全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...
HPB Surgery  2012 

The Underlying Mechanisms: How Hypothyroidism Affects the Formation of Common Bile Duct Stones—A Review

DOI: 10.1155/2012/102825

Full-Text   Cite this paper   Add to My Lib

Abstract:

For decades, one well-known risk factor for the development of gallbladder stones has been hypothyroidism. Recent studies have interestingly reported that the risk in particular for common bile duct (CBD) stones increases in clinical and subclinical hypothyroidism. There are multiple factors that may contribute to the formation and/or accumulation of CBD stones in hypothyroid patients, including decreased liver cholesterol metabolism, diminished bile secretion, and reduced sphincter of Oddi relaxation. This paper focuses on the mechanisms possibly underlying the association between hypothyroidism and CBD stones. The authors conclude that when treating patients with CBD stones or microlithiasis, clinicians should be aware of the possible hypothyroid background. 1. Introduction Several factors affecting bile content and bile flow are involved in the complex pathogenesis of gallstones. In hypothyroidism, not only the risk for gallbladder stones [1, 2], but also the risk for common bile duct (CBD) stones in particular is increased [3–5]. Impaired liver cholesterol metabolism [6], diminished bile secretion [7], and reduced sphincter of Oddi (SO) relaxation [8, 9] may contribute to the formation and/or accumulation of CBD stones in hypothyroid patients. In this paper the possible mechanisms underlying the association between hypothyroidism and CBD stones are being discussed. 2. Review Criteria PubMed was searched in April 2011 with the terms “hypothyroidism,” “subclinical hypothyroidism,” “thyroxine,” “thyroid function,” “gallstones,” “bile duct stones,” “sphincter of Oddi,” “biliary motility,” “cholesterol metabolism,” and “hepatic secretion” for full-length English language original publications and review articles published between 1950 and 2010 (initial inclusion criteria). Abstracts and articles not relevant to the topic were excluded. A total of 3472 publications were identified at the initial step, out of which 3396 were excluded and 76 were finally considered. The search was updated in August 2012. 3. Prevalence of Clinical and Subclinical Hypothyroidism in CBD Stone Patients Several recent studies report an association between hypothyroidism, or subclinical hypothyroidism, and CBD stones (Table 1). In a retrospective study on patients over 60 years of age [3], it was noted for the first time that CBD stone patients have significantly more diagnosed hypothyroidism (11%), not only when compared to control patients from whom gallstones had been excluded (2%), but also when compared to gallbladder stone patients without CBD stones (6%). In this study,

References

[1]  L. H. Honore, “A significant association between symptomatic cholesterol cholelithiasis and treated hypothyroidism in women,” Journal of Medicine, vol. 12, no. 2-3, pp. 199–203, 1981.
[2]  S. M. Strasberg, “The pathogenesis of cholesterol gallstones—a review,” Journal of Gastrointestinal Surgery, vol. 2, no. 2, pp. 109–125, 1998.
[3]  J. Inkinen, J. Sand, and I. Nordback, “Association between common bile duct stones and treated hypothyroidism,” Hepato-Gastroenterology, vol. 47, no. 34, pp. 919–921, 2000.
[4]  J. Laukkarinen, G. Kiudelis, M. Lempinen et al., “Increased prevalence of subclinical hypothyroidism in common bile duct stone patients,” Journal of Clinical Endocrinology and Metabolism, vol. 92, no. 11, pp. 4260–4264, 2007.
[5]  J. Laukkarinen, J. Sand, V. Autio, and I. Nordback, “Bile duct stone procedures are more frequent in patients with hypothyroidism. A large, registry-based, cohort study in Finland,” Scandinavian Journal of Gastroenterology, vol. 45, no. 1, pp. 70–74, 2010.
[6]  J. P. Andreini, W. F. Prigge, C. Ma, and R. L. Gebhard, “Vesicles and mixed micelles in hypothyroid rat bile before and after thyroid hormone treatment: evidence for a vesicle transport system for biliary cholesterol secretion,” Journal of Lipid Research, vol. 35, no. 8, pp. 1405–1412, 1994.
[7]  F. J. Field, E. Albright, and S. N. Mathur, “Effect of dietary cholesterol on biliary cholesterol content and bile flow in the hypothyroid rat,” Gastroenterology, vol. 91, no. 2, pp. 297–304, 1986.
