Научная статья на тему 'Age influence on features polycystic ovarian on hormonal homeostasis which leading to changes in bone metabolism and development of type 2 diabetes'

Age influence on features polycystic ovarian on hormonal homeostasis which leading to changes in bone metabolism and development of type 2 diabetes Текст научной статьи по специальности «Клиническая медицина»

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POLYCYSTIC OVARY SYNDROME / BONE METABOLISM / TYPE 2 DIABETES

Аннотация научной статьи по клинической медицине, автор научной работы — Safarova Sain Sattar

Polycystic ovary syndrome is a serious disease of women in reproductive age, but when woman enters the menopause affect any existing violation of hormonal homeostasis in the future condition of the body. The problem of optimization of diagnostics and preventive maintenance of a bone pathology when women are in the polycystic ovary syndrome in postmenopausal period lead to the development of diabetes mellitus (DM) type 2 and accelerate the development of osteoporosis demands more steadfast attention.

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Текст научной работы на тему «Age influence on features polycystic ovarian on hormonal homeostasis which leading to changes in bone metabolism and development of type 2 diabetes»

the cases was seen in north part of Albania, in Has and Kukes district. Has and Kukes are situated close to Kosovo boarder, and has an environment for ticks spreading CCHF due to its geographic structure, climate and lifestyle of people living there.

Tick bites are especially seen in livestock farmers and agriculturists [9]. In this study CCHF was diagnosed mostly in the housewife and agriculturists, who were usually young adults working in open field and taking care and cleaning of animal barns. It is interesting to note that except two cases, all the infected

patients were from the villages of northern part of Albania, close to Kosovo.

Various fatality rates for CCHF, of up to 80 %, have been reported in the literature [10]. In this study, the fatality rate was 0 %, which is lower. This may be because the diagnosis was set in the early phase of the disease, or because we have cases that are spread by Kosovo boarder.

To conclude from the results of our study we reported that economic condition, geographic structure, climate and habitat had an important role in the distribution of the infection in different area of Albania.

References:

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Maltezou H. C. and Papa A. Crimean-Congo hemorrhagic fever: epidemiological trends and controversies in treatment//BMC Med. - Jan. 2011. - Vol. 9. - P. 131.

Vescio F. M., Busani L., Mughini-Gras L., Khoury C., Avellis L., Taseva E., Rezza G. and Christova I. Environmental correlates of Crimean-Congo haemorrhagic fever incidence in Bulgaria//BMC Public Health. - Jan. 2012. - Vol. 12, no. 1. - P. 1116.

Peters C. J. and Shelokov A. Viral Hemorrhagic Fever. - 1986.

LeDuc J. W. Epidemiology ofhemorrhagic fever viruses//Rev. Infect. Dis. -1989. - Vol. 11, Suppl 4. - P. 730-735. Viral Hemorrhagic Fevers/CDC Special Pathogens Branch//[Electronic resource]. - Available from: http://www. cdc.gov/ncidod/dvrd/spb/mnpages/dispages/vhf.htm (Accessed: 21-Feb-2016).

Pinazo M. J., Muñoz J., Betica L., Delgado M. J. P., Gutierrez J. M., Radic L. B., Maretic T., Zekan S., Avsic-Zu-panc T., Sequeira E., Aymar E. S., Trilla A., Brustenga J. G., and Gascon J. Imported dengue hemorrhagic fever, Europe//Emerg. Infect. Dis. - Aug. 2008. - Vol. 14, no. 8. - P. 1329-1330.

Papa A., Bino S., Llagami A., Brahimaj B., Papadimitriou E., Pavlidou V., Velo E., Cahani G., Hajdini M., Pilaca A., Harxhi A. and Antoniadis A. Crimean-Congo hemorrhagic fever in Albania, 2001//Eur. J. Clin. Microbiol. Infect. Dis. - Aug. 2002. - Vol. 21, no. 8. - P. 603-606.

8. Bino S. Crimean-Congo Hemorrhagic fever (CCHF) Prevention and Control, 2006//[Electronic resource]. -Available from: https://www.google.com/search?q=haenni+2005&ie=utf-8&oe=utf-8#q=S.+Bino.+Crimean-Congo+Hemorrhagic+fever+ (CCHF)+Prevention+and+Control %2C (Accessed: 15-Feb-2015).

9. Appannanavar S. B. and Mishra B. An update on crimean congo hemorrhagic Fever//J. Glob. Infect. Dis. - Jul. 2011. - Vol. 3, no. 3. - P. 285-292.

