Железодефицитные новости

[Dr.Vad]

Уважаемые коллеги,

Этим сообщением открываю новую тему, где буду размещать тезисы недавних публикаций по железодефициту или ЖД анемии, имеющие определенный клинический интерес. Начну с работы из Швейцарии от известного специалиста, работы которого посвящены изучению связи железодефицита и нарушению функции щитовидной железы:

J Clin Endocrinol Metab. 2007 Jun 12;
Iron deficiency predicts poor maternal thyroid status during pregnancy.
Zimmermann MB, Burgi H, Hurrell RF.
Laboratory for Human Nutrition, Swiss Federal Institute of Technology (ETH) Zürich; Committee for Fluoride-Iodine Fortification of Salt, Swiss Academy of Medical Science, Bern, Switzerland.

Context: Pregnant women are often iron deficient, and iron deficiency has adverse effects on thyroid metabolism. Impaired maternal thyroid function during pregnancy may cause neurodevelopmental delays in the offspring. Objective: To investigate if maternal iron status is a determinant of TSH and/or TT4 concentrations during pregnancy Design and Outcome Measures: In a representative national sample of Swiss pregnant women (n=365) in the 2(nd) and 3(rd) trimester, samples of urine and blood were collected, and data on maternal characteristics and supplement use was recorded. Concentrations of TSH, TT4, hemoglobin, mean corpuscular volume, serum ferritin (SF), transferrin receptor (TfR) and urinary iodine (UI) were measured. Body iron stores were calculated and stepwise regressions done to look for associations. Results: The median UI (range) was 139 (30-433) microg/L. In the 3(rd) trimester, nearly 40% of women had negative body iron stores, 16% of woman had a TT4 <100 nmol/L and 6% had a TSH >4.0 mU/L. Compared to the women with positive body iron stores, the relative risk of a TT4 <100 nmol/L in the group with negative body iron stores was 7.8 (95% CI: 4.1; 14.9). Of the 12 women with TSH >4.0 mU/L, 10 of them had negative body iron stores. SF, TfR and body iron stores were highly significant predictors of TSH (standardized beta: -0.506, 0.602, and -0.589, respectively, all p<0.0001) and TT4 (standardized beta: 0.679, -0.589, and 0.659, respectively, all p<0.0001). Conclusions: Poor maternal iron status predicts both higher TSH and lower TT4 concentrations during pregnancy in an area of borderline iodine deficiency.

Полный текст доступен [Ссылки доступны только зарегистрированным пользователям ]

[Dr.Vad]

Эта работа еще раз показывает, что Мальтофер (трехвалентное железо) не всегда оптимальное лекарство для лечения ЖДА и достаточно порой просто сменить препарат на старый добрый сульфат или фумарат железа (II):

Hematology. 2007 Jun;12(3):255-6.
Ineffectiveness of oral iron hydroxide polymaltose in iron-deficiency anemia.
Ruiz-Argüelles GJ, Díaz-Hernández A, Manzano C, Ruiz-Delgado GJ.
Centro de Hematología y Medicina Interna de Puebla, Puebla, PUE, Mexico.

Two hundred and forty one patients with iron deficiency anemia (IDA) were identified in a single institution over a 24-year period; of these, 75 individuals were studied as the result of persistent IDA despite the administration of oral iron hydroxide polymatose (IP). The levels of hemoglobin when the patients were referred for study after being given oral IP had a median of 10.3 g/dl; after administration of oral iron fumarate during periods ranging from 1 to 14 months, the levels of hemoglobin rose to a median of 12.5 g/dl (p>0.01). Our data support previous observations made in other countries about the ineffectiveness of oral IP in the treatment of individuals with IDA and should alert the clinician to avoid unnecessary consultations and misdiagnosis.

[Dr.Vad]

Эту статью к новинкам отнести сложно, но в виду того, что только недавно удалось раскопать ее полный текст, приведу ее фрагменты: у студентов 16-19 лет (преимущественно девушек) на фоне коррекции железодефицита снизились головокружения, раздражимость, слабость/недомогание, депрессивные симптомы, чувствительность к холоду:

"There was a significant reduction after iron treatment in students with one abnormal laboratory test result, concerning the symptoms vertigo/dizziness, fatigue, irritability, over-exertion, depressive symptoms, indisposition, and sensitiveness to cold."