[8]  J. Inkinen, J. Sand, P. Arvola, I. P?rsti, and I. Nordback, “Direct effect of thyroxine on pig Sphincter of Oddi contractility,” Digestive Diseases and Sciences, vol. 46, no. 1, pp. 182–186, 2001.
[9]  J. Laukkarinen, J. Sand, S. Aittom?ki et al., “Mechanism of the prorelaxing effect of thyroxine on the sphincter of Oddi,” Scandinavian Journal of Gastroenterology, vol. 37, no. 6, pp. 667–673, 2002.
[10]  R. G?rtner, “Subclinical hyperthyroidism—does it have to be treated?” MMW-Fortschritte der Medizin, vol. 146, no. 39, pp. 37–39, 2004.
[11]  B. Biondi and I. Klein, “Hypothyroidism as a risk factor for cardiovascular disease,” Endocrine, vol. 24, no. 1, pp. 1–13, 2004.
[12]  J. S. Vassilakis and N. Nicolopoulos, “Dissolution of gallstones following thyroxine administration. A case report,” Hepato-Gastroenterology, vol. 28, no. 1, pp. 60–61, 1981.
[13]  J. M. Donovan, “Physical and metabolic factors in gallstone pathogenesis,” Gastroenterology Clinics of North America, vol. 28, no. 1, pp. 75–97, 1999.
[14]  L. Behar, K. Y. Lee, W. R. Thompson, and P. Biancani, “Gallbladder contraction in patients with pigment and cholesterol stones,” Gastroenterology, vol. 97, no. 6, pp. 1479–1484, 1989.
[15]  R. P. Jazrawi, P. Pazzi, M. L. Petroni et al., “Postprandial gallbladder motor function: refilling and turnover of bile in health and in cholelithiasis,” Gastroenterology, vol. 109, no. 2, pp. 582–591, 1995.
[16]  J. Laukkarinen, P. K??bi, J. Kalliovalkama et al., “Bile flow to the duodenum is reduced in hypothyreosis and enhanced in hyperthyreosis,” Neurogastroenterology and Motility, vol. 14, no. 2, pp. 183–188, 2002.
[17]  J. Laukkarinen, J. Sand, R. Saaristo et al., “Is bile flow reduced in patients with hypothyroidism?” Surgery, vol. 133, no. 3, pp. 288–293, 2003.
[18]  R. Polikar, A. G. Burger, U. Scherrer, and P. Nicod, “The thyroid and the heart,” Circulation, vol. 87, no. 5, pp. 1435–1441, 1993.
[19]  M. I. Surks and R. Sievert, “Drugs and thyroid function,” The New England Journal of Medicine, vol. 333, no. 25, pp. 1688–1694, 1995.
[20]  C. K. Glass and J. M. Holloway, “Regulation of gene expression by the thyroid hormone receptor,” Biochimica et Biophysica Acta, vol. 1032, no. 2-3, pp. 157–176, 1990.
[21]  M. A. Lazar and W. W. Chin, “Nuclear thyroid hormone receptors,” Journal of Clinical Investigation, vol. 86, no. 6, pp. 1777–1782, 1990.
[22]  V. K. K. Chatterjee and J. R. Tata, “Thyroid hormone receptors and their role in development,” Cancer Surveys, vol. 14, pp. 147–168, 1992.
[23]  M. A. Lazar, “Thyroid hormone receptors: multiple forms, multiple possibilities,” Endocrine Reviews, vol. 14, no. 2, pp. 184–193, 1993.
[24]  W. W. Chin, “Molecular mechanisms of thyroid hormone action,” Thyroid, vol. 4, no. 3, pp. 389–393, 1994.
[25]  D. R. Salter, C. M. Dyke, and A. S. Wechsler, “Triiodothyronine (T3) and cardiovascular therapeutics: a review,” Journal of Cardiac Surgery, vol. 7, no. 4, pp. 363–374, 1992.
[26]  J. Segal, “A rapid, extranuclear effect of 3,5,3'-triiodothyronine on sugar uptake by several tissues in the rat in vivo. Evidence for a physiological role for the thyroid hormone action at the level of the plasma membrane,” Endocrinology, vol. 124, no. 6, pp. 2755–2764, 1989.
