе с явлениями некоронарогенной ишемии, кардиомиопатии с нарушением кровообращения различной степени, со стороны нервной системы — вегетососудистые, вестибулярные нарушения; со стороны пищеварительной системы — поверхностные и атрофические гастропатии...

[Dr.Vad]

Некоторые из симптомов, которые могут быть признаками/следствием скрытого железодефицита:

слабость, повышенная утомляемость;
повышенная нервозность и боязливость;
раздражительность, недостаточная концентрация внимания;
снижение трудоспособности, снижение толерантности к физ. нагрузкам;
дневная сонливость;
психологическая лабильность, депрессивное настроение;
головные боли по утрам;
пониженный аппетит;
отвращение к некоторым (чаще мясным) продуктам питания, повышенная тяга к чрезмерному употреблению определенных продуктов питания (шоколад, сладости, газиров. напитки), субпродуктов (сырые макароны, лед) или непищевых веществ (волосы, песок, глина, побелка, шерстяные нитки);
тяжесть в пояснице/боли в спине к концу рабочего дня;
непроизвольное желание шевелить/двигать ногами перед засыпанием;
повышенная предрасположенность к инфекциям (в том числе герперические высыпания на лице, фурункулез, рецидивирующие вагинозы/молочница);
обильные менструальные кровопотери;
гипотония, склонность к обморокам в душной обстановке;
одышка и сердцебиение при обычных физических нагрузках;
зябкость рук и ног, немотивированный субфебрилитет;
сухость кожи;
локальный или генерализованный кожный зуд;
ломкость, выпадение волос;
ломкость и исчерченность ногтей;
трещины кожи ног и рук;
стоматит, глоссит, хейлит, кариес;
голубоватый оттенок склер (белочная оболочка глаза);
трyдности при проглатывании твердой пищи, таблеток;
снижение мышечного тонуса, мышечная слабость;
императивные позывы на мочеиспускание, недержание мочи при смехе и чихании, ночное недержание мочи;
неустойчивый стул, снижение желудочной секреции, атрофический гастрит.

[Dr.Vad]

Signs and Symptoms of Iron Deficiency

(Wintrobe's Clinical Hematology, 11th Edition, 2004)

