Download study of clinical and imaging profile in thyrotoxicosis

“STUDY OF CLINICAL AND IMAGING PROFILE IN THYROTOXICOSIS”
BY
DR. UMAR NAZIR KABLI
SYNOPSIS FOR REGISTRATION OF SUBJECT FOR DISSERTATION
UNDER GUIDANCE OF
GROUP CAPTAIN A.K.DASH
MD (GEN MED), DNB (MEDICINE), DRM (NUCL MED), MNAMS, SR ADV MEDICINE
HOD, DEPARTMENT OF NUCLEAR MEDICINE
COMMAND HOSPITAL AIR FORCE,BANGALORE
TO
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES
BENGALURU, KARNATAKA
IN PARTIAL FULLFILLMENT OF REGULATIONS FOR AWARD OF
MASTER DEGREE IN MEDICINE
DEPARTMENT OF MEDICINE,
COMMAND HOSPITAL AIR FORCE, BENGALURU-560007
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, BENGALURU, KARNATAKA.
ANNEXURE – II
PROFORMA FOR REGISTRATION OF TOPICS FOR DISSERTATION
1
Name of the Candidate and Dr. UMAR NAZIR KABLI
Address (in Block Letters)
POST GRADUATE STUDENT,
DEPARTMENT OF MEDICINE,
COMMAND HOSPITAL, AIR FORCE
BENGALURU, KARNATAKA.
2
Name of the Institution
COMMAND HOSPITAL, AIR FORCE
BENGALURU, KARNATAKA.
3
Course of Study and Subject
POST-GRADUATE
M.D. MEDICINE
4
Date of Admission to Course
01-07-2013
5
Title of the Topic
STUDY OFCLINICAL AND IMAGING PROFILE IN
VARIOUS TYPES OF THYROTOXICOSIS
6.
Brief resume of the intended work:
6.1
Aim of the Study:
To study the clinical and imaging profile in armed forces patients population .
6.2
Objective:
(i) To study the imaging profile in various types of thyrotoxicosis patients.
(ii) Special emphasis of various pattern of nuclear medicine imaging abnormalities in
various types of thyrotoxicosis presentations.
6.3
Need for the study:
Thyrotoxicosis is a reasonably common clinical entity in all strata of patient population leading to lot of
morbidity and mortality despite of all available modern and accurate diagnostic techniques. This is
most commonly due to delayed clinical diagnosis and subsequent treatment leading to
complications.Best part of this condition is that it is potentially curable disease with specific modalities
of conservative therapy.
The annual incidence of the disease is 0.5 cases per 1000 persons during a 20-year
period, with the peak occurrence in people aged 10-50 years. All thyroid diseases occur more
frequently in women than in men. An American study reported a prevalence of about 400 per 100,000
persons, with a lifetime risk of 1% in men and up to 2% in women. 60-80% of cases are due to Graves'
disease with a peak onset at 10-50 years; the remainder of cases are due largely to nodular thyroid
disease that appears later in life. It affects females more than males (ratio 9:1).A Scottish study found
an incidence of 0.77/1,000 annually in women and 0.14/1,000 annually in men.In England the
incidence of Graves' disease has been reported as 0.5 per 1,000 per year.Thyrotoxicosis is less
common in children than in adults.
Recent work has estimated the incidence of thyrotoxicosis at 80/100,000 per year in
women and 8/100,000 per year in men. Studies specifically estimating the incidence in childhood have
been reported in Sweden (0·7/100,000 per year, <16 years, 1990–1994),2 Poland (1·83/100,000 per
year, <16 years, 1989–1996, specifically Graves’ disease),3Denmark (0·79/100,000/year, <15 years,
1982–1988)4 and Hong Kong (6·5/100,000/year, <15 years, 1994–1998, specifically Graves’
disease).5 There are no comparable incidence studies of thyrotoxicosis in childhood in the USA,
although prevalence data are available for 0- to 17-year olds6 and 10- to 19-year olds.7 The studies
from Hong Kong, Sweden and Poland reported an apparent increase in cases over their study periods,
since 1989, although the reasons for this remain unclear. There are no data from the UK or Ireland on
the incidence of thyrotoxicosis in young people. Using the British Pediatric Surveillance Unit (BPSU),
we were able to measure the contemporary UK and Ireland incidence of childhood thyrotoxicosis to
record complete national population data and to describe in detail the presenting features of condition.
Indian patients with thyrotoxicosis have been observed to present with more severe weight loss leading
to emaciation, dyspnea, proximal muscle weakness, diarrhoea / hyperdefecation.
