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Test Code GFATS Glial Fibrillary Acidic Protein Alpha Subunit Antibody, Immunofluorescence Titer Assay, Serum


Necessary Information


Provide the following information:

-Relevant clinical information

-Ordering provider name, phone number, mailing address, and e-mail address



Specimen Required


Only orderable as a reflex. For more information see:  

ENS2 / Encephalopathy, Autoimmune Evaluation Serum 

DMS2 / Dementia, Autoimmune Evaluation, Serum 

EPS2 / Epilepsy, Autoimmune Evaluation, Serum 

MAS1 / Autoimmune Myelopathy Evaluation, Serum


Useful For

Reporting an end titer result in serum specimens

 

Distinguishing autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy from infectious meningoencephalitis and idiopathic inflammatory central nervous system (CNS) disorders such as multiple sclerosis, vasculitis and sarcoidosis, disorders commonly considered in the differential diagnosis

 

Alerting the clinician that the patient has an immune-mediated, steroid-responsive disorder and to search for a malignancy

Testing Algorithm

If immunofluorescence assay (IFA) pattern suggests GFAP, then GFAP IFA titer and GFAP cell-binding assay (CBA) are performed at an additional charge.

Method Name

Only orderable as a reflex. For more information see:

ENS2 / Encephalopathy, Autoimmune Evaluation Serum

DMS2 / Dementia, Autoimmune Evaluation, Serum

EPS2 / Epilepsy, Autoimmune Evaluation, Serum

MAS1 / Autoimmune Myelopathy Evaluation, Serum

 

Indirect Immunofluorescence Assay (IFA)

Reporting Name

GFAP IFA Titer, S

Specimen Type

Serum

Specimen Minimum Volume

1 mL

Specimen Stability Information

Specimen Type Temperature Time Special Container
Serum Refrigerated (preferred) 28 days
  Frozen  28 days
  Ambient  72 hours

Reject Due To

Gross hemolysis Reject
Gross lipemia Reject
Gross icterus Reject

Clinical Information

Antibody targeting glial fibrillary acidic protein (GFAP)-IgG is a biomarker of a subacute and progressive autoimmune meningitis, encephalitis, and myelitis that can mimic multiple sclerosis (MS) or other idiopathic inflammatory central nervous system (CNS) disorders such as sarcoidosis. Neurological manifestations include headache, optic neuropathy, transverse myelitis, cognitive decline, and cerebellar ataxia. Cerebrospinal fluid (CSF) is inflammatory. Cranial magnetic resonance (MR) imaging reveals linear perivascular enhancement oriented radially to ventricles. A paraneoplastic neurological context is common. Reported neoplasms accompanying neurological symptoms include adenocarcinomas (prostate and gastroesophageal), myeloma, melanoma, colonic carcinoid, parotid pleomorphic adenoma, and teratoma. If GFAP-IgG is detected by immunofluorescence assay (IFA), it is reflexed to a test for the alpha isoform of GFAP (GFAPalpha-IgG) by cell based assay.

Reference Values

Only orderable as a reflex. For more information see:

ENS2 / Encephalopathy, Autoimmune Evaluation Serum

DMS2 / Dementia, Autoimmune Evaluation, Serum

EPS2 / Epilepsy, Autoimmune Evaluation, Serum

MAS1 / Autoimmune Myelopathy Evaluation, Serum

 

<1:240

Interpretation

Seropositivity for autoantibody (positive) is supportive of autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy, a treatable form of meningoencephalomyelitis. A paraneoplastic basis should be considered, according to age, sex, and other risk factors.

 

Patients who are GFAP-IgG positive have increased risk of tumor. GFAP-IgG increases the likelihood of certain malignancies being found within 2 years of symptom onset (34%). The most common malignancy found is ovarian teratoma (22%).

 

GFAP meningoencephalomyelitis is immunotherapy-responsive. GFAP-IgG positive patients have better outcomes after treatment with corticosteroids.

 

The presence of GFAP-IgG alerts the clinician that the patient has an immune-mediated, steroid-responsive disorder and directs patient care accordingly. It also alerts the clinician to search for a malignancy.

Clinical Reference

1. Fang B, McKeon A, Hinson SR, et al: Autoimmune glial fibrillary acidic protein astrocytopathy: a novel meningoencephalomyelitis. JAMA Neurol 2016;73:1297-1307

2. Flanagan EP, Hinson SR, Lennon VA, et al: Glial fibrillary acidic protein immunoglobulin G as biomarker of autoimmune astrocytopathy: Analysis of 102 patients. Ann Neurol 2017;81:298-309

3. Iorio R, Damato V, Evoli A, et al:Clinical and Immunological characteristics of the spectrum of GFAP autoimmunity: a case series of 22 patients. J Neurol Neurosurg Psychiatry 2018 Feb;89(2):138-146 doi:10.1136/jnnp-2017-316583

Method Description

The patient's sample is tested by a standardized indirect immunofluorescence assay (IFA) that uses a composite frozen section of mouse cerebellum, kidney, and gut tissues. After incubation with sample and washing, fluorescein-conjugated goat antihuman IgG is applied. Neuron-specific autoantibodies are identified by their characteristic fluorescence staining patterns. Samples that are scored positive for any neuronal nuclear or cytoplasmic autoantibody are titrated to an endpoint. Interference by coexisting non-neuron-specific autoantibodies can usually be eliminated by serologic absorption.(Yu Z, Kryzer TJ, Griesmann GE, et al: CRMP-5 neuronal autoantibody: marker of lung cancer and thymoma-related autoimmunity. Ann Neurol 2001;49:146-154)

Day(s) Performed

Monday through Sunday

Report Available

10 days

Specimen Retention Time

28 days

Performing Laboratory

Mayo Clinic Laboratories in Rochester

Test Classification

This test was developed and its performance characteristics determined by Mayo Clinic in a manner consistent with CLIA requirements. It has not been cleared or approved by the US Food and Drug Administration.

CPT Code Information

86256

LOINC Code Information

Test ID Test Order Name Order LOINC Value
GFATS GFAP IFA Titer, S 93423-2

 

Result ID Test Result Name Result LOINC Value
605133 GFAP IFA Titer, S 93423-2

NY State Approved

Yes