[27]  C. A. Siegrist-Kaiser, C. Juge-Aubry, M. P. Tranter, D. M. Ekenbarger, and J. L. Leonard, “Thyroxine-dependent modulation of actin polymerization in cultured astrocytes. A novel, extranuclear action of thyroid hormone,” Journal of Biological Chemistry, vol. 265, no. 9, pp. 5296–5302, 1990.
[28]  P. R. Warnick, P. J. Davis, F. B. Davis, V. Cody, J. Galindo Jr., and S. D. Blas, “Rabbit skeletal muscle sarcoplasmic reticulum Ca2+-ATPase activity: stimulation in vitro by thyroid hormone analogues and bipyridines,” Biochimica et Biophysica Acta, vol. 1153, no. 2, pp. 184–190, 1993.
[29]  W. D. Lawrence, M. Schoenl, and P. J. Davis, “Stimulation in vitro of rabbit erythrocyte cytosol phospholipid-dependent protein kinase activity. A novel action of thyroid hormone,” Journal of Biological Chemistry, vol. 264, no. 9, pp. 4766–4768, 1989.
[30]  K. Sterling, “Direct thyroid hormone activation of mitochondria: the role of adenine nucleotide translocase,” Endocrinology, vol. 119, no. 1, pp. 292–295, 1986.
[31]  T. Ishikawa, T. Chijiwa, M. Hagiwara, S. Mamiya, and H. Hidaka, “Thyroid hormones directly interact with vascular smooth muscle strips,” Molecular Pharmacology, vol. 35, no. 6, pp. 760–765, 1989.
[32]  K. Ojamaa, C. Balkman, and I. L. Klein, “Acute effects of triiodothyronine on arterial smooth muscle cells,” Annals of Thoracic Surgery, vol. 56, Supplement 1, pp. S61–S67, 1993.
[33]  C. Limas and C. J. Limas, “Influence of thyroid status on intracellular distribution of cardiac adrenoceptors,” Circulation Research, vol. 61, no. 6, pp. 824–828, 1987.
[34]  F. B. Davis, P. J. Davis, and S. D. Blas, “Role of calmodulin in thyroid hormone stimulation in vitro of human erythrocyte Ca2+-ATPase activity,” Journal of Clinical Investigation, vol. 71, no. 3, pp. 579–586, 1983.
[35]  A. Rudinger, K. M. Mylotte, and P. J. Davis, “Rabbit myocardial membrane Ca2+-adenosine triphosphatase activity: stimulation in vitro by thyroid hormone,” Archives of Biochemistry and Biophysics, vol. 229, no. 1, pp. 379–385, 1984.
[36]  J. Jansen, E. C. H. Friesema, C. Milici, and T. J. Visser, “Thyroid hormone transporters in health and disease,” Thyroid, vol. 15, no. 8, pp. 757–768, 2005.
[37]  H. Heuer and T. J. Visser, “Minireview: pathophysiological importance of thyroid hormone transporters,” Endocrinology, vol. 150, no. 3, pp. 1078–1083, 2009.
[38]  R. A. Dickey and S. Feld, “Guest editorial: the thyroid-cholesterol connection: an association between varying degrees of hypothyroidism and hypercholesterolemia in women,” Journal of Women's Health, vol. 9, no. 4, pp. 333–336, 2000.
[39]  K. M. Kutty, D. G. Bryant, and N. R. Farid, “Serum lipids in hypothyroidism—a re-evaluation,” Journal of Clinical Endocrinology & Metabolism, vol. 46, pp. 55–56, 1978.
[40]  J. Elder, A. McLelland, D. S. O'Reilly, C. J. Packard, J. J. Series, and J. Shepherd, “The relationship between serum cholesterol and serum thyrotropin, thyroxine and tri-iodothyronine concentrations in suspected hypothyroidism,” Annals of Clinical Biochemistry, vol. 27, no. 2, pp. 110–113, 1990.
[41]  T. Kuusi, M. R. Taskinen, and E. A. Nikkila, “Lipoproteins, lipolytic enzymes, and hormonal status in hypothyroid women at different levels of substitution,” Journal of Clinical Endocrinology and Metabolism, vol. 66, no. 1, pp. 51–56, 1988.
[42]  C. J. Packard, J. Shepherd, G. M. Lindsay, A. Gaw, and M. R. Taskinen, “Thyroid replacement therapy and its influence on postheparin plasma lipases and apolipoprotein-B metabolism in hypothyroidism,” Journal of Clinical Endocrinology and Metabolism, vol. 76, no. 5, pp. 1209–1216, 1993.
