Laboratory diagnosis of endocrine

diseases and hypersensitivity

Yanzi Chang
Lihuili hospital
 Overview of endocrine system
• Including
- endocrine gland (e.g pituitary gland, thyroid, pancreas, adrenal
gland, gonad (testis and ovary))
- endocrine cells (distributed in gastrointestinal tract, heart, lung,
kidney, vessel)
• Mechanism of action
- Hormones combine with specific receptor on the cellular surface.
- A series of amplification effect in the cell.
• Range of action
- Specific e.g thyroid stimulating hormone(TSH), adrenocorticotrophic
hormone (ACTH)
- Extensive e.g thyroxine, growth hormone
 Outline
• Laboratory diagnosis for endocrine diseases
- Pituitary hormone
- Thyroid hormone
- Adrenal hormone
- sex hormone
- Lab diagnosis for common endocrine diseases
• Laboratory diagnosis for hypersensitivity
- Categories of hypersensitivity
- Laboratory diagnosis for common hypersensitivity diseases
 Pituitary hormone
• Anterior pituitary hormone
- Growth hormone (GH)
- adrenocorticotrophic hormone (ACTH)
- Thyroid stimulating hormone(TSH)
- Luteinizing hormone(LH)
- follicle stimulating hormone (FSH)
- Prolactin (PRL)
• Posterior pituitary hormone
- Antidiuretic hormone (ADH)
- Oxytocin
 Growth hormone
• Secreted by anterior pituitary.
• Function: stimulate skeletal growth, promote protein
synthesis, gluconeogenesis, lipid peroxidation,
absorption of calcium and phosphorus.
• Regulated by growth hormone releasing hormone
(GHRH) and growth hormone releasing inhibitory
hormone (GHIH, also called somatostatin, SS).
Released in a pulsatile manner (one peak every 1 to 4h,
increase after sleep and reach peak 1h deep sleep
later).
• Half-value period: 20-30min, (difficult to detect)
 IGF-I and IGFBP-3
• IGFs (Insulin-like growth factors), IGFBP-3(IGF binding
protein): GH dependent (synthetized by the liver after GH activates
liver cells). In blood, IGF-I (75%)combined with IGFBP-3.
• IGF-I:
- Half-value period: 2h
- relevant to age, and influenced by other hormone (e.g.
thyroxine and prolactin), nutrition intake.
• IGFBP-3:
- Reflects the total concentration of IGF-I and II.
- Not be influenced by age and nutrition intake.
• IGF-I and IGFBP-3 are the first selections in lab diagnosis for GH
disorder.
• Normal range:
- IGF-I:
Children: 31-160ug/L (1-2 years old)
Increase with the age, reach peak level in youthhood (11-16years
old).
Adults: decrease with the age.
- IGFBP-3
Newborn: 0.4-1.4mg/L, increase to 2-5mg/L in youthhood.
• Clinical significance:
- IGF-I and IGFBP-3 ↓↓, GH deficiency.
- IGF-I and IGFBP-3 ↑↑, gigantism in children or acromegaly in adults.
 adrenocorticotrophic hormone (ACTH)
• Secreted by anterior pituitary.
• Function: Stimulate adrenal cortex
to secret glucocorticoids, hypothalamus

mineralocorticoid, androgen.
• Regulated by corticotropic hormone
releasing hormone (CRH) and by serum
cortisol concentration. Released in daily
rhythmicity (low in night, peak in the
morning)
• Clinical significance: differentiate the
hyperadrenocorticism, hypoadrenocorticism
• ↑seen in primary hypoadrenocorticism, congenital
adrenal cortex hyperplasia, ectopic ACTH syndrome,
ectopic CRH tumor.
• ↓anterior pituitary hypofunction, primary
hyperadrenocorticism.
 Thyroid stimulating hormone, TSH

• Function: promotes the synthesis and release of

thyroxine, thyroid cell hyperplasia, gland enlargement.
• Regulated by thyrotropin releasing hormone (TRH),
negatively regulated by somatostatin and feedback from
thyroxine.
• Normal range: different according to the method.
• Clinical significance:
• The most important item to diagnose primary and
secondary hypothyroidism. The first item to evaluate
thyroid function with FT3 and FT4.
- ↑ primary hypothyroidism, ectopic TSH secretion, syndrome of
inappropriate TSH secretion, simple goiter, thyroiditis, hyperfunction
of anterior pituitary.
the item to observe effect of thyroxine replacement treatment.
- ↓hyperthyroidism, secondary hypothyroidism, hypofunction of
anterior pituitary, acromegaly, hypercortisolism. Large amount of
glucocorticoids treatment and anti-thyroid medicine.
 Luteinizing hormone (LH) and
follicle stimulating hormone (FSH)
LH
• Produced by anterior pituitary.
• Function: control the menstrual cycle. Induce ovulation FSH
and synthesis of corpus luteum (for female). Stimulate
the synthesis of testosterone (for male).