Symptom panorama in upper secondary school students and symptoms related to iron deficiency

Screening with laboratory tests, questionnaire and interventional treatment with iron

Scandinavian Journal of Primary Health Care, 2005; 23: 28-33

[Dr.Vad]

Еще одна работа от французов, известных своими изысканиями в области синдрома attention-deficit/hyperactivity и железодефицита: похоже, что у детей с наиболее выраженным этим расстройством часто присутствует и синдром беспокойных ног, а также наибольший железодефицит, оцениваемый по низкому уровню ферритина:

Sleep Med. 2007 Jul 17;
Impact of restless legs syndrome and iron deficiency on attention-deficit/hyperactivity disorder in children.
Konofal E, Cortese S, Marchand M, Mouren MC, Arnulf I, Lecendreux M.

OBJECTIVE: Increasing evidence suggests a significant comorbidity between attention-deficit/hyperactivity disorder (ADHD) and restless legs syndrome (RLS). Iron deficiency may underlie common pathophysiological mechanisms in subjects with ADHD plus RLS (ADHD+RLS). To date, the impact of iron deficiency, RLS and familial history of RLS on ADHD severity has been scarcely examined in children. These issues are addressed in the present study. METHODS: Serum ferritin levels, familial history of RLS (diagnosed using National Institutes of Health (NIH) criteria) and previous iron supplementation in infancy were assessed in 12 ADHD+RLS children, 10 ADHD children and 10 controls. RLS was diagnosed using NIH-specific pediatric criteria, and ADHD severity was assessed using the Conners' Parent Rating scale. RESULTS: ADHD symptom severity was higher, although not significantly, in children with ADHD+RLS compared to ADHD. The mean serum ferritin levels were significantly lower in children with ADHD than in the control group (p<0.0005). There was a trend for lower ferritin levels in ADHD+RLS subjects versus ADHD. Both a positive family history of RLS and previous iron supplementation in infancy were associated with more severe ADHD scores. CONCLUSIONS: Children with ADHD and a positive family history of RLS appear to represent a subgroup particularly at risk for severe ADHD symptoms. Iron deficiency may contribute to the severity of symptoms. We suggest that clinicians consider assessing children with ADHD for RLS, a family history of RLS, and iron deficiency.

Одна из предыдущих публикаций от этих авторов в полном доступе:

[Ссылки доступны только зарегистрированным пользователям ]

[Dr.Vad]

Еще одна публикация отражающая взаимосвязь ЖДА и повышенного гликогемоглобина: примечательна тем, что показывает на повышенные уровни малондиальдегида и фруктозамина у пациентов с ЖДА, корректирующиеся после терапии железом. Это может указывать на повышенный процесс гликирования гемоглобина при ЖДА, а не просто удельное повышение % гликогемоглобина вследствие уменьшения его негликированной фракции при анемии. (Если так, то выявление и коррекция латентного железодефицита у больных с СД теоретически может способствовать улучшению гликемического контроля по уровню HbA1c)

Biomed Pharmacother. 2007 Jul 23;
Increased plasma malondialdehyde and fructosamine in iron deficiency anemia: Effect of treatment.
Sundaram RC, Selvaraj N, Vijayan G, Bobby Z, Hamide A, Rattina Dasse N.
Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research, Dhanvantari Nagar, Pondicherry 605 006, India.

Glycation and lipid peroxidation are spontaneous reactions that are believed to play a key role in the pathogenesis of many clinical disorders. Glycation of proteins is enhanced by elevated glucose concentrations. However, increased glycated hemoglobin levels have been documented in iron deficiency anemic patients without any history of diabetes. Collective evidences reveal that lipid peroxidation can modulate protein glycation. This study was undertaken to unravel the possible association of malondialdehyde and fructosamine in iron deficient anemic patients and to observe the possible alteration in malondialdehyde and fructosamine levels in these patients after one month supplementation with iron. Twenty non-diabetic anemic patients and 16 age-matched healthy subjects were enrolled for this study. Plasma lipid peroxides, fasting glucose, fructosamine, iron, ferritin and hemoglobin were analyzed in both the groups. Partial correlation analysis was performed to predict the independent association of malondialdehyde and fasting glucose on fructosamine. In anemic patients, while fructosamine and malondialdehyde levels were found to be significantly increased, hemoglobin, iron and ferritin levels decreased significantly when compared to before treatment. Fructosamine was found to have a significant positive correlation with malondialdehyde even after nullifying the effect of glucose. After one month supplementation with iron, both fructosamine and malondialdehyde levels decreased significantly when compared to before treatment. There was a significant increase in iron, ferritin and hemoglobin levels in anemic patients after one month of treatment. In conclusion, an increased level of fructosamine and malondialdehyde was found in anemic patients. These data suggest that fructosamine levels are closely associated with malondialdehyde concentrations in iron deficient anemic patients.