[43]  G. C. Ness, L. C. Pendleton, Y. C. Li, and J. Y. L. Chiang, “Effect of thyroid hormone on hepatic cholesterol 7α hydroxylase, LDL receptor, HMG-CoA reductase, farnesyl pyrophosphate synthetase and apolipoprotein A-I mRNA levels in hypophysectomized rats,” Biochemical and Biophysical Research Communications, vol. 172, no. 3, pp. 1150–1156, 1990.
[44]  L. Scarabottolo, E. Trezzi, P. Roma, and A. L. Catapano, “Experimental hypothyroidism modulates the expression of the low density lipoprotein receptor by the liver,” Atherosclerosis, vol. 59, no. 3, pp. 329–333, 1986.
[45]  R. Day, R. L. Gebhard, H. L. Schwartz et al., “Time course of hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase activity and messenger ribonucleic acid, biliary lipid secretion, and hepatic cholesterol content in methimazole-treated hypothyroid and hypophysectomized rats after triiodothyronine administration: possible linkage of cholesterol synthesis to biliary secretion,” Endocrinology, vol. 125, no. 1, pp. 459–468, 1989.
[46]  E. C. S. Ellis, “Suppression of bile acid synthesis by thyroid hormone in primary human hepatocytes,” World Journal of Gastroenterology, vol. 12, no. 29, pp. 4640–4645, 2006.
[47]  O. Strand, “Influence of propylthiouracil and D- and L-thiiodothyronine on excretion of bile acids in bile fistula rats,” Proceedings of the Society for Experimental Biology and Medicine, vol. 109, pp. 668–672, 1962.
[48]  R. L. Gebhard and W. F. Prigge, “Thyroid hormone differentially augments biliary sterol secretion in the rat. II. The chronic bile fistula model,” Journal of Lipid Research, vol. 33, no. 10, pp. 1467–1473, 1992.
[49]  M. Cakir, E. Kayacetin, H. Toy, and S. Bozkurt, “Gallbladder motor function in patients with different thyroid hormone status,” Experimental and Clinical Endocrinology and Diabetes, vol. 117, no. 8, pp. 395–399, 2009.
[50]  F. Bergman and W. van der Linden, “Further studies on the influence of thyroxine on gallstone formation in hamsters,” Acta Chirurgica Scandinavica, vol. 131, no. 4, pp. 319–328, 1966.
[51]  W. Van Steenbergen, J. Fevery, R. De Vos, R. Leyten, K. P. M. Heirwegh, and J. De Groote, “Thyroid hormones and the hepatic handling of bilirubin. I. Effects of hypothyroidism and hyperthyroidism on the hepatic transport of bilirubin mono- and diconjugates in the Wistar rat,” Hepatology, vol. 9, no. 2, pp. 314–321, 1989.
[52]  H. Johansson, “Gastrointestinal motility function related to thyroid activity. An experimental study in the rat,” Acta Chirurgica Scandinavica, vol. 359, pp. 1–88, 1966.
[53]  W. R. Middleton, “Thyroid hormones and the gut,” Gut, vol. 12, no. 2, pp. 172–177, 1971.
[54]  R. L. Duret and P. A. Bastenie, “Intestinal disorders in hypothyroidism—clinical and manometric study,” The American Journal of Digestive Diseases, vol. 16, no. 8, pp. 723–727, 1971.
[55]  K. Kowalewski and A. Kolodej, “Myoelectrical and mechanical activity of stomach and intestine in hypothyroid dogs,” American Journal of Digestive Diseases, vol. 22, no. 3, pp. 235–240, 1977.
[56]  L. J. Miller, C. A. Gorman, and V. L. W. Go, “Gut-thyroid interrelationships,” Gastroenterology, vol. 75, no. 5, pp. 901–911, 1978.
[57]  R. B. Shafer, R. A. Prentiss, and J. H. Bond, “Gastrointestinal transit in thyroid disease,” Gastroenterology, vol. 86, no. 5, pp. 852–858, 1984.
[58]  S. Goto, D. F. Billmire, and J. L. Grosfeld, “Hypothyroidism impairs colonic motility and function. An experimental study in the rat,” European Journal of Pediatric Surgery, vol. 2, no. 1, pp. 16–21, 1992.