LH (IU/L) FSH(IU/L)
Males, 23-70 yr 1.2-7.8 1.4-15.4
Females
Follicular phase 1.7-15.0 1.4-9.9
Midcycle peak 21.9-56.6 0.2-17.2
Luteal phase 0.6-16.3 1.1-9.2
postmenopausal 14.2-52.3 19.3-100.6
• Clinical significance:

- LH and FSH: Evaluation of menstrual cycle, diagnosis of sterility,

hormone replacement treatment in postmenopausal period.

- If LH and FSH increase persistently, indicate primary ovarian failure.

If decrease, indicate secondary ovarian failure.

- Forecast for ovulation: 30h after LH increase, ovulation will happen.

 Prolactin (PRL)
• Produced by anterior pituitary and released in rhythmicity.
• Function: stimulate the production of milk, promote
breast’s growth.
• Clinical significance:
- ↑ mainly for the diagnosis of hyperprolactinemia (lead to
hypothalamic sex gland hypofunction. manifestation:
Female, anovulation; male, sexual dysfunction).
- ↑ seen in some breast cancer and pituitary tumor.
 Pituitary hormone
• Anterior pituitary hormone
- Growth hormone (GH)
- adrenocorticotrophic hormone (ACTH)
- Thyroid stimulating hormone(TSH)
- Luteinizing hormone(LH)
- follicle stimulating hormone (FSH)
- Prolactin (PRL)
• Posterior pituitary hormone
- Antidiuretic hormone (ADH)
- Oxytocin
 Antidiuretic hormone (ADH)
• Secreted by posterior pituitary. Activation element: blood
high osmotic, low blood volume, and low extracellular
fluid.
• Function: promote the distal tubule collecting duct to
reabsorb water.
• Clinical significance:
- ↑ seen in pituitary hyperfunction, renal insipidus,
dehydration. Also seen in some lung cancer
(heterogenous secretion) or other cancers.
- ↓ seen in central insipidus, nephrotic syndrome, large
amount of isotonic solution intake, body fluid increase.
 Outline
• Laboratory diagnosis for endocrine diseases
- Pituitary hormone
- Thyroid hormone
- Adrenal hormone
- sex hormone
- Lab diagnosis for common endocrine diseases
• Laboratory diagnosis for hypersensitivity
- Categories of hypersensitivity
- Laboratory diagnosis for common hypersensitivity diseases
 Thyroid hormone detection
• Thyroxine
deiodination
2DIT T4 +TG T4 +TBG T3 +TBG
FT4 Liver, kidney FT
3
T3 +TG T3 +TBG
FT3
Thyroid Circulation

DIT: diiodotyrosine
T4 : tetraiodothyronine
TG: thyroglobulin
TBG: thyroxine binding
globulin
rT3 : reverse triiodothyronine
 TT4, FT4 and TT3, FT3 , rT3
• TT4 and TT3 easily influenced by the quantity of
TBG. But FT4 and FT3 couldn’t be influenced by
TBG, so more susceptible and stable for
evaluating thyroid function.

• rT3: produced fromT4 deiodination in peripheral

tissue. More sensitive and specific in diagnosis
for hypothyroidism and hyperthyroidism.
• ↑seen in hyperthyroidism, congenital thyroid disease of grow in

quantity of binding globulin, thyroid hormone insensitivity syndrome,

Other diseases (primary biliary cirrhosis, severe liver or renal

diseases, severe infection, heart failure) , pregnancy, acyeterion or

estrogen intake.

• ↓ seen in hypothyroidism, iodine lack goiter, chronic lymphocytic

thyroiditis, low TBG level, other diseases (course of treatment for

hyperthyroidism, some cancers, heart failure.)

