Serum Urea or BUN what is the difference?

**Sourced from Quora – Credit to original author**

Urea is the principal nitrogenous waste product of metabolism and is generated from protein breakdown.

It is eliminated from the body almost exclusively by the kidneys in urine, and measurement of its concentration, first in urine and later in blood, has had clinical application in the assessment of kidney (renal) function for over 150 years.

Around the world, essentially the same method of urea analysis is used, but the result is expressed in two different ways . In the US and a few other countries, plasma or serum urea concentration is expressed as the amount of urea nitrogen. Although plasma or serum is used for the analysis, the test is still, somewhat confusingly, commonly referred to as blood urea nitrogen (BUN), and the unit of BUN concentration is mg/dL.

In all other parts of the world, urea is expressed as the whole molecule (not just the nitrogen part of the molecule) in SI units (mmol/L).

Since BUN reflects only the nitrogen content of urea (Molecular weight 28) and urea measurement reflects the whole of the molecule (Molecular weight 60), urea is approximately twice (60/28 = 2.14) that of BUN.

Thus BUN 10 mg/dL is equivalent to urea 21.4 mg/dL.

To convert BUN (mg/dL) to urea (mmol/L):

multiply by 10 to convert from /dL to /L and divide by 28 to convert from mg BUN to mmol urea, i.e. 10/28 = 0.357

So the conversion factor is 0.357

BUN mg/dL multiplied by 0.357 = urea (mmol/L)

Urea (mmol/L) divided by 0.357 = BUN (mg/dL)

Approximate reference (normal) range:

Serum/plasma urea 2.5-7.8 mmol/L

Serum/plasma BUN 7.0-22 mg/dL.


Kawasaki Disease

Typically <5y of age

Diagnosis considered when patients present with temperatures >38.5°C for more than 5 days, along with four of the five following associated clinical findings

  1. Bilateral conjunctival injection sparing the limbus, without exudate and starting with the onset of fever
  2. Cracked or fissured lips, with or without injected oral mucosa or strawberry tongue
  3. A generalized polymorphous rash
  4. Edema or erythema of the palms and soles, followed by periungual desquamation in the convalescent phase
  5. Painful cervical lymph node enlargement > 1.5 cm in diameter

10% patients develop coronary aneurysm but don’t fulfil the criteria = ‘incomplete’ KD

Incidence of coronary artery aneurysms = 25% in untreated patients

Mortality 2%;

With early detection & treatment – Prevalence 5% and mortality < 1%

Without treatment, manifestations of acute inflammation can last up to several weeks, with an increased risk for cardiac complications

Signs and symptoms in the acute phase of cardiac complications

Apart from the criteria above

fever with tachycardia out of proportion to the degree of fever

muffled heart tones, and gallop heart sounds.

ECG may reveal low-voltage R waves and flattening T waves, with possible prolongation of the PR and QT intervals

Q wave & repolarisation abnormalities = acute MI rare

ECHO = may reveal mild LV dilation along with a decrease in systolic function, mitral regurgitation, pericardial effusion, aortic root dilation, and mild aortic insufficiency

By 10th day = coronary dilatation seen in 50% of children with KD; Males at increased risk

50% of aneurysms tend to regress within the first 2 years via proliferation of intimal cells, but patients are still at increased risk for accelerated atherosclerosis.

Aspirin has been instrumental in suppression of the anti-inflammatory process, leading to a significant decrease in mortality from 2% to 0.5%.  (avoid high-risk sports activities to minimize the risk for bleeding). Initial dose of aspirin for effective anti-inflammatory action is 80-100 mg/kg, divided into four daily doses

Gamma-globulins decrease the frequency of coronary aneurysms compared with use of aspirin alone, as well as a reduction in morbidity and mortality when gamma-globulins are promptly administered. The recommended doses of intravenous gamma-globulin have been up to 2 g/kg, infused over 12-18 hours

Varicella and Neonate

Maternal Varicella Infection

VZIG (human varicella-zoster immunoglobulin) is recommended for infants born to a mother who develops chicken pox in the period 7 days before to 7 days after delivery. (The highest risk appears to be 5 days before to 2 days after delivery).

Exposed infants born before 28 weeks gestation or weighing less than 1000grams should be given VZIG as transfer of maternal IgG antibodies may be inadequate.

Infants > 28 weeks gestation may be VZV antibody negative, but should be serological tested, despite a maternal history of varicella or zoster.


