Приглашение к дискуссии: железодефицит и нарушения НС

[Mak]

Уважаемый Михаил Владимирович!



При наличии таких значений подозрение на железодефицит может натолкнуть низкий средний обьем эритроцита (80 фл и менее), пониженное содержание гемоглобина в эритроците (28 пг и ниже) и особенно наличие анизоцитоза: широта распределения эритроцитов более 14,5%.



Все эти показатели дает автомат. счетчик; если его нет, то отношение сывороточного железа к общей железосвязывающей способности сыворотки (норма 30-35%, менее 20-25% дефицитное состояние, более 45% -повышенное всасывание, вероятность перегрузки организма железом). Оба низкие при анемии - скорее всего ее генез - воспалительный.



О ферритине не упоминаю (и тем более о рецепторах к трансферрину и пр.), тк в большинстве лабораторий это исследование недоступно.



Спасибо, а как в показателях автоматического счётчика называются средний обьем эритроцита и содержание гемоглобина в эритроците?



И, если не сложно, как по показателям автоматического счётчика заподозрить В12 дефицит?

 

[IGM]

Уважаемый Алгор!



Опять-таки, не скажу конкретно за тонзиллит или или ВИЧ (отсутствуют данные), но существует небольшой клин. эвиденс, где коррекция железодефицита снижала частоту рецидива герпетич. инфекции и фурункулеза; по моим личным наблюдениям тоже есть свидетельства, что после коррекции ЖД снижается частота простудных заболеваний. Ничто не мешает этим и др. нозологиям сосуществовать вместе, но считаю, что и лечение должно быть направлено на коррекцию каждой из них.

Вспоминаются в связи с этим частые рекомендации наших больничных кардиологов моим пациентам с миеломной болезнью (обычно пожилые пациенты с ИБС): "все ваши сердечные беды от основного заболевания, вот вылечит вас гематолог - все и пройдет, а не вылечит - так и будете мучаться" Приходилось самому быть и кардиологом и гастроэнтероголом и невропатологом и при ОТСУТСТВИИ рекомендаций от этих специалистов после их консультации самому корректировать сопутствующую патологию.

 

[Solaire]

Спасибо, а как в показателях автоматического счётчика называются средний обьем эритроцита и содержание гемоглобина в эритроците?



И, если не сложно, как по показателям автоматического счётчика заподозрить В12 дефицит?



MCV - средний объем, который в фемто-литрах измеряется

МСН - гемолглобин в эритроците



B12 дефицит наверное по макроцитозу заподозрить и по высокому цветовому показателю. Хотя объем эритроцита еще при алкоголизме растет

 

[sve]

Уважаемый Михаил Владимирович!



Пру В12 дефицитной анемии MCV обычно более 100 и нередко 110-120, при фолатных - значения меньше 95-105 (норма 80-95 фл). Увеличивается и MCH - более 33 пг, тогда как средняя концентрация гемоглобина в эритроците (MCHC) на верхней границе 35-36 г/дл.



Повышение MCV неплохо коррелирует с уровнем гомоцистеина в крови (основной метаболит при дефиците кобаламина/фолата) и похоже является фактором риска при атеросклерозе. Если интересно, то 2 релевантных тезисов:



Acta Med Austriaca. 2002;29(2):57-60.



Erythrocyte mean cellular volume and its relation to serum homocysteine, vitamin B12 and folate.



Haltmayer M, Mueller T, Poelz W.



Department of Laboratory Medicine, Konventhospital Barmherzige Brueder, Seilerstaette 2, A-4014 Linz.



