MOLECULAR STUDY EARLY INFANTILE EPILEPTIC ENCEPHALOPATHY (SCN2A) SEQUENCING, WHOLE BLOOD

New Test in CIC Catalog

Test Code: 4069

Sample:	Whole blood - EDTA (5 ml)
Conservation:	Refrigerated
Method:	Sequencing Method
Set Up Days:	Daily
Plazo de Entrega:	60 days
Information:
Early infantile epileptic encephalopathy (EIEE) or Ohtahara syndrome is the earliest form of age-dependent encephalopathies, which include also West syndrome and Lennox-Gastaut syndrome. This rare syndrome is characterized by a very early onset, during the first months of life, with frequent tonic spasms and a suppression-burst pattern on electroencephalogram. Partial motor seizures may occur. Brain imaging usually discloses gross structural abnormalities in the majority of cases. Metabolic disorders were present in a few cases. The course is severe with early death or marked psychomotor retardation and intractable seizures with frequent evolution to West syndrome.
Links:
OMIM Entry - # 613721 - EPILEPTIC ENCEPHALOPATHY, EARLY INFANTILE, 11; EIEE11
Orphanet- Early infantile epileptic encephalopathy
OMIM Entry - - 182390 - SODIUM CHANNEL, VOLTAGE-GATED, TYPE II, ALPHA SUBUNIT; SCN2A

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FLUOXETINE AND DESMETHLYFLUOXETINE, SERUM

Modification Units and Reference values

Test code: 3177

PREVIOUS Units and Reference values	CURRENT  Units and Reference values
* FLUOXETINE:    Therapeutic level: 0.04 - 0.80 mg/L  * NORFLUOXETIN:    Therapeutic level: 0.15 - 0.50 mg/L	* FLUOXETINE:    Therapeutic level: 100 - 400 µg/L   NOTE:Norfluoxetine is an active metabolite, its level is important when: fluoxetine is very low or undetectable ; case of intoxication. When fluoxetine is in the therapeutic zone, the associated level of norfluoxetine confirm a good treatment response.

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MOLECULAR STUDY - MDR1 GENE EXPRESSION, WHOLE BLOOD

Erased test in CIC Catalog

Test Code: 7080

Discontinued for technical reason and decrease in demand.(Discontinued in: 02/10/2012)

HORMONAL STUDY, SALIVE

Erased test in CIC Catalog

Test Code: 3978

Discontinued for technical reason and decrease in demand.(Discontinued in: 03/07/2012)

IgG4 SPECIFIC ANTIBODIES FOR (Gm25) ASPERGILLUS VERSICOLOR

Erased test in CIC Catalog

Test Code: 3778

Discontinued for technical reasons due to low clinical significance of test results and the consequent decrease in demand.(Discontinued in: 26/04/2012)

OLANZAPINE, SERUM

Erased test in CIC Catalog

Test Code: 3596

Discontinued for technical reason and decrease in demand.(Discontinued in: 03/05/2012)

GALACTOSE, URINE

Erased test in CIC Catalog

Test Code: 3550

Discontinued for technical reason and decrease in demand.(Discontinued in: 05/06/2012)

IgE SPECIFIC ANTIBODIES FOR CANARY (Seric Proteins) (E199), SERUM

Erased test in CIC Catalog

Test Code: 3476

Discontinued for technical reasons due to low clinical significance of test results and the consequent decrease in demand.(Discontinued in: 21/05/2012)

IgG SPECIFIC ANTIBODIES FOR CANARY (Seric Proteins) (E199), SERUM

Erased test in CIC Catalog

Test Code: 1792

Discontinued for technical reasons due to low clinical significance of test results and the consequent decrease in demand.(Discontinued in: 08/05/2012)

MENINGOCOCCAL- BACTERIOSTATIC/BACTERICIDAL ACTIVITY , SERUM

Erased test in CIC Catalog

Test Code: 1906

Discontinued for technical reason and decrease in demand.(Discontinued in: 11/06/2012)

TIAGABINE (GABITRIL), SERUM

Erased test in CIC Catalog

Test Code: 1339

Discontinued for technical reasons due to low clinical significance of test results and the consequent decrease in demand.(Discontinued in: 09/07/2012)

