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 / @xirurgi_2025 / @xirurgi_2025 - 881 - файл
.pdf
76
3. Janata K, Holzer M, Domanovits H, Mullner M, Bankier A, Kurtaran A, et al. Mortality of
patients with pulmonary embolism. Wien Klin Wochenschr. 2002;114(17–18):766–72.
4. Heit JA, Mohr DN, Silverstein MD, Petterson TM, O'Fallon WM, Melton LJ 3rd. Predictors
of recurrence after deep vein thrombosis and pulmonary embolism: a population-based cohort
study. Arch Intern Med. 2000;160(6):761–8.
5. Baglin T, Luddington R, Brown K, Baglin C.Incidence of recurrent venous thromboembo-
lism in relation to clinical and thrombophilic risk factors: prospective cohort study. Lancet.
2003;362(9383):523–6.
6. Anderson FA Jr, Wheeler HB, Goldberg RJ, Hosmer DW, Patwardhan NA, Jovanovic B,
etal. A population-based perspective of the hospital incidence and case-fatality rates of deep
vein thrombosis and pulmonary embolism. The Worcester DVT study. Arch Intern Med.
1991;151(5):933–8.
7. Geerts WH, Pineo GF, Heit JA, Bergqvist D, Lassen MR, Colwell CW, etal. Prevention of
venous thromboembolism: the seventh ACCP conference on antithrombotic and thrombolytic
therapy. Chest. 2004;126(3 Suppl):338S–400S.
8. Falanga A, Russo L.Epidemiology, risk and outcomes of venous thromboembolism in cancer.
Hamostaseologie. 2012;32(2):115–25.
9. Silverstein MD, Heit JA, Mohr DN, Petterson TM, O’Fallon WM, Melton LJ 3rd. Trends in
the incidence of deep vein thrombosis and pulmonary embolism: a 25-year population-based
study. Arch Intern Med. 1998;158(6):585–93.
10. Engbers MJ, van Hylckama VA, Rosendaal FR.Venous thrombosis in the elderly: incidence,
risk factors and risk groups. J Thromb Haemost. 2010;8(10):2105–12.
11. Johnson SA, Eleazer GP, Rondina MT. Pathogenesis, diagnosis, and treatment of venous
thromboembolism in older adults. J Am Geriatr Soc. 2016;64(9):1869–78.
12. Larsson L, Grimby G, Karlsson J.Muscle strength and speed of movement in relation to age
and muscle morphology. J Appl Physiol Respir Environ Exerc Physiol. 1979;46(3):451–6.
13. Gensini GF, Rostagno C, Caciolli S.Treatment options for acute venous thromboembolism in
the older patient. Geriatrics. 1998;53(1):34–6. 9–40, 6–7
14. White RH, Gettner S, Newman JM, Trauner KB, Romano PS. Predictors of rehospitaliza-
tion for symptomatic venous thromboembolism after total hip arthroplasty. N Engl J Med.
2000;343(24):1758–64.
15. Bozzato S, Galli L, Ageno W. Thromboprophylaxis in surgical and medical patients. Semin
Respir Crit Care Med. 2012;33(2):163–75.
16. White RH, Zhou H, Romano PS.Incidence of symptomatic venous thromboembolism after
different elective or urgent surgical procedures. Thromb Haemost. 2003;90(3):446–55.
17. Caprini JA. Thrombosis risk assessment as a guide to quality patient care. Dis Mon.
2005;51(2–3):70–8.
18. Treasure T, Hill J.NICE guidance on reducing the risk of venous thromboembolism in patients
admitted to hospital. J R Soc Med. 2010;103(6):210–2.
19. Gould MK, Garcia DA, Wren SM, Karanicolas PJ, Arcelus JI, Heit JA, etal. Prevention of
VTE in nonorthopedic surgical patients: antithrombotic therapy and prevention of thrombosis,
9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines.
Chest. 2012;141(2 Suppl):e227S–77S.