10. Bodur H., Akinci E., Ascioglu S., Öngürü P. and Uyar Y. Subclinical infections with Crimean-Congo hemorrhagic fever virus, Turkey//Emerg. Infect. Dis. - Apr. 2012. - Vol. 18, no. 4. - P. 640-642.

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Safarova Sain Sattar, Azerbaijan Medical University, Associated professor, PHD

E-mail: [email protected]

Age influence on features polycystic ovarian on hormonal homeostasis which leading to changes in bone metabolism and development of type 2 diabetes

Abstract: Polycystic ovary syndrome is a serious disease of women in reproductive age, but when woman enters the menopause affect any existing violation of hormonal homeostasis in the future condition of the body. The problem of optimization of diagnostics and preventive maintenance of a bone pathology when women are in the polycystic ovary syndrome in postmenopausal period lead to the

development of diabetes mellitus (DM) type 2 and accelerate the development of osteoporosis demands more steadfast attention.

Keywords: polycystic ovary syndrome, bone metabolism, type 2 diabetes.

Polycystic ovary syndrome (PCOS) is a serious disease of women in reproductive age, but what happens when woman enters the menopause affect any existing violation of hormonal homeostasis in the future condition of the body [1].

There observed a change of the clinical picture of the disease which replaces the cosmetic problems, impaired fertility with metabolic disorder when women are in the polycystic ovary syndrome in postmenopausal period [2].

Hormonal changes in menopause developing in PCOS lead to the development of diabetes mellitus (DM) type 2 and accelerate the development of osteoporosis (OP), whilst the bone mass is reduced by lowering the rate of bone formation [3]. An important background for the formation of type 2 diabetes and the development of osteopathy is the presence of insulin resistance (IR) and obesity typical 60-70 % of patients with polycystic ovary syndrome [4].

The process of bone formation and resorption are closely controlled by hormones interactive regulation, which is carried out at the tissue level. Hormones ho-meostasis are among the main factors that determine bone mass and bone quality.

The most significant effect on bone mineral metabolism have estrogens because they activate osteoblasts, inhibit the production of interleukin activating the apop-tosis of osteoclasts, promote inhibition of bone resorption, reduces the sensitivity of bone tissue to absorbable effect of PTH to increase the sensitivity of bone tissue to vitamin D3, stimulate the synthesis of calcitonin regulate the processes of absorption and excretion of Ca, activate apoptosis of osteoclasts. Reduced estrogen levels leads to accelerated bone turnover and loss of bone substance [5]. So the connection of PCOS and osteoporosis are explainable. As mentioned, in PCOS ovaries do not release the required amount of estrogen, thus estrogen deficiency greatly affects the metabolism of calcium in the body. A lack of estrogenimpaire absorption of calcium in the intestine, enhance bone remodeling (whose dynamics exceed increasing age related) in combination with excessive osteoclast activity [2; 4]. The mechanism of these changes under the influence of reducing the concentration of estrogen is not fully understood, but in the end the bones become very fragile, causing hip osteopenia and osteoporosis of the lumbar spine. It should be noted that osteoporosis develops gradually and long time

may go unnoticed. The first characteristic of his clinical symptoms reach values of 10-15 years of osteopenic syndrome [6].

In recent years, a large number of studies on insulin resistance and PCOS have been carried out. The regulation of steroidogenesis in the ovaries takes place with the participation of insulin like growth factor, which was the basis for the definition of the concept of the role of insulin resistance in the pathogenesis of PCOS. Insulin resistance is an important feature of PCOS, in most cases characterized by the hyperinsulinemic insulin resistance. It is known as Type 2 diabetes in their pathogenesis associated with insulin resistance, which gives reason to believe PCOS jog factor in stimulating the development of type 2 diabetes [7].

These data provide a basis to conclude that insulin resistance underlies PCOS, hyperandrogenism as a consequence of this breach, and that hyperinsulinemia may play a leading role in the pathogenesis of PCOS. Most researchers associated hyperinsulinemia in PCOS with insulin resistance [1]. At the same time it does not exclude the possibility of dysfunction of ^-cells, which may be accompanied by hyperinsulinemia. Reduced sensitivity of peripheral tissues to insulin in PCOS observed 2-3 times more frequently than in the general population. All this gives grounds to link the pathogenesis of PCOS with the mechanisms of the emergence of type 2 diabetes and osteoporosis [8]. Thus, women with PCOS postmenopausal have a relatively high risk of the aforementioned diseases. However, the pathogenic mechanisms of this influence is not fully understood and require further refinement.

