Thyroid

Escape from Wolff-Chaikoff effect is presumed to be due to formation of inactive NIS dimers
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Though it is well known fact that initially FT4 is investigation of choice in the setting of antithyroid drug therapy for hyperthyroidism,when TSH recovers(≥ 3 months), it becomes the best method to follow on.
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How to calculate amount of daily iodine intake(DII) from urine iodine concentration?
-Median 24-hour urine volume is 0.9 ml/kg/hr
-24hr urine volume is 1.5 L
-Normal bioavailability of iodine is 92%
Hence DII= weight(kg) × 0.92×0.0009 L/kg/hr × 24 hr/day
Simplified,
DII=weight(kg) × 0.0234 × urine iodine(microgram/L)

For example, 100 µg/L urine iodine in a 50 kg man means DII of 117 µg.
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For diagnosing substernal extension of goiter investigation of choice is CT. 99mTcO4 doesnt help much as surrounding radioactivity of heart and great vessels is also high.Better to go for 123I scan.
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How to look for etiology of post-radioablative hypothyroidism,if previous records are not available,except for 99mTC04 scan showing diffuse uptake?
A:Clinically there are no residua of TAO/acropachy/pretibial myxedema.Anti-TSH-R abs even might not help as we know their titer decrease in accordance with decrease in thyroid volume.All this meaning ending up in presumptive diagnosis?
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Most common cause of acute thyroiditis is Staphylococcus aureus in adults and streptococcci in children,with mixed infections(anaerobes & gram negative bacteria) in almost 30%.My choice of antibiotics are vancomycin, piperacillin-tazobactam and metronidazole in combination.Corner stone management is hospital admission, parenteral antibiotics, I & D and not to forget to do barium swallow,CT/MRI to look for pyriform sinus (which is located normally just lateral to arytenoid cartilage) fistula.
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Growth of goiter during LT4 treatment for autoimmune thyroid disease indicates possibility of lymphoma and its should be FNAB
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Nodule with elevated TSH has 30% risk of carcinoma compared to a nodule with TSH in usual range.hence it is FNAB prior to LT4 suppressive therapy.
( K. Boelaert, J. Horacek, R. L. Holder, J. C. Watkinson, M. C. Sheppard, and J. A. Franklyn.Serum Thyrotropin Concentration as a Novel Predictor of Malignancy in Thyroid Nodules Investigated by Fine-Needle Aspiration.J. Clin. Endocrinol. Metab., Nov 2006; 91: 4295 - 4301.)
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One case ive encountered is 24 year-old-female with history of weight gain and found to have S.TSHof 3.2 µIU/ml with T4 of 4 ug/dl(N,5.5-11) who has been on LT4 150 µg/day.In such scenario ( total T4 is low and serum TSH is not elevated), TBG deficiency, central hypothyroidism, or euthyroid sick syndrome should be considered.Serum free T4 concentration is normal in TBG deficiency.
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Thyrotoxic Graves' disease with normal thyroidal 99m Tc pertechnetate uptake
Recently ive encountered one such case,a 26 year old goitrous male and not received antithyroid medications and having stare and upper eye lid retraction but no proptosis where biochemically and clinically patient was thyrotoxic and Tc scan was showing uptake in upper limit of normal (in contrast to low or no uptake in subacute/silent thyroiditis).Such things have been documented earlier(Annals of Nuclear Medicine,Vol 4,No2,43-48,1990) which interpret such cases are in initial phases of evolving thyrotoxicosis

