Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4437_Библиотеки_им_академика_М_И_Перельмана
.pdf
336
M. Sakr
cytology reliably exclude cancer? World J Surg.
2014;38:614–21.
183. Yoon JH, Kwak JY, Moon HJ, Kim MJ, Kim
EK. The diagnostic accuracy of ultrasound-guided
ne-needle aspiration biopsy and the sonographic
differences between benign and malignant thyroid
nodules 3cm or larger. Thyroid. 2011;21:993–1000.
184. Portereld JR Jr, Grant CS, Dean DS, Thompson
GB, Farley DR, Richards ML, etal. Reliability of
benign ne needle aspiration cytology of large thyroid nodules. Surgery. 2008;144:963–8.
185. Nou E, Kwong N, Alexander LK, Cibas ES,
Marqusee E, Alexander EK.Determination of the
optimal time interval for repeat evaluation after a
benign thyroid nodule aspiration. J Clin Endocrinol
Metab. 2014;99:510–6.
186. Sugitani I, Toda K, Yamada K, Yamamoto N,
Ikenaga M, Fujimoto Y. Three distinctly different
kinds of papillary thyroid microcarcinoma should be
recognized: our treatment strategies and outcomes.
World J Surg. 2010;34:1222–31.
187. Yu XM, Wan Y, Sippel RS, Chen H. Should all
papillary thyroid microcarcinomas be aggressively
treated? An analysis of 18,445 cases. Ann Surg.
2011;254:653–60.
188. Chow SM, Law SC, Chan JK, Au SK, Yau S, Lau
WH. Papillary microcarcinoma of the thyroid—
prognostic signicance of lymph node metastasis
and multifocality. Cancer. 2003;98:31–40.
189. Hay ID, Hutchinson ME, Gonzalez-Losada T,
McIver B, Reinalda ME, et al. Papillary thyroid
microcarcinoma: a study of 900 cases observed in a
60-year period. Surgery. 2008;144:980–7.
190. Roti E, Degli Uberti EC, Bondanelli M, Braverman
LE. Thyroid papillary microcarcinoma: a descriptive and meta-analysis study. Eur J Endocrinol.
2008;159:659–73.
191. Giordano D, Gradoni P, Oretti G, Molina E, Ferri
T. Treatment and prognostic factors of papillary thyroid microcarcinoma. Clin Otolaryngol.
2010;35:118–24.
192. Ito Y, Miyauchi A, Inoue H, Fukushima M, Kihara
M, Higashiyama T, et al. An observational trial
for papillary thyroid microcarcinoma in Japanese
patients. World J Surg. 2010;34:28–35.
193. Niemeier LA, Kuffner AH, Song C, Carty SE, Hodak
SP, Yip L, et al. A combined molecular-pathologic
score improves risk stratication of thyroid papillary
microcarcinoma. Cancer. 2012;118:2069–77.
194. O’Brien T, Gharib H, Suman VJ, van Heerden
JA. Treatment of toxic solitary thyroid nodules: surgery versus radioactive iodine. Surgery.
1992;112:1166–70.
195. Alexander EK, Heering JP, Benson CB, Frates MC,
Doubilet PM, Cibas ES, Marqusee E.Assessment of
nondiagnostic ultrasound-guided ne needle aspirations of thyroid nodules. J Clin Endocrinol Metab.
2002;87:4924–7.
196. Chen YT, Kitabayashi N, Zhou XK, Fahey TJ III,
Scognamiglio T. MicroRNA analysis as a potential
diagnostic tool for papillary thyroid carcinoma. Mod
Pathol. 2008;21:1139–46.
197. Hall TL, Layeld LJ, Philippe A, Rosenthal
DL.Sources of diagnostic error in ne needle aspiration of the thyroid. Cancer. 1989;63:718–25.
198. Nishimori H, Tabah R, Hickeson M, How
J. Incidental thyroid “PETomas”: clinical signicance and novel description of the self-resolving
variant of focal FDG-PET thyroid uptake. Can J
Surg. 2011;54:83–8.
199. Keutgen XM, Filicori F, Crowley MJ, Wang Y,
Scognamiglio T, Hoda R, etal. A panel of four miRNAs accurately differentiates malignant from benign
indeterminate thyroid lesions on ne needle aspiration. Clin Cancer Res. 2012;18:2032–8.
200. Gagel RF, Hoff AO, Cote GE. Medullary thyroid
carcinoma. In: Braverman L, Utiger R, editors.
Werner and Ingbar’s the thyroid. Philadelphia, PA:
Lippincott Williams and Wilkins; 2005. p.967–88.
201. Carey C, Skosey C, Pinnamaneni KM, Barsano
CP, DeGroot LJ. Thyroid abnormalities in children
of parents who have graves’ disease. Possible preGraves’ disease. Metabolism. 1980;29:369–74.
202. Agretti P, Ferrarini E, Rago T, Candelieri A, De
Marco G, Dimida A, et al. MicroRNA expression prole helps to distinguish benign nodules
from papillary thyroid carcinomas starting from
cells of ne-needle aspiration. Eur J Endocrinol.