Purpose of the study. The study of clinical and hormonal features in patients older than 50 years with PCOS and IR can, on the one hand, to open new perspectives in the study of the pathogenesis of the disease, and on the other — to improve recommendations for treatment and examination of this category of women.

Materials and methods. The study involved 45 patients 50-58 years of age (54 ± 2.5 years) with an intact uterus in postmenopausal women with PCOS and obesity visceral type.

All women were examined by the standard scheme: asking the history, gynecological examination, anthropometric measurements with calculation of body mass index (BMI) and the determination of the ratio of waist

circumference to hip circumference — OT/OB. Meno-pausal status of surveyed women was assessed by the Kupperman index.

Condition of bone mass is determined by measuring bone mineral density (BMD) by dual-energy X-ray absorptiometry (DEXA) in the lumbar spine (LI-LIV), femoral neck (Neck), greater trochanter — trochanter major (Troch), Triangle Ward (Ward). Diagnosis of osteoporosis was carried out according to WHO criteria — for T-criterion, i. e. standard deviation (SD) of standard indicators of peak bone mass in healthy women. The value SD to -1 regarded as the norm, from -1 to -2.5 SD — as osteopenia, above -2.5 SD — as osteoporosis.

Parameters calcium-phosphorus metabolism were evaluated by the concentration of calcium and inorganic phosphorus in serum, as well as their level of fasting urinary excretion relative to the excretion of creatinine (cal-cium-creatinine ratio (SSC) and a daily morning urine). On the state of bone formation activity was evaluated by the total content of alkaline phosphatase and osteocalcin in serum. The level of bone resorption was judged by the content of hydroxyproline in urine and excretion relative to creatinine excretion (ODA/Cr).

We used clinical, ultrasound, hormonal examination (determination of insulin levels, fasting glucose, free testosterone, LH, FSH, DAN, E2, PRL, TSH, T4).

Data analysis was performed using the methods of variation and mathematical statistics program "Biostat" in compliance with the general recommendations for medical and biological research.

Results of the study. Among the observed patients, mean age at menopause was — 46.4 years, which is 1.5-2 years earlier than among general population. The length of climacteric syndrome (CS) at the time of study was 4.8 ± 2.1 years. The prevalence of severe and moderate forms of the CS (67 %) over the light forms was found, which is not typical for this age. The symptoms of autonomic dysfunction detected in 93 %. Sweating, tendency to edema, flushing and palpitations were mostly observed. Urinary incontinence during physical exertion, vaginal dryness bothered 62.86 ± 9.52 % of surveyed women. Memory and mood impairment, including anxiety, apathy, tendency to depression, psychosomatic disorders were noted in 56 % of the cases.

Ultrasound revealed enlargement of the ovaries with multiple cystic formations. It revealed a significant increase in the level of free testosterone at 18 patients. The index of LH/FSH was 3 at 33 % of the patients. At 12 patients, it showed a significant increase in the level of DAN, indicating a mixed form of PCOS and obliterated adrenal genital syndrome. BMI among the surveyed women was 28.3 ± 1.4 kg., OT was 86 ± 5.3 cm., and MSA was 14.9 ± 2.8 u. e. Insulin anemia dynamics characterized by a decrease in insulin response (HOMAsecr — 162.5 ± 70.4; the integral index of insulin response was 5-4 ± 1.5).

The endocrine exchange disorders accounted for 77 %. It was revealed an increase in insulin level at 27 patients. It was diagnosed diabetes at 8 patients.

It was found that excess weight in menopause has direct correlation with diabetes and insulin resistance was in in reverse correlation with the IPC. A negative correlation was determined between hyperglycemia and bone mineral density of the femoral neck.

With PCOS at postmenopausal period, complicated by changes in bone and carbohydrate metabolism, there is a structural violation of trabecular and cortical bone, which is manifested by structural changes in lumbar spine and proximal femur on the DEXA [2, 9]. Study of bone metabolism markers at patients with PCOS in post menopause period showed that creatinine excretion in relation to hydroxyproline excretion increases in 72 % of cases that, given densitometry indicators, confirms the prevalence of bone resorption over bone formation process. Thus, with PCOS in postmenopausal period, the change in alkaline phosphatase activity and hydroxyproline content is detected before densitometry change indicators.

Among indicators of calcium-phosphorus metabolism and bone density, a sufficiently high degree of correlation was revealed only under certain parameters of bone mineral density (p < 0.001) and urinary calcium excretion relative to creatinine (p < 0.05), that indicates enhanced resorption of bone tissue.

This suggests that the presence of PCOS in the history of hormonal homeostasis aggravates the menopause, thereby contributing to the development of type 2 diabetes and osteoporosis in later stages of menopause.