Iron deficiency anemia, like all anemias, is not a disease but a manifestation of disease, and the clinical presentation may include features of the underlying disease process as well as those of the deficiency state. Many patients, however, seek medical attention because of symptoms of anemia alone. In a study from the 1960s, this mode of presentation was observed in 63% of 371 patients (220). Only 16% visited the physician because of symptoms of the disease causing the anemia. In the remaining 21%, anemia was discovered at the time of evaluation for an unrelated complaint.
The onset of iron deficiency anemia is usually insidious, and the progression of symptoms is gradual. As a result, patients accommodate remarkably well to advancing anemia and may delay a visit to their physicians for prolonged periods.
GROWTH
Iron deficiency impairs growth in infancy, and the growth rate is restored when the deficiency is corrected (188). In one group, 78 of 156 iron-deficient children fell below the twenty-fifth percentile of expected weight.
FATIGUE AND OTHER NONSPECIFIC SYMPTOMS
Iron deficiency anemia can be associated with irritability, palpitations, dizziness, breathlessness, headache, and fatigue. Fatigue is a particularly common complaint among patients. It is clear that even latent iron deficiency (i.e., iron deficiency without any anemia at all) may result in fatigue (302). A group of 44 nonanemic women reporting fatigue were treated both with iron and with placebo in random order. Symptomatic improvement in women receiving iron was significantly better than that of women given the placebo but only in women whose iron stores were depleted. Other investigators have been unable to confirm this observation (303,304), but many practitioners have cared for patients with recurrent iron deficiency who could tell when their stores became depleted because of symptoms that preceded anemia.
NEUROMUSCULAR SYSTEM
Despite the lack of symptoms at rest, investigators have demonstrated that even mild degrees of iron deficiency anemia impair muscular performance, as measured by standardized exercise tests (189,305,306). Total exercise time, maximal workload, heart rate, and serum lactate levels after exercise are all affected adversely in proportion to the degree of anemia. Furthermore, work performance and productivity at tasks requiring sustained or prolonged activity are impaired in iron-deficient subjects and improve when iron is administered (307,308). As a result, measures directed toward iron nutrition of a work force can produce important economic dividends, more than offsetting the costs of the treatment program (189,307).
Abnormalities in muscle metabolism are noted even when deficiency is mild (309). Blood lactate levels were measured in mildly iron-deficient female athletes after standardized exercise tests. Peak lactate levels fell significantly after 2 weeks of iron treatment. This observation led to the suggestion that iron deficiency forces the muscles to depend to a greater extent on anaerobic metabolism than occurs in normal subjects. In contrast, no abnormalities of muscle function were noted in six nonanemic patients with long-standing iron deficiency, induced for the treatment of polycythemia vera (310).
Animal studies confirm that muscle function is disturbed in iron deficiency. The spontaneous activity level of iron-deficient rats decreased (311), and short-term exercise tolerance in treadmill running tests was reduced (181,182,312,313), even at mild degrees of deficiency (314). These abnormalities could not be explained by anemia alone, because they persisted after anemia was corrected by exchange transfusion (181,182). All were corrected promptly when iron was administered.
A variety of behavioral disturbances has been observed in iron-deficient children (188,315,316,317,318 and 319). These children have been reported to be irritable and disruptive, with short attention spans and a lack of interest in their surroundings. Neurologic development in infants (320) and scholastic performance in older children (321) may be impaired. Cognitive performance is defective in iron-deficient rats (322). All of these behavioral abnormalities are ameliorated with the initiation of iron therapy.
The ability to maintain body temperature on exposure to cold is impaired in iron-deficient patients (323) and animals (324). Occasional patients experience neuralgia pains, vasomotor disturbances, or numbness and tingling. In children, iron deficiency has been associated with neurologic sequelae, including developmental delay, ischemic stroke, increased intracranial pressure, papilledema, and the clinical picture of pseudotumor cerebri (325). The pathogenesis is probably complex, involving severe anemia, thrombocytosis, and reduced levels of tissue iron enzymes.
EPITHELIAL TISSUES
Patients with long-standing iron deficiency may develop a constellation of symptoms characterized by defective structure or function of epithelial tissue. Especially affected are the nails, the tongue and mouth, the hypopharynx, and the stomach. These epithelial lesions tend to occur together in the same patients at the same time (326,327) but also may occur as isolated findings.
In iron-deficient subjects, the fingernails may become brittle, fragile, or longitudinally ridged, but these findings are quite nonspecific. Alterations more typical of iron deficiency are nail thinning, flattening, and ultimately the development of koilonychia, concave or “spoon-shaped” nails. Koilonychia is now rarely seen in clinical practice, but of 400 babies attending a well-baby clinic in West Virginia before 1970, 5.5% had koilonychia, and nearly all of these infants appeared to be iron-deficient (328). Koilonychia is a relatively nonspecific finding, which can also result from prolonged, repeated exposure to hot soapsuds and other caustic agents.
Oral abnormalities, including atrophy of the lingual papillae, are the most common of iron deficiency–induced epithelial changes. These may present as soreness or burning of the tongue, either spontaneously or stimulated by food or drink, and by varying degrees of redness (326). The filiform papillae over the anterior two-thirds of the tongue are the first to atrophy and may disappear completely. In severe cases, fungiform papillae also may be affected, leaving the tongue completely smooth and waxy or glistening (329). These changes are generally reversed after 1 to 2 weeks of iron therapy. Angular stomatitis, characterized by ulcerations or fissures at the corners of the mouth, is a less specific sign of iron deficiency, and it also occurs in riboflavin and pyridoxine deficiencies.