Cobalamin (B12) and folate deficiency is related to both increased erythrocyte mean cellular volume (MCV) and raised serum total homocysteine (tHcy) values. Furthermore, there are indications that B12 and folate serum values do not represent the tissue status of the two vitamins exactly. Therefore, a direct relationship between MCV and tHcy, if demonstrated, could support the hypothesis that tHcy is a better indicator for the cited vitamin status than the serum levels of B12 and folate. We studied MCV, gamma glutamyl transferase (GGT), serum B12, folate and tHcy values in 200 hospitalized patients. There was a significant correlation of MCV with GGT (r = 0.266, P < 0.001) and with tHcy (r = 0.248, P < 0.001), but not with serum B12 and folate. Stepwise multiple linear regression with MCV as dependent and GGT, B12, folate and tHcy as independent variables, respectively, revealed significant associations of MCV with GGT (B = 2.18, 95% CI 0.95-3.42, P = 0.001) and tHcy (B = 3.33, 95% CI 1.26-5.39, P = 0.002). By removing tHcy from this model, serum B12 became a significant predictor of MCV (B = -1.70, 95% CI -3.25 to -0.15, P = 0.032). Serum folate was not significantly associated with MCV in multivariate analysis. In conclusion, the present study confirms indications that serum B12 and folate values lack clinical sensitivity and specificity in diagnosing vitamin deficiency states by showing MCV was better associated to tHcy, than to B12 or folate serum levels. This observation demonstrates that tHcy may be useful in diagnosing patients with B12 and/or folate deficiency.



--------------------------------------------

Ann Vasc Surg. 2002 Jul;16(4):474-9.



Erythrocyte mean corpuscular volume associated with severity of peripheral arterial disease: an angiographic evaluation.



Haltmayer M, Mueller T, Luft C, Poelz W, Haidinger D.



Department of Laboratory Medicine, Konventhospital Barmherzige Brueder Linz, Linz, Austria.



Elevated erythrocyte mean corpuscular volume (MCV) may be a risk factor for peripheral arterial disease (PAD). The aim of the present study was to evaluate whether MCV was associated with the severity of atherosclerotic findings in the lower limbs of PAD patients, as measured by an angiographic scoring system based on vessel lumen reduction. One hundred male patients with symptomatic PAD were studied. MCV was significantly correlated with the angiographic score (rs = 0.247, p = 0.013). PAD patients with an angiographic score in the lower third were compared to those with values in the upper third using a logistic regression model with age, smoking, hypertension, MCV, homocysteine, and total cholesterol and triglycerides as independent variables. This model revealed significant odds ratios (OR) for MCV (OR = 2.02 for an increment of 5 fl, 95% CI = 1.08-3.8) and for age (OR = 2.41 for an increment of 10 years, 95% CI = 1.21-4.81) and facilitated classification of 71% of all subjects correctly. In conclusion, MCV may be associated with angiographically determined disease severity in patients with PAD. This finding supports the hypothesis that MCV is a risk factor for PAD, although the mechanism by which MCV may contribute to the presence and severity of the disease is not yet determined.

 

[tase4ka]

Уважаемый Александр!



Алкоголизм - один из факторов риска развития фолиеводефицита/-ной анемии.

 

[sbk2005]

Уважаемые коллеги!



Ухожу в отпуск, поэтому не смогу очень часто бывать на форуме (и заодно активно выявлять у всех обращающихся свой "любимый" ЖД). Те не менее по возможности постараюсь ответить на все Ваши замечания. Напоследок недавние тезисы с характерным названием (просто попались на глаза) - я бы правда перефразировал на "еще один повод предупреждать железодефицитную анемию у детей":



J Child Neurol. 2004 Jul;19(7):526-31.



Cerebral sinovenous thrombosis in children: another reason to treat iron deficiency anemia.



Benedict SL, Bonkowsky JL, Thompson JA, Van Orman CB, Boyer RS, Bale JF Jr, Filloux FM.



Division of Pediatric Neurology, Department of Pediatrics, The University of Utah and Primary Children's Medical Center, Salt Lake City, UT 84113, USA.



