What's going on with amyloid protein deposition

What is amyloid deposition? When it comes to amyloid protein deposition, many friends don’t know much about this issue. This is not surprising. After all, it is not common in our lives. Unless they suffer from this disease, few friends will have a detailed understanding of the problem of amyloid protein deposition. However, for our health, I hope that everyone can have a more detailed understanding of the causes and examination and diagnosis of amyloid protein deposition.

Causes of amyloid deposition:

The exact mechanism of amyloid formation has not been fully understood, but the prerequisite for the deposition of amyloid fibrils is that its precursor protein is produced in excessive amounts or has structural abnormalities. The precursor protein is incompletely degraded to become easily folded into reverse parallel β-sheet structure fragments. In familial amyloid polyneuropathy and hemodialysis-related amyloidosis, intact, undegraded TTR and β2-M molecules can also form amyloid fibrils. The primary structure of a protein is very important for its ability to form amyloid fibrils. For example, in hereditary amyloidosis, a single amino acid substitution can transform a wild-type molecule that is unable to form amyloid into a mutant molecule that can produce fibrils. In addition, there are some other factors that affect the deposition process and distribution of protofibrils, collectively referred to as amyloid enhancing factor (AEF), which may be related to individual differences in clinical practice. Mechanisms of amyloid formation.

Diagnosis

1. In addition to detailed inquiries about the current medical history, the patient should also focus on the past history and family history. The past history should include inquiries about whether the patient has a history of rheumatoid arthritis, inflammatory bowel disease, tuberculosis, suppurative osteomyelitis, and empyema, and renal dialysis treatment.

Macroglossia, periorbital purpura, unexplained cardiac enlargement and heart failure, hepatomegaly, proteinuria, systemic lymphadenopathy, intractable pleural effusion, and pancytopenia should all be considered to be the possibility of systemic amyloidosis.

2. Laboratory tests that are helpful for the diagnosis of systemic amyloidosis include: ① Bence-Jone protein test in urine; ② bone marrow puncture smear examination. In systemic amyloidosis AL type, the proportion of immature and mature plasma cells in the bone marrow exceeds 15%, and myeloma cells can also be seen; ③ AF type, determination of related variant proteins in plasma.

3. The diagnosis is to prove the deposition of amyloid protein in the tissue gaps. The most reliable method is to do a biopsy and pathological section examination of the diseased tissue.

Through this article's introduction to the causes and diagnostic methods of amyloid protein deposition, I believe that everyone has a certain understanding of the disease. Here I need to remind everyone that the harm of amyloid protein deposition is actually quite large. Therefore, if you are diagnosed with the disease, you must pay attention to active treatment.