The etiology behind the thyrotoxicosis need to be established based on patient
history, clinical diagnosis, biochemical and serological abnormalities and imaging abnormalities in USG
Neck and 99m Technetium Pertechnetate Thyroid Uptake study , thyroid scintigraphy. This is important
from the point of view that each one variety needs different approach of therapy.
7.
Materials And Methods
(i)
Study Design: Prospective study.
(ii)
Subjects: All patients (Symptomatic & Sub clinical cases) presenting to Command
Hospital (Air Force) Bangalore who are diagnosed/detected to have thyrotoxicosis.
( Number of subjects = 50)
(iii)
Inclusion Criteria:
·
·
(iv)
Newly detected thyrotoxicosis
Age ≥ 15 and ≤ 50 years.
Exclusion Criteria:
. Those who refuse to give informed consent.
Inability to come for follow up
(v)
Sample size: Total of Fifty cases in the age groups of 15 years and 50 years with
suspected thyrotoxicosis patients based on clinical suspicion/hematological
/hormonal profile/ USG neck abnormalities who present between one year period
between Sep 2013 and Sep 2014 will be taken up for the proposed study.
Methodology: All the patients with the diagnosis of thyrotoxicosis presenting to this hospital from
Sep 2013 to Sep 2014 will be enrolled after written informed consent. A predefined proforma will be
completed in every patient with a detailed clinical history, physical examination, and investigation
studies. The details of physical examination including anthropometric data, vital signs and complete
systemic evaluation will be recorded. All clinically suspected cases will undergo routine hematological
evaluation with Hb%, ESR, CBC. Further serological evaluation with Rheumatoid factor, ANA, AntiTPO Antibody etc will be done. The cases will undergo routine ECG, USG Neck evaluation followed by
99m Technetium Pertechnetate Thyroid scan and uptake study. Final diagnosis will be based on
nuclear medicine imaging in the given scenario.
(v) Statistical analysis: Appropriate statistical analysis of various clinical, biochemical and
imaging abnormalities will be carried out on completion of the study.
7.1 Does the Study require any investigations or interventions to be conducted on patients or
other humans or animals? If so please describe briefly.
Yes, 5 ml of venous blood will be collected for hematological and biochemical analysis as it is routinely
done for all Thyrotoxicosis patients for evaluation.
7.2 Has ethical clearance been obtained from your institution in case of 7.1?
Yes
Review of Literature
The term thyrotoxicosis refers to the clinical syndrome of hyper metabolism and hyperactivity those
results from excessive quantities of the thyroid hormones. The term hyperthyroidism is used to denote
sustained increased in thyroid hormone biosynthesis and secretion by the thyroid gland. While many
patients with thyrotoxicosis have hyperthyroidism, it is not so in others such as - those in whom it is
caused by thyroiditis or exogenous thyroid hormone administration. Thyrotoxicosis can range in
severity from subclinical hyperthyroidism to life threatening thyroid storm. Although we do not have
prevalence data, thyrotoxicosis is found in various age groups (children, elderly) and in different clinical
situations.
Aetiology of Thyrotoxicosis
The most common cause of thyrotoxicosis is Grave’s disease followed by toxic multinodular goiter
(TMNG), solitary toxicadenoma and thyroiditis. The other less common causes include TSH secreting
pituitary adenoma, struma ovarii, metastatic functional differentiated thyroid cancer and metatstatic
tumors within the thyroid gland causing destruction induced thyrotoxicosis (Table 1)
Table 1 : Causes of Thyrotoxicosis
A. Primary hyperthyroidism
Graves’ disease
Toxic multinodular goiter
Toxic adenoma
Functioning thyroid carcinoma metastases
Activating mutation of the TSH receptor
Activating mutation of Gsa (McCune-Albright syndrome)
Struma ovarii
Drugs: iodine excess (Jod-Basedow phenomenon)
B. Thyrotoxicosis without hyperthyroidism
Subacute thyroiditis
Silent thyroiditis
Other causes of thyroid destruction: amiodarone, radiation, infarction of adenoma
Ingestion of excess thyroid hormone (thyrotoxicosis factitia) or thyroid tissue
C. Secondary hyperthyroidism
TSH-secreting pituitary adenoma
Thyroid hormone resistance syndrome: occasional patients may have
features of thyrotoxicosis
Chronic gonadotropin-secreting tumors
Gestational thyrotoxicosis
Thyrotoxicosis factitia
Pathogenesis
Grave’s Disease: Grave’s disease is the commonest cause of thyrotoxicosis being more common in
females than males. It is caused by an activating antibody which targets the TSH receptor of the
thyroid follicular cells and stimulates thyroid hormone production, increase thyroid vascularity and
growth similar to thyrotropin, but without normal feedback inhibition. The TSH-R antibodies also bind to
the retro-orbital tissues producing a T-cell inflammatory response, release of cytokines, activation of
fibroblasts and accumulation of glycosaminoglycans leading to an infiltratory ophthalmopathy.