Iron deficiency anemia is a rare cause of cerebral sinovenous thrombosis in children. We report three cases of cerebral sinovenous thrombosis and iron deficiency anemia treated at Primary Children's Medical Center in Salt Lake City, Utah, between 1998 and 2001. The children were 9, 19, and 27 months old at the time of admission. Hemoglobin levels ranged from 6.6 to 7.0 g/dL, mean corpuscular volume levels from 45 to 56 fL, and platelet counts from 248,000 to 586,000/microL. Magnetic resonance imaging and magnetic resonance venography revealed thrombosis of the straight sinus and internal cerebral veins in all three children, with the addition of the vein of Galen, left transverse and sigmoid sinuses, and upper left internal jugular vein in one child. Recovery ranged from excellent to poor in 3 months to 3 years of follow-up. Four additional cases, ages 6 to 22 months, were found in the English-language literature. Evaluation for prothrombotic disorders was negative in all children, including the current cases. Treatments have included thrombectomy, corticosteroids, mannitol, heparin, low-molecular-weight heparin, warfarin, aspirin, blood transfusion, and iron supplementation, but there is no consensus regarding therapy, other than to correct the anemia and treat iron deficiency. Iron deficiency anemia, a preventable cause of cerebral sinovenous thrombosis, deserves consideration when cerebral sinovenous thrombosis is detected in young children.

 

[Вилисович]

Дефицит железа и нарушения миелинизации:



Iron deficiency is a common nutritional disorder, especially in children, affecting over 25% people worldwide (Cook et al., [1994]; Beard and Connor, [2003]). Iron deficiency during pregnancy in humans is frequently associated with prematurity and perinatal mortality (Beard, [2003]). Children who experienced iron deficiency suffer behavioral defects, such as impaired learning and memory function (Lozoff et al., [1987]; Baynes, [1996]). Iron deficiency in humans is reportedly associated with a decrease in auditory and visual evoked potentials attributed to hypomyelination (Algarin et al., [2003]). This attribution in consistent with magnetic resonance imaging in human infants indicating that altered iron status is associated with hypomyelination (Deregnier et al., [2000]). A relationship between iron and brain function has been more directly assessed in rodent models, in which iron deficiency is reportedly associated with persistent changes in resting energy status, neurotransmission, and myelination (Rao et al., [2003]). A direct effect of iron deficiency on myelin has been shown, which includes a decrease in lipids (Larkin and Rao, [1990]; Oloyede et al., [1992]; Kwik-Uribe et al., [2000]) and some proteins (Beard et al., [2003]).



Из J Neurosci Res. 2004 Sep 1;77(5):681-9. Effect of manipulation of iron storage, transport, or availability on myelin composition and brain iron content in three different animal models. Ortiz E, Pasquini JM, Thompson K, Felt B, Butkus G, Beard J, Connor JR.

 

[kangaroo]

Неврологические последствия дефицита железа у человека:



Из Yager JY, Hartfield DS.Neurologic manifestations of iron deficiency in childhood.

Pediatr Neurol. 2002 Aug;27(2):85-92.



Iron deficiency anemia and infant development



Lozoff and colleagues have performed extensive work on iron deficiency and neurodevelopment. Their work includes studying a group of Costa Rican children starting from infancy to adolescence to determine the effects of early iron deficiency anemia on development. The initial study began with a cohort of 191 well infants 12-23 months of age that had hematologic testing to determine hemoglobin and iron status. Bayley Scales of Infant Development were completed at baseline 1 week and 3 months after intramuscular or oral iron therapy with a placebo control group. The infants with moderately severe iron deficiency anemia (hemoglobin less than 100 g/L) had both lower mental and motor scores at baseline. No group had a significant change in test scores after 1 week of therapy of either oral or intramuscular iron. Anemia was corrected within 3 months of iron therapy in all treated infants, although 64% still had evidence of iron deficiency. The scores of infants with persistent iron deficiency at 3 months remained significantly lower than those of control subjects. The children who had correction of iron deficiency and anemia (36%) had no difference in test scores vs control subjects. The group concluded that those who did not have a reversal of iron deficiency within 3 months of treatment had more severe or chronic iron depletion before therapy was initiated. Iron treatment to correct anemia was not sufficient to reverse neurobehavioral changes, or perhaps more severe iron deficiency resulted in irreversible deficits. Subsequent work utilizing extended oral iron therapy for 6 months in iron-deficient anemic infants also demonstrated that cognitive deficits were irreversible even after 6 months of therapy.