MOLECULAR STUDY - MUTATION GEN BRCA 1 AND BRCA 2 (SCREENING 6 MUTATIONS), WHOLE BLOOD

New Test in CIC Catalog

Test Code: 4068

Sample:	Whole blood - EDTA (5 ml)
Conservation:	Refrigerated
Method:	Sequencing Method
Set Up Days:	Daily
Plazo de Entrega:	25 days

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BREATH TEST FOR HELICOBACTER PYLORI (UREA C-13)

Modification Reference values

Test code: 2454

PREVIOUS Reference values	CURRENT  Reference values
Negative : Index Less  than    2.0 Grey zone: Index between 2.0 - 4.0 Positive : Index Greater than  4.0	Negative : Index Less  than    2.0 Grey zone: Index between 2.0 - 3.5 Positive : Index Greater than  3.5

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MOLECULAR STUDY DEFICIENCY KALLMAN SYNDROME TYPE 6 (FGF8) SECUENCING, WHOLE BLOOD

New Test in CIC Catalog

Test Code: 4067

Sample:	Whole blood - EDTA (5 ml)
Conservation:	Refrigerated
Method:	Sequencing Method
Set Up Days:	Daily
Plazo de Entrega:	30 days
Information:
Kallmann syndrome (KS) is a congenital genetic disorder characterized by the association of hypogonadotropic hypogonadism (HH) due to gonadotropin-releasing hormone (GnRH) deficiency, and anosmia or hyposmia (with hypoplasia or aplasia of the olfactory bulbs). The prevalence is reported at 1/8,000 males and 1/40,000 females, but may be underestimated. Most cases are diagnosed at the time of puberty due to lack of sexual development, but KS may also be suspected in infancy in males with cryptorchidism and micropenis. The main clinical features consist of the absence of spontaneous puberty and a partial or total loss of the sense of smell (anosmia) in both sexes. Other possible signs include mirror movements of the upper limbs (bimanual synkinesis), unilateral (occasionally bilateral and lethal) renal aplasia, cleft lip or palate, dental agenesis, and hearing impairment. KS is caused by impaired development of the olfactory system and disrupted embryonic migration of the GnRH-synthesizing neurons from the olfactory epithelium to the hypothalamic region of the brain. The majority of reported cases were sporadic. Three modes of inheritance have been described in familial forms: X-linked recessive, autosomal dominant (with incomplete penetrance) and, more rarely, autosomal recessive. However, in an undetermined proportion of the patients, transmission may be digenic or oligogenic. To date, five causative genes have been identified: KAL1 (Xp22.3), responsible for the X-linked form, and FGFR1 (8p12) FGF8 (10q24), PROKR2(20p13), and PROK2 (3p21.1), which are involved in the autosomal forms. Other genes involved in KS remain to be discovered as mutations in the genes identified so far are detected in less than 30% of the patients. Diagnostic methods consist of hormone evaluation (sex hormone dosage and GnRH stimulation tests), as well as qualitative and quantitative evaluation of the sense of smell (olfactometry). Morphological analysis of the olfactory bulbs by magnetic resonance imaging (MRI) can be useful (especially in young children, whose sense of smell is difficult to evaluate). Differential diagnoses include isolated GnRH deficiency (normosmic idiopathic hypogonadotropic hypogonadism) and CHARGE syndrome, which combines KS with various additional developmental anomalies. Genetic counseling should be adapted to each family, taking into account the wide variability in clinical expression, even within the same family, as well as the possibility, in sporadic cases, of an FGFR1 neomutation. Hormonal replacement therapy is used to induce puberty, and later, fertility. There is no current treatment available for anosmia. With treatment, onset of puberty occurs in all cases, and fertility is achieved in most cases.
Links:
OMIM Entry - # 612702 - HYPOGONADOTROPIC HYPOGONADISM 6 WITH OR WITHOUT ANOSMIA; HH6
Orphanet- Kallmann syndrome
OMIM Entry - - 600483 - FIBROBLAST GROWTH FACTOR 8; FGF8

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MOLECULAR STUDY DEFICIENCY KALLMAN SYNDROME TYPE 5 (CDH7) SECUENCING, WHOLE BLOOD