2012;167:393–400.
203. Sabel MS, Staren ED, Gianakakis L, Dwarakanathan
S, Prinz RA. Use of ne needle aspiration biopsy
and frozen section in the management of the solitary
thyroid nodule. Surgery. 1997;122:1021–7.
204. Bartalena L, Fatourechi V.Extrathyroidal manifestations of graves’ disease: a 2014 update. J Endocrinol
Investig. 2014;37(8):691–700.
205. Devereaux D, Tewelde SZ. Hyperthyroidism
and thyrotoxicosis. Emerg Med Clin North Am.
2014;32(2):277–92.
206. Bahn RS, Burch HB, Cooper DS, Garber JR,
Greenlee MC, Klein I, et al. Hyperthyroidism and
other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and
American Association of Clinical Endocrinologists.
Endocr Pract. 2011;17(3):456–520.
207. Volpe R. The pathogenesis of graves’ disease.
Endocr Pract. 1995;1(2):103–15.
208. Smith TJ, Hegedüs L. Graves’ disease. N Engl J
Med. 2017;376(2):185.
209. Rastad J, Karlsson FA. Surgical management of
graves’ disease: preoperative preparation and extent
of surgery. Problems Gen Surg. 1997;14(4):132–54.
210. Nordyke RA, Gilbert FI Jr. Optimal iodine-131 dose
for eliminating hyperthyroidism in graves’ disease. J
Nucl Med. 1991;32(3):411–6.
211. Brito JP, Castaneda-Guarderas A, Gionfriddo MR,
Ospina NS, Maraka S, Dean DS, etal. Development
and pilot testing of an encounter tool for shared decision making about the treatment of graves’ disease.
Thyroid. 2015;25(11):1191–8.
t.me/Dr_Mouayyad_AlbtousH
12 Benign Thyroid Disease
337
212. Hedley AJ, Young RE, Jones SL, etal. Antithyroid
drugs in treatment of hyperthyroidism of graves’
disease: long-term follow up of 434 patients. Clin
Endocrinol. 1989;31:209–18.
213. McHenry CR, Slusarczyk SJ, Askari AT, et al.
Rened use of scintigraphy in the evaluation of
nodular thyroid disease. Surgery. 1998;124:656–62.
214. Lazarus JH.Silent thyroiditis and subacute thyroiditis. In: Braverman LE, Utiger RD, editors. Werner
and Ingbar’s the thyroid. 7th ed. Philadelphia: JB
Lippincott-Raven Publishers; 1996. p.577–91.
215. Mulligan DC, McHenry CR, Kinney W, et al.
Amiodarone-induced thyrotoxicosis: clinical presentations and expanded indications for thyroidectomy. Surgery. 1993;114:1114–9.
216. Vanderpump MPJ.The epidemiology of thyroid disease. Br Med Bull. 2011;99(1):39–51.
217. Weetman AP. Chronic autoimmune thyroiditis. In:
Braverman LE, Utiger RD, editors. The thyroid.
Lippincott, Philadelphia, PA: Williams & Wilkins;
2000. p.721–32.
218. Mizokami T, Wu Li A, El-Kaissi S, Wall
JR. Stress and thyroid autoimmunity. Thyroid.
2004;14:1047–55.
219. Khan A, Nosé V.Pathology of the thyroid gland. In:
Lloyd RV, editor. Endocrine pathology. Totowa, NJ:
Humana; 2004. p.153–89.
220. Gordin A, Maatela J, Miettinen A, Helenius T,
Lamberg B-A. Serum thyrotrophin and circulating thyroglobulin and thyroid microsomal antibodies in a Finnish population. Acta Endocrinol.
1979;l90:33–9.
221. Ling SM, Kaplan SA, Weitzman JJ, Reed GB, Costin
G, Landing BH. Euthyroid goiters in children.
Correlation of needle biopsy with other clinical and
laboratory ndings in chronic lymphocytic thyroiditis and simple goiter. Pediatrics. 1969;44:695–9.
222. Tunbridge WMG, Evered DC, Hall R, Appleton D,
Brewis M, Clark F, et al. The spectrum of thyroid
disease in a community. The Whickham survey. Clin
Endocrinol. 1977;7:481–6.
223. Vanderpump MP, French JM, Appleton D.The prevalence of hyperprolactinaemia and association with
markers of autoimmune thyroid disease in survivors
of the Whickham survey cohort. Clin Endocrinol.
1998;48(1):39–44.
224. Vanderpump MP, Tunbridge WM, French JM.The
incidence of thyroid disorders in the community: a
twenty-year follow-up of the Whickham survey. Clin
Endocrinol. 1995;43(1):55–68.
225. Staii A, et al. Hashimoto thyroiditis is more frequent than expected when diagnosed by cytology
which uncovers a pre-clinical state. Thyroid Res.
2010;3:11–6.
