SOVREMENNAYA PEDIATRIYA.2016.1(73):40-43; doi10.15574/SP.2016.73.40 

Particular qualities of intranasal structures conditions in children with type 1 diabetes 

Layko А., Gavrylenko Iu.

Shupyk National Medical Academy of Post-Graduate Education, Kiev, Ukraine 

Objective: To examine particular qualities of the intranasal structures state in children and adolescent patients with type 1 diabetes (T1D). 

Patients and methods. During the period of 2013–2015 161 patients with type 1 were examined having been treated at the endocrinology department of the National Children's Specialized Hospital OKHMATDET and Children's Hospital №6 (Kyiv). The study group included 138 (85.7%) patients with type-1 with the changes of intranasal structures, the control group — 23 (14.3%) patients with type-1 with no pathology of upper respiratory tract. Among children of the main group — 92 (66.67%) boys and 46 (33.33%) girls aged 6–17. All children received clinical and laboratory examination in accordance with the protocols, as well as endoscopy of the nasal cavity, nasopharynx, paranasal sinus computed tomography (if necessary). 

Results. The most pronounced changes of intranasal structures in children with T1D in the study group were identified in the form of the curvature of the nasal septum (IEF). Endoscopic examination of the nasal cavity and nasopharynx in children of the main group diagnosed the hypertrophy of the inferior turbinate in 54% of patients, acute rhinosinusitis — 12%, chronic adenoids, adenoid vegetations in 10%, polyps — 2%. Microcirculatory disorders according to the nail bed capillaroscopy in patients of the main group were observed 3 times more often than the control group. As a result of bulbar microscopy for children with T1D and IEF vascular changes in a single non-niformity of the caliber of vessels were identified in — 75%, unit sakkulyation venules — 50% maendricus tortuosity of the capillaries — 75%, as well as single-venular anastomoses arteriolo — 37.5%. Intra- and extravascular changes in this group of patients have not been identified. 

Conclusions. The results of studies in children with T1D indicate the need for timely early diagnosis of the state of intranasal structures and microcirculation to select appropriate methods of correction and treatment. 

Key words: nose, endoscopy, type 1 diabetes, children, adolescents. 

REFERENCES

1. Gavrylenko Iu. 2015. Clinical and epidemiological aspects of ENT diseases in children with diabetes mellitus type 1. International scientific journal. Pediatrics. Eastern Europe. 4(12): 68—75.

2. Dedov II, Petercova VA. 2006. Guidance on child's endocrinology. Moskow, Universum Pablsng: 600.

3. Laiko AA, Gavrylenko YuV, Stepanova OV. 2015. Investigation of the mucous membrane state of Kisselbah's zone in children with type 1 diabetes. Collection of scientific works of staff members of NMAPE. 24; 1: 435—442.

4. Zhmerenetsky KV, Kaplieva OV, Sirotina ZV, Yezerskyy RF. 2012. Place of microcirculation in the development of vascular disorders in children and adolescents. Far East Medical zhurnal. 2: 59—62.

5. Moldavskaya AA, Petrov VV, Avedisyan VE. 2007. Zonal features of structural organization of mucous membrane of cavity of nose of man are in early postnatal ontogenesis. 8: 19—21.

6. Mityuryaeva IA, Gavrylenko IuV, Gniloskurenko AV. 2015. State features of bulbar microscopy in children with type 1 diabetes end chronic ENT-patology. International Journal of Pediatrics, Obstetrics and Gynecology. 8; 1: 59—60.

7. Potenza M, Garliardi S, Nacci C et al. 2009. Endothelial dysfunction and diabetes: from mechanisms to therapeutic targets. Curr Med Chem. 16; 1: 94—112. http://dx.doi.org/10.2174/092986709787002853; PMid:19149564

8. Scardina G, Cacioppo A, Pisano T et al. 2011. In vivo evaluation of labial microcirculation in diabetics: a comparision of healthy subjects. Panminevra Med. 53: 81—85. PMid:21659973

9. Yang G, Lucas R, Caldwell R et al. 2010. Novel mechanisms of endothelia dysfunction in diabetes. J Cardiovasc Dis Res. 1; 2: 59—63. http://dx.doi.org/10.4103/0975-3583.64432; PMid:20877687 PMCid:PMC2945199