20. Falanga A, Russo L, Milesi V. The coagulopathy of cancer. Curr Opin Hematol.
2014;21(5):423–9.
21. Thodiyil PA, Kakkar AK.Variation in relative risk of venous thromboembolism in different
cancers. Thromb Haemost. 2002;87(6):1076–7.
22. Sorensen HT, Mellemkjaer L, Olsen JH, Baron JA.Prognosis of cancers associated with
venous thromboembolism. N Engl J Med. 2000;343(25):1846–50.
23. Rickles FR, Levine MN. Epidemiology of thrombosis in cancer. Acta Haematol.
2001;106(1–2):6–12.
24. Mismetti P, Laporte S, Darmon JY, Buchmuller A, Decousus H.Meta-analysis of low molecu-
lar weight heparin in the prevention of venous thromboembolism in general surgery. Br J Surg.
2001;88(7):913–30.
A. Falanga and V. Milesi

5 Risk ofVenous Thromboembolism inSurgical Elderly Patients
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
77
25. Kakkar AK, Haas S, Wolf H, Encke A.Evaluation of perioperative fatal pulmonary embo-
lism and death in cancer surgical patients: the MC-4 cancer substudy. Thromb Haemost.
2005;94(4):867–71.
26. Bergqvist D, Agnelli G, Cohen AT, Eldor A, Nilsson PE, Le Moigne-Amrani A, etal. Duration
of prophylaxis against venous thromboembolism with enoxaparin after surgery for cancer. N
Engl J Med. 2002;346(13):975–80.
27. Rasmussen MS, Jorgensen LN, Wille-Jorgensen P, Nielsen JD, Horn A, Mohn AC, et al.
Prolonged prophylaxis with dalteparin to prevent late thromboembolic complications in
patients undergoing major abdominal surgery: a multicenter randomized open-label study. J
Thromb Haemost. 2006;4(11):2384–90.
28. Kakkar VV, Balibrea JL, Martinez-Gonzalez J, Prandoni P, Group CS.Extended prophylaxis
with bemiparin for the prevention of venous thromboembolism after abdominal or pelvic surgery for cancer: the CANBESURE randomized study. J Thromb Haemost. 2010;8(6):1223–9.
29. Lyman GH, Khorana AA, Kuderer NM, Lee AY, Arcelus JI, Balaban EP, et al. Venous
thromboembolism prophylaxis and treatment in patients with cancer: American Society of
Clinical Oncology clinical practice guideline update. J Clin Oncol Off J Am Soc Clin Oncol.
2013;31(17):2189–204.
30. Farge D, Debourdeau P, Beckers M, Baglin C, Bauersachs RM, Brenner B, etal. International
clinical practice guidelines for the treatment and prophylaxis of venous thromboembolism in
patients with cancer. J Thromb Haemost. 2013;11(1):56–70.
31. Siragusa S, Armani U, Carpenedo M, Falanga A, Fulfaro F, Imberti D, etal. Prevention of
venous thromboembolism in patients with cancer: guidelines of the Italian Society for
Haemostasis and Thrombosis (SISET) (1). Thromb Res. 2012;129(5):e171–6.
32. Kearon C. Natural history of venous thromboembolism. Circulation. 2003;107(23 Suppl
1):I22–30.
33. Falck-Ytter Y, Francis CW, Johanson NA, Curley C, Dahl OE, Schulman S, etal. Prevention
of VTE in orthopedic surgery patients: antithrombotic therapy and prevention of thrombosis,
9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines.
Chest. 2012;141(2 Suppl):e278S–325S.
34. Hull RD, Pineo GF, Stein PD, Mah AF, MacIsaac SM, Dahl OE, etal. Extended out-of- hospital
low-molecular-weight heparin prophylaxis against deep venous thrombosis in patients after
elective hip arthroplasty: a systematic review. Ann Intern Med. 2001;135(10):858–69.