226. Inoue M, Taketani N, Sato T, Nakajima H.High incidence of chronic lymphocytic thyroiditis in apparently healthy school children: epidemiological and
clinical study. Endocrinol Jpn. 1975;22:483–7.
227. Yoshida H, Amino N, Yagawa K, Uemura K, Satoh
M, Miyai K, etal. Association of serum antithyroid
antibodies with lymphocytic inltration of the thy-
roid gland: studies of seventy autopsied cases. J Clin
Endocrinol Metab. 1978;46:859–64.
228. Gordin A, Saarinen P, Pelkonen A, Lamberg
B-A.Serum thyroglobulin and the response to thyrotropin releasing hormone in symptomless autoimmune thyroiditis and in borderline and overt
hypothyroidism. Acta Endocrinol. 1974;75:274–7.
229. Tunbridge WMG, Brewis M, French JM, Appleton
D, Bird T, Clark F, etal. Natural history of autoimmune thyroiditis. Br Med J. 1981;282:258–63.
230. Totterman TH, Maenpaa J, Gordin A, Makinen T,
Andersson AC. Blood and thyroid-inltrating lymphocyte subclasses in juvenile autoimmune thyroiditis. Clin Exp Immunol. 1977;30:193–7.
231. Moriuchi A, Yokoyama S, Kashima K, Andoh T,
Nakayama I, Noguchi S. Localized primary anyloid tumor of the thyroid developing in the course
of Hashimoto’s thyroiditis. Acta Pathol Jpn.
1992;42:210–6.
232. Shaw PJ, Walls TJ, Newman PK, Cleland PG,
Cartlidge NE. Hashimoto’s encephalopathy: a
steroid-responsive disorder associated with high
antithyroid antibody titers—report of ve cases.
Neurology. 1991;41:228–33.
233. Khardori R, Eagleton LE, Soler NG, McConnachie
PR. Lymphocytic interstitial pneumonitis
in autoimmune thyroid disease. Am J Med.
1991;90:649–52.
234. Tateno F, Sakakibara R, Kishi M, Ogawa
E. Hashimoto’s ophthalmopathy. Am J Med Sci.
2011;342(1):83–5.
235. Yoshihara A, Yoshimura Noh J, Nakachi A, Ohye H,
Sato S, Sekiya K, et al. Severe thyroid-associated
orbitopathy in Hashimoto’s thyroiditis. Report of
two cases. Endocr J. 2011;58(5):343–8.
236. Skillern PG, Crile G Jr, McCullaugh EP, Hazard JB,
Lewis LA, Brown H.Struma lymphomatosa: primary
thyroid failure with compensatory thyroid enlargement. J Clin Endocrinol Metab. 1956;16:35–9.
237. Becker KL, Ferguson RH, McConahey WM. The
connective-tissue diseases and symptoms associated with Hashimoto’s thyroiditis. N Engl J Med.
1963;268:277–81.
238. Bastenie PA, Vanhaelst L, Golstein J, Smets P, Keys
MJ, Karvonen MJ, Punsar S.Asymptomatic autoimmune thyroiditis and coronary heart-disease. Lancet.
1977;1:155–9.
239. Heinonen OP, Aho K, Pyorala K, Gordin A, Punsar
S, Puro K.Symptomless autoimmune thyroiditis in
coronary heart disease. Lancet. 1972;1:785–9.
240. Jankovic B, Le KT, Hershman JM.Clinical review:
Hashimoto’s thyroiditis and papillary thyroid carcinoma: is there a correlation? J Clin Endocrinol
Metab. 2013;98(2):474–82.
241. Lee JH, Kim Y, Choi JW, Kim YS. The association between papillary thyroid carcinoma and histologically proven Hashimoto’s thyroiditis: a
meta- analysis. Eur J Endocrinol. 2013;168(3):343–9.
242. Larson SD, Jackson LN, Riall TS, Uchida T,
Thomas RP, Qiu S, Evers BM. Increased incidence
of well-differentiated thyroid cancer associated with
t.me/Dr_Mouayyad_AlbtousH
338
M. Sakr
Hashimoto thyroiditis and the role of the PI3k/Akt
pathway. J Am Coll Surg. 2007;204(5):764–673.
243. Fava A, Oliverio R, Giuliano S, Parlato G,
Michniewicz A, Indrieri A, etal. Clinical evolution
of autoimmune thyroiditis in children and adolescents. Thyroid. 2009;19(4):361–7.
244. Muzza M, Degl’Innocenti D, Colombo C, Perrino
M, Ravasi E, Rossi S, Cirello V, Beck-Peccoz P,
Borrello MG, Fugazzola L. The tight relationship
between papillary thyroid cancer, autoimmunity and
inammation: clinical and molecular studies. Clin
Endocrinol. 2010;72:702–8.
245. Kim HS, Choi YJ, Yun JS. Features of papillary thyroid microcarcinoma in the presence and
absence of lymphocytic thyroiditis. Endoc Pathol.
2010;21:149–53.
