tripsinogyn gene (sp)

[Guest guest]

Hi All,

I went to the FNP today and we tried to talk about this gene and she

knew nothing of it. Since I am in effect letting her be my pancreas

doctor I need to educate her on this. I was asking to be tested for it,

but she has never heard of it. Didn't someone on the board post

something fabulous about it and it's connection to CP? If not I will

gather info on the web about it.

Thanks,

Sandy in Ca

>

>

[Guest guest]

Serum Complex of Trypsin-2 and a 1-antitrypsin: A New Sensitive Marker of Acute

Pancreatitis

Johan Hedström, M.D*., Jari Leinonen, M.Sc., and Ulf-Håkan Stenman, M.D.

Departmetnt of Clinical Chemistry, Helsinki University Central Hospital,

Helsinki, Finland

Introduction: Pathological intrapancreatic activation of trypsinogen to trypsin

occurs in acute pancreatitis (AP). When reaching blood, trypsin-2 forms a

complex with a1-antitrypsin (AAT). The trypsin-2-AAT complex can be specifically

measured by a recently developed double antibody sandwich assay.

Purpose: To estimate the diagnostic and prognostic accuracy of serum

determinations of trypsin-2-AAT in AP. Serum CRP, amylase and trypsinogen-2 were

used as reference methods.

Design: A retrospective study on consecutive patients during March 1992 to

November 1993.

Setting: Patients treated for AP and other acute abdominal disorders at the

Second Department of Surgery at Helsinki University Central Hospital.

Methods: 110 patients with AP and 66 patients with acute abdominal diseases of

extrapancreatic origin were studied. The final diagnosis of AP was based in

findings of upper abdominal pain accompanied by the typical appearance of AP in

ultrasonography or computed tomography (CT). Based on the clinical course, AP

was classified as mild (n=82) or severe (n=28). Trypinogen-2 and trypsin-2-AAT

were determined by time- resolved immunofluorometric assays (IFMA). The upper

reference limit was 12 µg/L. The ability of various tests to differentiate

between mild and severe AP and nonpnacreatic disease was estimated on the basis

of sensitivity and specificity at clinically relevant cut-off levels and the

validity of the test was further evaluated by receiver-operating characteristic

(ROC) curve analysis.

Results: At admission, all patients with AP had clearly elevated values of

trypsin-2-AAT (= 32 µ g/L), whereas only 5% of the controls had such values. In

AP, trypsinogen-2 and trypsin-2-AAT increased earlier than CRP and remained

elevated longer than amylase. There was also less overlapping between patients

with AP and controls for trypsin-2-AAT than for the other markers. Time course

profiles of trypsin-2-AAT showed that in severe cases it mostly peaked in the

initial sample and slowly decreased during the next days. In patients with mild

AP the peak was mostly observed in the second day. Of the markers studied,

trypsin-2-AAT showed the best accuracy (largest area under the ROC curve) both

in differentiating AP from controls and mild from severe disease. At

presentation, trypsin-2-AAT differentiated between mild and severe AP much more

accurately than CRP, AUC being 0.82 and 0.73, respectively.

Conclusion: Of the markers studied, trypsin-2-AAT displayed the best accuracy

for differentiating between AP and extrapancreatic disease as well as for

predicting a severe course of the disease at presentation. If available on

automated instrumentation and on emergency basis, the assay could markedly

improve the diagnosis of this common and potentially lethal disease.

On 7/14/2004 2:05:32 PM, pancreatitis wrote:

> Hi All,

>

> I went to the FNP today and we tried to talk about this gene and she

> knew nothing of it. Since I am in effect letting her be my pancreas

> doctor I need to educate her on this. I was asking to be tested for it,

> but she has never heard of it.

> Didn't someone on the board post

> something fabulous about it and it's

> connection to CP? If not I will

> gather info on the web about it.

>

> Thanks,

> Sandy in Ca

>

>

> >

> >