Probiotics and Prebiotics in children: what current literature states about their effect on respiratory diseases
Maria Gogou, Katerina Haidopoulou
President
A. Constantopoulos
Editorial board
Director
S. Antoniadis
Members
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E. Galanakis
A. Evangeliou
L. Thomaidou
M. Kanariou
A. Kapogiannis
S. Kitsiou-Tzeli
E. Mantadakis
P. Panagiotopoulou-Gartagani
A. Papadopoulou
V. Papaevagelou
A. Papathanassiou
A. Siamopoulou-Mavridou
A. Syrigou-Papavasiliou
Manuscript submission
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BOOK PRESENTATION
“A music from the past” by Afrodite Koidou
Kawasaki
Correspondence
Maria Gogou
Dimitriou Nika 44, 60100, Katerini
e-mail: mariaangogou@ gmail.com
Neurologic manifestations in Kawasaki disease
Maria Gogou, Andreas Giannopoulos
Abstract
Kawasaki disease is a frequent vasculitis in childhood associated with cardiovascular complications. However, its clinical phenotype can also include strokes, inflammation of Central Nervous System, dysfunction of cranial nerves, as well as behavioral disorders. According to the literature, early diagnosis of the disease and the proper treatment prevents the appearance of neurologic complications. Our article focuses on the neurologic manifestations of Kawasaki disease and the underlying mechanisms.
2nd Department of Pediatrics, University General Hospital AHEPA, Thessaloniki, Greece
Βιβλιογραφία
1. Dimitriades VR, Brown AG, Gedalia A. Kawasaki disease: pathophysiology, clinical manifestations, and management. Curr Rheumatol Rep 2014, 16:423
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3. Alves NR, Magalhães CM, Almeida Rde F, Santos RC, Gandolfi L, Pratesi R. Prospective study of Kawasaki disease complications: review of 115 cases. Rev Assoc Med Bras 2011, 57:295-300
4. Gitiaux C, Kossorotoff M, Bergounioux J, Adjadj E, Lesage F, Boddaert N, et al. Cerebral vasculitis in severe Kawasaki disease: early detection by magnetic resonance imaging and good outcome after intensive treatment. Dev Med Child Neurol 2012, 54:1160-3
6. Chen JL, Wang XM, Li Y, Shi K. Kawasaki disease complicated by ischemic cerebral stroke: a case report. Zhongguo Dang Dai Er Ke Za Zhi 2015, 17:642-3
7. Sabatier I, Chabrier S, Brun A, Hees L, Cheylus A, Gollub R, et al. Stroke by carotid artery complete occlusion in Kawasaki disease: case report and review of literature. Pediatr Neurol 2013, 49:469-73
8. Wang YM, Cao YC, Xu ZJ. Kawasaki disease complicated with cerebral infarction: a case report. Zhonghua Er Ke Za Zhi 2012, 50:628-9
9. Suda K, Matsumura M, Ohta S. Kawasaki disease complicated by cerebral infarction. Cardiol Young 2003, 13:103-5
10. Fujiwara S, Yamano T, Hattori M, Fujiseki Y, Shimada M. Asymptomatic cerebral infarction in Kawasaki disease. Pediatr Neurol 1992, 8:235-6
11. Laxer RM, Dunn HG, Flodmark O. Acute hemiplegia in Kawasaki disease and infantile polyarteritis nodosa. Dev Med Child Neurol 1984, 26:814-8
12. Boespflug O, Tardieu M, Losay J, Leroy D. Acute hemiplegia complicating Kawasaki disease. Rev Neurol (Paris) 1984, 140:507-9
13. Wada Y, Kamei A, Fujii Y, Ishikawa K, Chida S. Cerebral infarction after high-dose intravenous immunoglobulin therapy for Kawasaki disease. J Pediatr 2006, 148:399-400
14. Ahn JH, Phi JH, Kang HS, Wang KC, Cho BK, Lee JY, et al. A ruptured middle cerebral artery aneurysm in a 13-month-old boy with Kawasaki disease. J Neurosurg Pediatr 2010, 6:150-3
15. Yamazaki-Nakashimada MA, Rivas-Larrauri F, Alcántara-Salinas A, Hernández-Bautista V, Rodríguez-Lozano AL. Brain hemorrhage in a patient with Kawasaki disease. Rev Alerg Mex 2013, 60:38-40