246. Dvorkin S, Robenshtok E, Hirsch D, Strenov Y,
Shimon I, Benbassat CA. Differentiated thyroid
cancer is associated with less aggressive disease
and better outcome in patients with coexisting
Hashimotos thyroiditis. J Clin Endocrinol Metab.
2013;98(6):2409–14.
247. Marotta V, Guerra A, Zatelli MC, Uberti ED, Di
Stasi V, Faggiano A, etal. BRAF mutation positive
papillary thyroid carcinoma is less advanced when
Hashimoto’s thyroiditis lymphocytic inltration is
present. Clin Endocrinol. 2013;79(5):733–8.
248. Pankow BG, Michalak J, McGee MK.Adult human
thyroid weight. Health Phys. 1985;49:1097–103.
249. Glynne A, Thomson JA. Serum immunoglobulin levels in thyroid disease. Clin Exp Immunol.
1972;12:71–7.
250. Monteleone JA, Davis RK, Tung KSK, Ramos CV,
Peden VH.Differentiation of chronic lymphocytic
thyroiditis and simple goiter in pediatrics. J Pediatr.
1973;83:381–5.
251. Kawakami Y, Fisfalen M-E, DeGroot LJ.Proliferative
responses of peripheral blood mononuclear cells
from patients with autoimmune thyroid disease to
synthetic peptide epitopes of human thyroid peroxidase. Autoimmunity. 1992;13:17–26.
252. Zhang, et al. Clinical features of papillary thyroid cancer in ht patients from an area wih a high
prevalence of Hashimoto’s disease. BMC Cancer.
2012;12:610–5.
253. Fiore, et al. Hashimoto’s thyroiditis is associated
with papillary thyroid carcinoma: role of TSH and
treatment with L-thyroxine. Endocr Relat Cancer.
2011;18:429–37.
254. Krysiak R, Okopien B. The effect of levothyroxine and Selenomethionine on lymphocyte
and monocyte cytokine release in women with
Hashimoto’s thyroiditis. J Clin Endocrinol Metab.
2011;96:2206–15.
255. Wozniak, etal. Maltoma of the thyroid in a man with
Hashimoto’s thyroiditis. J Clin Endocrinol Metab.
1999;4:84–8.
256. Miller BS, Paul G.Image in endocrinology: thyroid
lymphoma arising from Hashimoto’s thyroiditis. J
Clin Endocrinol Metab. 1991;10:3711–2.
257. Takano T, Miyauchi A, Matsuzuka F, Yoshida H,
Kuma K, Amino N. Diagnosis of thyroid malignant lymphoma by reverse transcription-polymerase
chain reaction detecting the monoclonality of immunoglobulin heavy chain messenger ribonucleic acid.
J Clin Endocr Metab. 2000;85:671–5.
258. Vickery AL, Hamlin E Jr. Struma lymphomatosa (Hasimoto’s thyroiditis): observations on
repeated biopsies in 16 patients. N Engl J Med.
1961;264:226–9.
259. Bozkurt NC, Karbek B, Ucan B, Sahin M, Cakal E,
Ozbek M, etal. The association between severity of
vitamin D deciency and Hashimoto’s thyroiditis.
Endocr Pract. 2013;21:1–14.
260. McConahey WM, Woolner LB, Black BM, Keating
FR Jr. Effect of desiccated thyroid in lymphocytic
(Hashimoto’s) thyroiditis. J Clin Endocrinol Metab.
1959;19:45–9.
261. Karges B, Muche R, Knerr I, Ertelt W, Wiesel T,
Hub R, Neu A, Klinghammer A, Aufschild J, Rapp
A, Schirbel A, Boehm BO, Debatin KM, Heinze
E, Karges W. Levothyroxine in euthyroid autoimmune thyroiditis and type 1 diabetes: a randomized, controlled trial. J Clin Endocrinol Metab.
2007;92(5):1647–52.
262. Caturegli P, De Remigis A, Rose NR.Hashimoto thyroiditis: clinical and diagnostic criteria. Autoimmun
Rev. 2014;4–5:391–7.
263. Kahaly GJ, Diana T, Glang J, Kanitz M, Pitz S,
König J.Thyroid stimulating antibodies are highly
prevalent in Hashimoto’s thyroiditis and associated Orbitopathy. J Clin Endocrinol Metab.
2016;101(5):1998–2004.
264. Kim KW, Park YJ, Kim EH, Park SY, Park DJ, Ahn
SH, etal. Elevated risk of papillary thyroid cancer in
Korean patients with Hashimoto’s thyroiditis. Head
Neck. 2011;33(5):691–5.
265. Amino N, Tada H, Hidaka Y. Postpartum autoimmune thyroid syndrome: a model of aggravation of
autoimmune disease. Thyroid. 1999;9:705–13.
266. Stagnaro-Green A. Clinical review 152: postpartum thyroiditis. J Clin Endocrinol Metab.
2002;87:4042–7.
267. Volpe R.The management of subacute (de Quervain)
thyroiditis. Thyroid. 1993;3:253–5.