A small percentage of these patients with ophthalmopathy have a similar process of activation of
dermal fibroblasts in the anterior leg leading to the development of a pretibial myxoedema.
Toxic multinodular goiter (TMNG) is the second leading cause of thyrotoxicosis and is more common
in our country as compared to other regions. It generally arises in a multinodular thyroid gland that
subsequently develops autonomously functioning nodules over time. It is more prevalent in populations
with greater iodine deficiency. TMNG develops in older individuals, with a longstanding previous
multinodular goiter in which one of the nodules attains functional autonomy. Several different
mechanisms could contribute to this process. One of the common mechanisms is somatic mutation in
the TSH receptor gene leading constitutive receptor activation and upregulation of the cAMP signaling,
has been described in upto 60% of these patients.
Toxic adenoma: The solitary toxic adenoma causes hyperthyroidism in slightly younger individuals
and also results from a similar process of constitutive activation of the TSH receptor due to mutations
in the TSH receptor gene. The course of the disease evolves similar to that of the TMNG with the
nodule autonomy developing after the nodule has been present for a considerable period of time.
Clinical features of thyrotoxicosis (Table 2)
Subclinical hyperthyroidism is defined by normal circulating levels of free T4 and T3 and low levels of
TSH. It is caused by the same conditions that account for the majority of cases of overt
hyperthyroidism i.e. Graves’ disease, toxic multinodular goiter, and solitary functioning thyroid nodules.
Subclinical hyperthyroidism is associated with an increased risk of atrial fibrillation and mortality,
osteopenia/osteoporosis in postmenopausal women and mild hyperthyroid symptoms.
Thyrotoxicosis results in a hypermetabolic state with energy production exceeding the energy
expenditure leading to increased heat production presenting as heat intolerance perspiration and fever.
Even though there is greater energy expenditure there is generalized weakness and fatigue
Table 2: Clinical features of thyrotoxicosis
---------------------------------------------------------------------------------------------------------------------------------Symptoms
Signs
---------------------------------------------------------------------------------------------------------------------------------Hyperactivity, irritability,
Tachycardia; atrial fibrillation in the elderly
Dysphoria
Heat intolerance and sweating
Tremor
Palpitations
Goiter
Nervousness, fatigue and
Warm, moist skin
weakness
Muscle weakness, proximal
Dysnoea
Myopathy
Weight loss with increased
Hyperreflexia
appetite
Lid retraction or lag
Diarrhea / Hyperdefecation
Gynecomastia
Polyuria
Loss of libido
Oligomenorrhea
Laboratory diagnosis
1. Thyroid hormone assay
Biochemical confirmation of thyrotoxicosis is based on the finding of a suppressed TSH (<0.05 μU/mL)
in combination with elevated serum total or free T4 and T3 levels in patients with clinically evident
thyrotoxicosis. Although a TSH assessment alone may be appropriate for routine screening in an
asymptomatic patient, the suspicion of thyrotoxicosis warrants the additional assessment of T4 and T3.
In cases in which subclinical hyperthyroidism is suspected, TSH measurement may be used as a first
diagnostic step, with subsequent T4 and T3 assessment if TSH is suppressed. Laboratory
measurement of total T3 and total T4 reflects mainly protein-bound hormone concentrations. There are
several conditions altering the protein binding of T4. (Table 4) These protein-binding abnormalities
affect the index tests (free T4 index and free T3 index) and may give inaccurate values when changes
in protein binding are present. For these reasons, free T4 assays are preferred over the total hormone
estimation and index tests; however their availability may not be universal. 5 The ratio of T4 to T3
frequently has a characteristic pattern in different thyrotoxic states. Evaluation of the T4/T3ratio may be
a useful tool in the initial diagnosis of thyrotoxicosis when radioactive iodine uptake testing is not
readily available or is contraindicated. Graves’ disease and toxic nodular goiter typically present with
increased T3 production, with a T3/T4 ratio greater than 20. With thyrotoxicosis caused by thyroiditis,
iodine exposure, or exogenous levothyroxine intake, however, T4 is the predominant hormone and the
T3/T4 ratio is usually less than 20. A small number of thyrotoxic patients may present with an increase
in serum free T3 and normal T4. This is referred to as “T3 toxicosis”.
Thyroid antibodies:
Although the antithyroids peroxidise and anti-thyroglobulin antibodies may be elevated in almost all
cases of thyrotoxicosis, measurement of the TSH-R antibodies may be helpful in the diagnosis and
management of Grave’s disease in certain situations. It may be helpful in prediction of postpartum
Graves’ disease and neonatal thyrotoxicosis. It has also been used to predict chances of relapse in
patients treated with antithyroid medications and in the identification of orbitopathy in the absence of
obvious features of thyrotoxicosis.