16. Ishida A, Matsuo S, Kawamura S, Nishikawa T. Subarachnoid hemorrhage due to nonbranching aneurysm of the middle cerebral artery in a young adult with a history of Kawasaki disease. Surg Neurol Int 2014, 5:5
17. Du ZD, Wang Q, Liu XY. Intracranial hemorrhage in children in the acute stage of Kawasaki disease. Zhonghua Er Ke Za Zhi 2005, 43:542-3
18. Tanaka S, Sagiuchi T, Kobayashi I. Ruptured pediatric posterior cerebral artery aneurysm 9 years after the onset of Kawasaki disease: a case report. Childs Nerv Syst 2007, 23:701-6
19. Hoshino K, Morooka K, Imai H, Takagi K, Arimoto K, Saji T. Neurological involvements with transient gait disturbance in subacute phase of Kawasaki disease; a case report. No To Hattatsu 1995, 27:315-9
20. Kawasaki T, Arakawa Y, Sugino T, Mitsuhara T, Funaki T, Kikuchi T, et al. Three Cases of Moyamoya Disease with a History of Kawasaki Disease. No Shinkei Geka 2015, 43:1005-10
21. Du Z. A case of neonatal incomplete Kawasaki disease complicated with aseptic meningitis. Zhonghua Er Ke Za Zhi 2014, 52:63-4
22. Türel O, Güzeltaş A, Aydoğmuş C, Hatipoğlu N, Hatipoğlu H, Siraneci R. Kawasaki disease presenting as meningitis in a two months old infant. Anadolu Kardiyol Derg 2011, 11:369-70
23. Saint-Faust M, Benoit P, Bourlon F, Bloch C, De Ricaud D. Kawasaki disease in a young infant: difficulties for diagnosis and early complications. Arch Pediatr 2007, 14:1427-30
24. Husain E, Hoque E. Meningoencephalitis as a presentation of Kawasaki disease. J Child Neurol 2006, 21:1080-1
25. Takagi K, Umezawa T, Saji T, Morooka K, Matsuo N. Meningoencephalitis in Kawasaki disease. No To Hattatsu 1990, 22:429-35
26. Burgner D, Curtis N. Kawasaki disease as a cause of encephalitis. Arch Dis Child. 2011, 96:988-9
27. Dengler LD, Capparelli EV, Bastian JF, Bradley DJ, Glode MP, Santa S, et al. Cerebrospinal fluid profile in patients with acute Kawasaki disease. Pediatr Infect Dis J 1998, 7:478-81
28. Yeom JS, Park JS, Seo JH, Park ES, Lim JY, Park CH, et al. Initial characteristics of Kawasaki disease with cerebrospinal fluid pleocytosis in febrile infants. Pediatr Neurol 2012, 47:259-62
29. Kemmotsu Y, Nakayama T, Matsuura H, Saji T. Clinical characteristics of aseptic meningitis induced by intravenous immunoglobulin in patients with Kawasaki disease. Pediatr Rheumatol Online J 2011, 9:28
30. García Norniella B, Morán Poladura M, Fernández Díaz M, Fernández Fernández E, Suárez Castañón C. Aseptic meningitis secondary to intravenous immunoglobulin treatment in Kawasaki disease. An Pediatr (Barc) 2011, 75:79-80
31. Boyce TG, Spearman P. Acute aseptic meningitis secondary to intravenous immunoglobulin in a patient with Kawasaki syndrome. Pediatr Infect Dis J 1998, 17:1054-6
32. Nooraine J, Iyer RB, Raghavendra S. Intravenous immunoglobulin induced meningoencephalitis. Neurol India 2014, 62:98-9
33. Larralde M, Santos-Muñoz A, Rutiman R. Kawasaki disease with facial nerve paralysis. Pediatr Dermatol 2003, 20:511-3
34. Li ST, Chiu NC, Ho CS, Chen MR. Facial palsy in Kawasaki disease: report of two cases. Acta Paediatr Taiwan 2008, 49:24-7
42.Delafay MC, Matoussi Z, Remy-Piccolo V, Gay C, Veyrier M, Stéphan JL. Kawasaki disease and cranial nerve involvement: two cases. Arch Pediatr 2015, 22:853-6
43. Poon LK, Lun KS, Ng YM. Facial nerve palsy and Kawasaki disease. Hong Kong Med J 2000, 6:224-6
44. Thapa R, Mallick D, Biswas B, Chakrabartty S. Transient unilateral oculomotor palsy and severe headache in childhood Kawasaki disease. Rheumatol Int 2011, 31:97-9
