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Food Intolerance and Malabsorption Syndrome in Children: Signs and Symptoms

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Tetiana Yaroshevska at Dnepropetrovsk State Medical Academy
Tetiana Yaroshevska
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Tetiana Yaroshevska*
Department of Childhood Diseases, SI Dnepropetrovsk Medical Academy HM of Ukraine, Ukraine
*Corresponding author: Tetiana Yaroshevska, Associate Professor, Department of Childhood Diseases, SI Dnepropetrovsk Medical Academy HM of
Ukraine, Dnipro, Ukraine
Submission: May 11, 2018; Published: September 07, 2018
Food Intolerance and Malabsorption Syndrome in
Children: Signs and Symptoms
Introduction
Issues of food intolerance formation in children are currently
        
[1-3]. Environmental pollution can negatively affect quality of food.

body is not adapted to during the evolution (e.g. stabilizers, preser-
  -
tomical and physiological features that are predisposing to forma-
tion of malabsorption syndrome, such as delayed start of digestive
enzyme systems, violation of gastrointestinal motility regulation,
immaturity of the intestinal microbiocenosis, high intestinal pen-
etration and others.

can be latent. Patients are being miss-supervised by various spe-

of suffering remains unclear and the prescription of treatment is
being delayed [3]. The most common clinical manifestation of mal-
absorption syndrome is polyfecalia and this symptom can be easily
        -

-
 -
cemia-related spasmophilia, lack of body mass, reduction of height
and delay in sexual development. Accumulation of under-digested
metabolic products leads to the formation of intoxication syndrome
-
ty, tearfulness, pallor of the skin, periorbital cyanosis. Intoxication
can also cause tachycardia, aphthous stomatitis, violations of bio-
chemical indicators of liver and kidney function [2,4]. Toxic damage
of the nervous system has characteristic symptoms, such as tics,
tremor of the extremities and eyelids. Also, gastro-esophageal re-
  
recurrent abdominal and pelvic pain or cystalgia.
The most common causes of malabsorption syndrome are cys-
       -
          
amination of feces come to be a key to understand the syndrome of

increase in feces pH, putrefactive odor and creatorrhea. Carbohy-
drate malabsorption is characterized by an acidic smell, decrease
in  level, and amylorrhea. And in cases of fat malabsorption,
       

amylorrhea and creatorrhorea attract doctor’s attention rarely and
are usually explained by the presence of an intestinal dysbacterio-
-
-

Currently the capabilities of laboratory diagnosis of these diseases
   
protein antibodies, antiendomysial and anti-tissue transglutami-
nase IgA antibodies, hydrogen respiratory test and also genetic test
 
adult-type hypolactasia [3]. At the same time, it can be assumed
    
 
direction is prospecting [5].
Conclusion
Mentioned above does not include all the causes of
malabsorption syndrome and food intolerance in children.
Diagnostic research can be long and complicated. But usage of a
       
      
         

quality of life of sick children.
References
1.         
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785-796.
2.          
Pediatrics, pp. 1954-1956.
Mini Review
Research in
Pediatrics & Neonatology
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Volume - 2 Issue - 5
ISSN: 2576-9200
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How to cite this article: Tetiana Y. Food Intolerance and Malabsorption Syndrome in Children: Signs and Symptoms. Res Pediatr Neonatol. 3(1). RPN.000549.2018.
DOI: 10.31031/RPN.2018.03.000551
Volume - 3 Issue - 1
3.              
Diabetes insipidus-diagnosis and management. Horm Res Paediatr

4.     


5. 

6.  

7.       
        
     

8.      

9.      
Pediatrics, pp. 1882-1883.
10. 

11.          
  
328.
12.        
       

13.         

14.           

15.         

16.           