[Dr.Vad]

The association of dysphagia, angular stomatitis, and lingual abnormalities with hypochromic anemia was reported as early as the beginning of the twentieth century. Dysphagia affects women more often than men and is relatively uncommon in patients younger than age 30 years. However, it has been observed in adolescents (188,326) and even toddlers (author's unpublished observations). Patients with sideropenic dysphagia (also known as Paterson-Kelly syndrome and Plummer-Vinson syndrome) note a gradual onset of difficulty swallowing and describe discomfort localized to the area of the neck near the cricoid cartilage. They experience dysphagia with solid foods but have little problem with liquids. If not treated, the dysphagia worsens, and ultimately the diet is so restricted that it interferes with the maintenance of balanced nutrition.
The most common anatomic lesion is a “web” of mucosa at the juncture between the hypopharynx and the esophagus (330). These webs, which may be multiple, usually extend from the anterior wall into the lumen of the esophagus, but they may encircle the lumen completely, forming a cufflike structure. In some patients, a benign stricture is noted, and the opening into the esophagus at the cricoid area may be reduced to the size of a pinhole or slit. Postcricoid webs may occur in the absence of documented iron deficiency, but nearly all affected patients were iron-deficient in one investigative series (327). Both webs and strictures may be demonstrated by radiographic examination (lateral view) of the neck after barium swallow. Multiple exposures or cineradiography are required for optimal demonstration of these abnormalities.
At biopsy, the webs appear to be constructed of normal epithelium with underlying loose connective tissue, sometimes showing a chronic inflammatory reaction. In a small percentage, hyperchromatic nuclei and increased mitotic activity are observed in the basal cell layer. Biopsy of the strictures demonstrates chronic, nonspecific inflammation and degeneration of striated muscle. Carcinoma in the postcricoid area has been noted as a late complication of the syndrome in 4 to 16% of patients (326).
For relief of the dysphagia, clinicians often must rupture the webs, dilate the stenosis, or both, although treatment with iron supplements often relieves dysphagia in mild cases if the associated webs are small (331,332).
The variation in the prevalence of sideropenic dysphagia suggests that factors other than iron deficiency may contribute to oroesophageal abnormalities. Genetic factors may be important, as may some unrecognized coexisting nutritional abnormalities.
Gastric biopsy demonstrates the presence of gastritis of varying severity in a substantial fraction of iron-deficient patients. These lesions are nonspecific and often asymptomatic and may be indistinguishable from those seen in association with pernicious anemia. Varying degrees of reduction in gastric secretion are associated with the gastritis. As gastric damage progresses, patients lose the ability to secrete acid, pepsin, and intrinsic factor. Achlorhydria has been reported to occur in infants and children as well as in adults (188). Antibodies to gastric parietal cells have been described in approximately one-third of patients with iron deficiency (326,333). Although the mechanism of production of these antibodies is not understood, they appear to be a manifestation, rather than a cause, of gastritis.
IMMUNITY AND INFECTION
The relationship between iron deficiency and infection is complex (334,335 and 336). Iron deficiency clearly results in at least two abnormalities in the immune response: defective lymphocyte-mediated immunity and impaired bacterial killing by phagocytes. Evidence of defective cellular immunity includes as much as a 35% reduction in the number of circulating T cells. Both helper and suppressor T cells are affected (337). In addition, iron-deficient subjects do not respond as well as normal subjects to certain skin test antigens, such as to Candida, diphtheria, and Trichophyton. These abnormalities can be corrected by the administration of iron. No abnormalities have been noted in testing with tuberculin or dinitrochlorobenzene. Ribonucleotide reductase is an iron-containing enzyme required for the synthesis of DNA for cell division. Some authors have suggested that reduced levels of this enzyme might lead to impaired ability of the T cells to proliferate, thereby accounting for the defects in cell-mediated immunity, but others have reported changes in cytokine production in iron-deficient patients.
The nitroblue tetrazolium dye test of phagocyte function yielded abnormal results in iron-deficient children, and the abnormality could be corrected by iron administration (338,339). Furthermore, a decrease in the magnitude of the “oxidative burst” accompanying phagocytosis was observed (340). Finally, killing of several types of pathogenic bacteria by neutrophils was defective (338,341).
The sequence of changes in neutrophil function was studied as iron deficiency developed in rats. Myeloperoxidase activity was reduced to a greater extent and responded more slowly to iron therapy than did defects in the oxidative burst (342). Because the oxidative burst is considerably more important in bacterial killing than is myeloperoxidase, the observations suggest that the neutrophil conserves its most important function as the deficiency develops. The defect in the oxidative burst could be demonstrated only with the use of agents that induced phagocytosis; no defect was noted when the burst was stimulated by soluble agents. Thus, phagocytosis, rather than the oxidative burst itself, may be at fault.
Taken together, these abnormalities provide a basis for an expectation that resistance to infection may be impaired in iron deficiency. Conversely, considerable data suggest that iron deficiency and iron sequestration by binding proteins protect against infection by depriving the invading organisms of the metal. Thus, optimal immune function is highly dependent on iron balance; both iron-deficient and iron-overloaded hosts are at higher risk for infection.
PICA
Pica is a striking symptom of iron deficiency. Hippocrates wrote that a “craving to eat earth” was associated with “corruption of the blood.” Abnormal eating patterns were also a prominent manifestation of chlorosis.
Pagophagia, defined as the purposeful eating of at least one tray of ice daily for 2 months, is a common form of pica. In one study, the ingestion of ice averaged nearly 2 kg/day, and some patients ate an astounding 4 to 9 kg/day (343). This dramatic symptom was relieved within 1 to 14 days after iron was administered. Another study found that pagophagia was a symptom of iron deficiency in 23 of 38 consecutive adult patients, and iron therapy was curative (344). Pica is especially striking when the patient consumes bizarre, nonfood substances (226).
Crosby estimated the incidence of pica in his iron-deficient patients to be 50% (345). Approximately one-half of them ate ice; the rest experienced “food pica.” The latter consists of compulsively eating one food, often something that is brittle and makes a crunching sound when chewed (346). Because patients may be ashamed of this compulsive habit, they often do not volunteer the information during the medical interview. Direct, tactful inquiry is necessary to elicit the history of pica.
GENITOURINARY SYSTEM
Disturbances in menstruation are common in iron deficiency, and not infrequently, iron deficiency results from, or is exacerbated by, excessive menstrual blood loss. Beeturia, the excretion of a pink to red pigment in the urine after the ingestion of beets, has been reported to be more common in iron-deficient patients than in normal subjects (347). However, it is likely that a significant fraction of the normal population also has this symptom (348).
SKELETAL SYSTEM
Changes in the skull similar to those found in association with thalassemia or chronic hemolytic anemia have been reported in children with iron deficiency anemia of long duration (349,350). The diploic spaces may be widened, and the outer tables thinned, at times with vertical striations producing a hair-on-end appearance. In addition, abnormalities of the long bones are noted, especially the metacarpals and phalanges, with expansion of the medulla and thinning of the cortices (350). These changes likely result from expansion of the erythroid marrow during bone growth and development.