[Dr.Vad]

Pediatrics. 2007 Sep;120(3):568-575.
Iron Deficiency in Early Childhood in the United States: Risk Factors and Racial/Ethnic Disparities.
Brotanek JM, Gosz J, Weitzman M, Flores G.
Department of Pediatrics, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9063.

BACKGROUND. Iron deficiency affects 2.4 million US children, and childhood iron-deficiency anemia is associated with behavioral and cognitive delays. Given the detrimental long-term effects and high prevalence of iron deficiency, its prevention in early childhood is an important public health issue. OBJECTIVES. The study objectives were to (1) identify risk factors for iron deficiency in US children 1 to 3 years old, using data from the most recent waves of the National Health and Nutrition Examination Survey IV (1999-2002) and (2) examine risk factors for iron deficiency among Hispanic toddlers, the largest minority group of US children. PATIENTS AND METHODS. Analyses of the National Health and Nutrition Examination Survey IV were performed for a nationally representative sample of US children 1 to 3 years old. Iron-status measures were transferrin saturation, free erythrocyte protoporphyrin, and serum ferritin. Bivariate and multivariable analyses were performed to identify factors associated with iron deficiency. RESULTS. Among 1641 toddlers, 42% were Hispanic, 28% were white, and 25% were black. The iron deficiency prevalence was 12% among Hispanics versus 6% in whites and 6% in blacks. Iron deficiency prevalence was 20% among those with overweight, 8% for those at risk for overweight, and 7% for normal-weight toddlers. Fourteen percent of toddlers with parents interviewed in a non-English language had iron deficiency versus 7% of toddlers with parents interviewed in English. Five percent of toddlers in day care and 10% of the toddlers not in day care had iron deficiency. Hispanic toddlers were significantly more likely than white and black toddlers to be overweight (16% vs 5% vs 4%) and not in day care (70% vs 50% vs 43%). In multivariable analyses, overweight toddlers and those not in day care had higher odds of iron deficiency. CONCLUSIONS. Toddlers who are overweight and not in day care are at high risk for iron deficiency. Hispanic toddlers are more likely than white and black toddlers to be overweight and not in day care. The higher prevalence of these risk factors among Hispanic toddlers may account for their increased prevalence of iron deficiency.

'Исследование американских ученых впервые выявило связь между патологическим ожирением и недостатком железа в организме. По результатам анализов, 20% тучных детей страдают от низкого содержания железа в организме, в то время как только 7% детей с нормальным весом больны железодефицитной анемией...'

[Ссылки доступны только зарегистрированным пользователям ]

[Dr.Vad]

Индукция железодефицита путем эксфузий крови в 2 раза сокращает развитие печеночно-клеточного рака у больных с хр. гепатитом С:

J Gastroenterol. 2007 Oct;42(10):830-6.
Long-term phlebotomy with low-iron diet therapy lowers risk of development of hepatocellular carcinoma from chronic hepatitis C.
Kato J, Miyanishi K, Kobune M, Nakamura T, Takada K, Takimoto R, Kawano Y, Takahashi S, Takahashi M, Sato Y, Takayama T, Niitsu Y.
Fourth Department of Internal Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan.

