Subaraknoid kanama sırasında asidotik kanla oluşan tiroid harabiyeti: Deneysel çalışma

Yıl 2020, Cilt: 4 Sayı: 4, 255 - 258, 01.04.2020

Ozgur Caglar , Erdem Karadeniz , Sevilay Özmen , Elif Oral Ahıskalıoğlu , Mehmet Aydin

https://doi.org/10.28982/josam.709558

Öz

Amaç: Metabolik asidoz tiroid fonksiyonlarını olumsuz etkileyebilir. Bu çalışmanın amacı subaraknoid kanama (SAK) sonrası oluşan asidozun tiroid bezinde yaptığı harabiyeti göstermektir.
Yöntemler: Çalışma, son SAK deneylerinden seçilen yirmi tavşan verilerinden seçildi. Tiroid bezlerini analiz etmek için kontrol grubu olarak beş tavşan (n=5) seçildi; 1 cc salin enjekte edilen SHAM grubu (n=5) ve SAK sonrası asidoz oluşan tavşanlardan seçilen on tavşandan oluşan çalışma grubu (n=10) saptadı. Deney prosedürleri öncesinde, deney sırasında ve sonrasında TSH, T3, T4 ve düşük pH değerleri kaydedildi. Tiroid bezlerinin normal ve dejenere epitel hücresinin yoğunlukları stereolojik yöntemler kullanılarak hesaplandı. pH ve tiroid hormon değerleri, dejenere epitel hücre yoğunlukları arasındaki ilişki istatistiksel olarak analiz edildi.
Bulgular: Kanın pH değerleri kontrolde 7,35 (0,037), SHAM'da 7,32 (0,05), SAK grubunda 7,21 (0,012) SAH grubunda tespit edildi. Duvar yüzeyi/hücre yüzeyi olarak hesaplanan foliküllerin milimetre kare başına normal/dejenere epitel hücre sayısı hesaplandı. Normal tiroid foliküllerinde normal epitel hücre sayısı 5.000 (750) idi. Dejenere epitel hücre sayısı normal grupta 50 (9) idi; SHAM grubunda 154 (30) ve çalışma grubunda 460 (80) olarak hesaplandı. Tüm sonuçlar için kontrol grubu ile SHAM ve SAH grupları arasında istatistiksel olarak anlamlı fark bulundu (P<0,001).
Sonuç: SAK'ın en ölümcül komplikasyonlarında biri olan asidoz nörovasküler ağ dejenerasyonuyla tiroid bezinde hasar oluşturabilir.

Anahtar Kelimeler

Subaraknoid kanama, Asidoz, Tiroid bezi harabiyeti

Destroyed thyroid by acidic blood during subarachnoid hemorrhage: Experimental study

Öz

Aim: Metabolic acidosis can negatively affect thyroid functions. The aim of this study is to show the damage in the thyroid gland caused by acidosis following subarachnoid hemorrhage (SAH).
Methods: Twenty rabbits were chosen from our recent SAH studies. Five healthy rabbits were included in the control group, five were included in the SHAM group, which received 1 ml of saline, and ten rabbits, chosen from SAH-induced animals with decreased blood pH, constituted the study group. TSH, T3, T4 and blood pH values were recorded before, during and after the experimental procedures. Densities of the normal and degenerated epithelial cell of thyroid glands were estimated using stereological methods. The relationship between blood pH and thyroid hormone values, and degenerated epithelial cell densities were analyzed statistically.
Results: pH values of blood were measured as 7.35 (0.037), 7.32 (0.05), and 7.21 (0.012) in the control, SHAM and SAH groups, respectively. The estimation of normal and degenerated epithelial cells per square milimeter of follicles was calculated as wall surface/cell surface. The mean normal epithelial cell count was 5,000 (750) in normal thyroid follicles. Mean degenerated epithelial cells counts were 50 (9) in the normal group, 154 (30) in the SHAM group and 460 (80) in the study group. For all results there was statistically significant difference between the control, SHAM and SAH groups (P<0.001).
Conclusions: Acidosis, one of the most fatal complications of SAH, may damage the thyroid gland with neurovascular network degeneration.