268. Fatourechi V, Aniszewski JP, Fatourechi GZ, et al.
Clinical features and outcome of subacute thyroiditis
in an incidence cohort: Olmsted County, Minnesota,
study. J Clin Endocrinol Metab. 2003;88:2100–5.
269. Taylor HC, Sheeler LR. Recurrence and heterogeneity in painless thyrotoxic lymphocytic thyroiditis. Report of ve cases. J Am Med Assn.
1982;248:1085–8.
270. Papi G, LiVolsi VA.Current concepts on Riedel thyroiditis. Am J Clin Pathol. 2004;121:S50–63.
271. Gan YU, Lam SL. Imaging ndings in acute neck
infections due to pyriform sinus stula. Ann Acad
Med Singap. 2004;33:636–40.
272. Farwell AP. Infectious thyroiditis. In: Braverman
LE, Utiger RD, editors. Werner & Ingbar’s the thy-
t.me/Dr_Mouayyad_AlbtousH
12 Benign Thyroid Disease
339
roid: a fundamental and clinical text. Lippincott,
Philadelphia: Williams & Wilkins; 2000. p.1044–50.
273. Miyauchi A, Matsuzuku F, Kuma K, Takai
S.Piriform sinus stula: an underlying abnormality
common in patients with acute suppurative thyroiditis. World J Surg. 1990;14:400–5.
274. Jeng LB, Lin JD, Chen MF.Acute suppurative thyroiditis: a ten-year review in a Taiwanese hospital.
Scand J Infect Dis. 1994;26:297–300.
275. Preziati D, La Rosa L, Covini G, Marcelli R,
Rescalli S, Persani L, etal. Autoimmunity and thyroid function in patients with chronic active hepatitis
treated with recombinant interferon alpha-2a. Eur J
Endocrinol. 1995;132:587–93.
276. Roti E, Minelli R, Giuberti T, Archelli S, Schianchi
C, Gardini E, etal. Multiple changes in thyroid function in patients with chronic active HCV hepatitis
treated with recombinant interferon-alpha. Am J
Med. 1996;172:482–7.
277. Harjai KJ, Licata AA.Effects of amiodarone on thyroid function. Ann Intern Med. 1997;126:63–73.
278. McDermott A, Onyeaka CV, Macnamara
M.Surgery-induced thyroiditis: fact or ction? Ear
Nose Throat J. 2002;81:408–10.
279. Manson CM, Cross P, De Sousa B. Postoperative necrotizing granulomas of the thyroid.
Histopathology. 1992;21:392–3.
280. Kobayashi A, Kuma K, Matsuzuka F, Hirai K, Fukata S,
Sugawara M.Thyrotoxicosis after needle aspiration of
thyroid cyst. J Clin Endocrinol Metab. 1992;75:21–4.
281. Porter N, Beynon HL, Randeva HS.Endocrine and
reproductive manifestations of sarcoidosis. QJM.
2003;96:553–61.
282. Röher HD, Schulte KM. Operative therapie bei
thyreoiditis. In: Rothmund M, Harder F, Siewert
JR, editors. Praxis der viszeralchirurgie: endokrine
chirurgie. Berlin Heidelberg New York: Springer;
2000. p.199–202.
283. Kon YC, DeGroot LJ. Painful Hashimoto’s thyroiditis as an indication for thyroidectomy: clinical
characteristics and outcome in seven patients. J Clin
Endocrinol Metab. 2003;88:2667–72.
t.me/Dr_Mouayyad_AlbtousH
Malignant Thyroid Disease
MahmoudSakr
13
13.1 Introduction
The wide spectrum of aggressiveness of thyroid
cancer is extra-ordinary, ranging from differentiated malignancies in which most patients live out
close to their normal lifespan to anaplastic varieties that are almost universally lethal [1].
13.1.1 Classication ofThyroid
Neoplasms
13.1.1.1 World Health Organization
(WHO) Classication
A classication of thyroid tumors, as suggested
by WHO is shown in Table13.1 [2].
13.1.1.2 Pathological Classication
Most thyroid tumors arise from the follicular
cells, and most are well-differentiated. Poorly
differentiated and undifferentiated types are rare
(Table 13.2). Well-differentiated carcinomas
include papillary and follicular carcinomas.
13.1.2 Incidence ofThyroid Cancer
Thyroid cancer is the most common endocrine
cancer [3], and its incidence has continuously
M. Sakr (*)
Department of Surgery, Faculty of Medicine,
Alexandria University, Alexandria, Egypt
increased in the last three decades all over the
world [4]. Based on recent data, thyroid cancer,
in general, is the fth most common cancer in
women [5]; in Italy, it is the second most frequent
cancer in women below 45years of age [6]. The
incidence of thyroid cancer in the USA more than
doubled over the past 30years. Only in few countries (Norway, Sweden) thyroid cancer incidence
has decreased [4]. Genetic factors, environmental
inuences, and access to medical care can easily
explain the high variability in the thyroid cancer
incidence by geographic area and ethnicity.