35. Pengo V, Crippa L, Falanga A, Finazzi G, Marongiu F, Palareti G, etal. Questions and answers
on the use of dabigatran and perspectives on the use of other new oral anticoagulants in patients
with atrial brillation. A consensus document of the Italian Federation of Thrombosis Centers
(FCSA). Thromb Haemost. 2011;106(5):868–76.
36. Eriksson BI, Dahl OE, Rosencher N, Kurth AA, van Dijk CN, Frostick SP, etal. Dabigatran
etexilate versus enoxaparin for prevention of venous thromboembolism after total hip replacement: a randomised, double-blind, non-inferiority trial. Lancet. 2007;370(9591):949–56.
37. Eriksson BI, Dahl OE, Huo MH, Kurth AA, Hantel S, Hermansson K, etal. Oral dabigatran
versus enoxaparin for thromboprophylaxis after primary total hip arthroplasty (RE-NOVATE
II*). A randomised, double-blind, non-inferiority trial. Thromb Haemost. 2011;105(4):721–9.
38. Eriksson BI, Dahl OE, Rosencher N, Kurth AA, van Dijk CN, Frostick SP, et al. Oral dabi-
gatran etexilate vs. subcutaneous enoxaparin for the prevention of venous thromboembolism after total knee replacement: the RE-MODEL randomized trial. J Thromb Haemost.
2007;5(11):2178–85.
39. Committee R-MW, Ginsberg JS, Davidson BL, Comp PC, Francis CW, Friedman RJ, etal. Oral
thrombin inhibitor dabigatran etexilate vs north American enoxaparin regimen for prevention
of venous thromboembolism after knee arthroplasty surgery. J Arthroplast. 2009;24(1):1–9.
40. Eriksson BI, Quinlan DJ, Eikelboom JW.Novel oral factor Xa and thrombin inhibitors in the
management of thromboembolism. Annu Rev Med. 2011;62:41–57.
41. Eriksson BI, Borris LC, Friedman RJ, Haas S, Huisman MV, Kakkar AK, etal. Rivaroxaban
versus enoxaparin for thromboprophylaxis after hip arthroplasty. N Engl J Med.
2008;358(26):2765–75.

78
42. Kakkar AK, Brenner B, Dahl OE, Eriksson BI, Mouret P, Muntz J, et al. Extended dura-
tion rivaroxaban versus short-term enoxaparin for the prevention of venous thromboembolism after total hip arthroplasty: a double-blind, randomised controlled trial. Lancet.
2008;372(9632):31–9.
43. Lassen MR, Ageno W, Borris LC, Lieberman JR, Rosencher N, Bandel TJ, etal. Rivaroxaban
versus enoxaparin for thromboprophylaxis after total knee arthroplasty. N Engl J Med.
2008;358(26):2776–86.
44. Turpie AG, Lassen MR, Davidson BL, Bauer KA, Gent M, Kwong LM, etal. Rivaroxaban
versus enoxaparin for thromboprophylaxis after total knee arthroplasty (RECORD4): a randomised trial. Lancet. 2009;373(9676):1673–80.
45. Lassen MR, Raskob GE, Gallus A, Pineo G, Chen D, Portman RJ.Apixaban or enoxaparin for
thromboprophylaxis after knee replacement. N Engl J Med. 2009;361(6):594–604.
46. Lassen MR, Raskob GE, Gallus A, Pineo G, Chen D, Hornick P, etal. Apixaban versus enoxa-
parin for thromboprophylaxis after knee replacement (ADVANCE-2): a randomised doubleblind trial. Lancet. 2010;375(9717):807–15.
47. Lassen MR, Gallus A, Raskob GE, Pineo G, Chen D, Ramirez LM, etal. Apixaban versus enoxa-
parin for thromboprophylaxis after hip replacement. N Engl J Med. 2010;363(26):2487–98.