Diabetes

Diabetic foot
1.Probe-to-bone test in the diagnosis of osteomyelitis has sensitivity of 90% compared to radiograph's sensitivity of 55% and MRI's sensitivity of 100%.
2.When diameter of plantar ulcer is> 2cm and depth >3 mm risk of osteomyelitis is high.
3.Layers of epidermis,mnemonic:Corn Lovers Grow Several Bales(from superficial to deep)
-Stratum Corneum
-Stratum Lucidum
-Stratum Granulosum
-Stratum Spinosum
-Stratum Basale(germinativum)
4.Claw toe:All joints plantar flexed;(metatarsophalangeal(MTPJ) & proximal(PIPJ) and distal interphalangeal joints(DIPJ).
Mallet toe:Only DIPJ is plantar flexed
Lumbricals normally extend PIPJ & DIPJ while they flex MTPJ.Loss of lumbricals action leads to clawtoes
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Screening for CAD in diabetes
What Diabetes care 30:2729,2007 recommends rather hesitatingly as screening test is EBCT/mutislice CT(Cardiac) to look for CAC score,and proceed for further evaluation if score is >400.There is no recommendation for the frequency to rescreen for those with CAC <400.
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Gatifloxacin and dysglycemia
Gatifloxacin has been associated with both hypoglycemia and hyperglycemia.With the exception of a slight increase in the risk of hypoglycemia with levofloxacin, these risks were not shared by other fluoroquinolones. Dysglycemic events were not restricted to patients receiving drug treatment for diabetes.Although the mechanism of these apparently competing adverse effects is not fully understood, studies in animals suggest that although gatifloxacin can promote insulin release and hypoglycemia by blocking the ATP-sensitive potassium channels of pancreatic islet cells, it can also trigger the vacuolation of pancreatic beta cells, leading to reduced insulin levels and hyperglycemia.
( N Engl J Med 2006; 354:2725-2726, Jun 22, 2006. )
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Biguanide and lactic acidosis(>5 mmol/l)
Lactic acidosis often has non specific and subtle symptoms like myalgias, malaisiae,somnolence and abdominal distress and also may be associated with bradyarrhythmia and hypotension.Biguanides reduce pyruvate dehydrogenase activity and mitochondrial transport of reducing agents, enhancing anaerobic metabolism.Metformin is readily removed by hemodialysis, which would be appropriate for severe, life-threatening acidosis. Metformin is a cation at physiologic pH and cimetidine,digoxin, procainamide, quinidine, ranitidine, iodinated contrast media, and amiloride might compete with renal tubular secretion of metformin at the site of organic cation transport.Metformin is dialyzable .Hence prompt hemodialysis is life saving measure.