• Hypothyroidism: rT3 ↓, FT4 ↓, TT4 ↓ , TT3 and FT3 could
be normal.
• Hyperthyroidism: rT3 ↑ ↑ , FT3 ↑ ↑, TT3↑ ↑, FT4 ↑ TT4 ↑
• T3 –type hyperthyroidism (overactive thyroid adenoma,
multiple nodular enlargement of thyroid gland) : FT3 ↑ ↑,
TT3↑ ↑, FT4 andTT4 normal.
• Evaluation of thyroxine replacement treatment : normal
rT3 , FT3, TT3 indicate appropriate quantity. If rT3 , FT3,
TT3 ↑ indicate overtreatment.
• Evaluation of anti-thyroid treatment :If rT3 ,FT4 ,TT4 ↓
indicate overtreatment.
 Thyroid relevant protein and autoantibody

• TG, thyroglobulin
• Synthetized in thyroid, combined with thyroxine for
storage.
• Mainly used to be a symbol for differentiating thyroid
carninoma (↑ ↑)from in thyroid adenoma, subacute
thyroiditis, hishimoto thyroiditis, Graves’ disease (↑)
 Thyroid relevant protein and autoantibody

• TBG, thyroxine binding globulin

• In serum, for thyroxine’s tranportation. TT4 and TT3 easily
influenced by the quantity of TBG.
• Clinical significance: to evaluate the discrepancy
between TSH or clinical symptom with T3, T4
concentration.
- T4/ TBG could eliminate TBG’s influence.
- The ratio 3.1-4.5, indicate thyroid function normal.
- The ratio 0.2-2.0, Hypothyroidism should be considered.
- The ratio 7.6-14.8, hyperthyroidism should be
considered.
 Thyroid relevant protein and autoantibody

• TPOAb, thyroid peroxidase antibody

- TPO exists in thyroid, and play role in thyroxine
synthesis.
- ↑ seen in 90% chronic Hishimoto thyroiditis, 70%
Graves’ disease. Also seen in type I DM.
• TGAb, thyroglobulin antibody
- Antibody to TG.
- ↑ seen in 60-70% chronic Hishimoto thyroidtis and
primary myxoedema, 20-40% Graves’ disease.
 Thyroid relevant protein and autoantibody

• Thyrotropin receptor antibody, TRAb

- Antibody to TSH receptor on the thyroid cell membrane.
Once binding to TSH receptor, could induce Graves’
disease. Could be seen in 95% Graves’ disease
patients.
- Clinical significance:
- Diagnosis for Graves’ disease and evaluating prognosis
of Graves’ disease.
 Outline
• Laboratory diagnosis for endocrine diseases
- Pituitary hormone
- Thyroid hormone
- Adrenal hormone
- sex hormone
- Lab diagnosis for common endocrine diseases
• Laboratory diagnosis for hypersensitivity
- Categories of hypersensitivity
- Laboratory diagnosis for common hypersensitivity diseases
 Detection for adrenal hormone

glomerulosa Mineralocorticoid(Aldo
sterone)
fasciculate Glucocorticoid
Adrenal cortex
(cortisol)
reticulary sex hormone, minor
cortisol
Adrenal medulla pheochromocyte Noradrenaline (90%)
Adrenaline (10%)

Adrenal cortex hormone was released in daily rhythmicity.

 Detection for adrenal cortex hormone

• Aldosterone, ALD
• Mineralocorticoid, secreted by adrenal glomerulosa.
Released in daily rhythmicity and influenced by body’s
position.
• Function: to act on the distal convoluted tubule, maintain
homeostasis (preserve sodium and eject potassium).
• Primary aldosteronism: caused by adrenal cortex
hyperplasia or tumor.
• Secondary aldosteronism: caused by effective blood
volume decrease, renal blood volume decrease, e.g
heart failure, nephrotic syndrome, hypertension, ascites
due to cirrhosis, long term low sodium diet.
 Detection for adrenal cortex hormone
• ↑ seen in aldosteronism: primary aldosteronism
(most>500pmol/L), secondary aldosteronism
(most>1000pmol/L).
• ↓ seen in adrenal insufficiency, hypophyseal
insufficiency, high sodium diet…
 Detection for adrenal cortex hormone

• Cortisol
• Urine 17-hydroxysteroid (17-OH)
• Urine 17-ketosteroid (17-KS)
 Detection for adrenal cortex hormone
• Cortisol:
- Glucocorticoid, secreted by adrenal fasciculate and reticulary, in
daily rhythmicity.
- 90% cortisol binding with CBG (cortisol binding globulin), 5%-10%
free cortisol will be discharged in urine.
• Detection tests:
- Serum cortisol: 8am (Cmax), 2am (Cmin)
- 24h urine free cortisol (24hUFC): stable concentration, not be
influenced by daily rhythmicity.
- Serum cortisol and 24hUFC: first screening tests for dysfunction of
adrenal cortex.
 Detection for adrenal cortex hormone

