Introduction
Various systemic diseases can affect the gastrointestinal (GI) tract, including rheumatological and dermatological conditions. These extra-intestinal manifestations often precede the diagnosis of the primary disease and can significantly impact the quality of life. Recent research has greatly expanded the understanding of the mechanisms behind GI involvement in systemic diseases, allowing for earlier diagnosis and better management. This comprehensive article will provide an overview of the GI manifestations of key rheumatological diseases such as systemic lupus erythematosus, rheumatoid arthritis, Sjögren's syndrome, systemic sclerosis, vasculitis as well as dermatological diseases like psoriasis.
What Is the Epidemiological Pattern of This Disease?
GI involvement is common in systemic rheumatological diseases, occurring in 50-70 percentage of systemic lupus erythematosus (SLE) patients, 20 percentage of rheumatoid arthritis (RA) patients, up to 30 percentage of Sjögren's syndrome patients, nearly all systemic sclerosis patients, 40-60 percentage of small vessel vasculitis patients and 40 percentage of psoriasis patients with inflammatory bowel disease. Symptoms can precede the diagnosis of the primary disease in months to years. Serious complications like perforations, hemorrhage, pancreatitis, and protein-losing enteropathy may arise and require prompt diagnosis and management.
What Is the Root Cause of GI Manifestations In Systemic Diseases?
The pathogenesis of GI manifestations in systemic diseases is multifactorial and not completely understood. Proposed mechanisms include immune complex deposition, vasculitis, smooth muscle atrophy and fibrosis, dysmotility, autonomic neuropathy, endothelial activation, and side effects of medications. Antibodies against phospholipids, muscle proteins, and epithelial cells have been detected in affected patients. Histologically, nonspecific inflammation, vascular damage, granulomas, fibrosis, and amyloid deposition may be seen. Genetic susceptibility and shared inflammatory pathways, like Tumor Necrosis Factor-alpha (TNF-alpha), likely underlie the association with inflammatory bowel disease.
What Are the GI Manifestations in Systemic Lupus Erythematosus?
In SLE, the most common GI complaints are nausea, vomiting, abdominal pain, diarrhea, and dysphagia. Vasculitis, protein-losing enteropathy, intestinal pseudo-obstruction, and perforation can occur. On endoscopy, mucosal erythema, edema, erosions, and ulcerations are sometimes observed. Smooth muscle atrophy and fibrosis lead to dysmotility, while antibodies cause damage to gut epithelial cells.
Treating GI manifestations involves immunosuppression with steroids and other agents to control overall disease activity. Antibiotics for superimposed infections, nutritional support, and addressing medication side effects are key. Surgery may be needed for obstruction or perforation. Tight control of inflammation helps minimize GI complications.
What Are the GI Manifestations in Rheumatoid Arthritis?
The most frequent GI complaints in RA are dysphagia, heartburn, nausea, abdominal pain, and constipation. Amyloidosis, gastric antral vascular ectasia, and cholestatic liver disease may arise. Endoscopy shows nonspecific gastritis and duodenitis in many cases. Reduced gut motility from autonomic neuropathy and myenteric plexus inflammation contributes to symptoms like dysphagia and constipation. Vasculitis also plays a role, while drugs like Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) can worsen inflammation. Treatment focuses on controlling joint inflammation with Disease Modified Anti-Rheumatic Drugs (DMARDs) and biologics. GI-sparing pain medications should be used when possible.
What Are the GI Manifestations in Sjögren’s Syndrome?
GI manifestations in Sjögren's syndrome include dysphagia, nausea, abdominal pain, and diarrhea. Autoimmune pancreatitis, Primary Biliary Cholangitis (PBC), and Primary Sclerosing Cholangitis (PSC) occur in a subset. Lymphocytic infiltration of glands leads to exocrine pancreatic insufficiency and mucosal inflammation. Cryoglobulinemic vasculitis is also implicated. Treatment focuses on managing sicca symptoms, immunosuppression to control disease activity, and pancreatic enzyme supplementation. Biliary stenting or ursodeoxycholic acid may be used for chronic cholestasis. Careful screening for nutritional deficiencies is warranted.
What Are the GI Manifestations in Systemic Sclerosis?