[Dr.Vad]

The deleterious effects of iron deficiency and iron deficient anaemia are due partly to impaired delivery of oxygen to the tissues and partly to a deficiency of iron containing compounds, especially enzymes, in various tissues. Restlessness and irritability in children who are deficient in iron has been related to increased concentrations of catecholamines, which return to normal after treatment with iron. Lower IQ scores have been found in UK and American adolescent girls who are deficient in iron. Abnormalities in response to infection have been shown in people who are deficient in iron, where decreased neutrophil function and impaired T cell proliferation occurs. Studies in humans have confirmed the findings from animals of reduced work capacity and poor work performance in iron deficient anaemia. Reduced thermoregulation has also been confirmed in people who are iron deficient where norepinephrine concentration was increased, and differences were found in concentrations of epinephrine, dopamine, triiodothyronine, and thyroxine. Normal concentrations for these parameters were restored after iron supplementation. Hair loss has been reported in women with iron deficiency, which responded to iron supplementation. The quantity of non-haem iron in the brain is to a large extent independent of the iron stores in the body. Overall, 10% of the iron complement of the adult brain is present at birth, and by the age of 10 this has reached 50%; however, not until the early 20s is the full adult complement achieved. Although most of the deleterious effects of iron deficiency can be reversed by appropriate iron supplementation, of concern is the possibility that if during the adolescent years a shortfall exists, then, as in rats, humans may not be able to make up the deficiency by iron supplementation, and adolescent girls may enter adult life with a compromised complement of iron in the brain.