New Test in CIC Catalog

Test Code: 4066

Sample:	Whole blood - EDTA (5 ml)
Conservation:	Refrigerated
Method:	Sequencing Method
Set Up Days:	Daily
Plazo de Entrega:	55 days
Information:
Kallmann syndrome (KS) is a congenital genetic disorder characterized by the association of hypogonadotropic hypogonadism (HH) due to gonadotropin-releasing hormone (GnRH) deficiency, and anosmia or hyposmia (with hypoplasia or aplasia of the olfactory bulbs). The prevalence is reported at 1/8,000 males and 1/40,000 females, but may be underestimated. Most cases are diagnosed at the time of puberty due to lack of sexual development, but KS may also be suspected in infancy in males with cryptorchidism and micropenis. The main clinical features consist of the absence of spontaneous puberty and a partial or total loss of the sense of smell (anosmia) in both sexes. Other possible signs include mirror movements of the upper limbs (bimanual synkinesis), unilateral (occasionally bilateral and lethal) renal aplasia, cleft lip or palate, dental agenesis, and hearing impairment. KS is caused by impaired development of the olfactory system and disrupted embryonic migration of the GnRH-synthesizing neurons from the olfactory epithelium to the hypothalamic region of the brain. The majority of reported cases were sporadic. Three modes of inheritance have been described in familial forms: X-linked recessive, autosomal dominant (with incomplete penetrance) and, more rarely, autosomal recessive. However, in an undetermined proportion of the patients, transmission may be digenic or oligogenic. To date, five causative genes have been identified: KAL1 (Xp22.3), responsible for the X-linked form, and FGFR1 (8p12) FGF8 (10q24), PROKR2(20p13), and PROK2 (3p21.1), which are involved in the autosomal forms. Other genes involved in KS remain to be discovered as mutations in the genes identified so far are detected in less than 30% of the patients. Diagnostic methods consist of hormone evaluation (sex hormone dosage and GnRH stimulation tests), as well as qualitative and quantitative evaluation of the sense of smell (olfactometry). Morphological analysis of the olfactory bulbs by magnetic resonance imaging (MRI) can be useful (especially in young children, whose sense of smell is difficult to evaluate). Differential diagnoses include isolated GnRH deficiency (normosmic idiopathic hypogonadotropic hypogonadism) and CHARGE syndrome, which combines KS with various additional developmental anomalies. Genetic counseling should be adapted to each family, taking into account the wide variability in clinical expression, even within the same family, as well as the possibility, in sporadic cases, of an FGFR1 neomutation. Hormonal replacement therapy is used to induce puberty, and later, fertility. There is no current treatment available for anosmia. With treatment, onset of puberty occurs in all cases, and fertility is achieved in most cases.
Links:
OMIM Entry - # 612370 - HYPOGONADOTROPIC HYPOGONADISM 5 WITH OR WITHOUT ANOSMIA; HH5
Orphanet- Kallmann syndrome
OMIM Entry - - 608892 - CHROMODOMAIN HELICASE DNA-BINDING PROTEIN 7; CHD7

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MOLECULAR STUDY DEFICIENCY KALLMAN SYNDROME TYPE 3 AND 4 (PROKR2,PROK2) SECUENCING, WHOLE BLOOD