Other laboratory abnormalities in thyrotoxicosis
Thyrotoxicosis may also cause hyperglycemia, hypercalcemia, elevated alkaline phosphatase,
leukocytosis, and elevated liver enzymes. The hyperglycemia is typically mild and is caused by
catecholamine-induced inhibition of insulin release and increased glycogenolysis. Mild hypercalcemia
and elevated alkaline phosphatase occur as well because of direct TSH stimulation of osteoblastic
bone resorption mediated by the NF-KB-RANKL pathway
Table 4: Causes of elevated serum thyroxine concentrations
A. Thyrotoxicosis
1. Increased Serum protein binding
2. Increased serum thyroxine binding globulin concentrations
B. Inherited
1. Estrogens: pregnancy, exogenous, tumoral production
2. Hepatitis, hepatoma
3. HIV infection
4. Carcinoma of pancreas, hepatoma
5. Psychiatric and Medical Illness
C. Drugs
1. Methadone, heroin, clofibrate, 5-flurouracil
2. Familial dysalbuminemic hyperthyroxinemia
3. Increased serum transthyretin binding or concentrations
4. Propranolol (high doses)
5. Amiodarone
D. Radiographic contrast agents used for cholecystography
Fig-1: 99m Technetium Pertechnetate Scintigraphy image showing
multiple photopenic defects in both the lobes and hot nodules in the
left lobe suggestive of toxic multinodular goiter
Imaging Studies
Different imaging modalities may assist in the determination of the etiology of thyrotoxicosis. The most
important of these are the thyroid nuclear imaging studies and anatomic studies like thyroid ultrasound.
A. Non radio isotope imaging methods
I.
II.
III.
Ultrasonography
Computerized Tomography
MRI
B. Radio isotope Scintigraphy methods
I.
II.
III.
IV.
V.
99m Technetium based study in Gamma Camera
201 Thallium based
131 Iodine based
123 Iodine based
18 F- FDG PET imaging study
Nuclear medicine Scintigraphy
Radioactive iodine uptake and scanning is a very useful tool in the diagnostic evaluation of
thyrotoxicosis. After ingestion of the tracer usually I131 or I123, the emitted g radiation allows external
detection, calculation of fractional uptake and scintigraphic imaging of the thyroid gland. The uptake is
measured at 6 hr and 24 hr and the normal values range between 5 – 15% for the
6 hr uptake and 5-25% for the 24 hr uptake. Technetium-99m (Tc-99m) pertechnetate imaging is
preferably being used now, since it is actively trapped in thyroid follicular cells like iodine and has the
advantage of a rapid turnover requiring the uptake and scan to be completed within 20-30 min with a
much lower dose of radioactivity. However, it has limitations in terms of detecting organification
defects. However in due course of time, the practice of studies with Radio iodine has come down due
to prolonged duration (> 24 hours per single study), harmful Beta radiation exposure along with high
energy Gamma radiation of 360 Kev, unsuitability in lactating patients.Further the availability of radio
iodine isotope particularly 123 Iodine is very difficult due to limited production worldwide.Radio iodine
does not give any information on vascularity of affected thyroid glands.
Thyroid ultrasonography
Thyroid sonography may be useful in the diagnostic evaluation of thyrotoxicosis. Sonographic
assessment can identify thyroid nodules and goiter that may not be readily apparent on examination.
Additionally, sonographic Doppler flow assessment may provide particularly useful information about
several thyrotoxic states. An index of blood flow per unit area has been used to distinguish between
Graves’ disease and thyrotoxicosis caused by non-hypermetabolic destructive thyroiditis. Using a
thyroid blood flow area of 8% or greater had a sensitivity of 95% and a specificity of 90% for the
prediction of Graves’ disease. This may also be helpful in differentiating the thyroid peroxidase,
compared to PTU which causes reversible inhibition and also a single dose of methimazole has been
shown to provide measurable intrathyroidal concentrations lasting up to 20 hours.
Recent studies.
The assessment of thyroid blood flow by color flow Doppler ultrasonography is valuable in the
differentiation of best of the thyrotoxicosis from Grave’s disease. According to a study by Kumar et al
.the study was carried out in 65 people, between jun2007 to mar 2008.
Table 5 : Shows the radio iodine uptake and pattern of distribution in various disorders causing
thyrotoxicosis.