(BMJ 2001;322:1355-1357)

[Dr.Vad]

Очень свежий и толковый обзор по ЖДА:

Killip S, Bennett JM, Chambers MD.
Iron deficiency anemia.
Am Fam Physician. 2007 Mar 1;75(5):671-8

[Ссылки доступны только зарегистрированным пользователям ]

[Dr.Vad]

Zimmermann MB, Hurrell RF.
Lancet. 2007 Aug 11;370(9586):511-20.


Epidemiology

WHO estimates that 39% of children younger than 5 years, 48% of children between 5 and 14 years, 42% of all women, and 52% of pregnant women in developing countries are anaemic,6 with half having iron deficiency anaemia.7 According to WHO, the frequency of iron deficiency in developing countries is about 2·5 times that of anaemia.6 Iron deficiency is also common in women and young children in industrialised countries. In the UK, 21% of female teenagers between 11 and 18 years, and 18% of women between 16 and 64 years are iron deficient.8 In the USA, 9–11% of non-pregnant women aged between 16 and 49 years are iron deficient, and 2–5% have iron deficiency anaemia, with more than twofold higher frequency in poorer, less educated, and minority populations.9 In pregnant women of low-income areas in the USA, the frequency of iron deficiency anaemia in the first, second, and third trimesters is 2%, 8%, and 27%, respectively.9 In France, iron deficiency and iron deficiency anaemia affect 29% and 4% of children younger than 2 years;10 in the USA, 2% of children between 1 and 2 years have iron deficiency anaemia.1

Adverse effects

The high frequency of iron deficiency anaemia in the developing world has substantial health and economic costs. In an analysis of ten developing countries, the median value of physical productivity losses per year due to iron deficiency was about US$0·32 per head, or 0·57% of the gross domestic product.54 In the WHO African subregion, it is estimated that if iron fortification reached 50% of the population, it would avert 570 000 disability adjusted life years (DALYs) every year.55 During the first two trimesters of pregnancy, iron deficiency anaemia increases the risk for preterm labour, low birthweight, infant mortality, and predicts iron deficiency in infants after 4 months of age.[56] and [57] Estimates are that anaemia accounts for 3·7% and 12·8% of maternal deaths during pregnancy and childbirth in Africa and Asia, respectively.58 Data for the adverse effects of iron deficiency on cognitive and motor development in children are equivocal because environmental factors limit their interpretation.[59], [60] and [61] Several studies reported adverse effects of iron deficiency anaemia on infant development that might be only partly reversible.[59] and [60] Other studies suggest that no convincing evidence exists that iron deficiency anaemia affects mental or motor development in children younger than 2 years, but that iron deficiency adversely affects cognition in school children.61 Anaemic school-children have decreased motor activity, social inattention, and decreased school performance.60 Whether adverse effects of iron deficiency on neuromotor development are due to anaemia or absence of iron in the developing brain is unclear.62 Iron deficiency anaemia increases susceptibility to infections, mainly of the upper respiratory tract, which happen more often and have a longer duration in anaemic than in healthy children.63 A recent study showed no positive effect of iron supplementation on physical growth during childhood.64 The response to iodine prophylaxis is reduced in goitrous children with deficiencies of both iodine and iron,[65] and [66] probably because of impairment of the haem-dependent enzyme, thyroid peroxidase.67 Iron supplementation can increase low serum retinol concentrations in iron-deficient children.[68] and [69] Iron deficiency might increase the risk for chronic lead poisoning in children exposed to environmental lead.70 In adults, physical activity is reduced,71 and manual labourers in developing countries are more productive if they are given iron and treated for hookworm and other infections.72 Iron deficiency, even in the absence of anaemia, might cause fatigue and reduce work performance.[73] and [74]

[Galunyap]

а где бы на русском взять выше написанное?

[Dr.Vad]

Оптимально - обратиться к мед. переводчику, на русском нигде таких материалов мне не попадалось...

[Dr.Vad]

нормы ферритина и др. маркеров железного статуса организма в США по возрастам и национальностям 1999-2000

Iron-Status Indicators

[Ссылки доступны только зарегистрированным пользователям ]