الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Trigger finger is caused by a disproportion between the tendon and its sheath, specifically in the A1 pulley. It causes hand pain and disability. The most common form of the trigger finger is the primary type, which is far more common in the middle aged women than men. Secondary type of trigger finger is often encountered in patients with chronic illnesses such as diabetes, rheumatoid arthritis, gout, renal disease and hypothyroidism. However, the exact etiology remains controversial.
The aim of the work was to study the histopathological changes of affected tendon sheath, trying to understand the nature of the cause and the histopathology of trigger finger after exclusion of rheumatoid diseases and congenital trigger finger.
This study was carried out on twenty patients with trigger finger disease.
Our results revealed that:
- The mean of age were 37.4 ± 7.4 years. Two patients (10.0%) were in the age group (21-30 years), twelve patients were in the age group (31-40 years) and s patients (30.0%) were in the age group (41-50 years).
- Eighteen patients (90.0%) were females and the remaining two patients (10.0%) were males.
- The majority of the patients (65.0%) were housewives, four patients were employee (20.0%), two patients were teachers (10.0%) and one patient was farmer (5.0%).
- The right side was affected in fifty patients (75.0%) and the left was affected in five patients (25.0%).
- The ring finger was affected in two patients (10.0%), middle finger in six patients (30.0%) and thumb in twelve patients (60.0%).
- All the patients were right handed.
- Local injection of corticosteroids as a line of conservative treatment was performed in five patients (25.0%). De Quervain disease was present in two patients (10.0%).
- Previous local injury was present in nineteen patients (95.0%).
Histopathology study showed that:
- One patient forming vascularized granulation tissue, seven patients showed moderate, tiny, and congested vessels with absent thick wall and twelve patients showed mild forming mildly separated tiny vessels with thin wall.
- Synovial sheath was atrophied in fourteen patients and present in six patients. Among these six patients; three patients showed hypertrophic complex papelloid with heavy chronic inflammation in one patient, mild in one patient and negative for inflammatory cells in one patient. In the other three patients; the histopathylogy show synovium forming in thin flat epitheliallayer with underneath loose fibrovascular stroma with negative inflammatory cells.
- Stromal fibrosis was severe forming dense collagen deposition with hyaline degeneration in fifteen patients. Three patients of them showed superadded myxoid degeneration and chondroid metaplasia, while the remaining twelve patients dense collagen was covered with hyaline degeneration. In five patients, the stromal fibrosis was moderate with hyaline matrix.