The second study followed the same cohort of infants at 5 years of age. The retention rate was 85%. All children, regardless of iron status in infancy, had comparable nutritional status. The children with moderately severe anemia in infancy had lower mental and motor scores in most areas compared with their nonanemic peers. It was suggested that prolonged severe iron deficiency in infancy is associated with poor developmental outcome at 5 years of age.



The third study followed the same cohort at 11-14 years of age. Again 87% of original patients were re-evaluated. All children had normal growth and nutritional status without evidence of iron deficiency. The group with iron deficiency in infancy again demonstrated a variety of deficits with lower verbal and full-scale intelligence quotient scores and had specific problems in writing and mathematics. Lower motor scores were also demonstrated. Those children who had iron deficiency in infancy were more likely to have repeated a grade or require special services, such as tutoring. These children were also more likely to have behavior problems.



Walter et al. studied a cohort of 196 Chilean infants from infancy to 5 years of age. Again, iron-deficient anemic infants had lower baseline mental and psychomotor scores that were not corrected after 3 months of iron therapy. Further analysis of the data suggested that prolonged iron deficiency and severe anemia in infancy result in irreversible developmental changes despite correction of anemia. In follow-up at 5 years of age, the formerly iron-deficient group scored significantly lower in fine motor skills on the Woodcock-Johnson preschool cluster scale, and these children also had neurologic immaturity with "soft signs" demonstrated on physical examination.



Others researchers have also followed formerly iron-deficient infants through their school and adolescent years. One group demonstrated that 7-year-old Israeli children who were anemic in infancy had lower achievement scores than peers. Another group demonstrated a significant association between iron deficiency in infancy and mental retardation at 10 years of age in American children.



Lozoff has performed other work with iron-deficient infants and children. Short-term effects of iron therapy in infants with iron deficiency have been studied. Again anemic children had significantly lower baseline mental and motor scores compared with control subjects. The differences were most marked in the 19-24-month-old age group who presumably had more severe and protracted iron deficiency. These deficits persisted after 1 week of iron treatment. Similar results were achieved in the group of Chilean infants studied by Walter.



Lozoff’s study also demonstrated that behavioral abnormalities in iron-deficient anemic infants are rapidly reversible. At baseline the anemic infants exhibited several abnormalities that resolved after 1 week of iron therapy, with "increased fearfulness" being the only difference remaining between treatment and control groups. Lozoff has looked further at behavior of iron-deficient infants and has concluded that anemic infants are "functionally isolated" as a result of altered interaction with their physical and social environment. This in turn interferes with their natural development, resulting in motor and cognitive delay. Other authors have also attributed abnormal test scores to a behavioral deficit observed with iron deficiency anemia.



Although most studies have revealed that the deficits observed in infants with iron deficiency anemia are irreversible, not all studies are in agreement. Reversal of mental and psychomotor deficits found at baseline testing after 4 months of iron treatment in a group of 12 to 18-month-old Indonesian infants has been demonstrated. Also Moffat et al. demonstrated a transient decline in psychomotor development and no changes in behavior or mental development in a cohort of iron-deficient inner-city Canadian infants.



Marginal iron deficiency and infant development



Mild iron deficiency without anemia also results in developmental abnormalities. Short-term effects of intramuscular iron treatment of 9 to 12-month-old infants with marginal iron deficiency demonstrated baseline developmental scores of those with iron deficiency to be lower than nonanemic control subjects. One week after treatment the scores of the iron-deficient group improved significantly from baseline, whereas those of the control group did not. Interestingly, a behavioral deficit was not evident in this cohort of infants with marginal iron deficiency. These results were also found in another study of infants with marginal iron deficiency in which there was no difference in overall behavior, except "excessive fearfulness". Although the abnormalities may seem subtle and reversible in those children with mild iron deficiency, children with marginal iron deficiency in infancy who did not improve with iron therapy had lower achievement scores when tested at 5 years of age.