Recent reports indicated a similar age-specic
trend by racial/ethnic groups. Although the lowest rates of thyroid cancer are observed in blacks,
the greatest rate of PTC acceleration occurs in
black females [7].
In any case, the continuously increasing rate
of thyroid cancer is nearly exclusively due to
increases in the incidence of PTC, with no signicant change for the follicular, medullary, or
anaplastic histotypes. The increase mainly
regards small tumors, although large tumors have
also increased [8, 9]. In spite of the steadily
increased incidence, thyroid cancer “mortality”
is reported stable at approximately 0.5 cases per
100,000 persons [10].
Some experts believe that the worldwide
increase of thyroid cancer is due to the increased
diagnostic intensity [11]. Others believe that a
“true increase,” due to environment and lifestyle
changes, is also possible [8, 9, 12–15].
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
M. Sakr (ed.), Head and Neck and Endocrine Surgery,
https://doi.org/10.1007/978-3-031-64102-2_13
t.me/Dr_Mouayyad_AlbtousH
341
342
Table 13.1 WHO classication of thyroid neoplasms
I. Primary tumors
1. Epithelial tumors
– Tumors of follicular cells
– Tumors of C- (and related neuroendocrine) cells
– Tumors of follicular/C-cells
2. Sarcoma
3. Lymphoma
Miscellaneous
II. Secondary tumors
III. Tumor-like lesions
1. Tumors with oncocytic (Hürthle cell) features
2. Tumors with clear cell features
3. Tumors with squamous features
4. Tumors with mucinous features
Table 13.2 Pathological classication of thyroid neoplasms
Grade of malignancy Pathological histotypes
I. Well-differentiated (low-grade malignancy) 1. Usual papillary thyroid carcinoma (PTC)
II. Intermediate differentiation 1. Medullary thyroid carcinoma (MTC)
III. Poorly differentiated (high- grade malignancy) Anaplastic (undifferentiated) carcinoma
– Benign (follicular adenoma)
– Malignant (carcinoma)
* Differentiated:
Follicular carcinoma–Papillary carcinoma
* Poorly differentiated
* Undifferentiated (anaplastic)
– Medullary carcinoma
– Others
– Oncocytic (Hürthle cell) adenoma
– Oncocytic (Hürthle cell) carcinoma
– papillary (Hürthle cell) oncocytic tumors
2. Micro-carcinoma (<1cm)
3. Follicular variant of PTC
4. Usual follicular thyroid carcinoma (FTC)
5. Hurthle cell carcinoma
2. Diffuse sclerosing variant of PTC
3. Columnar cell variant of PTC
4. Insular carcinoma
5. Tall cell variant of papillary carcinoma
M. Sakr
13.1.3 Screening
There are two primary methods to screen for thy-
roid cancer such as (1) neck palpation during a
physical examination, which can identify palpable nodules, and (2) ultrasound (US), which can
identify both palpable and non-palpable nodules,
especially those <1 cm. US can also identify
characteristics of a “suspicious” nodule [16].
Screening with both palpation and US can also
identify abnormal cervical LNs that may represent metastatic thyroid cancer.
Screening for thyroid cancer could result in
early detection of malignant thyroid nodules that
are easily treatable, before the cancer spreads
beyond the thyroid gland. Early detection could
make treatment more effective, with potentially
less harm than if administered later. Potential
t.me/Dr_Mouayyad_AlbtousH
harms of screening include false-positive results,
which may lead to unnecessary diagnostic tests.
Screening may also result in “over-diagnosis”
because it can detect very small and/or indolent
tumors that might never affect a person’s morbidity or mortality [17, 18]. Over-diagnosis might
also lead to over-treatment [19].
At present, there is no screening program to
detect thyroid cancer for the general population.
Screening is possible for familial MTCs associated with specic oncogene mutations. The
genetic basis of papillary, follicular, and anaplastic thyroid cancer has been investigated and
the roles and potential prognostic value of several genes, for example, RET, TRK, ras, BRAF,
and p53, have been identied. Testing for these
genes is not routinely available in clinical practice [20].
13 Malignant Thyroid Disease
343
While screening generally is not possible, a
family history for thyroid cancer should be taken
in each case, and if there is a strong familial incidence of thyroid cancer or association with other
cancers, genetic advice should be considered in
appropriate cases from the regional genetics
service.
13.1.4 Risk Factors ofThyroid
Carcinoma
13.1.4.1 History-Taking
It is important to focus on gender, age, duration
of the swelling and, more importantly, its rate of
growth, history of neck irradiation, and family
history of thyroid cancer. Fowler et al. (1989)
found that a family history of thyroid disease was
present in 41% of their patients with thyroid nodules [21]. Male gender carries 2–3 times the risk
of thyroid cancer as compared to women [22,
23]. At an age below 20years, the risk of malig-
nancy is doubled, whilst above 70years, the risk
of malignancy is quadrupled [22, 23].
