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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 However, it has been observed in adolescents (188,326) and even toddlers (author's unpublished observations).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.
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 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.
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).
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.
Вадим Валерьевич.