45.Smith KA, Yunker WK. Kawasaki disease is associated with sensorineural hearing loss: a systematic review. Int J Pediatr Otorhinolaryngol 2014, 78:1216-20
46. Novo A, Pinto S, Prior AC, Alvares S, Soares T, Guedes M. Kawasaki disease and sensorineural hearing loss: an (un)expected complication. Eur J Pediatr 2012, 171:851-4
47. Knott PD, Orloff LA, Harris JP, Novak RE, Burns JC. Sensorineural hearing loss and Kawasaki disease: a prospective study. Am J Otolaryngol 2001, 22:343-8
48. Sundel RP, Cleveland SS, Beiser AS, Newburger JW, McGill T, Baker AL, et al. Audiologic profiles of children with Kawasaki disease. Am J Otol 1992, 13:512-5
49. Magalhães CM, Magalhães Alves NR, Oliveira KM, Silva IM, Gandolfi L, Pratesi R. Sensorineural hearing loss: an underdiagnosed complication of Kawasaki disease. J Clin Rheumatol 2010, 16:322-5
50. Kara A, Beşbaş N, Tezer H, Karagöz T, Devrim I, Unal OF. Reversible sensorineural hearing loss in a girl with Kawasaki disease. Turk J Pediatr 2007, 49:431-3
51. Yoshikawa H, Abe T. Febrile convulsion during the acute phase of Kawasaki disease. Pediatr Int 2004, 46:31-2
52. Okanishi T, Enoki H. Transient subcortical high-signal lesions in Kawasaki syndrome. Pediatr Neurol 2012, 47:295-8
53. Hikita T, Kaminaga T, Wakita S, Ogita K, Ikemoto H, Fujii Y. Regional cerebral blood flow abnormalities in patients with kawasaki disease. Clin Nucl Med 2011, 36:643-9
54. Terasawa K, Ichinose E, Matsuishi T, Kato H. Neurological complications in Kawasaki disease. Brain Dev 1983, 5:371-4
55. Takanashi J, Shirai K, Sugawara Y, Okamoto Y, Obonai T, Terada H. Kawasaki disease complicated by mild encephalopathy with a reversible splenial lesion (MERS).
56. King WJ, Schlieper A, Bindi N, Cappelli M, Korneluk Y, Rowe PC. The effect of Kawasaki Disease on cognition and behaviour. Arch Pediatr Adolesc Med 2000, 154:463–468
57. Carlton-Conway D, Ahluwalia R, Henry L, Michie C, Wood L, Tulloh R. Behaviour sequelae following acute Kawasaki Disease. BMC Pediatrics 2005, 5:14
58. Dhillon R, Newton L, Rudd PT, Hall SM. Management of Kawasaki disease in the British Isles. Arch Dis Child 1993, 69:631–8
59. Nishad P, Singh S, Sidhu M, Malhi P. Cognitive and behaviour assessment following Kawasaki disease--a study from North India. Rheumatol Int 2010, 30:851-4
e-mail: kaloumenou@ gmail.com
Correspondence
Irene Kaloumenou
Τ +306979671174
e-mail:kaloumenou@gmail. com
Premature adrenarche: pathophysiology, clinical implications and treatment
Adrenarche is the term for the maturational increase of the zona reticularis of the adrenal cortex. It is called: the puberty of the adrenal. The zona reticularis begins to form in the central adrenal cortex at the third year of age and mostly secrets cortisol. At about the fifth to sixth year of age, in both boys and girls, it begins to develop into a continuous zone. Within about a year, the adrenarchal increase in the adrenal androgen production becomes perceptible. Clinically adrenarche is the term applied to the appearance of axillary and pubic hair (pubarche), sebaceous gland and apocrine gland development as well as an increase in adult-type body odor. Premature adrenarche refers to the early maturational increase of the zona reticularis in girls younger than 8 years old and boys younger than 9 years old.
Depatment of Εndocrinology - Growth and Development, Children’s Hospital P. & A. Kyriakou, Athens, Greece
Συντομογραφίες:
DHEA:
DHEA-S:
SGA: Small for gestational
SGA / LBW
(PCOS).
1. Mesiano S, Jaffe RB. Developmental and functional biology of the primate fetal adrenal cortex. Endocr Rev 1997;18(3 Suppl):378-403.