History of rapid growth in a few weeks
[24–26] and the presence of associated symptoms such as difculty in swallowing or breathing would suggest a compressive effect or
involvement of the esophagus or trachea.
Hoarseness of voice strongly indicates RLN
palsy and malignancy [24]. Other associated diseases should also be noted. These are summarized in Table13.3 [27].
There is a 40% absolute risk of malignancy for
a thyroid nodule with previous exposure to irradiation, particularly during childhood. Low dose
carries a 100 life-time risk of malignancy, while
high dose carries a 300 times increased life-time
risk. The latency period is 10–15years, and cancer mostly occurs 20–30 years after radiation
exposure [24, 25].
13.1.4.2 Local Examination
The larger the tumor size, especially when >4cm,
and the presence of obstructive symptoms indicate higher risk of malignancy [23, 26]. Firm/
hard consistency or xed swelling indicates high
risk, while a soft, mobile, or cystic swelling indicates a low risk of malignancy [26]. “Hard” nodules may also result from calcications in benign
adenomas, and “xation” of the thyroid can also
occur with severe chronic thyroiditis [26].
The presence of cervical lymphadenopathy
indicates high risk of malignancy (Table13.3). In
fact, the most signicant physical ndings suggestive of malignancy are the unilateral, rm,
non-tender, discrete lymph nodes (LNs); these
may result from metastatic thyroid cancer, most
commonly papillary thyroid carcinoma (PTC)
[26].
13.1.4.3 General Examination
Thyroid malignancy also metastasizes to the
lungs in 10% of individuals, sometimes occuring
without LN spread, especially in patients with
follicular thyroid carcinoma (FTC). Other sites of
Table 13.3 Risk factors for thyroid cancer [27]
Risk factors
History-taking Physical examination
– Male gender
– Age<20 or>70years
– Low-iodine diet (endemic goiter)
– Radiation exposure (during childhood)
– Family history of thyroid cancer
– Hashimoto’s thyroiditis (risk of lymphoma)
– Family or personal history of thyroid adenoma
– Multiple endocrine neoplasia (MEN II a,b)
– Gardner syndrome
– Familial adenomatous polyposis
– Cowden’s disease (hamartoma tumor syndrome)
– Non-polyposis colon cancer syndrome (NPCC)
t.me/Dr_Mouayyad_AlbtousH
– True vocal cord xation
– Very rm or hard nodules
– Fixation to skin, surrounding musculature, and
extra-capsular spread
– Associated cervical lymph nodes (LNs)
– Recent rapid growth
– Large nodules (>4cm)
– Persistent diarrhea (MTC)
344
M. Sakr
spread include the spinal cord, base of the tongue,
and bone, especially the skull, tibia, and costochondral junction. If medullary thyroid carcinoma (MTC) is suspected in conjunction with
multiple endocrine neoplasia (MEN)-2A and
MEN-2B, the characteristic features of MEN
syndrome may also be evident.
13.1.4.4 Flexible Laryngoscopy
Flexible laryngoscopy is important to assess
vocal cord movements. The so-called “classic”
red ag physical nding is true vocal cord paralysis. However, this nding by itself can be of limited help in assessing malignant potential as the
three main causes of unilateral vocal cord paralysis can be broadly categorized as iatrogenic,
malignant, and idiopathic. Reviews of unilateral
cord paralysis quote gures for malignancy ranging from 7% to 25% with the vast majority due to
lung cancer. If lung cancer is excluded, all other
malignancies, including thyroid cancer, represent
well under 10% of unilateral vocal cord paralysis. In contrast, idiopathic causes account for
30–40% of vocal cord paralysis cases.
13.2 Well-Dierentiated Thyroid
Cancer (WDTC)
13.2.1 Introduction
Well-differentiated thyroid carcinoma (WDTC)
refers to both PTC and FTC, which arise from the
thyroid follicular cell. Among many unique features of DTC, two require special mention. First,
age is the most important prognostic factor. It is
interesting to note that the mortality in patients
with thyroid cancer in the younger age group is
extremely low, while that in the elderly patient is
quite high. There is no other human cancer that
parallels this biological behavior. This is the only
cancer where age is included in the staging system. There is no stage III and IV cancer in patients
below the age of 45years [28–30]. Second, the
presence of nodal metastasis has almost no prognostic implication, whilst in the majority of cancers the presence of nodal metastasis decreases
the survival by almost 50% [31].
The mortality of DTC remains low; most
deaths are directly related to the high-risk group,
generally elderly patients with poorly differentiated histology or locally aggressive tumors.
There is considerable debate and controversy
about the management of the disease [32]. There
are vigorous proponents of routine total thyroidectomy (TT), whereas other authors recommend
less than TT, depending on the prognostic factors
and risk groups [33].
13.2.2 Staging
The TNM staging of WDTC is summarized in
Table 13.4. Staging according to age with
45years as the cut point is listed in Table13.5.
The 10-year cancer-specic mortality rate is
shown in Table13.6.