A. Falanga and V. Milesi

Part II
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Endocrine Surgery

Thyroid andParathyroid Diseases
inElderly Patients
SilvestroCanonico, MassimoDe Falco,
andGiuseppeSantangelo
6.1 Thyroid Diseases
The thyroid undergoes a physiological cellular senescence, involving a progressive
weight and volume loss, together with an increase of brous components, reduction
in follicle size and amount, decrease of colloid production and increase of inltrating lymphocytes [1–3].
Functional changes occur simultaneously, consisting of increased TSH serum
levels and a reduction of T3 and Ft3 circulating levels, likewise increased rT3 levels,
which is a metabolically inactive hormone. FT4 and T4 levels are set to be
unchanged. Peripheral organs decrease their susceptibility to thyroid hormones,
combined with an increasing rate of antithyroid antibodies.
The signicance of thyroid hormonal changes in the geriatric population is not
perfectly clear yet. It was suggested that they may be a protection mechanism
against the physiological catabolism of aging. According to this hypothesis higher
TSH levels may be related to a longer lifespan. In conclusion, it is difcult to
unequivocally understand laboratory ndings of the thyroid function in elderly
subjects [1–3].
The clinical suspicion of thyroid disease in geriatric patients is not different from
that of younger people. Primary hyperthyroidism consists of an increase of FT3 and
FT4 serum levels combined with TSH reduction. On the other hand, primary hypothyroidism consists of a reduction of FT3 and FT4 levels combined with an increased
TSH serum concentration [4]. The difculty in interpreting the results analytically
arises from subclinical thyroid dysfunctions in the aim of nding appropriate therapeutic management.
6
S. Canonico (*) • M. De Falco • G. Santangelo
Department of Medical, Surgical, Neurological, Metabolic and Geriatric Sciences,
University of Campania Region “Luigi Vanvitelli”, 81100 Caserta, Italy
e-mail: silvestro.canonico@unicampania.it; massimo.defalco@unicampania.it;
giuseppesantangelo@email.it
© Springer International Publishing AG, part of Springer Nature 2018
A. Crucitti (ed.), Surgical Management of Elderly Patients,
https://doi.org/10.1007/978-3-319-60861-7_6
81

82
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
S. Canonico et al.
Geriatric people are characterized by an increasing rate of patients with high
antithyroid antibodies and subclinical hypothyroidism. Subclinical hypothyroidism
itself has advantages to the aging human body as the reduction of catabolism.
Clinical studies also show that there is no link with the decaying of brain cortical
functions: thus, if no symptoms are reported and in cases of moderate subclinical
hypothyroidism, no pharmacological treatment would be recommended.
Subclinical hyperthyroidism is classied into two degrees. The rst degree is
recognized when TSH levels are persistently ranging from 0.1 to 0.39mIU/L and
is related to an increased incidence of atrial brillation. In the second degree, TSH
levels are always less than 0.1mIU/L with an increased rate of mortality related
to coronary artery disease, increased incidence of atrial brillation, heart failure,
and fractures [5–9]. So, a rst grade of subclinical hyperthyroidism is related to
an increased incidence of atrial brillation, therefore, subclinical hyperthyroidism
in geriatric patients must be treated with antithyroid drugs, or with
131
I radio meta-
bolic therapy [5].
6.2 Goiter
The term goiter refers to an abnormal and irreversible enlargement of the thyroid
gland. Once diagnosed, goiter reveals its benign nature and can be classied into
multinodular (Fig.6.1) or nodular and toxic or non-toxic goiter. The genesis of a
goiter has its roots in genetic, environmental, food and drug factors all combining
with each other. Whether in endemic or non-endemic goiter areas the prevalence of
a goiter is higher in the geriatric population than in the younger population. Mostly
in Western countries, this can be related to several conditions, such as recurrences
in patients who had previously undergone partial thyroidectomy, or increased use of
instrumental investigations due to other geriatric diseases. A continuous enlarging
goiter may become symptomatic over time, and in these cases diagnosis is required.