Cause of
Fractional uptake in
Pattern of distribution of tracer
Thyrotoxicosis
24 hr (%)
in thyroid
__________________________________________________________________________________
Grave’s Disease
35-95
Homogenous
Toxic nodular goiter
20-60
Restricted to regions of autonomy
Subacute thyroiditis
0-2
Little or no uptake
Silent thyroiditis
0-2
Little or no uptake
0-2
Little or no uptake
Thyrotoxicosis
0-2
Little or no uptake
Struma ovarii
0-2
Uptake in ovary
Follicular carcinoma
0-5
Uptake in tumor metastasis
30-80
Homogenous
(uni or multinodular)
Iodine-induced
Thyrotoxicosis
Factitious or iatrogenic
TSH induced
Thyrotoxicosis
Fig. 2 : Ultrasonography showing multinodular goiter
Radioactive Iodine: Radioactive thyroid ablation is becoming the most widely used definitive treatment
for thyrotoxicosis due to Grave’s disease or toxic multinodular goiter. It has the advantage of allowing
the discontinuation of the use of thionamides with worrisome side effects such as agranulocytosis,
hepatotoxicity or vasculitis. The major long term side effect of radioactive iodine therapy is permanent
hypothyroidism. Short term side effects include acute exacerbation of thyrotoxicosis, radiation
thyroiditis presenting as anterior neck tenderness or gastritis and sialadenitis. Pre-treatment with
thionamides has been shown to reduce the risk of post-treatment thyrotoxicosis.
However the efficacy of radioactive iodine treatment may also be reduced. This is particularly true with
PTU, whereas with methimazole and carbimazole this effect was not significant as long as these
agents were discontinued 3-5 days before treatment. The response to radioactive iodine is not
immediate, usually requiring about 2-3 months. Most patients therefore require antithyroid medication
to be continued for a few months until hypothyroidism develops. Persistence of hyperthyroidism
beyond 6 months after therapy may require re-treatment with radioactive iodine to achieve complete
ablation. One of the major concerns has been the risk of second malignancy after the use of
radioactive iodine therapy particularly in children. These concerns have been with relation to the
development of leukaemia or malignant lymphoma, thyroid cancer and cancers of the small bowel.
This risk is shown to relatively small and not consistently demonstrated across all studies. The risk of
thyroid malignancies is eliminated when an ablative approach to therapy is used with a goal to render
the patient hypothyroid, with no significant residual functional thyroid tissue
Treatment of Thyrotoxicosis
The approach to treatment of thyrotoxicosis depends on the etiology of thyrotoxicosis and consists of
the use of agents that block the synthesis of thyroid hormone in the thyroid gland, the generation of
active T3 from the pro-hormone T4 or blocking its actions at the end organs.
Thionamides
The thionamides are the most commonly used agents which belong to two different categories, the
imidazole derivatives – carbimazole and methimazole and the thiouracil derivative – propyl thiouracil
(PTU). The thionamides act by inhibing the thyroid peroxidase–mediated oxidation of iodide, iodine
organification, and iodotyrosine coupling. Also, thionamides inhibit the thyroperoxidase-catalyzed
coupling process through which iodotyrosine residues are combined to form T4 and T3. PTU also
possesses the extra thyroidal action of blocking conversion of T4 to T3 in peripheral tissues through
inhibition of type 1 deiodinase, which may be of benefit in cases of thyroid storm or severe
thyrotoxicosis. Methimazole and PTU have different pharmacologic properties that should be
considered while making a choice of therapy. The serum half-life of methimazole is 6 to 8 hours,
whereas the half-life of PTU is 1 to 2 hours. These short half-lives would suggest that the thionamides
should be administered in divided daily doses. However, methimazole is effective even when given
once daily, since it interferes with iodine organification more effectively by irreversibly inhibiting therapy
and in patients with transient toxicosis due to thyroiditis where they form the primary therapy.
Situations favoring surgical therapy over radioactive iodine therapy for
hyperthyroidism Absolute indications
1. Suspicious of biopsy proven malignant nodules
2. Co-morbidity requiring surgery e.g. Hyperparathyroidism
3. Contraindication to radioactive iodine ablation
4. Pregnancy or lactation
5. Young children
6. Severe intolerance to antithyroid medications
7. Large compressive / obstructive goiter
Relative indications
1. Severe Grave’s ophthalmopathy
2. Patients desiring pregnancy within 6-12 months of treatment
3. Patients unable to continue close follow up
4. Patients incompletely treated by radioactive iodine ablation
Conclusions
Thyrotoxicosis is a potentially common problem in our Indian population especially females.In
view of females getting exposed to various types of physiological stress during life time such as
menstruation, pregnancy and lactation, an early diagnosis of thyrotoxicosis is mandatory .Therapeutic
options have a great bearing in female thyrotoxicosis patients with pregnancy and lactation because of
limitations that exist in treatment with Radio iodine. Patients need to stop breast feeding permanently
after a low dose therapy with Radio Iodine. Further pregnancy is only recommended to be planned
after one year of last radio iodine dose.