Cases

This 35 year- old- female elsewhere diagnosed having toxic multinodular goiter(TMNG) with biochemical confirmation of hyperthyroidism was put on methimazole without prior scintigraphy.Now i want to know whether its is really TMNG or nodular variant of Graves' disease.What is the best test to do without withdrawing the medication?
A:TSH-R antibodies
PN: Titer of TSH-R abs decrease during treatment with antithyroid drugs.So how much sensitive this test will be?
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A 60 year- old- man presented with left side hemiparesis due to bleed in right basal ganglionic area and he is found to have multinodular goiter.TSH was <0.01mIU/ml with normal FT4 & FT3.Heart rate was 90/minute & with no signs of TAO.TSH-R antibodies are negative.Patient's relatives refused scintigraphy due to economic constraints.On 6th day he developed atrial fibrillation which was controlled with amiodarone injection.Now whether he should be treated with antithyroid drugs and if so in what doses? PN: I have put him on methimazole 20 mg/day and patient is yet to turn for follow-up. ******************************************************************************
A 40 year- old- man diagnosed with tuberculosis meningitis when he had seizures & fever was treated subsequently with anti tuberculous drugs and prednisolone 30mg/day else where (which was tapered over 3 months).Now he presented with generalized weakness gradually increasing in severity after steroid withdrawal.Review of previous MRI brain shows partial empty sella turcica on 2 images done 6 months apart.ITT obviously is not a choice.250 microgm Synacthen stimulation test at 8 am shows basal value of 430 nmol/L with 30- & 6- minute values being 650 nmol/L and 740 nmol/L respectively.His TSH is 7.4 mIU/mL(N,0.3-5.0) with low FT4 and low-normal FT3. Serum TPO antibodies are within normal range.Serum IGF-1 was low compared to age and sex matched range.Other anterior pituitary hormones are within normal range and testosterone(8 am) was 18nmol/L.I have put him on LT4 and plan to repeat FT4 after 6weeks.My plan is to evaluate for GH deficiency.Doubt is about the role of IGF-1 as screening test in such setting where patient is clinically euthyroid but hormonal profile is of central hypothyroidism.Hypothyroidism irrespective of etiology is known to cause decreased GH secretion and impaired responsiveness to IGF-1 (but not impaired response of IGF-1 generation to GH). I think when FT4 is normal & repeat IGF-1 is still low, it indirectly indiactes damage to somatotrophs. PN: S. IGF-1 has no role as screening test for GH deficiency in the setting of hypothyroidism.We have to do thyroid function tests before embarking on IGF-1.Already it is well known fact that normal S.IGF-1 does not rule out GH deficiency.
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A 28-year-old female with complaints of hirsutism,oligomenorrhea of 15 years duration has been diagnosed as PCOS and on treatment with metformin,OCPs and laser treatment for hair, has no contributive family history.Her last menstrual period was 6 month back when on metformin.As PCOS is a diagnosis of exclusion baseline investigations were done. 8am 17-OHP was 30 ng/ml with E2 of 1200 pmol/L. S.LH & FSH were o.17 & o.o1 µIU/ml and S.PRL of 69.2 ng/ml with S.TSH of 2.24µIU/ml.Other investigations are normal.She recently noticed serous discharge from her breasts.To establish the diagnosis of LOCAH,current Williams doesnt recommend to do ACTH stimulation test once 17OHP levels are > 8 ng/ml;but as 2006 JCEM article by Dr.Maria New still advocates it.Any how my plan is to put her on dexamethasone 0.25mg bedtime,as she now desires fertility.Also i want her endometrium to be evaluated by a gynecologist.About breast discharge and slightly elevated PRL,this might be due to elevated E2 ( feature of such PCOS- & related states).Once she is on treatment,in due course i prefer to repeat E2 & PRL.
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A 64- year-old female has been consulting me for DM & hypothyroidism for past 3 days because her previous endocrinologist is sick. She has past history of rheumatic heart disease and subsequently detected to have DCMP and has been on diuretics and digoxin. She has under gone hysterectomy 20 years back for fibroid uterus and ovaries were preserved She is known case of Left side carcinoma of breast(Ductal ca),under gone radical mastectomy(1998) with ER & PR positivity but HER2 was not done. Subsequently she received local RT, Doxorubicin based CT (4 CYCLES) and thereafter treated with tamoxifen for 2 years(at NTR cancer center). She was off treatment for 2 years and when she complained of new growth on right breast,investigations else where done showed lung and bone metastases. CT guided FNAC from lung nodules evinced metastasis. The new growth was assumed to be metastasis and no local procedure was done. She has been on once monthly zolendronate 4mg and anastrozole 1mg/day for past 8 months. When I saw her for first time this was the basic picture and I asked her to undergo biopsy of right breast mass as in most cases its new primary event rather than metastasis and if she is found to have HER2 positivity can benefit from Trastuzumab. Also as response rate is better with letrozole compared to anastrozole, I asked her to switch the medications. MRI(with contrast) breast is advised. About DM,her s.creatinine is 1.6 mg/dl and is on insulin with TSH of 8.3 úIU/ml and LT4 dose was escalated. Also S.TPO abs are requested.
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Does this patient has insulinoma?
One of most common dilemmas an Endocrinoologist do face is differentiating psychiatric diseases which have predominant manifestations of giddiness&/or sweating from causes of hypoglycemia.In an outpatient practice,nearly 99% such cases being referred are of former type.But it is mandatory to establish or rule out endocrine diagnosis.The gold standard test is 72-hour fast for insulinoma,for which the doctor always has a needle of suspicion.But without good resident doctor & nursing care it is difficult to evaluate such cases and often patient's relatives complain that he is not able to tolerete after few hours and if not convinced properly ends in premature termination of test.The alternatives we have got are C-peptide suppression test,which carries a fear of irreversible damage that too with not so good diagnostic sensitivity.Another option is glucagon stimulation test,which is safer .But it is notoriously difficult to find a chemist in this country who sells that drug.I dont know why it has so much limited availability.Ofcourse, tolbutamide is out of question!!!