amoxicillin-potassium-clavulanate-combination and Crohn-Disease

Amicrobial pustulosis of the folds (APF) is a recently described entity characterized by relapsing pustular lesions predominantly involving the cutaneous flexures and scalp. This disease typically occurs in association with systemic lupus erythematosus and a variety of other autoimmune diseases. We here describe an APF-like pustular eruption predominantly affecting the scalp, face and trunk, occurring during long-term infliximab treatment for Crohn's disease. Immunohistochemical staining of skin biopsy specimens for myxovirus resistance protein A, a marker for type 1 interferon-inducible proteins, showed increased staining in the epidermis and dermal mononuclear inflammatory infiltrate. Our observation further extends the spectrum of cutaneous adverse reactions potentially related to anti-tumor necrosis factor-α, the clinical context in which APF can occur as well as its clinical presentations.

Topics: Acute Generalized Exanthematous Pustulosis; Amoxicillin-Potassium Clavulanate Combination; Antibodies, Monoclonal; Crohn Disease; Dermatologic Agents; Female; Gastrointestinal Agents; GTP-Binding Proteins; Humans; Infliximab; Myxovirus Resistance Proteins; Neutrophils; Prednisolone; Severity of Illness Index; Treatment Outcome; Tumor Necrosis Factor-alpha; Young Adult

Topics: Adult; Aged; Amoxicillin-Potassium Clavulanate Combination; Anti-Bacterial Agents; Ciprofloxacin; Clarithromycin; Comorbidity; Crohn Disease; Enterobacteriaceae Infections; Female; Hafnia alvei; Humans; Immunocompromised Host; Male; Pneumonia, Bacterial; Pulmonary Disease, Chronic Obstructive; Rare Diseases; Treatment Outcome; Young Adult

The administration of indometacin to rats increases intestinal permeability and induces inflammatory pathology of the small bowel. This represents a potential model for Crohn's disease.. To analyse the pathogenic role of T cells, tumour necrosis factor and bacterial flora in indometacin-induced changes in small bowel permeability and inflammation.. Rats were given indometacin, 13 mg/kg, on day 1 and day 2. The effects of antibiotic (metronidazole, aztreonam and amoxicillin/clavulanic acid), anti- tumour necrosis factor and interleukin-10 therapy were evaluated. The parameters used were weight change, serum haemoglobin, chromium-51 ethylenediaminetetra-acetate permeability and macro-and microscopic score on day 5. Results in conventionally harboured rats were compared with those in T-cell-free rats. Additional in vitro experiments were carried out to test the effect of metronidazole on tumour necrosis factor production.. Indometacin administration resulted in small bowel ulcers and inflammation, independently of T cells. Metronidazole was more potent than amoxicillin/clavulanic acid and anti-tumour necrosis factor in improving the indometacin-induced small bowel inflammation. Only part of the efficacy was through improvement of increased intestinal permeability. Aztreonam and interleukin-10 had no effect. Metronidazole also suppressed in vitro lipopolysaccharide-induced tumour necrosis factor production, suggesting a therapeutic effect of this drug through the inhibition of tumour necrosis factor.. These data implicate anaerobic bacteria and tumour necrosis factor production, but not T cells, as essential elements of the pathogenesis of indometacin-induced small bowel inflammation. Tumour necrosis factor is also involved in the change in intestinal permeability. Metronidazole was the most efficacious drug in this model, probably because it suppressed anaerobic bacteria and directly inhibited tumour necrosis factor production.

Topics: Amoxicillin-Potassium Clavulanate Combination; Animals; Anti-Bacterial Agents; Anti-Inflammatory Agents, Non-Steroidal; Aztreonam; Bacteria, Anaerobic; Crohn Disease; Disease Models, Animal; Drug Therapy, Combination; Female; Indomethacin; Inflammation; Interleukin-10; Metronidazole; Monobactams; Permeability; Rats; Rats, Wistar; T-Lymphocytes; Tumor Necrosis Factor-alpha