New Test in CIC Catalog

Test Code: 4065

Sample:	Whole blood - EDTA (5 ml)
Conservation:	Refrigerated
Method:	Sequencing Method
Set Up Days:	Daily
Plazo de Entrega:	30 days
Information:
Kallmann syndrome (KS) is a congenital genetic disorder characterized by the association of hypogonadotropic hypogonadism (HH) due to gonadotropin-releasing hormone (GnRH) deficiency, and anosmia or hyposmia (with hypoplasia or aplasia of the olfactory bulbs). The prevalence is reported at 1/8,000 males and 1/40,000 females, but may be underestimated. Most cases are diagnosed at the time of puberty due to lack of sexual development, but KS may also be suspected in infancy in males with cryptorchidism and micropenis. The main clinical features consist of the absence of spontaneous puberty and a partial or total loss of the sense of smell (anosmia) in both sexes. Other possible signs include mirror movements of the upper limbs (bimanual synkinesis), unilateral (occasionally bilateral and lethal) renal aplasia, cleft lip or palate, dental agenesis, and hearing impairment. KS is caused by impaired development of the olfactory system and disrupted embryonic migration of the GnRH-synthesizing neurons from the olfactory epithelium to the hypothalamic region of the brain. The majority of reported cases were sporadic. Three modes of inheritance have been described in familial forms: X-linked recessive, autosomal dominant (with incomplete penetrance) and, more rarely, autosomal recessive. However, in an undetermined proportion of the patients, transmission may be digenic or oligogenic. To date, five causative genes have been identified: KAL1 (Xp22.3), responsible for the X-linked form, and FGFR1 (8p12) FGF8 (10q24), PROKR2(20p13), and PROK2 (3p21.1), which are involved in the autosomal forms. Other genes involved in KS remain to be discovered as mutations in the genes identified so far are detected in less than 30% of the patients. Diagnostic methods consist of hormone evaluation (sex hormone dosage and GnRH stimulation tests), as well as qualitative and quantitative evaluation of the sense of smell (olfactometry). Morphological analysis of the olfactory bulbs by magnetic resonance imaging (MRI) can be useful (especially in young children, whose sense of smell is difficult to evaluate). Differential diagnoses include isolated GnRH deficiency (normosmic idiopathic hypogonadotropic hypogonadism) and CHARGE syndrome, which combines KS with various additional developmental anomalies. Genetic counseling should be adapted to each family, taking into account the wide variability in clinical expression, even within the same family, as well as the possibility, in sporadic cases, of an FGFR1 neomutation. Hormonal replacement therapy is used to induce puberty, and later, fertility. There is no current treatment available for anosmia. With treatment, onset of puberty occurs in all cases, and fertility is achieved in most cases.
Links:
OMIM Entry - # 244200 - HYPOGONADOTROPIC HYPOGONADISM 3 WITH OR WITHOUT ANOSMIA; HH3
OMIM Entry - # 610628 - HYPOGONADOTROPIC HYPOGONADISM 4 WITH OR WITHOUT ANOSMIA; HH4
Orphanet- Kallmann syndrome
OMIM Entry - - 607002 - PROKINETICIN 2; PROK2
OMIM Entry - - 607123 - PROKINETICIN RECEPTOR 2; PROKR2

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MOLECULAR STUDY DEFICIENCY KALLMAN SYNDROME TYPE 2 (FGFR1) SECUENCING, WHOLE BLOOD

New Test in CIC Catalog

Test Code: 4064

Sample:	Whole blood - EDTA (5 ml)
Conservation:	Refrigerated
Method:	Sequencing Method
Set Up Days:	Daily
Plazo de Entrega:	40 days
Information:
Kallmann syndrome (KS) is a congenital genetic disorder characterized by the association of hypogonadotropic hypogonadism (HH) due to gonadotropin-releasing hormone (GnRH) deficiency, and anosmia or hyposmia (with hypoplasia or aplasia of the olfactory bulbs). The prevalence is reported at 1/8,000 males and 1/40,000 females, but may be underestimated. Most cases are diagnosed at the time of puberty due to lack of sexual development, but KS may also be suspected in infancy in males with cryptorchidism and micropenis. The main clinical features consist of the absence of spontaneous puberty and a partial or total loss of the sense of smell (anosmia) in both sexes. Other possible signs include mirror movements of the upper limbs (bimanual synkinesis), unilateral (occasionally bilateral and lethal) renal aplasia, cleft lip or palate, dental agenesis, and hearing impairment. KS is caused by impaired development of the olfactory system and disrupted embryonic migration of the GnRH-synthesizing neurons from the olfactory epithelium to the hypothalamic region of the brain. The majority of reported cases were sporadic. Three modes of inheritance have been described in familial forms: X-linked recessive, autosomal dominant (with incomplete penetrance) and, more rarely, autosomal recessive. However, in an undetermined proportion of the patients, transmission may be digenic or oligogenic. To date, five causative genes have been identified: KAL1 (Xp22.3), responsible for the X-linked form, and FGFR1 (8p12) FGF8 (10q24), PROKR2(20p13), and PROK2 (3p21.1), which are involved in the autosomal forms. Other genes involved in KS remain to be discovered as mutations in the genes identified so far are detected in less than 30% of the patients. Diagnostic methods consist of hormone evaluation (sex hormone dosage and GnRH stimulation tests), as well as qualitative and quantitative evaluation of the sense of smell (olfactometry). Morphological analysis of the olfactory bulbs by magnetic resonance imaging (MRI) can be useful (especially in young children, whose sense of smell is difficult to evaluate). Differential diagnoses include isolated GnRH deficiency (normosmic idiopathic hypogonadotropic hypogonadism) and CHARGE syndrome, which combines KS with various additional developmental anomalies. Genetic counseling should be adapted to each family, taking into account the wide variability in clinical expression, even within the same family, as well as the possibility, in sporadic cases, of an FGFR1 neomutation. Hormonal replacement therapy is used to induce puberty, and later, fertility. There is no current treatment available for anosmia. With treatment, onset of puberty occurs in all cases, and fertility is achieved in most cases.
Links:
OMIM Entry - # 147950 - HYPOGONADOTROPIC HYPOGONADISM 2 WITH OR WITHOUT ANOSMIA; HH2
Orphanet- Kallmann syndrome
OMIM Entry - - 136350 - FIBROBLAST GROWTH FACTOR RECEPTOR 1; FGFR1