Further, the diagnostic yield of various types of thyrotoxicosis based on radio isotope imaging along
with clinical suspicion and biochemical profile of thyroid hormones is phenomenal. This has improved
the outcome of modern treatment of thyrotoxicosis. At the same time this has brought down the
morbidity of affected treatment with early diagnosis and initiation of specific therapy.
REFERENCES
. Bahn Rebecca S ; Burch Henry B, Cooper David S; 2011ATA/AACE Guidelines
hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American
thyroid association and American association of clinical endocrinologists :Endocr Pract; ;Vol 17
No. 3 1-64
2. Larsen PR, Davies TF, Hay ID, Wilson JD, Foster DW, Kronenberg HM et al (eds).: The thyroid
gland. Williams Textbook of Endocrinology. Philadelphia, WB Saunders Co, 9th Ed, 1998; 389515.
3. So WY, Yeung VT, Chow CC, et al: TSH secreting pituitary adenoma: A rare cause of
thyrotoxicosis. Int J Clin Pract; 1998; 52:62- 64.
4. Franklyn JA. The management of hyperthyroidism. N Engl J Med. 1994; 330(24): 1731-8.
5. Siegel RD, Lee SL. Toxic nodular goiter; Toxic adenoma and toxic multinodular goiter. Endocrinol
Metab Clin North Am.1998; 27:151-68.
6. Weetman AP; Graves’ disease. N Engl J Med. 2000; 343:1236-48.
7. Loh KC. Amiodarone-induced thyroid disorders: a clinical review. Postgrad Med J ; 2000; 76:13340.
8. Mittra ES, Niederkohr RD, Rodriguez C, et al. Uncommon causes of thyrotoxicosis. J Nucl Med.
2008; 49:265-78.
9. Hari Kumar K V,Pasupuleti,Jayaraman M,Abhyuday V: Role of thyroid Doppler in
differential Diagnosis Of Thyrotoxicosis; Endocr Pract Jan Feb 2009;15;1,6,9
9.
Signature of the Candidate
10. Remarks of the Guide
The topic is relevant to current problem of
Thyrotoxicosis in India. It is pertinent to assess
the risk factors, clinical and diagnostic features
and outcome of thyrotoxicosis in 10 to 50 age
group of people. I will be glad to guide Dr. Umar
Nazir Kabli in his work.
11. Name & Designation
11.1
Guide
GP CAPT A.K DASH
M.D (Medicine) DNB ( Medicine) ,DRM
SENIOR ADVISOR (MED)
PROFESSOR OF MEDICINE
COMMAND HOSPITAL,AIR FORCE,
BENGALURU.
11.2
Signature
…………………
11.3
Co-Guide (If any)
Nil
11.4
Signature
NOT APPLICABLE
11.5
Head of the Department
BRIG M S PRAKASH
M.D(Medicine),D.M. (Nephrology)
CONSULTANT & HOD(MED)
PROFESSOR,
HEAD OF DEPARTMENT,
DEPARTMENT OF MEDICINE,
COMMAND HOSPITAL, AIR FORCE,
BENGALURU.
11.6
Signature
…………………
12
12.1 Remarks of the Principal
12.2 Signature
………………..
CERTIFICATE OF ACCEPTANCE BY THE GUIDE
1.
I
GP CAPT A K DASH , here by accept DR UMAR NAZIR KABLI as a candidate of
MD (MEDICINE) course. The title of his dissertation is as follows:-
“STUDY OF CLINICAL AND IMAGING PROFILE IN THYROTOXICOSIS”
1. He will be under my guidance during the period of his study and thesis work.
Date:
GP CAPT A.K DASH
M.D. (MED) , D.N.B. (MED), DRM (NUC MED)
SENIOR ADVISOR (MEDICINE & NUCL MED)
PROFESSOR AND HEAD OF THE
DEPARTMENT OF NUCLEAR MEDICINE,
COMMAND HOSPITAL,
AIR FORCE,
BENGALURU
CERTIFICATE FROM ETHICAL COMMITTEE
1. The committee has examined the scope including the aim, objectives, method of data
collection & human/animal intervention of the following study to be carried out by Dr. UMAR
NAZIR KABLI under the guidance of GP CAPT A K DASH , title of which is
“STUDY OF CLINICAL AND IMAGING PROFILE IN THYROTOXICOSIS”
2.
The committee has no objection for undertaking this study at Command Hospital Air
force, Bangalore, 560007.