2. Korth-Schutz S, Levine LS, New MI. Dehydroepiandrosterone sulfate (DS) levels, a rapid test for abnormal adrenal androgen secretion. J Clin Endocrinol Metab 1976;42:1005.
3. De Peretti E, Forest MG. Pattern of plasma dehydroepiandrosterone sulfate levels in humans from birth to adulthood: evidence for testicular production. J Clin Endocrinol Metab 1978;47:572.
6. Mouritsen A, Aksglaede L, Soerensen K, Hagen CP, Petersen JH, Main KM, et al. The pubertal transition in 179 healthy Danish children: associations between pubarche, adrenarche, gonadarche, and body composition. Eur J Endocrinol 2012; 168(2 Suppl):129-136.
7. Parker LN Adrenarche. Endocrinol Metab Clin North Am 1991;20: 71-83.
8. Dhom G. The prepuberal and puberal growth of the adrenal (adrenarche). Beitr Pathol 1973;150(4 Suppl):357-377.
9. Parker LN. Control of Adrenal androgen secretion. Endocrinol Metab Clin North Am 1991;20:(2 Suppl) 401-421.
10. Brunelli VL, Chiumello G, David M, Forest MG. Adrenarche does not occur in treated patients with congenital adrenal hyperplasia resulting from 21-hydroxylase deficiency. Clin Endocrinol (Oxf) 1995;42(5 Suppl):461-466.
11. Weber A, Clark AJ, Perry LA, Honour JW, Savage MO. Diminished adrenal androgen secretion in familial glucocorticoid deficiency implicates a significant role for ACTH in the induction of adrenarche. Clin Endocrinol (Oxf) 1997;46(4 Suppl):431-437.
12. Ibanez L, Potau N, Marcos MV, de Zegher F. Corticotropin-releasing hormone: a potent androgen secretagogue in girls with hyperandrogenism after precocious pubarche. J C Endocrinol Metab 1999;84(12 Suppl):4602-4606
13 Parker LN, Lifrak ET, Odell WD. A 60,000 molecular weight human pituitary glycopeptide stimulates adrenal androgen secretion. Endocrinology 1983; 113(6 Suppl):2092-2096.
14 . Anderson DC. The adrenal androgen-stimulating hormone does not exist. Lancet 1980 30;2(8192):454-456.
15 Biason-Lauber A, Zachmann M, Schoenle EJ. Effect of leptin on CYP17 enzymatic activities in human adrenal cells: new insight in the onset of adrenarche. Endocrinology 2000; 141(4 Suppl):1446-1454.
16 Clarke D, Fearon U, Cunningham SK, Mc Kenna TJ. The steroidogenic effects of beta-endorphin and joining peptide: a potential role in the modulation of adrenal androgen production. J Endocrinol 1996;151(2 Suppl):301-307.
17. Parker LN, Sack J, Fisher DA, Odell WD. The adrenarche: prolactin, gonadotropins, adrenal androgens, and cortisol. J Clin Endocrinol Metab 1978;46(3 Suppl):396-401.
18 Remer T, Manz F. Role of nutritional status in the regulation of adrenarche. J Clin Endocrinol Metab 1999;84(11 Suppl):3936-3944.
19. Whitworth EJ, Kosti O, Renshaw D, Hinson JP. Adrenal neuropeptides: regulation and interaction with ACTH and other adrenal regulators. Microsc Res Tech 2003;61(3 Suppl):259-267.
20 Lebrethon MC, Jaillard C, Naville D, Begeot M, Saez JM. Effects of transforming growth factor-beta 1 on human adrenocortical fasciculata-reticularis cell differentiated functions. J Clin Endocrinol Metab 1994;79(4 Suppl):1033-1039.
21 Voutetakis A, Livadas S, Sertedaki A, Maniati-Christidi M, Dacou-Voutetakis C. Insufficient adrenarche in patients with combined pituitary hormone deficiency caused by a PROP-1 gene defect. J Pediatr Endocrinol Metab 2001;14(8 Suppl):1107-1111.
22. Taha D, Mullis PE, Ibanez L, de Zegher F. Absent or delayed adrenarche in Pit-1/POU1F1 deficiency. Horm Res 2005;64(4 Suppl):175-179.
