Normal range: Negative
Comment IgA endoysial antibody is found in untreated coeliac disease. Because it is not seen in any other disease group or in control populations, it is more specific than anti- gliadin antibody. The presece of endomysial antibody is thought to be indicative of damage to the jejunal mucosa and the level decreased with adherence to agluten-free diet
Sample: serum
Normal range: Negative
Comment Autoimmune anti – double stranded DNA antibody levels are usually significantly elevated in active SLE. Specificity for SLE is high and correlates with disease activity and with the occurrence of glomerulonephritis and it is a good marker to monitor the progression (increasing levels) and remission (decreasing levels) of SLE
Sample: serum
Normal range: Negative
Comment: Used to evaluate adrenal insufficiency and Addison’s disease. Serum antibodies to adrenal cortical cells, usually of all three zones, are seen in 60 % of patients with idiopathic Addison’s disease. They are also present in patients with fungal, tuberculous, or metastatic destruction of the adrenals. Antiadrenal antibodies can be present in idiopathic hypoparathyroidism and Hashimoto disease
Sample: serum
Normal range: Negative
Comment: Antibodies against ganglioside are found in various types of peripheral neuropathy. These include Guillain-Barrie’ syndrome, Miller Fisher syndrome (a variant of Guillain-Barrie’ with descending neuropathy). Also seen in Motor neuron disease and chronic inflammatory demyelinating polyneuropathy
:Test profile
:The following antibodies are examined
GM1 : Monosialoganglioside GM1
GM2 : Monosialoganglioside GM2
GM3 : Monosialoganglioside GM3
GD1a : Disialoganglioside GD1a
GD1b : Disialoganglioside GD1b
GT1b : Trisialoganglioside GT1b
GQ1b : Tetrasialoganglioside GQ1b
Clinical significance: Motor neuron disease associated with GM1, up to 70% of cases. Guillain-Barrie‘ syndrome associated with GM1 in up to 30% of cases, and with less frequency to GM3, GD1a, GD1b, GT1b and GQ1b. Sensory neuropathy associated with GD1b. Miller Fisher syndrome (a variant of Guillain-Barrie’ with descending neuropathy) associated with GQ1b in 90% of the cases
Sample: serum
3-7 yrs
8-76 IU/L
8-14 yrs
6-89 IU/L
> 14 yrs
8-52 IU/L
Comment: Results are elevated in sarcoidosis, more often when the disease is active and are of value in assessing the response of sarcoidosis to corticosteroid therapy.
A marked decreased is found in some patients on prednisone. A falling ACE level had been considered a favorable prognostic sign. Rising levels were thought to reflect activity uncontrolled by therapy, but its prognostic value in identification of subjects with progressive disease is limited. It also is used in investigation for Gaucher disease and maybe useful for monitoring noncompliance with ACE inhibitor treatment. ACE is thought to be produced by epithelioid cells and macrophages; elevations are found in a variety of Granulomatous disease
Sample: Serum
:Normal range
Children: 0.1-0.5 ng/mL
Male: 0.6-2.7 ng/mL
Female: 0.5-2.7 ng/mL
Comment: There is diurnal variation. Useful in diagnosis and management of congenital adrenal hyperplasia. Also of value in theinvestigation of hirsutism or virilism in females, when high levels may indicate either an adrenal cortical tumor or hypersecretion of ACTH
Sample: serum
:Normal range
24hr urine: Results are in relation to the volume collected
(Spot urine: < 460 IU/L (< 7.67 mkat/L
Comment: Raised levels parallel serum amylase unless there is renal failure. When the plasma enzyme is bound to a high molecular weight carrier. (macroamyasaemia), urine amylase is normal. Urine amylase may remain elevated for up to 2 wk after an episode of acute pancreatitis and may suggest formation of a pseudocyst
Sample: 24hr urine, spot urine
Normal range: up to 220 u/l
Comment: Useful in diagnosis of acute pancreatitis; desirable to support the clinical significance of elevated serum lipase. Serum amylase is used to work up abdominal pain, epigastric tenderness, nausea, and vomiting, findings which characterize acute pancreatitis as well as acute surgical emergencies such as gastrointestinal perforation (eg, peptic ulcer with perforation) or bowel infract. Pancreatitis in an individual may or may not be related to alcoholism . hypercalcemia related to pancreatitisis recognized with hyper – parathyrodism and other entities. About 80% of subjects with acute pancreatitis have increased serum a mylase within 24 hours. Both amylase and lipase assays are recommended in organophosphate posing. Causes of high serum pancreatic enzymes include acute pancreatitis, chronic pancreatitis, pancreatic ascites, pancreatic abscess, neoplasm, in or adjacent to pancreas, and common duct stones
Sample: Serum
Normal range: Ascetic & pleural fluids amylase activity are identical to, or slightly less than, serum activity
Comment: Ascetic fluidamylase level is increased in pancreatitis, intestinal obstruction or infraction, strangulated bowel, perforated hollow viscus, biliary tract disease, carcinoma of ovary, ruptured ectopic pregnancy, disseminated secondary neoplasm, peritonitis, pancreatic cyst or pseudocyst. Pleural fluid amylase levels are associated with leakage from the abdominal cavity or the presence of an amylase- producing lung tumor; bronchus, pancreatic or ovarian tumor, rupture of esophagus, perforation of thoracic duct, pulmonary tuberculosis, embolism, or infraction, and congestive heart failure
Sample: Body fluid
(Normal range: 0.2-0.8 mg/ml (12-47 mmol/L
Comment: Ammonia and alpha- ketoglutarate with NADH yield glutamate; glutamate and ammonia yield glutamine. Cerebrospinal fluid glutamine levels are useful in hepatic encephalopathy and with Reye syndrome. In the HHH syndrome, hyperammonemia is intermittent; it presents in infancy often, but symptoms can be delayed. Metabolic acidosis with ketosis are found in organic acidemias, in which hyperammonemia is found. Plasma amino acids, urine organic acids, and amino acids are indicated with NH3, biotinidase, and Carnitine. Recently, hyperinsulinaemic hypoglycaemia with persistent hyperammonia has been described. This disorder is not associated with any of the abnormalities of amino acids or organic acids observed in urea cycle enzyme defects, and is thought to be due to mutations in glutamate dehydrogenase
Sample: EDTA, vacutainer, ice, deliver immediately