In systemic sclerosis, symptoms include dysphagia, Gastero Esophagal Reflex Disorder (GERD), early satiety, bloating, malabsorption, and diarrhea. Serious complications, like pseudo-obstruction can occur. Vascular injury and collagen deposition in the GI wall impair motility, while fibrosis destroys glandular tissue. High-dose Proton Pump Inhibitors (PPIs) and prokinetics are used for GERD and dysmotility. Immunosuppression helps stabilize disease. Enteral feeding may be required when dysphagia is severe. Screening for bacterial overgrowth and nutritional deficiencies is important.
What Are the GI Manifestations in Vasculitis?
Abdominal pain, GI bleeding, and perforation are common in small vessel vasculitis like Polyarteritis Nodosa (PAN), Henoch-Schönlein Purpura (HSP), and Microscopic Polyangiitis (MPA). Large vessel vasculitis causes aneurysms and ischemia. Inflamed vessels develop microaneurysms that can rupture, erode, or stenose.
Endoscopy is often normal, but imaging may reveal bowel wall thickening, obstruction, or perforation. Biopsies show vasculitis in a minority. High-dose steroids induce remission, while immunosuppressants maintain it. Surgery is reserved for severe complications like perforation or hemorrhage that are unresponsive to medical therapy.
What Are the GI Manifestations in Psoriasis?
Up to 40 per cent of psoriasis patients develop inflammatory bowel disease, especially Crohn’s. This likely results from shared genetic risks and inflammatory mediators like TNF-alpha. Symptoms include abdominal pain, diarrhea, and bleeding. Endoscopy shows nonspecific inflammation. Topical treatments and phototherapy are used for mild skin diseases. Systemic agents like Methotrexate, Cyclosporine, and TNF inhibitors treat moderate to severe disease and can also improve Irritable Bowel Disease (IBD). Tight control of skin inflammation may prevent future GI manifestations.
How Is Evaluation Done for GI Manifestations in Systemic Diseases?
Evaluation of GI complaints in systemic disease patients begins with a thorough history and physical exam. Warning signs like anemia, weight loss, and bleeding warrant prompt investigation. Initial tests include a complete blood count, comprehensive metabolic panel, erythrocyte sedimentation rate, C-reactive protein, and stool studies for infection.
Further workup with imaging, such as Computed Tomography (CT) enterography or video capsule endoscopy, is considered for persistent symptoms. Upper endoscopy and colonoscopy with biopsies are useful to rule out vasculitis, IBD, infections, and malignancy. Rarely exploratory laparotomy is needed to diagnose ischemic or perforated bowel.
How Is Management Done for GI Manifestations in Systemic Diseases?
Treatment focuses on controlling the underlying systemic inflammation with immunosuppressive medications. Concomitant infections should be treated with appropriate antimicrobials. Nutritional support, pancreatic enzymes, bile acid supplements, and other symptomatic measures also play a role.
Surgery may be required for obstructions, perforations, or uncontrolled hemorrhages unresponsive to medical treatment. Aggressive management of the primary disease can improve or resolve many GI manifestations. However, GI complications may persist even with systemic remission due to irreversible fibrotic damage. Ongoing monitoring for nutritional deficiencies, infections, side effects of medications, and disease recurrence is essential.
What Are the Future Directions?
Further research is needed to elucidate better the pathophysiological mechanisms behind GI involvement in rheumatic and skin diseases. Studies of therapies targeted at specific inflammatory mediators and fibrosis pathways may identify novel treatments to supplement conventional immunosuppression. Developing clinical prediction tools to identify high-risk patients may facilitate earlier diagnosis and prevent complications. More sensitive and specific diagnostic modalities could aid in the prompt recognition of GI vasculitis, protein-losing enteropathy, and myenteric plexus. Increased awareness and vigilance regarding GI manifestations by providers can significantly improve patient outcomes.
Conclusion
In summary, GI involvement is common in patients with systemic rheumatological and dermatological diseases. Presentations range from mild complaints like nausea and diarrhea to severe complications like hemorrhage and perforation. A multidisciplinary, collaborative approach is key to optimally managing systemic inflammation and resultant GI dysfunction. Prompt recognition and treatment of GI disease have the potential to greatly improve the quality of life in this complex patient population. Further research and increased awareness will continue to advance patient care in this important realm.