HOD MEDICINE
COUNSELLOR
E-SUPPORT
OIC AFMRC
OIC PG CELL
CERTIFICATE FROM HEAD OF THE INSTITUTION
Permission is hereby accorded to the student Dr. UMAR NAZIR KABLI, to undergo MD
(MEDICINE) course being conducted at COMMAND HOSPITAL AIR FORCE BENGALURU
affiliated to Rajiv Gandhi University of Health Sciences commencing from May 2012 under
the guidance of GP CAPT A K DASH
PROFESSOR AND HOD, DEPARTMENT OF
NUCLEAR MEDICINE, COMMAND HOSPITAL AIRFORCE BENGALURU-560007.
COMMANDANT & PRINCIPAL
COMMAND HOSPITAL
AIR FORCE
BANGALORE-560007
INFORMED CONSENT FORM
Student Researcher: Dr. UMAR NAZIR KABLI
Title of Project:
“STUDY OF CLINICAL AND IMAGING PROFILE IN VARIOUS TYPES OF
THYROTOXICOSIS PATIENTS”
I am asking for your voluntary participation in my M.D. Medicine Dissertation project. Please read the
following information about the project. If you would like to participate, please sign in the appropriate
place below.
You are being asked to participate in this study being conducted in Command Hospital, Bengluru,
because you satisfy our eligibility criteria which are:
(1) Diagnosis of THYROTOXICOSIS.
(2) Male and Female Age > 20 to _< 50 years
You will be one of the patients we plan to recruit in this study during SEP 13 TO SEP 2013
Purpose of the project: In the present study, we plan to see the clinical profile of thyrotoxicosis in
age group of 20 to 50 yrs patients.
The study design: Subjects will be enrolled after informed written consent.
Time required for participation: thrice, 01, 03 and 06 months
Potential Risks of Study: There are no potential risks associated with the study.
Possible benefits to you: You are not expected to get any benefit from being on this research
study, other than the treatment benefit and free investigations/tests. We cannot guarantee, however
that you will receive any benefits from this study.
Cost to the participant: You will not be required to pay for the medications or lab tests. You will not
be paid for your traveling expenses / you will not be paid to participate in this research study. No
extra medication or investigation will be involved in the study.
How confidentiality will be maintained: Any information that is obtained in connection with this
study and that can be identified with you will remain confidential and will be disclosed only with your
permission or as required by law.
How will your decision to not participate in the study affect you?
Your decision not to participate in this research study will not affect your medical care or your
relationship with the investigator or the institution. Your doctor will still take care of you and you will
not loose any benefits to which you are entitled.
Can you decide to stop participating in the study once you start?
The participation in this research is purely voluntary and you have the right to withdraw from this
study at any time during the course of the study without giving any reasons. However, it is advisable
that you talk to the research team prior to stopping the treatment. You may be advised about how
best to stop the treatment safely. If you withdraw, you may be asked to undergo some additional tests
to which you may or may not agree. Though advisable that you give the investigators the reason for
withdrawing, it is not mandatory.
Can the investigator take you off the study?
You may be taken off the study without your consent if you do not follow instructions of the
investigators or the research team or if the investigator thinks that further participation may cause you
harm.
If you have any questions about this study, feel free to contact:
Principal investigator: GP CAPT A.K DASH MD (MED),DNB(MED),DRM(NUC MED), SR ADV (
MEDICINE& NUCL MED)
PROFESSOR (MEDICINE) AND HOD, DEPARTMENT OF NUCLEAR MEDICINE, COMMAND
HOSPITAL, AIR FORCE, BENGALURU.
Investigator: Dr. UMAR NAZIR KABLI, Post Graduate student, Department of medicine,
Command hospital Air Force, Bengluru, Karnataka.
Phone/email: 08105747956, [email protected].
Voluntary Participation:
Participation in this study is completely voluntary. If you decide not to participate there will not be any
negative consequences. Please be aware that if you decide to participate, you may stop participating
at any time and you may decide not to answer any specific question.
You will be given a copy of this form to keep.
YOU ARE MAKING A DECISION WHETHER OR NOT TO PARTICIPATE. YOUR SIGNATURE
INDICATES THAT YOU HAVE DECIDED TO PARTICIPATE, HAVING READ AND UNDERSTOOD
THE INFORMATION PROVIDED ABOVE.
Name of Research Participant:
Signature:
Date:
[By signing this form I am attesting that I have read and understood the information above and I freely
give my consent to participate in this study.]
Signature of Witness
(if any):
Name and Signature of Investigator
Dr. UMAR NAZIR KABLI,
Post Graduate student,
Department of Medicine,
Command Hospital, Bengaluru.
PATIENT ASSESSMENT PROFORMA
Date:
S. No.
Personal details:
Name
:
Age
:
Sex
:
Diagnosis
:
Address
:
History
Chief complaints: 1.
2.
3.