Fig. 6.1 Multinodular goiter in over-65 aged woman

6 Thyroid andParathyroid Diseases inElderly Patients
83
6.2.1 Non-Toxic Goiters
A goiter can be dened as non-toxic when thyroid functional levels range from
normal to partly decreased: the second condition may be the consequence of a
concurrent autoimmune thyroiditis. Goiter size is likely to be larger in geriatric
patients than in young people. A more frequent mediastinal widening also affects
older patients [1, 3, 10–12]. Both phenomena are due to the continuous enlargement of the goiter over time.
If a hypothyroidism is recognized, symptoms can be characterized by bodyweight gain, asthenia and fatigue, hypersomnia, cold intolerance, myxedema, constipation, skin and appendages disorders, psychiatric depression, altered
consciousness or impaired concentration ability, and heart failure. Geriatric patients
often report less symptoms than the younger patients with fatigue and asthenia
occurring more frequently in the former. Comorbidities as well as the few symptoms related to goiter may be interpreted as expression of non-thyroid primary diseases, delaying the diagnosis of hypothyroidism and resulting in a higher risk of
heart failure, atherosclerosis, and insurgent coma. On the other hand, in cases of
regular functions, symptoms may only be mechanical, such as dyspnea, dysphagia,
and rarely dysphonia [1, 10–12].
Most patients suffering with a goiter, even if affected by an extended goiter, are
reported as asymptomatic or fairly paucisymptomatic. This is probably related to a
physiological adaptation of the neck tissues to a slow and progressive enlargement
of the thyroid gland over time. In fact, many asymptomatic patients suffering from
tracheal deviation or compression, due to mediastinal widening, report a subjective
feeling of breathing improvement after being treated with total thyroidectomy.
The physiological reduction of sensitivity and possible coexisting respiratory
diseases can make it difcult to interpret the real severity of goiter-related symptoms in geriatric patients. Dysphagia, mainly occurring when the left back lobe of
the thyroid enlarges, is directly related to the compression of cervical esophagus,
but sometimes this diagnosis is difcult in elderly patients. Indeed, a cricopharyngeal dysphagia, linked to a neuromuscular incoordination of the mechanical swallowing process, is not unusual in older patients because it can be generally interpreted
as a paraphysiological age-related deciency, if no other potentially linked neurological, muscular, or vascular pathologies are diagnosed.
Dysphonia has more frequently to be interpreted as a neoplastic inltration of
one of the inferior laryngeal nerves rather than its extrinsic compression. However,
in geriatric patients a clinical diagnosis of dysphonia must take into account either
a possible primary or secondary larynx disease, or because of a reduced agingrelated vocal ability, in absence of other specic diseases.
To assess the thyroid function, the dosage of TSH, FT3, and FT4 is necessary
together with the measurement of Ab-hTg and Ab-TPO with the aim of diagnosing
a possible concurrent autoimmune chronic thyroiditis [3].
Instrumental diagnosis consists rstly of an US-scan that evaluates the glandular
size, the number, location, and features of possible lumps, the evidence of tracheal
dislocation, a potential mediastinal widening and the lymphatic state. A chest and

84
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
S. Canonico et al.
thorax CT scan is required in cases of substernal widening. The diagnostic is to be
completed by performing a needle biopsy, in cases of solid lumps with suspicious
characteristics.