[59]  G. L. Eastwood, L. E. Braverman, E. M. White, and T. J. Vander Salm, “Reversal of lower esophageal sphincter hypotension and esophageal aperistalsis after treatment for hypothyroidism,” Journal of Clinical Gastroenterology, vol. 4, no. 4, pp. 307–310, 1982.
[60]  K. O. Adeniyi, O. O. Ogunkeye, S. S. Senok, and F. V. Udoh, “Influence of the thyroid state on the intrinsic contractile properties of the bladder muscle,” Acta Physiologica Hungarica, vol. 82, no. 1, pp. 69–74, 1994.
[61]  K. Ojamaa, J. D. Klemperer, and I. Klein, “Acute effects of thyroid hormone on vascular smooth muscle,” Thyroid, vol. 6, no. 5, pp. 505–512, 1996.
[62]  J. Zwaveling, M. Pfaffendorf, and P. A. Van Zwieten, “The direct effects of thyroid hormones on rat mesenteric resistance arteries,” Fundamental and Clinical Pharmacology, vol. 11, no. 1, pp. 41–46, 1997.
[63]  W. H. Dillmann, “Biochemical basis of thyroid hormone action in the heart,” American Journal of Medicine, vol. 88, no. 6, pp. 626–630, 1990.
[64]  G. A. Brent, “Mechanisms of disease: the molecular basis of thyroid hormone action,” The New England Journal of Medicine, vol. 331, no. 13, pp. 847–853, 1994.
[65]  K. W. Park, H. B. Dai, K. Ojamaa, E. Lowenstein, I. Klein, and F. W. Sellke, “The direct vasomotor effect of thyroid hormones on rat muscle resistance arteries,” Anesthesia and Analgesia, vol. 85, no. 4, pp. 734–738, 1997.
[66]  P. Sandblom, W. L. Voegtlen, and I. C. Ivy, “The effects of CCK on the choledochoduodenal mechanism (sphincter of Oddi),” American Journal of Physiology, vol. 113, pp. 175–180, 1935.
[67]  J. Sand, H. Tainio, and I. Nordback, “Peptidergic innervation of human sphincter of Oddi,” Digestive Diseases and Sciences, vol. 39, no. 2, pp. 293–300, 1994.
[68]  J. Sand, P. Arvola, V. J?ntti et al., “The inhibitory role of nitric oxide in the control of porcine and human sphincter of Oddi activity,” Gut, vol. 41, no. 3, pp. 375–380, 1997.
[69]  J. Sand, I. Nordback, P. Arvola, I. P?rsti, A. Kalloo, and P. Pasricha, “Effects of botulinum toxin A on the sphincter of Oddi: an in vivo and in vitro study,” Gut, vol. 42, no. 4, pp. 507–510, 1998.
[70]  J. Sand, P. Arvola, I. P?rsti et al., “Histamine in the control of porcine and human sphincter of Oddi activity,” Neurogastroenterology and Motility, vol. 12, no. 6, pp. 573–579, 2000.
[71]  J. Sand, P. Arvola, and I. Nordback, “Calcium channel antagonists and inhibition of human sphincter of Oddi contractions,” Scandinavian Journal of Gastroenterology, vol. 40, no. 12, pp. 1394–1397, 2005.
[72]  V. P. Fomin, B. E. Cox, and R. Ann Word, “Effect of progesterone on intracellular Ca2+ homeostasis in human myometrial smooth muscle cells,” American Journal of Physiology, vol. 276, no. 2, part 1, pp. C379–C385, 1999.
[73]  M. Wakasugi, T. Noguchi, Y. I. Kazama, Y. Kanemaru, and T. Onaya, “The effects of sex hormones on the synthesis of prostacyclin (PGI2) by vascular tissues,” Prostaglandins, vol. 37, no. 4, pp. 401–410, 1989.
[74]  D. J. Beech, “Actions of neurotransmitters and other messengers on Ca2+ channels and K+ channels in smooth muscle cells,” Pharmacology and Therapeutics, vol. 73, no. 2, pp. 91–119, 1997.
[75]  A. R. Shepard and N. L. Eberhardt, “Molecular mechanisms of thyroid hormone action,” Clinics in Laboratory Medicine, vol. 13, no. 3, pp. 531–541, 1993.
[76]  B. G. Allen and M. P. Walsh, “The biochemical basis of the regulation of smooth-muscle contraction,” Trends in Biochemical Sciences, vol. 19, no. 9, pp. 362–368, 1994.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133