• Clinical significance:
- ↑ (Serum cortisol and 24hUFC) seen in adrenal hyperfunction,
bilateral adrenal hyperplasia or tumor, ectopic ACTH secretion, and
the increase lose daily rhythmicity.
- ↓ (Serum cortisol and 24hUFC) seen in adrenal hypofunction,
anterior pituitary hypofunction, but the decrease maintain daily
rhythmicity.
 Detection for adrenal cortex hormone
• Urine 17-hydroxysteroid (17-OH)
- the metabolite of adrenal cortisol.
- Total level in 24h reflects the change of cortisol.
- ↑ seen in adrenal hyperfunction, e.g. Cushing syndrome,
ectopic ACTH secretion, primary adrenal tumor.
- ↓seen in primary hypofunction, e.g. Addison’s disease,
anterior pituitary hypofunction…
 Detection for adrenal cortex hormone

• urine 17-ketosteroid (17-KS),

- The metabolite of androgen.
- Female and kids: from adrenal cortex.
- Male: 17-KS (2/3) from adrenal cortex. 1/3 from testis.
- ↑ seen in adrenal hyperfunction, e.g. Cushing syndrome,
ectopic ACTH secretion, primary adrenal tumor.
- ↓seen in primary hypofunction, e.g. Addison’s disease,
anterior pituitary hypofunction…
 Detection for adrenal medullary hormone

• 24h Urine Catecholamine (CA)

- Comprised of noradrenaline, adrenaline, dopamine
- Reflect adrenal medullary function and excitability of sympathetic
nerve.
• Clinical significance
- ↑seen in pheochromocytoma, adrenal medullary hyperplasia…
- ↓seen in Addison’s disease
• 24h Urine vanillylmandelic acid (VMA)
- Metabolite of CA
- Clinical significance
Similar to CA
 Outline
• Laboratory diagnosis for endocrine diseases
- Pituitary hormone
- Thyroid hormone
- Adrenal hormone
- sex hormone
- Lab diagnosis for common endocrine diseases
• Laboratory diagnosis for hypersensitivity
- Categories of hypersensitivity
- Laboratory diagnosis for common hypersensitivity diseases
 Detection for sex hormone
• Progesterone
• Estrogen: estradiol, E2
• Androgen: testosterone
• Human chorionic gonadotropin, hCG
 Detection for sex hormone

• Progesterone
LH
• Clinical significance
- To evaluate placenta’s function, FSH

corpus luteum’s function, to detect

Follicular development
ovulatory period.
Estrogen
- ↑physiologic indicate ovulation.
↑pathologic seen in corpus luteum progesterone
tumor, ovarian cyst, ..
- ↓pathologic seen in pituitary function
endometrium
failure, ovarian function failure, luteal
insufficiency, placenta dysplasia,
foetus death.
 Detection for sex hormone
• Estradiol, E2
• Secreted by testis, ovary and placenta, change with age and
menstrual cycle.
• Function: to promote female sex organ’s development, maintain
normal secondary sex characteristics, and influence body’s
metabolism.
• ↑Female sexual precocity, male feminization, ovary tumor, pituitary
tumor. Also seen in pregnancy, cirrhosis.
• ↓seen in primary and secondary sex gland hypofunction.
 Detection for sex hormone

• Testosterone
• The most important male androgen. Secreted by testis in
daily rhythmicity. (peak time 8am)
• ↑male sexual precosity, congenital adrenal hyperplasia,
Adrenal cortical hyperfunction, Polycystic ovary
syndrome,
• ↓ primary small testopathy (klinefelter), testicular
development disorder, male Turner’s syndrome.
 Detection for sex hormone
• Human chorionic gonadotropin, hCG
• One glycoprotein hormone produced by placental villi
tissue.
• Normal range: female: <=4U/L, male <=3U/L
• For diagnosis in pregnancy:
- 1w after pregnancy(menelipsis). hCG will increase one times every
two days.
- In the early 3 months, abnormal increase indicate Choriocarcinoma,
Hydatidiform mole, Multiple pregnancy.
- If decrease in early 3 months, indicate abortion, foetus death,
ectopic pregnancy.
• For diagnosis of other diseases:
- In non-pregnant female, increase seen in the tumors of germ cells,
ovary, bladder, pancreas, stomach, lung, liver, et al.
 Outline
• Laboratory diagnosis for endocrine diseases
- Pituitary hormone
- Thyroid hormone
- Adrenal hormone
- sex hormone
- Lab diagnosis for common endocrine diseases
• Laboratory diagnosis for hypersensitivity
- Categories of hypersensitivity
- Laboratory diagnosis for common hypersensitivity diseases
 Application of diagnostic test on common
endocrine diseases