13.2.3 Management ofWDTC
13.2.3.1 Surgical Treatment
Fine needle aspiration cytology (FNAC) should
be used in the planning of surgery. Patients with a
Table 13.4 TNM classication according to tumor,
nodes, and metastases
Primary tumor (pT)
pT1
Intra-thyroidal tumor, ≤1cm in greatest
dimension
pT2 Intra-thyroidal tumor, >1–4cm in greatest
dimension
PT3 Intra-thyroidal tumor, >4cm in greatest
dimension
pT4 Tumor of any size, extending beyond thyroid
capsule
pTX Primary tumor cannot be assessed
Regional LNs (cervical or upper mediastinal)
N0 No nodes involved
N1 Regional nodes involved
N1a Ipsilateral cervical nodes
N1b Bilateral, midline, or contra-lateral cervical
nodes or mediastinal nodes
NX Nodes cannot be assessed
Distant metastases
M0 No distant metastases
M1 Distant metastases
MX Distant metastases cannot be assessed
t.me/Dr_Mouayyad_AlbtousH
13 Malignant Thyroid Disease
345
Table 13.5 TNM classication of papillary or follicular
carcinoma by age
Stage Under 45years 45years and older
Stage I Any T, any N, M0 pT1, N0, M0
Stage II Any T, any N, M1 pT2, N0, M0
pT3, N0, M0
Stage III pT4, N0, M0
Any pT, N1, M0
Stage IV Any pT, any N, M1
Undifferentiated or anaplastic carcinomas are Stage IV
Table 13.6 10-year mortality rate of WDCT (PTC or
FTC) [165]
Stage 10-year cancer-specic mortality (%)
I 1.7
II 15.8
III 30
IV 60
PTC >1cm or with high-risk FTC should undergo
near-TT or TT, while those with PTC ≤1cm or
low-risk FTC may be treated with thyroid lobectomy (hemi-thyroidectomy) alone. Serum thyroglobulin (Tg) should be checked in all
postoperative patients with DTC, but not sooner
than 6weeks after surgery. Patients will normally
start on L-T4 100 μg daily after the operation.
This should be stopped 2weeks before
131
I abla-
tion or therapy.
Most patients with a tumor >1cm, who have
undergone a near-TT/TT, should have
131
I ablation. Pregnancy and breast-feeding should always
be excluded before administering
131
I. Breastfeeding should be stopped 4weeks and preferably 8weeks before
131
I ablation or treatment and
should not be resumed. A post-ablation scan
(3–10 days after
131
I ablation) should be
performed.
Patients treated with
131
I will require L-T4
therapy in a dose sufcient to suppress the serum
TSH to <0.1mIU/L.L-T4 can be started 3days
131
after
I in a dose sufcient to suppress TSH to
<0.1 mIU/L. In low-risk patients, TSH
<0.5mIU/L is acceptable.
Re-assessment with a whole-body scan
(WBS) after stopping L-T4 for 4weeks and stimulated serum Tg is indicated no earlier than
6months after
the tracer is detectable, a
131
I ablation. If abnormal uptake of
131
I treatment dose
should be given and a posttreatment scan
(3–10 days after
131
I treatment) performed. The
patient should then restart L-T4.
13.2.3.2 Radioactive Iodine (RAI)
Ablation andTreatment
ofWDTC
Following a TT or near-TT, some RAI uptake is
usually demonstrable in the thyroid bed.
131
I-induced destruction of this residual thyroid
tissue is known as “radioiodine remnant ablation.” “Radioiodine therapy” refers to administra-
131
tion of
I with the intention to treat recurrent or
metastatic disease. The principles and procedures
are similar for the administration of
131
I for abla-
tion or treatment.
Preparation for
131
I Ablation or Therapy
Patients should adopt a low I2 diet for 2weeks
prior to
131
I and other sources of excess I2 should
be eliminated (e.g., recent CT with contrast)
[34]. If
131
I can be administered within
3–4 weeks of thyroidectomy, no thyroid hormone replacement is required in the interim
period. This would usually allow TSH to rise to
>30 mIU/L at the time of ablation. For most
centers, however, the interval between thyroidectomy and
131
I ablation will be longer. In such
cases, patients should start T3 (20mg tds) after
surgery; this should be stopped 2weeks before
planned ablation to allow serum TSH to increase
to >30 mIU/L.
If there is doubt about completeness of surgery, a pre-ablation scan can be performed to
assess remnant size [35]. Demonstration of large
thyroid remnants should lead to consideration of
further surgery before
Pregnancy must be excluded before
131
I ablation.
131
I ablation. Breast-feeding must be discontinued
4weeks, preferably 8 weeks before
131
I ablation
or treatment and should not be resumed.
Pretreatment sperm banking should be considered in male patients likely to have >2 high-dose
131
I therapies [36]. Adequate hydration at the time
of treatment and for several days afterwards, regular emptying of the urinary bladder, and avoidance of constipation helps to prevent a reduction
in sperm count.
t.me/Dr_Mouayyad_AlbtousH
Соседние файлы в папке Библиотека им академика М.И. Перельмана