Children and adolescents with iron deficiency



Older children with iron deficiency also have cognitive impairment. Preschool children with iron deficiency with or without anemia have been shown to have problems with inattention resulting in difficulties with higher cognitive function. Other studies have demonstrated lower scores on cognitive testing of iron-deficient anemic adolescents. One large study involved a survey of 5,398 American children from 6 to 16 years of age from 1988 to 1994. Three percent were iron deficient, with the highest prevalence occurring in adolescent females. Children with iron deficiency with or without anemia were more than twice as likely to have mathematics problems.

 

[Н.И.П.]

Pediatric stroke



Pediatric stroke is uncommon, occurring in approximately 2.0-3.0/100,000 children per year. A recent review of pediatric stroke demonstrated no etiology in 20-36% of patients with ischemic stroke and 16% of patients with hemorrhagic stroke. Stroke in association with iron deficiency has been reported in the pediatric and adult literature in a number of case reports, and includes ischemic and thrombotic events. Children with cyanotic congenital cardiac disease are well recognized as being at increased risk of venous thrombosis. Interestingly enough, this has not been demonstrated in adult patients with cyanotic congenital heart disease. Hartfield et al. reported a series of six otherwise well children, 6-18 months of age, who presented with an ischemic stroke or venous thrombosis after a viral prodrome. All patients had iron deficiency as their underlying etiology after other known causes of stroke were excluded.



Three hypotheses have been proposed to explain the association between iron deficiency and stroke.



Thrombocytosis secondary to iron deficiency has been proposed as one mechanism. Iron regulates platelet production by inhibiting thrombocytosis. Hence, with mild-to-moderate iron deficiency, thrombocytosis occurs. Severe iron deficiency can cause thrombocytopenia. In adults, thrombocytosis secondary to conditions such as myeloproliferative disorders are a cause of thrombotic events. This differs from children in whom reactive thrombocytosis is benign.



A second theory is that iron deficiency results in a hypercoagulable state. The microcytic poorly deformable red blood cells increase blood viscosity and increase risk of venous thrombosis. This is the presumed mechanism for venous thrombosis in children with congenital cardiac disease whose hyperviscosity as a result of hypoxemia is exacerbated by iron deficiency. This particular group of children also had cerebrovascular dilatation, which slows blood flow and further promotes thrombosis.



Finally, transient hemiplegia and cerebellar infarct have been attributed to anemic hypoxia. The anemic state is well tolerated until a viral illness increases metabolic demands that cannot be met in the face of anemia. Decreased iron-dependent enzymes necessary to metabolic processes may contribute to impaired energy metabolism and oxygen utilization. This finding results in ischemic damage to areas of the brain supplied by end arteries and may manifest as transient hemiplegia or infarct. This theory is supported by resolution of transient hemiplegia after blood transfusion in patients with iron deficiency anemia.



Breath-holding spells



Breath-holding episodes have also been associated with iron deficiency. Episodes occur in up to 27% of children. Although benign in nature, breath-holding episodes result in much parental anxiety. The pathophysiology is unclear, although autonomic dysregulation resulting in vagally mediated cardiac arrest and subsequent cerebral anoxia has been proposed. Anemia has been suggested to exacerbate the likelihood of breath-holding episodes because the lower hemoglobin results in more rapid cerebral anoxia secondary to decreased oxygen-carrying capacity. Also, iron-deficient children are more irritable, which increases the likelihood of a spell.



Holowach et al. demonstrated a correlation between breath-holding episodes and anemia in a retrospective study. One-hundred and sixty children 3 months to 3 years of age with breath-holding episodes were reviewed over a 10-year period. Two control groups were used, including one group of 192 children with febrile seizures or myoclonus and a group of 572 hospitalized children with other medical conditions. Hemoglobin values were compared between the groups. Of those with breath-holding episodes, 23.5% had hemoglobin concentrations less than 79 gm/L compared with 2.6% of the children with seizures and 6.9% of hospitalized children. Other researchers have also demonstrated an association between iron deficiency anemia and breath-holding episodes with a decrease or resolution of the episodes after iron therapy.