References:

1. Glueck C. J., Wang P., Fontaine R., Tracy T., Sieve-Smith L. Metformin-induced resumption of normal menses in 39 of43 (91 %) previously amenorrheic women with polycystic ovary syndrome//Metabolism. - 1999. - 48: 1-10.

2. Rojas J., Chavez M., Olivar L., Rojas M., Morillo J., Mejias J. and others. Polycystic Ovary Syndrome, Insulin Resistance, and Obesity: Navigating the Pathophysiologic Labyrinth//Int. J. of Repr. Med. - Vol. 2014: 1-17.

3. Diamanti-Kandarakis E., Dunaif A. Insulin resistance and the polycystic ovary syndrome revisited: an update on mechanisms and implications//Endocr Rev. - 2012. - 33(6): 981-1030.

4. Schmidt J., Dahlgren E., Brannstrom M., Landin-Wilhelmsen K. Body composition, bone mineral density and fractures in late postmenopausal women with polycystic ovary syndrome - a long-term followup study//ClinEn-docrinol (Oxf). - 2012. - 77(2): 207-214.

5. Glintborg D., Hermann A. P., Andersen M. Bone mineral density and vitamin D in PCOS and hirsutism//Expert Rev Endocrinol Metab. - 2013. - 8(5): 449-459.

6. Glintborg D., Andersen M., Hagen C., Heickendorff L., Hermann A. P. Association of pioglitazone treatment with decreased bone mineral density in obese premenopausal patients with polycystic ovary syndrome: a randomized, placebo-controlled trial//J ClinEndocrinolMetab. - 2008. - 93(5): 1696-1701.

7. Teede H., Deeks A. and Moran L. Polycystic ovary syndrome: a complex condition with psychological, reproductive and metabolic manifestations that impacts on health across the lifespan//BMC Medicine. - 2010. -Vol. 8, article 41.

8. Gambineri A., Pelusi C., Vicennati V., Pagotto U. and Pasquali R. Obesity and the polycystic ovary syndrome// International Journal of Obesity. - 2002. - Vol. 26, no. 7. - P. 883-896.

9. Toprak S., Yönem A., Cakir B. et al. Insulin resistance in nonobese patients with polycystic ovary syndrome// Hormone Research. - 2001. - Vol. 55, no. 2. - P. 65-70.

Shostenko Alla Anatolievna, Bukovyna State Medical University, Assistant of the Children's Dental Surgery department, Chernivtsi, Ukraine

E-mail: [email protected]

Anatomic and physiological peculiarities of the buccal region

Abstract: Anatomic structures of the human buccal region provide significant functions of our body, like chewing, articulation, esthetic importance. Sufficient knowledge of the peculiarities of its structure due to the age aspect allows diagnostics and surgical correction of the facial inborn and acquired disorders [1; 2]. Keywords: buccal region, anatomic structures, buccal muscle.

Buccal region is a complex of soft tissues limited by a lower edge of the mandible, lower edge of the eye-socket, front edge of the manducatory muscle, naso-buccal, mouth buccal skin folds. On a comparatively little area numerous anatomic structures are located, like terminal section of the parotid duct, the Bichat's fat pad, blood and lymphatic vessels, nerves. It's worth to mention a high age and sex difference of the area anatomic development. Detailed data about development, variant and microsurgical anatomy, topography peculiarities and microscopic structure of the soft tissues is a morphological basis for understanding of the etiopathogenesis of the inborn disorders and acquired facial diseases [3; 5]. Tissues of the area are also an object of cosmetic surgical interventions and autoplastic material in oral surgery and oncology; that draws scientists' attention to the complex anatomic investigations of the side facial section aiming to develop new methods of surgical correction [6; 7].

Buccal muscle starts from the exterior surface of the alveolar processes of the maxillae and mandible are attached to the pterygomandibular raphe at the place of its connection with the superior pharyngeal constrictor muscle [10]. From outside the buccal space is limited by mimic muscles — major and minor zygomatic muscles. These muscles stretch front medially connecting to the front edge of the upper jaw limiting buccal area from the oral. At the front the space is bordered from oral area by orbicularis oris and levator labii superioris. The buccal space very often connects with the cellular space of the manductory muscle because the fascia parotidea is not joined on its medial surface which causes its connection with the fascia buccopharyngea. They are so called genuine medial and lateral borders of the buccal cellular space. Proximally it doesn't have distinct borders and turns into adipose tissue of the fossa temporalis, and distally — in mandibular cellular space where inflammatory processes may spread. Adipose cells in the back section of the

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