23 Agarwal G, Bhatia V, Cook S, Thomas PQ. Adrenocorticotropin deficiency in combined pituitary hormone deficiency patients homozygous for a novel PROP1 deletion. J Clin Endocrinol
Metab 2000;85(12 Suppl):4556-4561
24. Ong KK, Potau N, Petry CJ et al. Opposing influences of prenatal and postnatal weight gain on adrenarche in normal boys and girls. J Clin Endocrinol Metab 2004;89(6 Suppl):2647-2651.
25 Neville KA, Walker JL. Precocious pubarche is associated with SGA, prematurity, weight gain, and obesity. Arch Dis Child. 2005;90(3 Suppl):258-261.
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27 Nimkarn, S., Gangishetti PK, Yau M,, and New MI 21-Hydroxylase deficient Congenital Adrenal Hyperplasia In: Pagon RA, Adam MP, Ardinger HH, Wallace SE, Amemiya A, Bean LJH, Bird TD, Fong CT, Mefford HC, Smith RJH, Stephens K, editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2016.
2002 Feb 26 [updated 2016 Feb 4]
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29. Ibáñez L, Potau N, Zampolli M, Riqué S, Saenger P, Carrascosa A. Hyperinsulinemia and decreased insulin-like growth factor-binding protein-1 are common features in prepubertal and pubertal girls with a history of premature pubarche. J Clin Endocrinol Metab. 1997;82(7 Suppl):2283-2288.
30. Ibáñez L, Ong K, Valls C, Marcos MV, Dunger DB, de Zegher F. Metformin treatment to prevent early puberty in girls with precocious pubarche. J Clin Endocrinol Metab. 2006;91(8 Suppl):2888-2891.
31. Coviello AD, Legro RS, Dunaif A. Adolescent girls with polycystic ovary syndrome have an increased risk of the metabolic syndrome associated with increasing androgen levels independent of obesity and insulin resistance. J Clin Endocrinol Metab 2006;91(2 Suppl):492-497.
32. Saenger P, Reiter EO. Premature adrenarche: a normal variant of puberty? J Clin Endocrinol Metab 1992;74(2 Suppl):236-238.
33. Rosenfield RL, Lipton RB, Drum ML. Thelarche, pubarche and menarche attainment in children with normal and elevated body mass index. Pediatrics 2009;123-184
34. Herman-Giddens ME, Slora EJ, Wasserman RC, Bourdony CJ, Bhapkar MV, et al. Secondary sexual characteristics and menses in young girls seen in office practice: a study from the Pediatric Research in Office Settings network. Pediatrics 1997;99:505-512.
35. Zukauskaite S, Lasiene D, Lasas L, Urbonaite B, Hindmarsh P. Onset of breast and pubic hair development in 1231 preadolescent Lithuanian school-girls. Arch Dis Child 2005;90: 932-936.
36. Atay Z, Turan S, Guran T, Furman A, Bereket A. The prevalence and risk factors of premature thelarche and pubarche in 4- to 8-year-old girls. Acta Paediatr 2012;101: e71-75.
37. Kang MJ, Lee JS, Kim HY, Jung HW, Lee YA, Lee SH, Seo JY, Kim JH, Chung HR, Kim SY, Shin CH, Yang SW. Contributions of CAG repeat length in the androgen receptor gene and androgen profiles to premature pubarche in Korean girls. Endocr J. 2016 Oct 6. [Epub ahead of print].
e-mail:
Correspondence
Elpis-Athina Vlachopapadopoulou
T. 213 2009851
F.213 200953
M. 6932247228
e-mail: elpis.vl@gmail.com
Epidemiology, diagnosis and management of type 2 diabetes mellitus in children and adolescents
Since the early 1990s, the prevalence of type 2 diabetes mellitus (T2DM) has increased in children and adolescents worldwide and is linked to the rise in the prevalence of childhood obesity. Therefore, it is essential for health care providers to identify and treat these children, given that T2DM and its comorbidities are risk factors for vascular disease, fatty liver and renal insufficiency, later in life. Given that approximately 40 percent of patients are asymptomatic, the American Diabetes Association (ADA) recommends screening criteria for T2DM among asymptomatic children. Screening tests include fasting plasma glucose (FPG), hemoglobin A1c (HbA1c). Oral glucose tolerance test (OGTT) is recommended as further investigation, especially when clinical suspicion for diabetes remains high, despite a FPG or A1c that is non-diagnostic. Diabetes mellitus is diagnosed based on the ADA criteria: HbA1c ≥6.5 percent (47 mmol/mol) or fasting plasma glucose (FPG) ≥126 mg/dL (7 mmol/L) or two-hour plasma glucose ≥200 mg/dL (11.1 mmol/L) during an OGTT or in a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L). Οptimal treatment should use a combination of diet, exercise and pharmacologic interventions. Individualized nutrition therapy in addition with increased physical exercise are crucial component of the successful management of T2DM in order to achieve glycemic control. Metformin, is recommended as initial treatment while insulin therapy is recommended for selected patients.