17.              
Management of insipidus and adipsia in the child diabetes. Best Pract

 Submit Article
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A Novel Mutation in the AVPR2 Gene in a Palestinian Family with Nephrogenic Diabetes Insipidus
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Full-text available
  • Jan 2017
Nephrogenic diabetes insipidus (NDI) is a urinary concentrating defect resulting from resistance of the collecting duct to the antidiuretic action of vasopressin (AVP). The X-linked recessive form is the most frequent genetic cause of inherited NDI and can be caused by mutations in the gene encoding the V2 vasopressin receptor (AVPR2). A Palestinian male infant presented in the neonatal period with failure to thrive, vomiting, irritability, fever, and polyuria, and had biochemical findings consistent with NDI. The diagnosis of NDI was established based on the clinical picture, absent response to desmopressin, and a similarly affected elder brother. Sequencing of the AVPR2 gene for the patient and his affected brother revealed a novel missense mutation with replacement of G by A in codon 82 located in exon 2 (TGC → TAC), causing a cysteine to tyrosine substitution (C82Y). Testing of the mother showed that she was the carrier of that mutation. This is the identified AVPR2 mutation in a Palestinian family. Knowledge of these mutations will allow genetic counseling and early diagnosis of affected males.
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Central diabetes insipidus
Article
Full-text available
  • Dec 2016
  • Nagoya J Med Sci
Central diabetes insipidus (CDI), characterized by polyuria and polydipsia, is caused by deficiency of arginine vasopressin (AVP), an antidiuretic hormone which acts on V2 receptors in kidney to promote reabsorption of free water. CDI is classified into three subtypes; idiopathic, secondary and familial. A previous study suggests that infundibulo-neurohypophysitis might be an underlying cause of idiopathic CDI. Among secondary CDI, the tumors in the central nervous system such as craniopharyngioma and germ cell tumors are the most frequent causes. Familial CDI is inherited mostly in an autosomal dominant mode, and the number of causal mutations in the AVP gene locus reported so far exceeds 80. CDI is treated with desmopressin, an analogue of vasopressin, and the tablet is preferred to the nasal form because it is easier to administer. It is also shown that the oral disintegrating tablet formula increases QOL and decreases the incidence of hyponatremia in CDI patients. In some CDI patients, the osmoreceptors in the hypothalamus do not function and patients do not sense thirst. These adipsic CDI patients are treated with desmopressin and adjusting the amount of daily water intake based on body weight measurement; but controlling the water balance is extremely difficult, and morbidity and mortality are shown to be high in these patients.
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Central diabetes insipidus: Clinical profile that suggests organicity in Peruvian children: Lima - Peru 2001-2013
Article
Full-text available
Background: Central diabetes insipidus (CDI) is a heterogeneous disease caused by arginine vasopressin deficiency; its management implies a profound understanding of the pathophysiology and the clinical spectrum. The aim of the study was to describe the clinical characteristics that indicate organicity in children and adolescents with central diabetes insipidus treated at the Department of Endocrinology from The Child Health's Institute during 2001 to 2013. Methods: Cross-sectional, retrospective study. 79 cases of patients diagnosed with CDI (51 males and 28 females) from 1 month to 16 years of age were reviewed. For the descriptive analysis, measures of central tendency and dispersion were used; groups of organic and idiopathic CDI were compared using χ2-test and t-test. A p-value<0.05 was considered significant. Results: The average age of patients was 8.1±4.2 years. Organic causes were intracranial tumors, 44 (55.7%), Langerhans cell histiocytosis (LCH), 11 (13.9%) and cerebral malformations in 7 (8.9%) patients, while the idiopathic group was 14 (17.7%) patients. Regarding clinical characteristics suggestive of organicity, headache (p=0.02) and visual disturbances (p=0.01) were found statistically significant. The anterior pituitary hormonal abnormalities were documented in 34 (52.3%) organic CDI patients. Furthermore, we did not find a significant difference in the average daily dose of desmopressin between patients with permanent vs. transitory CDI (0.81±0.65 vs. 0.59±0.62; p=0.363). Conclusions: The main clinical features suggestive of organicity in pediatric patients with central diabetes insipidus were headache and visual disturbances; furthermore, anterior pituitary hormonal abnormalities suggest an underlying organic etiology.
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Pathophysiology, diagnosis and management of nephrogenic diabetes insipidus
Article
Full-text available
  • Jun 2015
  • NAT REV NEPHROL
Healthy kidneys maintain fluid and electrolyte homoeostasis by adjusting urine volume and composition according to physiological needs. The final urine composition is determined in the last tubular segment: the collecting duct. Water permeability in the collecting duct is regulated by arginine vasopressin (AVP). Secretion of AVP from the neurohypophysis is regulated by a complex signalling network that involves osmosensors, barosensors and volume sensors. AVP facilitates aquaporin (AQP)-mediated water reabsorption via activation of the vasopressin V2 receptor (AVPR2) in the collecting duct, thus enabling concentration of urine. In nephrogenic diabetes insipidus (NDI), inability of the kidneys to respond to AVP results in functional AQP deficiency. Consequently, affected patients have constant diuresis, resulting in large volumes of dilute urine. Primary forms of NDI result from mutations in the genes that encode the key proteins AVPR2 and AQP2, whereas secondary forms are associated with biochemical abnormalities, obstructive uropathy or the use of certain medications, particularly lithium. Treatment of the disease is informed by identification of the underlying cause. Here we review the clinical aspects and diagnosis of NDI, the various aetiologies, current treatment options and potential future developments.
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Genetics of Diabetes Insipidus
Article
  • Feb 2017
  • ENDOCRIN METAB CLIN
Diabetes insipidus is a disease characterized by polyuria and polydipsia due to inadequate release of arginine vasopressin from the posterior pituitary gland (neurohypophyseal diabetes insipidus) or due to arginine vasopressin insensitivity by the renal distal tubule, leading to a deficiency in tubular water reabsorption (nephrogenic diabetes insipidus). This article reviews the genetics of diabetes insipidus in the context of its diagnosis, clinical presentation, and therapy.
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Diabetes insipidus in infants and children
Article
  • Feb 2016
Diabetes insipidus, the inability to concentrate urine resulting in polyuria and polydipsia, can have different manifestations and management considerations in infants and children compared to adults. Central diabetes insipidus, secondary to lack of vasopressin production, is more common in children than is nephrogenic diabetes insipidus, the inability to respond appropriately to vasopressin. The goal of treatment in both forms of diabetes insipidus is to decrease urine output and thirst while allowing for appropriate fluid balance, normonatremia and ensuring an acceptable quality of life for each patient. An infant's obligate need to consume calories as liquid and the need for readjustment of medication dosing in growing children both present unique challenges for diabetes insipidus management in the pediatric population. Treatment modalities typically include vasopressin or thiazide diuretics. Special consideration must be given when managing diabetes insipidus in the adipsic patient, post-surgical patient, and in those undergoing chemotherapy or receiving medications that alter free water clearance.
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Diabetes insipidus in children
Article
Diabetes insipidus (DI) is one of the common disorders affecting sodium and water homeostasis, and results when ADH is either inadequately produced, or unable to negotiate its actions on the renal collecting tubules through aquaporins. The diagnostic algorithm starts with exclusion of other causes of polyuria and establishing low urine osmolality in the presence of high serum osmolality. In this paper, we have reviewed the diagnosis, etiology and management of DI in children, with special emphasis on recent advances in the field.
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