This observation was further substantiated by a double-blind placebo-controlled study of iron treatment for breath-holding episodes with 33 treatment and 34 placebo patients who demonstrated a response to iron therapy. More than 50% of the treatment group had no further breath-holding episodes, and another 36.4% had a partial response with 50% fewer episodes. None of the placebo group had a complete response, and 5.9% had a partial response. The lower the hemoglobin at onset, the more likely the patient was to respond. It was concluded that iron is an important treatment for breath-holding episodes in children, especially those with iron deficiency.



Pseudotumor cerebri



Since the 1800s, pseudotumor cerebri secondary to iron deficiency has been a recognized phenomena. It is most common in young females. The mechanism by which this occurs is unclear, although one theory suggests that tissue hypoxia leads to increased capillary permeability and primary brain edema, after which subsequent papilledema as a result of the increased intracranial pressure occurs. Other researchers have suggested that abnormalities in hemodynamics result in increased cerebral blood flow, causing increased intracranial pressure and papilledema. Also depletion of iron-containing enzymes has also been hypothesized to play a role. In infancy, these changes may manifest as a bulging fontanel rather than papilledema. Pseudotumor cerebri in this setting is reversible with iron therapy.



Another neurologic abnormality observed with iron deficiency anemia is bilateral cranial nerve VI palsy. This is proposed to be a consequence of increased intracranial pressure or focal pontine ischemia.

 

[д-р Куршакова]

MCV - средний объем, который в фемто-литрах измеряется



Это описка. Фентолитр - 10 в минус 15 степени литра.

MCV - mean cellular volume (mean corpuscular volume).

 

[Да-шутка]

Уважаемый Алон!



В том то вся и проблема, что встречается написание как ...volume of about 10-15 L (1 femtoliter)...metric unit of volume the femtolitre (US femtoliter)..., так и ...fentoliter. fl. 0.000000000000001L ... fl = Fentoliter



В отечественной периодике все же чаще встречаются феМтолитры.

 

[ds]

Ну и бог с ним

 

[bimba]

Genes, Low Iron Tied to Restless Legs in Kids



NEW YORK (Reuters Health) - Family history and iron deficiency appear to play important roles in childhood restless legs syndrome, according to a new study.



Restless legs syndrome (RLS) is a neurological condition that causes unpleasant sensations in the legs and an irresistible urge to move the limbs to relieve the discomfort, particularly at night. As a result, people with the condition often have sleep disturbances that make for daytime drowsiness.



Though family history and low iron stores in the body have been thought to play a role in at least some cases of restless legs syndrome, until now there has been little research on children with the disorder.



Traditionally, there's been a tendency for pediatricians to describe children with leg discomfort as having "growing pains," Dr. Suresh Kotagal, the lead author of the new study, told Reuters Health.



"But some may actually have restless legs," said Kotagal, a pediatric neurologist at the Mayo Clinic in Rochester, Minnesota.



The new study, which included 32 children with RLS, is the largest of its kind to date, according to Kotagal. He and colleague Dr. Michael H. Silber report the findings in the Annals of Neurology.



The researchers evaluated the records of 538 children seen in their sleep disorders clinic between 2000 and 2004. Six percent were found to have RLS.



Of these 32 children, 72 percent had a parent with RLS, most often a mother.



In addition, blood iron levels were lower than expected among the children who were tested, according to the report. One-third of the children were near the bottom of the established norms for their age and sex, while three-quarters were in the bottom half of that range.



Iron deficiency has been found in adults with restless legs, Kotagal noted, but at a lower rate than was seen in these children. It's unknown whether diet or a genetic predisposition to low iron is at work, he said.



Iron deficiency may contribute to RLS by way of its relationship with dopamine, a brain chemical that helps regulate movement. "Iron is a co-factor for the synthesis of dopamine in the brain," Kotagal explained, and scientists believe that dopamine deficiency is involved in restless legs.