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MOLECULAR STUDY DEFICIENCY KALLMAN SYNDROME TYPE 1 (KAL1) SECUENCING, WHOLE BLOOD

New Test in CIC Catalog

Test Code: 4063

Sample:	Whole blood - EDTA (5 ml)
Conservation:	Refrigerated
Method:	Sequencing Method
Set Up Days:	Daily
Plazo de Entrega:	40 days
Information:
Kallmann syndrome (KS) is a congenital genetic disorder characterized by the association of hypogonadotropic hypogonadism (HH) due to gonadotropin-releasing hormone (GnRH) deficiency, and anosmia or hyposmia (with hypoplasia or aplasia of the olfactory bulbs). The prevalence is reported at 1/8,000 males and 1/40,000 females, but may be underestimated. Most cases are diagnosed at the time of puberty due to lack of sexual development, but KS may also be suspected in infancy in males with cryptorchidism and micropenis. The main clinical features consist of the absence of spontaneous puberty and a partial or total loss of the sense of smell (anosmia) in both sexes. Other possible signs include mirror movements of the upper limbs (bimanual synkinesis), unilateral (occasionally bilateral and lethal) renal aplasia, cleft lip or palate, dental agenesis, and hearing impairment. KS is caused by impaired development of the olfactory system and disrupted embryonic migration of the GnRH-synthesizing neurons from the olfactory epithelium to the hypothalamic region of the brain. The majority of reported cases were sporadic. Three modes of inheritance have been described in familial forms: X-linked recessive, autosomal dominant (with incomplete penetrance) and, more rarely, autosomal recessive. However, in an undetermined proportion of the patients, transmission may be digenic or oligogenic. To date, five causative genes have been identified: KAL1 (Xp22.3), responsible for the X-linked form, and FGFR1 (8p12) FGF8 (10q24), PROKR2(20p13), and PROK2 (3p21.1), which are involved in the autosomal forms. Other genes involved in KS remain to be discovered as mutations in the genes identified so far are detected in less than 30% of the patients. Diagnostic methods consist of hormone evaluation (sex hormone dosage and GnRH stimulation tests), as well as qualitative and quantitative evaluation of the sense of smell (olfactometry). Morphological analysis of the olfactory bulbs by magnetic resonance imaging (MRI) can be useful (especially in young children, whose sense of smell is difficult to evaluate). Differential diagnoses include isolated GnRH deficiency (normosmic idiopathic hypogonadotropic hypogonadism) and CHARGE syndrome, which combines KS with various additional developmental anomalies. Genetic counseling should be adapted to each family, taking into account the wide variability in clinical expression, even within the same family, as well as the possibility, in sporadic cases, of an FGFR1 neomutation. Hormonal replacement therapy is used to induce puberty, and later, fertility. There is no current treatment available for anosmia. With treatment, onset of puberty occurs in all cases, and fertility is achieved in most cases.
Links:
OMIM Entry - # 308700 - HYPOGONADOTROPIC HYPOGONADISM 1 WITH OR WITHOUT ANOSMIA; HH1
Orphanet- Kallmann syndrome
OMIM Entry - - 300836 - KAL1 GENE; KAL1

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ANTIBODIES ANTI-RNA POLYMERASE-III, SERUM

New Test in CIC Catalog

Test Code: 4060

Sample:	Serum (1 ml)
Conservation:	Refrigerated
Method:	Enzyme Immunoassay (LOINC®: EIA)
Set Up Days:	Daily
Plazo de Entrega:	15 days