6.2.2 Toxic Goiters
The denition of toxic goiter refers to a pathological condition of thyroid enlargement associated with overproduction of thyroid hormones. According to the presence
of lumps in the area of parenchyma, goiters can be classied into diffuse toxic goiters
or toxic nodular goiters (uninodular or multinodular) [10–13]. In both geriatric and
in young patients, diffuse toxic goiter is also known as Graves Flajani Basedow disease and as a consequence of its genesis, it is autoimmune. In fact, some people are
genetically predisposed with anti-TSH receptor auto-antibodies which can bind to
their target, the thyroid, and have a stimulatory activity resulting in miming thyrotropin action. There are sub-populations of auto-antibodies which show some differences both in binding afnity and in intrinsic activity, and they are predisposed to
differ over time. This explains why the disease can present an erratic intensity over
time, both increasing and decreasing. In diffuse toxic goiters, there is a parenchymal
compactness, due to an extreme colloidal reduction. The thyroid is more vascularized with lymphocytic inltration. Toxic nodular goiters can be either uninodular or
multinodular. A uninodular thyroid toxic nodule, also called Plummer’s disease,
typically consists of a single increasing toxic nodule, that produces thyroid hormones, autonomously functioning from the hypothalamic pituitary axis. Such autonomous hyperactivity is conferred to the solitary nodule by a somatic mutation
activating the TSH receptor in single cells. The pathogenic mechanism is identical in
multinodular toxic goiters. The only difference is the somatic mutation, occurring in
one or even more pre-existing nodules, which turns them “autonomous.”
Toxic goiter, mainly multinodular, is generally more frequent in elderly patients
than in young individuals: the nodular mutation to “autonomously functioning” is
more likely to happen in old nodules, that is to say in elderly people. Such a phenomenon is far more frequent in endemic iodine deciency areas.
Symptomatology of toxic goiters is always functional, but at times can also be
mechanical. The most common symptoms are tachycardia, palpitation, weight
loss, heat intolerance, tachypnea, tremor, diarrhea, and nervousness; widespread
itching, and less frequently urticaria and fever. Patients suffering from GravesFlajaniial myxedema.
symptoms, even if variable in their intensity, in geriatric patients only one or two
symptoms can be detected. Tachycardia, weight loss, and tachypnea are among the
most commonly reported symptoms in the elderly. Furthermore, apathy rather than
nervousness appears in about 35% of geriatric patients suffering from hyperthyroidism. The clinical picture, already subtle in itself, should then be interpreted in the
light of potential existing co-morbidities and drug treatments, which can make the
Basedow disease can also have ophthalmopathy, acropachia, and pretib-
While hyperthyroidism in young patients generally manifests with numerous

6 Thyroid andParathyroid Diseases inElderly Patients
85
diagnosis of hyperthyroidism difcult or delayed [1–5, 10, 11]. If present, mechanic
symptoms are related to the goiter size and depend on the individual patient’s degree
of susceptibility: compressive dyspnea, dysphagia, and rarely dysphonia.
The laboratory diagnosis consists of a reduced or annulled TSH dosage with a
high FT3 and FT4 dosage. It is important to consider that a condition of low or
annulled levels of THS, occurring with high FT3 and T3 levels and normal FT4
levels—also known as T3 toxicosis—is more likely to occur in geriatric patients
than in young patients. It is appropriate to add the anti-receptors TSH antibody dosage to the normal one. The former is specically employed to diagnose GravesFlajani- Basedow disease, both in its diffuse and nodular versions.
US scan represents the rst instrumental exam. It allows assessment of the
gland size, potential traces of lumps with their characteristics, the degree of parenchyma and lumps vascularization, and the trachea condition. If a mediastinal
extrication is taking place, a chest and thorax CT scan is recommended to complete the second level diagnosis, allowing an optimal evaluation of the goiter’s
mediastinal portion.
99m
A radiolabel
Tc scan enables evaluation of whether the hypercaptation
involves all the parenchymal gland or just a portion of one or more lumps. A needle
biopsy is required in cases of suspicious scanned lumps. Indeed, it has been proven
that 2–6% of patients diagnosed with papillary thyroid carcinomas were also carriers of the TSH receptors mutation. This demonstrates that papillary carcinomas can
also manifest as autonomous lumps.
6.2.3 Treatment
Surgical treatment is recommended in cases of mechanical symptoms, tracheal dislocation and mediastinal extrication. The risk related to surgery is as high in geriatric patients as in young patients [10–13]. However, there are some specic
age-related complications, in the presence of more enlarged goiter, mediastinal widening, glands hyperactivity, relapse, and thyroiditis. Even when dealing with geriatric patients, a surgical treatment of the multinodular goiter is considered best
practice, unless general or local conditions make surgery-related risks higher than
the expected benet.