• Dysfunction of GH
• Dysfunction of thyroid
• Cushing’s syndrome
• Adrenal insufficiency
 Application of diagnostic test on common
endocrine diseases -Dysfunction of GH

• Growth retardation
- ↓ IGF-1, 96% sensitivity, 54% specificity.
- ↓ IGFBP-3, 97% sensitivity, 95% specificity.
• Acromegaly or Pituitary gigantism
- ↑ IGF-I
- ↑ IGFBP-3
 Application of diagnostic test on common
endocrine diseases- Dysfunction of thyroid

• Hyperthyroidism
- Caused by Graves’ disease (85%), Nodular goiter with hyperthyroidism,
Subacute thyroiditis with hyperthyroidism.
• Hypothyroidism
- Primary hypothyroidism: caused by chronic thyroiditis, middle or late
period of subacute thyroiditis, Thyroid resection, anti-thyroid drug
treatment, Iodine deficiency
- Secondary hypothyroidism: TRH and (or) TSH release deficiency from
hypothalamus or pituitary damage caused by tumor, operation,
radiotherapy
 Clinical suspicion of hyperthyroidism

Determination of serum TSH,FT3, FT4

TSH ↓ TSH ↓ TSH ↑or normal

All normal
FT3, FT4 normal FT3, FT4 ↑ FT3, FT4 ↑

Iodine uptake Iodine uptake

ratio ↑ ratio ↑
TRAb(-) TRAb(+)
Excluding
hyperthyroidism
Pituitary TSH-
Subclinical secreting tumors,
hyperthyroidism
ectopic TSH-
Subacute Graves secreting
thyroiditis, thyroid syndrome,
carcinoma, disease Refetoff
postpartum syndrome
thyroiditis, struma
ovarii, iatrogenic
hyperthyroidism

Fig. laboratory diagnostic strategy for hyperthyroidism

 Clinical suspicion of hypothyroidism

Determination of serum TSH,FT3, FT4

TSH ↓or normal, FT4 ↓ TSH ↑, FT4 ↓ TSH ↑, FT4 normal

Investigation of Primary
pituitary and hypothyroidism
adrenal function

Primary
Secondary Determinations of subclinical
hypothyroidism autoantibodies hypothyroidism

negative positive

Other etiology Hashimoto’s

thyroiditis

Fig. laboratory diagnostic strategy for hypothyroidism

 Application of diagnostic test on common endocrine
diseases- Cushing’s syndrome

• Also called hypercortisolism

• Clinical manifestation: moon face, acne, central obesity, hypertension,
osteoporosis.
• Etiology: hypothalamus or pituitary causes (Cushing disease, 70%),
adrenal hyperplasia or tumor(15%), ectopic secretion (CRH or ACTH,15%
)
• Diagnosis for Cushing’s syndrome
- 24h urine free cortisol (24hUFC):
<100ug (excluding Cushing’s syndrome)
>120ug (support diagnosis of Cushing’s syndrome, accuracy>90% )
- Daily rhythmicity: no obvious difference between at 8am and 8pm.
• Diagnosis for the causes of Cushing’s syndrome
- Serum ACTH detection:
adrenal tumor (↓ ↓), Cushing’s disease (↑ or normal), ACTH
secreting tumor(↑ ↑ )
- High dose dexamethasone suppression test
Method: Patients take dexamethasone at midnight, detect the serum
cortisol at 8am.
↓ ↓cortisol, indicates secretion suppression: Cushing’s disease
no secretion suppression: adrenal tumor, ectopic ACTH secretion,
large adrenal nodular hyperplasia
- CRH stimulating test
↑ ↑cortisol, reactivity, 90% Cushing’s disease
no reactivity, adrenal tumor, most ectopic ACTH secretion
 Differential diagnosis for Cushing syndrome
Cushing Adrenal Adrenal cortical Ectopic ACTH
disease cortical carcinoma syndrome
adenoma
Serum and urine ↑ ↑ ↑↑ ↑↑↑
cortisol
24h Urine 17-OH ↑↑ ↑↑ ↑↑↑ ↑↑↑↑