Anahtar Kelimeler

Subarachnoid Hemorrhage, Acidosis, Destroyed thyroid gland

Kaynakça

• 1. Ozmen S, Altinkaynak K, Aydin MD, Ahiskalioglu A, Demirci T, Özlü C, et al. Toward understanding the causes of blood pH irregularities and the roles of newly described binuclear neurons of carotid bodies on blood pH regulation during subarachnoid hemorrhage: Experimental study. Neuropathology. 2019;39(4):259-67.
• 2. Bederson JB, Germano IM, Guarino L. Cortical blood flow and cerebral perfusion pressure in a new noncraniotomy model of subarachnoid hemorrhage in the rat. Stroke. 1995;26(6):1086-92.
• 3. Demirci T, Aydin MD, Caglar O, Aydin N, Ozmen S, Nalci KA, et al. First definition of burned choroid plexus in acidic cerebrospinal fluid-filled brain ventricles during subarachnoid hemorrhage: Experimental study. Neuropathology. 2020.
• 4. Välimäki M, Liewendahl K, Nikkanen P, Pelkonen R. Hormonal changes in severely uncontrolled type 1 (insulin-dependent) diabetes mellitus. Scandinavian journal of clinical and laboratory investigation. 1991;51(4):385-93.
• 5. Chan LY-S, Fok WY, Sahota D, Lau TK. Cord blood thyroid-stimulating hormone level and risk of acidosis at birth. European Journal of Obstetrics & Gynecology and Reproductive Biology. 2006;124(2):173-7.
• 6. Takahashi S, Mitamura R, Itoh Y, Suzuki N, Okuno A. Hashimoto encephalopathy: etiologic considerations. Pediatric neurology. 1994;11(4):328-31.
• 7. Mallipedhi A, Vali H, Okosieme O. Myxedema coma in a patient with subclinical hypothyroidism. Thyroid. 2011;21(1):87-9.
• 8. Mayfield RK, Sagel J, Colwell JA. Thyrotoxicosis without elevated serum triiodothyronine levels during diabetic ketoacidosis. Archives of Internal Medicine. 1980;140(3):408-10.
• 9. Molfino A, Beck GJ, Li M, Lo JC, Kaysen GA, Investigators F. Association between change in serum bicarbonate and change in thyroid hormone levels in patients receiving conventional or more frequent maintenance haemodialysis. Nephrology. 2019;24(1):81-7.
• 10. Akarsu M, Yoldemir ŞA, Altun Ö, Dikker O, Özcan M, Çil EÖ, et al. The effects of overt hypothyroidism on adipose tissue and serum betatrophin levels. Journal of Surgery and Medicine. 2019;3(9):631-4.
• 11. ahmad Mirboluk A, Rohani F, Asadi R, Eslamian MR. Thyroid function test in diabetic ketoacidosis. Diabetes & Metabolic Syndrome: Clinical Research & Reviews. 2017;11:S623-S5.
• 12. Rashidi H, Ghaderian SB, Latifi SM, Hoseini F. Impact of diabetic ketoacidosis on thyroid function tests in type 1 diabetes mellitus patients. Diabetes & Metabolic Syndrome: Clinical Research & Reviews. 2017;11:S57-S9.
• 13. Schlienger J, Anceau A, Chabrier G, North M, Stephan F. Effect of diabetic control on the level of circulating thyroid hormones. Diabetologia. 1982;22(6):486-8.
• 14. Castells S. Thyroid function in juvenile diabetes. Pediatric Clinics of North America. 1984;31(3):623-34.
• 15. Dürig J, Fiedler W, De Wit M, Steffen M, Hossfeld D. Lactic acidosis and hypoglycemia in a patient with high-grade non-Hodgkin's lymphoma and elevated circulating TNF-α. Annals of Hematology. 1996;72(2):97-9.
• 16. Kawashima H, Kraut JA, Kurokawa K. Metabolic Acidosis Suppresses 25-Hydroxyvitamin D 3-1α-Hydroxylase in the Rat Kidney: Distinct Site And Mechanism Of Action. The Journal of Clinical Investigation. 1982;70(1):135-40.
• 17. Bronner F. Calcium homeostasis. Disorders of mineral metabolism: Elsevier; 1982. p. 43-102.
• 18. Mizuno J, Yonenaga K, Mimura Y, Arita H, Hanaoka K. Hyperthermia and metabolic acidosis during subtotal thyroidectomy for a patient with Basedow's disease. Masui The Japanese journal of Anesthesiology. 2008;57(7):897-900.
• 19. Haas M, Reinacher D, Li J, Wong N, Mooradian A. Regulation of apoA1 gene expression with acidosis: requirement for a transcriptional repressor. Journal of Molecular Endocrinology. 2001;27(1):43-57.