4. Others
SYMPTOMS
PRESENT(P)/ ABSENT(A)
Past history: Any major illness/injury/operations,
Family history; Goiter, thyrotoxicosis, Diabetes, Rheumatoid Arthritis?
Age of Onset: At which Thyrotoxicosis in the family detected
Personal history:
1. Current place of residence (For last 2 Years)
2. Diet:
3. Smoking:
4. Alcohol consumption:
5. Cocaine abuse:
6. Any other habits:
Physical examination
Ht:
cms.
Wt :
Kgs.
BMI-
Kg/ M2
1. General examination
Built and nutrition:
Xanthoma:
Pallor
Xanthelasma
Hyperhidrosis
Clubbing:
Icterus:
Edema:
Lymphadenopathy
Hair
Pulse:
/min, Type of pulse-
Blood pressure:
/
mm Hg
Respiratory rate:
2. Eye Examination:
3. Neck Examination:
ThyromegalyVascular bruitThyroid nodulesRetro sternal extension-
/Grade-
/min
Temperature:
Exophthalmos- (+)/(-) , Other Eye signs-
4. Skin -
Systemic examination
1. Cardiovascular system:
2. Respiratory system:
3. Central nervous system:
HMFTremorsPower of Muscles DTJ-
4. Abdomen:
Investigations:
ESRCBC-.
Biochemistry:
1. Blood Sugar(F)2.
PPBS-
Lipid Profile- TC-
3. Electrolytes-
, HDL-
Na+-
,LDL-
,TG-
,VLDL-
, K+ -
4. Serum CalciumThyroid ProfileSerum T3Serology1. ANA-
ng/ml ,
Serum T4-
µg/dl
,
TSH-
µIU/ml
2. Anti TPO Antibody
ECG
USG THYROID GLAND
THYROID SCAN (TECHNETIUM 99m Per Technetate UPTAKE AND SCAN)
Name and Signature of the Investigator:
Dr. UMAR NAZIR KABLI,
Post Graduate student,
Department of Medicine,
Command Hospital, Bengluru.
INFORMED CONSENT FORM
CONSENT FORM
Patient information sheet for participation in the study
Read the following carefully
You are being asked to participate in a research study. Make sure that you understand what your participation
will involve. Ask as many questions you may have to your doctor, before you sign this document.
In case of an emergency or any other problems with the study kindly contact:
Dr Umar Nazir Kabli 8105747956
Background information
In the cancer research field, imaging has emerged as the most prolific topic in the last decade with work
connecting it with risk reduction in thyrotoxicosis.
THE STUDY IS PURELY BASED ON DIAGONOSTIC TESTS. HENCE YOU/YOUR PATIENT ARE NOT AT ANY RISK.
Procedures
If you agree to participate in the study, the events described below will take place.
1.
When presenting to Nuclear Medicine and Endocrinology/Gen Med OPD and as referred cases from
various clinicians ,your blood sample will be collected subsequently to measure your serum T3, T4 and TSH
levels.
2.
Grading of your Disease (THYROTOXICOSIS) would be recorded.
Potential side effects
Nil, as study does not interfere with your treatment and is meant only to gather data.
You will not be identified in any published reports on this study. Within the study, you will be identified only by
a numerical code for identification. Confidentiality of your participation will be maintained to the extent provided
by existing law.
Refusal or withdrawal of participation
This study is based on routinely recommended investigation for thyrotoxicosis.However,your participation in
this study is voluntary. You may refuse to participate in, or withdraw from the study at any time without penalty
or loss of benefits or right to medical care to which you may otherwise be entitled. Your agreement to
participate does not waive any of your rights.
Questions/ patient rights
You will be completely free to make inquires. If you have any other questions about the study you should
contact anyone of the investigators.
“A STUDY OF IMAGING MODALITIES IN THYROTOXICOSIS”
INFORMED CONSENT FORM
I confirm that Dr UMAR NAZIR KABLI has explained to me the purpose of the research, the study procedure
and I am willing to undergo in this study. Alternatives to my participation in the study have also been
discussed. I have read and I understand this consent form. I agree to give my consent to participate as a
subject in this study.
………………………
…………………………
…………..
….……….
Patient Name
Patient’s Signature
Date
Time
I acknowledge the receipt of a copy of this consent form
………………………
…………………………
…………..
….……….
Patient Name
Patient’s Signature
Date
Time
………………………
…………………………
Name of Legally Acceptable
LAR’s signature
Representative
…………..
Date
….……….
Time
I have explained to ………………………………………….. the purpose of this research
………………………
…………………………
…………..
….……….
Investigator’s Name Investigator’s Signature
Date
Time
………………………
…………………………
…………..
….……….
Witness Name
Witness Signature
Date
Time