Eirini Dikaiakou
Elpis-Athina Vlachopapadopoulou
Stefanos Michalacos Department of Endocrinology-Growth and Development, Children’s Hospital P.A. Kyriakou, Athens, Greece
2.
Συντομογραφίες:
T2DM: Τype 2 Diabetes Mellitus
T1DM: Τype 1 Diabetes Mellitus
ADA: American Diabetes Association
FPG: Fasting Plasma
Glucose
HbA1c: Hemoglobin
A1c
TNF-a: Tumor Necrosis
Factor-a ΔΜΣ:
OGTΤ: Oral Glucose Tolerance Test
MODY: Maturity-onset diabetes of the young
GAD: Anti-glutamic Acid Decarboxylase
IA2: Anti-tyrosine Phosphatase
IAA: Anti-insulin antibodies
ZnT8: Beta cell-specific autoantibody to Zinc Transporter 8
FDA: Food and Drug Administration
DPP-IV: Dipeptidyl peptidase 4 (DPP-4)
SGLT2: Sodium-glucose co-transporter 2
AHA: American Heart Association
LDL-C: Low-density lipoprotein cholesterol
HDL-C: High-density lipoprotein cholesterol
125 mg/dL (≥5,6 mmol/L to 6,9 mmol/L). •
(≥7., mmol/L to 11,0 mmol/L)
1,75 g/kg (μέγιστη
OGTT. • Τιμές HbA1C μεταξύ 5,7% and 6,4% (39 to 46 mmol/mol) έχουν
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Probiotics and Prebiotics in children: what current literature states about their effect on respiratory diseases
Maria Gogou, Katerina Haidopoulou
Abstract
Gut microbiota is known to play a significant role in the normal function of all systems. At the same time the use of probiotics and prebiotics has been found to improve the clinical parameters in a variety of disorders. The aim of this review is to investigate the effect of probiotics and prebiotics use on airways disorders in childhood. According to the literature, the administration of probiotics and prebiotics contributes to a reduction in frequency and severity of respiratory infections among children, as well as to the improvement of symptoms in allergic rhinitis. On the contrary, a clear effect on asthma prevention has not been proven, yet.
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e-mail: nikiparask@gmail. com
Correspondence
Niki Paraskevopoulou
Thivon and Papadiamantopoulou Str., 11527 Athens T. +302132013417
Hereditary hemochromatosis is one of the most frequent genetic disorders in Caucasians, characterized by excessive accumulation of iron in the liver, heart and endocrine glands resulting in irreversible organ damage. It is associated with mutation of proteins involved in iron metabolism. There are 4 types of hemochromatosis depending on the mutation and the clinical presentation. Type 2 or juvenile hemochromatosis is associated with mutations of hemojuvelin (HJV) (type 2A) or rarely of hepcidin (HAMP) (type 2B) and is more severe than the other types. Clinical manifestations are evident during the 2nd decade of life or earlier.
We describe the case of a 5-year old boy with juvenile hemochromatosis type 2A who presented with slightly increased transaminases levels and an abnormal profile of iron metabolism (high Fe and ferritin levels and transferrin saturation). Molecular analysis confirmed the diagnosis. The patient has been started on a frequent therapeutic phlebotomy program with satisfactory response after 12 months of treatment.
2nd Department of Pediatrics, Aghia Sophia Children’s Hospital, Athens
Vassilios Papadakis
Department of Pediatric Hematology - Oncology, Aghia Sophia Children’s Hospital, Athens
Συντομογραφίες:
TS: (transferrin
saturation): κορεσμός
τρανσφερρίνης
HFE: (high Fe):
πρωτεΐνη HFE
HJV: (hemojuvelin):
αιμοτζουβελίνη
HAMP: (hepcidin):
εψιδίνη
TfR2:(transferrin
receptor 2):
2
FPN:(ferroportin):
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