Maternal varicella is not a contra-indication to breast feeding

Neonatal exposure to non-maternal Varicella Zoster

If the neonate has a significant exposure to chickenpox or shingles from a source other than the mother – e.g. Father, sibling, member of staff or another mother on the unit.

The mother should be asked about a past history of chickenpox or shingles. Babies of mother with a positive history will not require treatment. Mothers with no history or who are unsure should be tested for VZV antibodies. If the mother is seronegative, the infant will need a dose of VZIG, but does not need to be separated from its mother or siblings. If positive no further action is required.

If infant between 28 weeks to 36 weeks – the infant should be tested for VZV antibody. Even if the mother is seropositive, or has a past history of infection. The VZV antibody may not have crossed the placenta, be low or undetectable, despite the mother having had VZV exposure. If the infant is seronegative, it will require a dose of VZIG.

However, if <28 weeks and <1000kg. They should be given VZIG, as soon as exposure known. As transfer of maternal IgG antibodies may be inadequate, or non-existent. Even if the mother gives a positive history of having had the infection. Testing is also recommended in these infant, but not absolutely necessary.(Health Protection Agency).

Infants of mothers with shingles are not at risk as they will be protected by maternal antibodies.

Health Protection Agency

Risk assessment for neonates or infants with a confirmed significant exposure to chickenpox or shingles












Neonates whose mothers develop chickenpox (but not shingles) in the period 7 days before to 7 days after delivery


Not required for mother or infant


Administer VZIG within 7 days of delivery OR within 7 days of onset of disease in the mother, whichever is later




Infants (<1yr) who have remained in hospital since birth with any one of the following:


-born before 28 weeks gestational age OR


– weighed less than 1000g at birth OR


-infants who have severe congenital or other underlying condition that require prolonged intensive or special care during the first year of life


Test for VZV antibody status in the infant only


Administer VZIG within 7 days if found to be VZV antibody-negative by a qualitative assay or <150 mIU/ml by a quantitative assay




Neonates exposed to chickenpox or shingles (other than in the mother) in the first 7 days of life.


Test either mother (preferred) or neonate for VZV antibody status for infants whose mothers have a negative or uncertain history


Administer VZIG within 7 days if found to be VZV antibody-negative by a qualitative assay or <150 mIU/ml by a quantitative assay

Treatment of neonates with varicella

If severe chickenpox develops despite VZIG, high dose intravenous aciclovir treatment of 20mg/kg every eight hours for at least seven days should be started as soon as possible.

Prophylactic intravenous aciclovir should also be considered in addition to VZIG for infants whose mothers develop chickenpox four days before to two days after delivery as they are at the highest risk of fatal outcome despite VZIG prophylaxis

Amiodarone & Thyroid

Source –

Amiodarone causes a wide spectrum of effects on the thyroid.

  • Amiodarone inhibits type 1 5′-deiodinase enzyme activity, thereby decreasing the peripheral conversion of T4 to triiodothyronine (T3) and reducing the clearance of both T4 and reverse T3 (rT3). Consequently, the serum levels of T4 and rT3 increase and the serum levels of T3 decrease by 20-25%.
  • Amiodarone inhibits entry of T4 and T3 into the peripheral tissue. Serum T4 levels increase by an average of 40% above pretreatment levels after 1-4 months of treatment with amiodarone. This, in itself, does not constitute evidence of hyperthyroidism (thyrotoxicosis).
  • Inhibition of type 2 5′-deiodinase enzyme activity in the pituitary due to feedback regulation is seen in the first 1-3 months and leads to an increase in thyroid-stimulating hormone (TSH) levels. This is not an indication for T4 replacement in these patients. Serum TSH levels return to normal in 2-3 months as T4 concentrations rise sufficiently to overcome the partial block in T3 production. The response of TSH to thyroid-releasing hormone (TRH) may be reduced.
  • Amiodarone and its metabolites may have a direct cytotoxic effect on the thyroid follicular cells, which causes a destructive thyroiditis.
  • Amiodarone and its metabolite desethylamiodarone can act as a competitive antagonist of T3 at the cardiac cellular level.

In summary, serum T4 levels rise by 20-40% during the first month of therapy and then gradually fall toward high normal. Serum T3 levels decrease by up to 30% within the first few weeks of therapy and remain slightly decreased or low normal. Serum rT3 levels increase by 20% soon afterward and remain increased. Serum thyrotropin (TSH) levels usually rise after the start of therapy but return to normal in 2-3 months.