BACKGROUND: We have previously demonstrated that in patients with chronic hepatitis C (CHC), iron depletion improves serum alanine aminotransferase (ALT) levels as well as hepatic oxidative DNA damage. However, it has not been determined whether continuation of iron depletion therapy for CHC favorably influences its progression to hepatocellular carcinoma (HCC). METHODS: We conducted a cohort study on biopsy-proven CHC patients with moderate or severe liver fibrosis who failed to respond to previous interferon (IFN) therapy or had conditions for which IFN is contradicted. Patients were divided into two groups: subjects in group A (n = 35) underwent weekly phlebotomy (200 g) until they reached a state of mild iron deficiency, followed by monthly maintenance phlebotomy for 44-144 months (median, 107 months), and they were advised to consume a low-iron diet (5-7 mg iron/day); group B (n = 40) comprised CHC patients who declined to receive iron depletion therapy. RESULTS: In group A, during the maintenance phase, serum ALT levels decreased to less than 60 IU/l in all patients and normalized (<40 IU/l) in 24 patients (69%), whereas in group B no spontaneous decrease in serum ALT occurred. Hepatocarcinogenesis rates in groups A and B were 5.7% and 17.5% at the end of the fifth year, and 8.6% and 39% in the tenth year, respectively. Multivariate analysis revealed that iron depletion therapy significantly lowered the risk of HCC (odds ratio, 0.57) compared with that of untreated patients (P = 0.0337). CONCLUSIONS: Long-term iron depletion for CHC patients is a promising modality for lowering the risk of progression to HCC.

[Dr.Vad]

Публикация будушего года от французских коллег - прием железа снижает остроту синдрома гиперактивности/нарушения внимания у детей с латентным железодефицитом:

Pediatr Neurol. 2008 Jan;38(1):20-26.
Effects of Iron Supplementation on Attention Deficit Hyperactivity Disorder in Children.Konofal E, Lecendreux M, Deron J, Marchand M, Cortese S, Zaïm M, Mouren MC, Arnulf I.
Hôpital Robert Debré, Service de Psychopathologie de l’Enfant et de l’Adolescent, Paris, France; Hôpital Pitié Salpetrière, Fédération des Pathologies du Sommeil, APHP, Paris, France.

Iron deficiency has been suggested as a possible contributing cause of attention deficit hyperactivity disorder (ADHD) in children. This present study examined the effects of iron supplementation on ADHD in children. Twenty-three nonanemic children (aged 5-8 years) with serum ferritin levels <30 ng/mL who met DSM-IV criteria for ADHD were randomized (3:1 ratio) to either oral iron (ferrous sulfate, 80 mg/day, n = 18) or placebo (n = 5) for 12 weeks. There was a progressive significant decrease in the ADHD Rating Scale after 12 weeks on iron (-11.0 +/- 13.9; P < 0.008), but not on placebo (3.0 +/- 5.7; P = 0.308). Improvement on Conners' Parent Rating Scale (P = 0.055) and Conners' Teacher Rating Scale (P = 0.076) with iron supplementation therapy failed to reach significance. The mean Clinical Global Impression-Severity significantly decreased at 12 weeks (P < 0.01) with iron, without change in the placebo group. Iron supplementation (80 mg/day) appeared to improve ADHD symptoms in children with low serum ferritin levels suggesting a need for future investigations with larger controlled trials. Iron therapy was well tolerated and effectiveness is comparable to stimulants.

[Dr.Vad]

Железодефицит или ЖД анемия может быть наиболее частой причиной генерализованного зуда:

Am J Clin Dermatol. 2008;9(1):39-44
Generalized pruritus: a prospective study concerning etiology.
Polat M, Oztas P, Ilhan MN, Yalçin B, Alli N.
1st Dermatology Department, Ankara Numune Education and Research Hospital, Ankara, Turkey.

BACKGROUND: Generalized pruritus can often be the primary manifestation of systemic disease. OBJECTIVE: To determine how frequently generalized pruritus had a systemic etiology in an outpatient population seen in a dermatology department and whether any identifiable patient characteristics meant a systemic explanation of generalized pruritus was more likely. METHODS: A prospective controlled study of 55 patients with generalized pruritus and 41 healthy age- and sex-matched control subjects. Clinical data were collected from patients and laboratory parameters investigated in both patients and healthy control subjects to determine the frequency of systemic disease in each group. RESULTS: Of 55 patients, 12 had a systemic cause of pruritus. Pruritus was the initial symptom of systemic disease in eight of these patients. The underlying diseases included hypothyroidism, chronic lymphocytic leukemia, hepatitis C, hepatitis B, diabetes mellitus, lung cancer, uremia, and iron deficiency anemia. Of these, iron deficiency anemia was the most common cause. Compared with the control group, mean serum hemoglobin, iron, and cyanocobalamin (vitamin B(12)) levels in patients with generalized pruritus were lower. No other patient characteristics were statistically associated with systemic causes of pruritus. CONCLUSION: Generalized pruritus was the initial symptom of a systemic disease in 8 of 55 patients presenting to a dermatology outpatient clinic with this complaint. A number of underlying diseases were identified, of which the most common was iron deficiency anemia.