24h Urine 17-KS ↑↑ ↑ or normal ↑↑↑ ↑↑↑

High dose Most could Couldn’t be Couldn’t be Most couldn’t

dexamethason be suppressed suppressed be suppressed
e suppression suppressed
test
Serum ACTH Morning: ↓ ↓ ↑↑↑
minor↑
Evening: no
apparent
decrease
CRH stimulating Normal or No reaction No reaction No reaction,
test overreaction minor reaction

ACTH reaction Half reaction, Most no reaction reaction

stimulating test (higher than half no
normal) reaction
 Application of diagnostic test on common
endocrine diseases-adrenal insufficiency
• Primary adrenal insufficiency (Addison’s disease)
Adrenal pathology lead to secretion deficiency and feedback serum
ACTH ↑
• Secondary adrenal insufficiency: hypothalamus or pituitary damage
ACTH ↓
• Diagnostic tests:
- ACTH and serum cortisol detection:
primary disease: basic ACTH(↑)>150ng/L, cortisol<100ug/L
secondary disease: ACTH normal or ↓
- Urine 17-OH, 17-KS : ↓or normal
- Rapid ACTH stimulation test:
method: cortrosyn (artificial ACTH-like substance) i.v. 45min later,
detecting serum cortisol.
result: >=200ug/L normal
<200ug/L indicate dysfunction of pituitary adrenal axis
 Diagnosis of hypersensitivity diseases
• Summay of four types of hypersensitivity
According to speed, mechanism, clinical characteristics,
hypersensitivity could be divided into four types.
Type mechanism Disease

I IgE antibody 1. Occur and disappear Systemic: drug allergic

mediated, no immediately.(also called shock(penicillin), serum
complement immediate hypersensitivity allergic shock.
participation reaction) 2. Lead to Local: allergy in respiratory
physiologic dysfunction, tract, gastrointestinal tract,
seldom lead to severe tissue skin.
damage. 3. Apparent
individual difference and
genetic background
II IgM or IgG antibody Lead to cell lysis or tissue Tranfusion reaction,
binding to the damage hemolytic
antigen on target Commenly no genetic disease of newborn,
cell’s surface. background. autoimmune hemolytic
Complement, NK
cell, and anemia, Drug allergic
macrophage hypocytosis, Good pasture
involved. syndrome, Graves’
disease,
Type mechanism Disease
III Soluble immune Lead to local Local immune complex
complex deposite inflammation and tissue diseases: Arthus
on local or damage(local Congestion reaction, Arthus-like
systemic capillary and edema, necrosis, reaction.
basement infiltration of neutrophils ) Systemic immune
membrane, complex diseases: SLE,
activate Rheumatoid arthritis,
complement. Post streptococcal
Neutrophils, glomerulonephritis
basophilic cell,
platelet involved.
IV Effective T cell Also called delayed type Infectious DTH: TB,
binding to specific hypersensitivity virus
antigen, lead to reaction,DTH Contact dermatitis: after
mononuclear cell contacting Small
infiltration and molecular hapten, e.g
tissue damage Paints, dyes, cosmetics,
drug (penicillin)
 Diagnosis for common hypersensitivity
diseases
• Bronchial asthma
- Chronic allergic inflammation. Its mechanism thought relevant to
exogenous allergen stimulate production of IgE antibody. Type I
hypersensitivity.
• Diagnosis:
• Prick test
- Gold standard for allergy diagnosis. To identify IgE-mediated
reaction (type I), such as inhalant allergy, food allergy.
- To place allergen and control(+ve and -ve)
on the skin (Inside of the forearm)
- Pierced using needle
- To see the result 15min later.
- Positive: at least 2mm greater than –ve
Control.
• allergic shock
• Common causes: drug(penicillin, streptomycin, procaine), serum
• Diagnosis test
- Intradermermal test:
- Inject the allergen (0.01-0.02ml) into intracutaneous (Inside of the
forearm)
- To see the results 15-25min later.
- Positive: local blush, erythema, wheal,
sense tingles. Or systemic reaction.
• PPD (purified protein derivative)test:
- method: 0.1ml(0.1mg TB protein), Intradermal injection, observe
whether there would be red, swollen or scleroma 48h later.
if there are scleroma, detect the diameter of scleroma.
- negative: non-response or smaller than control.
- Weak positive(+): red and swollen.
- Positive(++) red and swollen with scleroma(0.5-1cm)
• hemolytic disease of newborn (HDN)
• Diagnosis test:
• Rh antibody test
- Normal value: titer <=32
- When titer>=64, if blood group incompatible between
the mother and fetal, the new born baby probably to
suffer HDN.
Thanks