Cgi
| Chronic Granulomatous Inflammation | |
|---|---|
| Synonyms | N/A |
| Pronounce | N/A |
| Specialty | N/A |
| Symptoms | Persistent inflammation, tissue damage |
| Complications | Fibrosis, organ dysfunction |
| Onset | Variable |
| Duration | Chronic |
| Types | N/A |
| Causes | Infectious agents, autoimmune diseases, foreign bodies |
| Risks | Genetic predisposition, environmental factors |
| Diagnosis | Biopsy, imaging studies |
| Differential diagnosis | N/A |
| Prevention | N/A |
| Treatment | Corticosteroids, immunosuppressants, surgery |
| Medication | N/A |
| Prognosis | Variable |
| Frequency | N/A |
| Deaths | N/A |
Chronic Granulomatous Inflammation (CGI) is a type of chronic inflammation characterized by the formation of granulomas, which are small aggregates of macrophages that have transformed into epithelioid cells. This condition can occur in response to a variety of stimuli, including persistent infectious agents, foreign bodies, and certain autoimmune diseases.
Pathophysiology
Chronic granulomatous inflammation is a complex immune response that occurs when the immune system attempts to isolate substances it perceives as foreign but is unable to eliminate. The formation of granulomas is a hallmark of this type of inflammation. Granulomas are composed of macrophages, which transform into epithelioid cells and often fuse to form multinucleated giant cells. These structures are surrounded by a collar of lymphocytes and sometimes fibroblasts.
The process begins with the activation of macrophages by T-helper cells, particularly the Th1 subset, which secrete cytokines such as interferon-gamma (IFN-γ). This cytokine milieu promotes the transformation of macrophages into epithelioid cells and the formation of multinucleated giant cells. The persistent presence of the inciting agent leads to chronic inflammation and tissue damage.
Causes
Chronic granulomatous inflammation can be caused by a variety of factors, including:
- Infectious agents: Certain bacteria, fungi, and parasites can cause granulomatous inflammation. Notable examples include Mycobacterium tuberculosis, which causes tuberculosis, and Histoplasma capsulatum, which causes histoplasmosis.
- Autoimmune diseases: Conditions such as sarcoidosis and Crohn's disease are associated with granuloma formation.
- Foreign bodies: The presence of foreign materials, such as sutures or silica, can lead to granuloma formation as the body attempts to wall off the foreign substance.
Clinical Presentation
The clinical presentation of chronic granulomatous inflammation varies depending on the underlying cause and the organs involved. Common symptoms include:
- Persistent fever
- Fatigue
- Weight loss
- Localized pain or discomfort
- Organ-specific symptoms, such as cough and dyspnea in pulmonary involvement or abdominal pain in gastrointestinal involvement
Diagnosis
The diagnosis of chronic granulomatous inflammation typically involves a combination of clinical evaluation, imaging studies, and histopathological examination. A biopsy of the affected tissue is often necessary to confirm the presence of granulomas. Imaging studies, such as X-rays, CT scans, or MRI, may be used to assess the extent of organ involvement.
Treatment
The treatment of chronic granulomatous inflammation depends on the underlying cause. General approaches include:
- Corticosteroids: These are often used to reduce inflammation and suppress the immune response.
- Immunosuppressants: Drugs such as methotrexate or azathioprine may be used in autoimmune conditions.
- Antimicrobial therapy: In cases of infectious granulomatous inflammation, appropriate antibiotics or antifungal medications are used.
- Surgical intervention: In some cases, surgical removal of the granulomatous tissue may be necessary.
Prognosis
The prognosis of chronic granulomatous inflammation varies widely depending on the cause and the organs involved. Some conditions, such as sarcoidosis, may resolve spontaneously, while others, like tuberculosis, require prolonged treatment. Chronic inflammation can lead to complications such as fibrosis and organ dysfunction.
See Also
External Links
- [Link to relevant medical resources]
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Contributors: Prab R. Tumpati, MD