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In the face of a separately extended PT, how should this report examiner deal with it?

Author: Xiang Lihua

Unit: Department of Clinical Laboratory, Xiangya Changde Hospital

As we all know, PT reaction exogenous coagulation pathway and co-coagulation pathway, APTT response endogenous coagulation pathway and common pathway, PT than APTT involves less clotting factors, then let's look at this coagulation result.

Are you confused about this result? How should we analyze the coagulation results of such PT alone?

Case after

Patient, male, 6 years. Main complaint: Intermittent nosebleed for 2 years, abnormal coagulation function was found for 12 days. Past history: physical fitness, no history of exposure to infectious diseases such as hepatitis, tuberculosis, and typhoid fever. Physical examination: body temperature 36.4 °C, pulse 92 times / min, breathing 23 times / min, clear, no petechiae, ecchymosis on the skin of the whole body. Laboratory tests for admission:

Coagulation routine

biochemistry

In the face of a separately extended PT, how should this report examiner deal with it?

Blood routine

In the face of a separately extended PT, how should this report examiner deal with it?

Case studies

In conjunction with the patient's laboratory tests and medical history, the common causes of PT prolongation are reviewed, and the figure below shows a brief coagulation waterfall chart.

In the face of a separately extended PT, how should this report examiner deal with it?

Source: A hundred schools of thought

In summary, under the premise that the experimental results are reliable, the possible causes of PT prolongation are:

1. Exogenous coagulation factor FVII. deficiency and FVII inhibitor.

2. Vitamin K deficiency, resulting in a decrease in vitamin K dependence factors FII., FVII., FIX., FX. Examples include warfarin or rat poisoning (VK antagonists), inadequate intake, biliary tract diseases, and cephalosporin antibiotics.

3. Coagulation factor II. and V deficiency.

4. Liver disease (combined with the patient's medical history and liver function can be basically excluded).

The detection of coagulation factors and coagulation factor mutations needs to be further improved.

Full set of coagulation factors: FVII.0.1%, yu is normal. No abnormalities were found in the detection of coagulation factor II and V mutations. Total extrogen results: no pathogenic or suspected pathogenic variants that can definitively explain the patient's phenotype were detected.

Final diagnosis: deficiency of coagulation factor VII.

summary

Coagulation factor VII. (FVII.) is involved in the exogenous coagulation pathway and is a vitamin K-dependent coagulation factor that is synthesized in the liver. In the event of tissue vascular damage, tissue factors (TF) are released into the bloodstream, FVII. binds to it, the molecular configuration changes, the active site is exposed, and it becomes an activated FVII.

TF binds to FVII. and Ca2+ to form the TF-FVII.a-Ca2+ complex. In turn, FX and FIX are activated, so that the endogenous and exogenous coagulation pathways are activated, which has important physiological and pathological significance, and is one of the important starting factors of the exogenous coagulation pathway.

Therefore, when clinical coagulation disorders with prolonged PT and non-vitamin K-dependent type are present, FVII deficiency should be considered and actively improved for coagulation factor activity to confirm the diagnosis.

In the face of a separately extended PT, how should this report examiner deal with it?

PT extends APTT's normal laboratory analysis pathmap

Source: Wang Lanlan, editor-in-chief of medical laboratory project selection and clinical application

Edited by: Yeah Reviewer: Xiao Ran

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