[Dr.Vad]

Железодефицитная анемия может быть причиной повышенного риска желчнокаменной болезни:

Ann Hematol. 2009 Jan;88(1):17-20.
Patients with iron deficiency anemia have an increased prevalence of gallstones.
Pamuk GE, Umit H, Harmandar F, Yeşil N.
Division of Hematology, Trakya University Medical Faculty, Edirne, Turkey.

We determined the frequency of gallstones (GS) in iron deficiency anemia (IDA) patients and evaluated factors that could affect GS formation-like lipid levels and gallbladder (GB) motilities of the patients. One hundred and eleven IDA patients (88 females, 23 males; median age, 42) and 81 healthy controls (68 females, 13 males; median age, 42) were included into our study. The clinical findings of all IDA patients were recorded down; biochemical values and body mass index (BMI) were determined; and abdominal ultrasonography was performed. In addition, GB emptying was monitored by ultrasound at 30-min intervals for 2 h after a mixed meal in randomly chosen, age-matched 25 IDA patients and 26 controls. Fasting volume (FV), residual volume (RV), and ejection fraction (EF) for all GBs were determined. The frequency of GS plus cholecystectomy was significantly higher in IDA patients (15 cases, 13.5%) than in the control group (five cases, 6.2%, p = 0.048). IDA patients with GS plus cholecystectomy were older than those without GS plus cholecystectomy (p < 0.001). FV and EF did not differ between IDA and control groups (p > 0.05). On the other hand, RV was significantly higher in IDA group than in controls (p = 0.035). The frequency of GS in IDA patients was significantly higher than in controls. The increased prevalence of GS in IDA might be explained with impaired GB motility.

[Dr.Vad]

Железодефицитная анемия может быть причиной рецидивирующего среднего отита у детей 0,5-4 года: чем ниже уровень гемоглобина, тем больше число рецидивов в год, коррекция анемии приводила к снижению частоты рецидивов у большинства детей:

The association between iron-deficiency anemia and recurrent acute otitis media.
Golz A, Netzer A, Goldenberg D, Westerman ST, Westerman LM, Joachims HZ.
Am J Otolaryngol. 2001 Nov-Dec;22(6):391-4.

Department of Otolaryngology-Head and Neck Surgery, Rambam Medical Center and the Faculty of Medicine, Haifa, Israel.

PURPOSE: This study was designed to examine the association between iron-deficiency anemia and the frequency of recurrent acute otitis media in children, and to evaluate the effect of restoring normal hemoglobin levels on the frequency of acute otitis media attacks.
MATERIALS AND METHODS: A total of 680 children with frequent episodes of acute otitis media were enrolled in the study. The levels of the hemoglobin were measured in both these children and in 200 healthy children with no history of infections. All children with hemoglobin levels lower than 9.5 g/dL received iron supplementation until they reached a level of at least 11 g/dL, and the subsequent frequency of middle ear infections was recorded.
RESULTS: The 680 children had an average of 8.3 +/- 2.7 episodes of acute otitis media per year per child, and an average hemoglobin level of 11.4 +/- 2.7 g/dL, whereas the controls had an average hemoglobin level of 13.1 +/- 2.5 g/dL. Twenty percent had hemoglobin levels below 9.5 g/dL. These children had more episodes of acute otitis media when compared with children with average levels. By increasing the hemoglobin level in these children, the frequency of the episodes of acute otitis media decreased significantly.

[Dr.Vad]

Недавняя работа от турецких коллег: одна из возможных причин повышенных кровопотерь во время месячных у женщин с ЖДА - снижение агрегации тромбоцитов на арахидоновую кислоту (аспириноподобное действие), которая возвращается к норме после лечения препаратами железа:

Pathophysiol Haemost Thromb. 2008;36(2):80-3.
Effect of Iron Therapy on Platelet Function among Iron-Deficient Women with Unexplained Menorrhagia.
Akay OM, Akin E, Mutlu FS, Gulbas Z.
Department of Hematology, Eskisehir Osmangazi University Medical School, Eskisehir, Turkey.