Surgical options to treat multinodular goiter, in the case of bilateral pathology,
are a total or subtotal thyroidectomy. On the other hand, a thyroid lobectomy may
be performed in cases of monolateral pathology. The option of a subtotal thyroidectomy prevails when relapse risk is lower because of a reduced lifespan. Such surgical procedure does not entail the risk of a bilateral recurrent paralysis and drastically
reduces the risk of iatrogenic hypoparathyroidism [10–13]. When threatening conditions evidently contraindicate a surgical treatment, either totally or partially, the
optional alternative treatment is almost always an alcohol injection. Cystic nodules
accountable for the mechanic symptomatology or tracheal dislocation can be treated
with such procedure. Solid nodules can be reduced by thermoablation, radiofrequency, high-intensity focused ultrasound and microwave [14–17].

86
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
S. Canonico et al.
Regarding toxic goiters, the primary therapeutic objective is to obtain euthyroidism by the administration of antithyroid drugs, notably methimazole. Obtaining a
normal thyroid function is the precondition even in carrying out surgery. In case of
contraindications to surgery and if mechanic symptomatology remains, although a
normal thyroid functionality is achieved, an
131
I radiometabolic therapy would be
appropriate. This enables the resolution of the hyperthyroidism state and the reduction of lump volume. Nonetheless, the same options that are considered as appropriate to treat non-toxic goiters can be employed [10–17].
6.3 Malignant Tumors
The cancers that can be generated from the follicular thyroid epithelium are papillary and follicular cancers, presenting some differences, and the anaplastic thyroid
cancer. Other forms (lymphomas, miscellaneous tumors, metastatic tumors, nonclassied tumors) are rare. Parafollicular cells can instead give rise to medullary
cancer. From an etiopathogenetic standpoint, familial predisposition and prior exposure to ionizing radiation of the cervical-mediastinal region are recognized as risk
factors. The incidence of malignant thyroid cancers is currently ranging from 5 to 7
cases out of 100.000 people a year, with an F/M ratio corresponding to 3.5/1.
According to several contributions, the rate is indeed much higher in the elderly
than in young people, the rate being reported as progressively increasing with aging
[18, 19]. This is explained by the fact that each isotype has more frequent aggressive
variants in elderly people. Anaplastic cancer and its various forms are almost always
found in geriatric people, as far as differentiated forms are concerned (papillar and
the follicular cancer) these are both characterized by more frequent histologic
aggressive variants.
Nearly 80% of malignant thyroid cancers are papillar cancers which constitute
the most frequent isotype in all ages, including geriatric people, who have an
increase of the most aggressive biological variants (oxyphilic, tall, sclerosing,
columnar and insular cells) [
frequency of BRAF
V600E
(notably in patients highly exposed to ionizing radiation). Both older age and
V600E
BRAF
mutation, if detected, combine with a more aggressive biological behavior. Papillar cancer is likely to metastasize via the lymphatic system. Such a process
is more frequent in geriatric patients and in children under 14years together with a
possible diffusion to the neck lymph node stations [19]. However, only in geriatric
patients does such an element negatively affect the prognosis. Bone and lungs
hematogenous metastases are much rarer.
Follicular cancer represents 10% of malignant thyroid cancers, occurs in iodine
deciency areas, and is more likely to metastasize via hematogen, mainly affecting lungs and bones. Slightly differentiated cancer and anaplastic cancer are
higher in iodine deciency areas and they represent near 1% of malignant thyroid
cancers, both often being the development of differentiated papillar and follicular
untreated forms.
20]. The genotype of papillar cancer consists of a great
somatic mutation and RET/PTC gene rearrangements
Соседние файлы в папке @xirurgi_2025