Two forms of AIT have been described. Type 1 usually affects patients with latent or preexisting thyroid disorders and is more common in areas of low iodine intake. Type 1 is caused by iodine-induced excess thyroid hormone synthesis and release (Jod-Basedow phenomenon). Type 2 occurs in patients with a previously normal thyroid gland and is caused by a destructive thyroiditis that leads to the release of preformed thyroid hormones from the damaged thyroid follicular cells. However, mixed forms of AIT may occur in an abnormal thyroid gland, with features of destructive processes and iodine excess.

The most likely mechanisms of AIH are an enhanced susceptibility to the inhibitory effect of iodine on thyroid hormone synthesis and the inability of the thyroid gland to escape from the Wolff-Chaikoff effect after an iodine load in patients with preexisting Hashimoto thyroiditis. In addition, iodine-induced damage to the thyroid follicles may accelerate the natural trend of Hashimoto thyroiditis toward hypothyroidism. Patients without underlying thyroid abnormalities are postulated to have subtle defects in iodine organification that lead to decreased thyroid hormone synthesis, peripheral down regulation of thyroid hormone receptors, and subsequent hypothyroidism.

Wolff–Chaikoff Effect

The Wolff–Chaikoff effect is an autoregulatory phenomenon that inhibits organification in the thyroid gland, the formation of thyroid hormones inside the thyroid follicle, and the release of thyroid hormones into the bloodstream. This becomes evident secondary to elevated levels of circulating iodide. The Wolff–Chaikoff effect is an effective means of rejecting a large quantity of imbibed iodide, and therefore preventing the thyroid from synthesizing large quantities of thyroid hormone. Excess iodide transiently inhibits thyroid iodide organification.

In individuals with a normal thyroid, the gland eventually escapes from this inhibitory effect and iodide organification resumes; however, in patients with underlying autoimmune thyroid disease, the suppressive action of high iodide may persist.

The Wolff–Chaikoff effect lasts several days (around 10 days), after which it is followed by an “escape phenomenon,” which is described by resumption of normal organification of iodine and normal thyroid peroxidase function. “Escape phenomenon” is believed to occur because of decreased inorganic iodine concentration secondary to down-regulation of sodium-iodide symporter (NIS) on the basolateral membrane of the thyroid follicular cell.

The Wolff–Chaikoff effect can be used as a treatment principle against hyperthyroidism (especially thyroid storm) by infusion of a large amount of iodine to suppress the thyroid gland. Iodide was used to treat hyperthyroidism before antithyroid drugs such as propylthiouracil and methimazole were developed. Hyperthyroid subjects given iodide may experience a decrease in basal metabolic rate that is comparable to that seen after thyroidectomy.

Jod-Basedow phenomenon

The Jod-Basedow effect is hyperthyroidism following administration of iodine or iodide, either as a dietary supplement or as contrast medium.

This phenomenon is thus iodine-induced hyperthyroidism, typically presenting in a patient with endemic goiter (due to iodine deficiency), who relocate to an iodine-abundant geographical area. People who have Graves disease, toxic multinodular goiter, or various types of thyroid adenoma are also at risk of Jod-Basedow effect when they ingest extra iodine. The Jod-Basedow effect also been seen as a side effect of administration of the iodine-containing contrast agents, or amiodarone, an antiarrhythmic drug.

The Jod-Basedow effect does not occur in persons with normal thyroid glands who ingest extra iodine in any form.

The Jod-Basedow effect typically occurs with comparatively small increases in iodine intake, in people who have thyroid abnormalities that cause the gland to function without the control of the pituitary (i.e., a thyroid gland that is not normally suppressed by thyroid hormone driven loss of TSH secretion from the pituitary). In some ways the Jod-Basedow phenomenon is the opposite of the Wolff-Chaikoff effect.

However, (unlike the Wolff-Chaikoff effect), the Jod-Basedow effect does not occur in persons with normal thyroid glands, as thyroid hormone synthesis and release in normal persons is controlled by pituitary TSH secretion, (which does not allow hyperthyroidism when extra iodine is ingested).

Investigation for Developmental Regression

Measurements: Length, Weight, OFC

Blood: FBC, Ferritin, U&E, LFT, Bone, CK, TSH, Free T4, Vitamin D level, Ammonia, Lactate, Pyruvate, Acylcarnitines, Plasma amino acids, White cell enzymes, VLCFAs, Urate, Biotinidase

Urine: Sulfite stick test, Amino and Organic acids, Oligosaccharides, GAGs

Radiology: MRI head