This study was performed to evaluate the effect of iron therapy on platelet function among women with unexplained menorrhagia in order to better understand possible interactions between iron deficiency anemia and platelet behavior and menorrhagia. Platelet aggregation and adenosine triphosphate (ATP) release induced by 5.0 mM adenosine diphosphate (ADP), 0.5 mM arachidonic acid (AA), 1.0 mg/ml ristocetin and 2 microg/ml collagen were studied by whole-blood platelet lumi-aggregometer in 50 menorrhagic women before and after oral iron therapy and in 22 women of the control group. There was a significant increase in AA- induced platelet aggregation (p < 0.05) and a decrease in ristocetin-induced platelet aggregation (p < 0.01) after treatment. Pre- and posttreatment platelet aggregation responses to ADP and collagen were not significantly different (p > 0.05). Pre- and posttreatment platelet secretion responses to all agonists disclosed no significant difference (p > 0.05). There was no significant difference between the study group after treatment and the control group in respect to platelet aggregation and ATP secretion values induced by all agonists (p > 0.05). We conclude that iron deficiency anemia in women causes AA-induced platelet dysfunction, which may give rise to increased menstrual blood loss and can be reversed by iron repletion.

[Dr.Vad]

Еще один эвиденс, что в основе зуда неясной этиологии наиболее часто может быть латентный железодефицит:

J Eur Acad Dermatol Venereol. 2008 May;22(5):615-618
Positivity of iron studies in pruritus of unknown origin.
Bharati A, Yesudian PD.

We audited 21 patients with Pruritus of unknown origin (PUO), obtaining case-notes from 4 hospitals in Merseyside, United Kingdom. The investigations done in these patients included full blood count (FBC), erythrocyte sedimentation rate (ESR), urea and electrolytes (U & E), liver function tests (LFT), glucose, ferritin, iron studies, thyroid function tests (TFT), IgE, RAST, immunoglobulins and chest X-ray (CXR).

The age range was 27 to 89 years (mean, 66.7 years), with 15 female and 6 male patients. The average number of investigations done for each patient was 5.3 (range, 0–9). The mean number of investigations per patient varied from hospital to hospital (range, 2.5–6.8).

Ferritin, iron studies or both had been done in 17 patients and an abnormality found in 8 (47%). Ferritin was abnormal in 4 (44%) of 9 patients and iron studies in 4 (36%) of 11 patients. LFTs showed an abnormality in 20%, whereas the positivity rate was less for other investigations. CXR, immunoglobulins and RAST were normal in all patients.

The causes of PUO are wide-ranging and include chronic renal failure, cholestasis, iron deficiency and internal malignancy. The mechanism underlying the association between iron deficiency and PUO remains unclear. Restoring the serum ferritin to normal levels by iron supplementation therapy has been reported to result in the resolution of pruritus of iron deficiency.

In our audit, none of the investigations were found to be significantly useful except ferritin and iron studies. With the high positivity rate in our audit for iron studies and ferritin, we recommend that they should be done in all patients with PUO.

[Dr.Vad]

Идиопатическая интракраниальная гипертензия в 10% случаев может быть обусловлена железодефицитной анемией, коррекция анемии в большинстве случаев приводит к излечению:

Eur Neurol. 2009 Jun 12;62(2):105-108.
Idiopathic Intracranial Hypertension Associated with Iron Deficiency Anaemia: A Lesson for Management.
Mollan SP, Ball AK, Sinclair AJ, Madill SA, Clarke CE, Jacks AS, Burdon MA, Matthews TD.
The Birmingham Neuro-Ophthalmology Unit, Birmingham and Midland Eye Centre, City Hospital, Birmingham, UK.