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PREGABALIN, SERUM

Modification Units and Reference values

Test code: 1154

PREVIOUS Units and Reference values	CURRENT  Units and Reference values
PEAK CONCENTRATION: 6 - 52 µmol/L (dosing of 100 - 600 mg per day)	2 - 8 mg/L

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INTERLEUKIN 1 ALPHA (IL1 ALPHA) , SERUM

Erased test in CIC Catalog

Test Code: 1144

Discontinued for technical reason and decrease in demand.(Discontinued in: 03/02/2012)

HISTOCOMPATIBILITY LYMPHOCYTE ANTIGEN - DRw52 (HLA-DRw52)

Erased test in CIC Catalog

Test Code: 901

Discontinued for technical reasons (commercial reagents not available) and decrease in demand.(Discontinued in: 04/06/2012)

CHOLESTEROL- FREE, SERUM

Erased test in CIC Catalog

Test Code: 519

Discontinued for technical reason and decrease in demand.(Discontinued in: 19/03/2012)

COCCIDIOIDES INMITIS ANTIBODIES, SERUM

Erased test in CIC Catalog

Test Code: 316

Discontinued for technical reasons due to low clinical significance of test results and the consequent decrease in demand.(Discontinued in: 10/07/2012)

MOLECULAR STUDY TRANSCOBALAMIN DEFICIENCY (TCN2) SEQUENCING, WHOLE BLOOD

New Test in CIC Catalog

Test Code: 4059

Sample:	Whole blood - EDTA (5 ml)
Conservation:	Refrigerated
Method:	Sequencing Method
Set Up Days:	Daily
Plazo de Entrega:	30 days
Information:
Transcobalamin II (TCII) deficiency is an autosomal recessive disease marked by defective intestinal absorption of vitamin B12. Homozygous TCII deficiency causes non-specific symptoms in one- and two-month-old infants (e.g. vomiting, poor growth) and infections due to an immune deficiency (hypogammaglobulinemia). The main symptom is megaloblastic anemia. Serum cobalamins, however, are normal, since the major circulating form, methyl vitamin B12, is bound to another transport protein (transcolabamin I). Specific treatment consists of massive per os or parenteral intake of vitamin B12. Symptoms disappear completely, except when the diagnosis is delayed and neurological signs have become permanent.
Links:
OMIM Entry - # 275350 - TRANSCOBALAMIN II DEFICIENCY
Orphanet- Transcobalamin II deficiency
OMIM Entry - - 613441 - TRANSCOBALAMIN II; TCN2

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HYPOCRETIN-1, CSF

New Test in CIC Catalog

Test Code: 4058

Sample:	CSF (2 ml)
Conservation:	Frozen
Method:	Radioimmunoassay (LOINC®: RIA)
Set Up Days:	Daily
Plazo de Entrega:	30 days

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VENLAFAXINE, SERUM

Modification Reference values 

Test code: 3603

PREVIOUS Reference values	CURRENT   Reference values
30 - 180 µg/L	30 - 180 µg/L LOD(Limit of detetion):        2.5 µg/L    LOQ(Limit of quantification):  5   µg/L

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MEVALONIC ACID, URINE

Modification Reference values 

Test code: 1564

PREVIOUS Reference values	CURRENT   Reference values
0.1 - 11.4 mmol/mol Creat.	0.0 - 11.4 mmol/mol Creat.

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POLIOMAVIRUS BK/JC DNA, WHOLE BLOOD

New Test in CIC Catalog

Test Code: 4057

Sample:	Whole blood - EDTA(2 ml)
Conservation:	Refrigerated
Method:	Real-Time PCR
Set Up Days:	Daily
Plazo de Entrega:	5 days

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IgE SPECIFIC ANTIBODIES FOR CRANBERRY (f341) FOOD, SERUM

New Test in CIC Catalog

Test Code: 4056

Sample:	Serum (1 ml)
Conservation:	Refrigerated
Method:	ImmunoCAP (LOINC®: IMMUNOCAP)
Set Up Days:	Daily
Plazo de Entrega:	6 days

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BONE ALKALINE PHOSPHATASE, SERUM

New Test in CIC Catalog

Test Code: 4055

Sample:	Serum (1 ml)
Conservation:	Refrigerated
Method:	Chemiluminescence (LOINC®: CL)
Set Up Days:	T,,,Th,
Plazo de Entrega:	20 days

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