Medications that boost dopamine levels in the central nervous system are used as part of RLS treatment, though there is also some evidence that treating iron deficiency improves some patients' symptoms, Kotagal noted.



It's unclear, though, he said, whether preventing iron deficiency in children at risk of RLS due to family history can in turn prevent the syndrome from developing.



Restless legs can take a toll on a child's quality of life and education, since the condition typically gets in the way of a good night's sleep. Kotagal noted that research suggests some children with attention-deficit hyperactivity disorder, or ADHD, may also have restless legs syndrome -- leading to the question, he said, of whether RLS-related sleep disturbances are causing those children's attention problems.



In this study, 87 percent of the children with RLS had problems falling asleep or staying asleep.



SOURCE: Ann Neurol. 2004 Dec;56(6):803-7.



Childhood-onset restless legs syndrome.



Kotagal S, Silber MH.



Division of Child and Adolescent Neurology, Mayo Clinic, Rochester, MN, USA



The clinical characteristics of childhood-onset restless legs syndrome are described. 32 of 538 subjects (5.9%) examined in our sleep disorders center received diagnoses of restless legs syndrome. They were classified based on published criteria into probable (n = 9/32 or 28%) and definite (n = 23/32 or 78%) categories. Apart from an earlier age of diagnosis of the probable group, no differences were found between the two categories. Sleep onset or sleep maintenance insomnia was the most common symptoms, being present in 28 of 32 subjects (87.5%). Inattentiveness was seen in 8 of 32 subjects (25%). Serum ferritin levels were measured in 24 of 32 subjects and were below 50 microg/L in 20 of 24 subjects (83%). A family history of restless legs syndrome was present in 23 of 32 (72%) subjects, with mothers almost three times more likely to be affected than fathers (p = 0.02). We conclude that iron deficiency and a strong family history are characteristic of childhood-onset restless legs syndrome.

 

[olgaz2]

При железодефицитной анемии у матери нарушается нейро-психическое развитие ребенка

и затрудняются взаимоотношения между мамой и ребенком:



J Nutr. 2005 Apr;135(4):850-5.



Mother-infant interactions and infant development are altered by maternal iron deficiency anemia.



Perez EM, Hendricks MK, Beard JL, Murray-Kolb LE, Berg A, Tomlinson M, Irlam J, Isaacs W, Njengele T, Sive A, Vernon-Feagans L.



School of Child and Adolescent Health, University of Cape Town, Cape Town, South Africa;



The aim of this study was to determine whether iron deficiency anemia (IDA) in young South African mothers alters mother-infant interactions and the infant's development. The study was a prospective, randomized, controlled intervention trial with 3 groups of mothers: nonanemic controls and anemic mothers administered either placebo (25 mg ascorbic acid and 10 mug folate) or daily iron treatment (125 mg FeSO(4) plus ascorbate and folate). Mothers of full-term, normal birth weight infants (n = 81) were followed from 10 wk to 9 mo postpartum. Maternal iron status, socioeconomic level, mother-infant interaction [Parent/Caregiver Involvement Scale (PCIS scale)], and infant development (Griffiths scale) were assessed. At baseline, anemic mothers tended (P < 0.10) to be less responsive to, and more controlling of, their infants. Infants of anemic mothers were developmentally delayed at 10 wk in hand-eye movement and overall quotient. Despite normalization of maternal iron status with supplementation in some mothers, the developmental delays were not diminished at 9 mo. At 9 mo, anemic mothers were significantly more "negative" towards their babies, engaged less in goal setting, and were less "responsive" than control mothers. In contrast, the behavior of anemic mothers given iron treatment toward their children was similar to that of the control mothers on all 11 scales of the PCIS. In conclusion, IDA altered mother-child interactions at both 10 wk and 9 mo postpartum. Additionally, infants whose mothers were anemic in the early postpartum scored worse on developmental tests at 10 wk and 9 mo of age.