Aim: To document the causal association of iron deficiency anaemia (IDA) and intracranial hypertension (IH). Methods: A consecutive case note review of patients with a clinical diagnosis of idiopathic intracranial hypertension (IIH) and anaemia presenting to a tertiary referral unit over a 2.5-year period. Demographics, aetiology and clinical details were recorded and analysed. Results: Eight cases were identified from 77 new cases presenting with IIH. All 8 had documented microcytic anaemia with clinical evidence of raised intracranial pressure. There was no evidence of venous sinus thrombosis on MRI and MR venography in 7 subjects and on repeated CT venography in 1. On correction of anaemia alone, 7 cases resolved. One patient with severe progressive visual loss underwent ventriculoperitoneal shunt in addition to treatment of anaemia, with good outcome. The incidence of this association is 10.3%. Conclusion: These cases present an association between IDA and IH, in the absence of cerebral sinus thrombosis. As a clinically significant proportion of cases presenting with signs of IIH have IDA, we recommend all patients presenting with IIH have full blood counts and if they are found to be anaemic, they should be treated appropriately.
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Еще более ранний эвиденс по теме с обзором всех опубликованных случаев:

We found 30 well-documented cases with isolated anemia and papilledema in the English and French literature. Among those, 13 were excluded from our analyses (11 had confounding disorders and 2 had cerebral venous thrombosis). In the remaining 17 cases isolated raised ICP associated with anemia was the most likely diagnosis, although in none of these cases was cerebral venous thrombosis excluded. A lumbar puncture confirmed raised ICP in only 10 cases. The remaining 7 cases did not have a lumbar puncture, therefore raised ICP could not be confirmed; however, the clinical presentations were highly suggestive of raised ICP associated with anemia. There were 14 women and 3 men, with a mean age of 24 years, range 4 to 56; 6 were obese; all had bilateral papilledema, associated with cotton–wool spots (CWS) in 8, peripapillary hemorrhages in 9, and retinal or preretinal hemorrhages in 4; 11 had chronic headaches, 1 had tinnitus, 5 had VIth nerve palsies, and 4 complained of dizziness. The ICP was elevated in all 10 patients in whom a lumbar puncture was performed (mean opening pressure of 385 mm; range, 220–600). All 17 cases had severe anemia, with a mean hemoglobin of 5.4 g/dl, range, 17 to 25 secondary to iron deficiency in 11, B12 deficiency in 1, combined B12 and folate deficiencies in 1, aplastic anemia in 3, and transient erythroblastopenia in 1. Treatment included successful reversal of the anemia in all 17, and lumbar puncture in 10 patients. Visual prognosis was good in 15 patients and unknown in 2.

Anemia and papilledema.
Biousse V, Rucker JC, Vignal C, Crassard I, Katz BJ, Newman NJ.
Am J Ophthalmol. 2003 Apr;135(4):437-46.

[Dr.Vad]

Железодефицитная анемия может нарушать регенерацию энтероцитов тонкого кишечника и приводить виллозной (сосочковой) атрофии, тем самым вызывая мальабсорбцию и нарушение усвоения пероральных препаратов - в/в коррекция препаратом железа привела к ликвидации анемии и полной регенерации нормальной слизистой кишечника:

Nutr Hosp. 2009 Oct;24(5):618-621.

Atrophy of the intestinal villi in a post-gastrectomy patient with severe iron deficiency anemia.
Lizarraga A, Cuerda C, Junca E, Bretón I, Camblor M, Velasco C, García-Peris P.

Nutrition Unit, Hospital General Universitario Gregorio Marañón, Madrid, España.

Background & aims: Iron deficiency anemia is a common complication of gastric surgery that in certain patients can be refractory to treatment with oral iron and needs to be treated parenterally. Methods: A 48-year woman underwent gastric surgery for a gastric ulcer. She was referred to the nutrition unit for the study and treatment of a 3-year iron deficiency anemia refractory to oral iron supplementation. Blood tests, endoscopy and jejunal biopsy were made to study the case. Results: Intestinal villi atrophy in the absence of celiac disease was the result. She was treated with intravenous iron, resolving the villous atrophy and thus oral iron supplementation could be effective. Conclusion: This case illustrates that iron deficiency may cause villous atrophy. In this setting, parenteral iron administration is necessary to correct the haematological and non-hematological alterations associated with this deficiency.

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А lack of iron alters the efficiency of cell proliferation and regeneration.(10) After bone marrow germinal blood cells, enterocytes have the second highest proliferation rate. Iron deficiency can have non-hematological manifestations, some of which may affect the gastrointestinal tract. Structural and functional abnormalities of the intestine including villous atrophy,(4,5) reduced absorption of D-xylose,(4,5) decrease in intestinal disaccharidase,(6) and alteration in intestinal permeability(7,8) have been previously reported.