RESUMO
Onset of inflammatory bowel disease [IBD] is nowadays seen as an interplay or a combination of genetic susceptibility, disturbed intestinal immunity, and environmental factors including gut microbiome. However, the initiation of inflammation and progression to IBD pathogenesis in a given individual is poorly understood. In this case report we describe the clinical course of a 17-year-old female patient developing symptoms suggestive of IBD after 'autovaccine therapy', in which sterilised samples of the patient's own stool were injected subcutaneously for improvement of her general immunity. The patient presented with a severe onset of disease, which was first suspected to be ulcerative colitis on outpatient examination and was later corrected to IBD with Crohn's-like features due to high systemic inflammation, mixed lymphocytic-granulocytic infiltrates in gastric biopsies, and further characteristics suggestive of Crohn's disease. A prolonged and complicated course was seen with intermittent steroid dependency in the long term. Numerous publications postulate that [auto-]immune reactions against resident bacterial stool flora may play a role in IBD. It is possible that in this patient tolerance to endogenous bacteria was disrupted by systemic pro-inflammatory mechanisms induced by autovaccination.
Assuntos
Autovacinas/efeitos adversos , Fezes/microbiologia , Doenças Inflamatórias Intestinais/imunologia , Adolescente , Feminino , Humanos , Doenças Inflamatórias Intestinais/diagnóstico , Doenças Inflamatórias Intestinais/microbiologia , Injeções SubcutâneasRESUMO
BACKGROUND: Adverse food reactions (AFR) have has recently attracted increased attention from the media and are now more commonly reported by patients. Its classification, diagnostic evaluation, and treatment are complex and present a considerable challenge in clinical practice. Non-immune-mediated types of food intolerance have a cumulative prevalence of 30% to 40%, while true (immune-mediated) food allergies affect only 2% to 5% of the German population. METHOD: We selectively searched the literature for pertinent publications on carbohydrate malabsorption, with special attention to published guidelines and position papers. RESULTS: Carbohydrate intolerance can be the result of a rare, systemic metabolic defect (e.g., fructose intolerance, with a prevalence of 1 in 25,000 persons) or of gastrointestinal carbohydrate malabsorption. The malabsorption of simple carbohydrates is the most common type of non-immune-mediated food intolerance, affecting 20% to 30% of the European population. This condition is caused either by deficient digestion of lactose or by malabsorption of fructose and/or sorbitol. Half of all cases of gastrointestinal carbohydrate intolerance have nonspecific manifestations, with a differential diagnosis including irritable bowel syndrome, intolerance reactions, chronic infections, bacterial overgrowth, drug side effects, and other diseases. The diagnostic evaluation includes a nutritional history, an H2 breath test, ultrasonography, endoscopy, and stool culture. CONCLUSION: The goals of treatment for carbohydrate malabsorption are to eliminate the intake of the responsible carbohydrate substance or reduce it to a tolerable amount and to assure the physiological nutritional composition of the patient's diet. In parallel with these goals, the patient should receive extensive information about the condition, and any underlying disease should be adequately treated.
Assuntos
Testes Respiratórios/métodos , Erros Inatos do Metabolismo dos Carboidratos/diagnóstico , Carboidratos da Dieta/efeitos adversos , Endoscopia Gastrointestinal/métodos , Fezes/química , Síndromes de Malabsorção/diagnóstico , Ultrassonografia/métodos , Erros Inatos do Metabolismo dos Carboidratos/classificação , Diagnóstico Diferencial , Humanos , Síndromes de Malabsorção/classificação , Síndromes de Malabsorção/etiologia , Anamnese/métodosRESUMO
BACKGROUND: Up to the present date, the treatment of recurrent chronic fistulas occurring with Crohn's disease represents a challenging task for both internists and surgeons alike. METHODS: Conservative methods of treatment using steroids, dietotherapy, antibiotics or immunosuppressive agents are not particularly effective in treating fistulas. Treatment with anti-tumor necrosis factor-alpha (TNFalpha) antibodies results in more remissions of fistulas. However, its use requires appropriate medical experience and causes substantial costs. Surgical procedures such as fistula sanitation or protective ileostomy are often obfuscated by the recurrence of the condition. The efficiency of anti-TNFalpha antibodies for the treatment of active Crohn's disease has been evidenced through several multicenter, double-blind, placebo-controlled studies. RESULTS: Here we report the successful anti-TNFalpha treatment of a patient suffering from chronic, fistulizing, therapy-resistant Crohn's disease and a concomitant chronic autoimmune thrombocytopenia. The chimeric anti-TNFalpha antibody infliximab markedly reduced the disease activity of Crohn's disease, and, in addition, substantially increased the platelet counts. After infliximab application, no other treatment of autoimmune thrombocytopenia was required. After infliximab therapy, autoantibodies to dsDNS could be observed. However, there were no signs of a lupus-like disease. CONCLUSION: This report indicates a favorable therapeutic response of autoimmune thrombocytopenia associated to Crohn's disease.
Assuntos
Anticorpos Monoclonais/uso terapêutico , Doença de Crohn/complicações , Doença de Crohn/tratamento farmacológico , Fármacos Gastrointestinais/uso terapêutico , Púrpura Trombocitopênica Idiopática/complicações , Fístula Retal/etiologia , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Adulto , Humanos , Infliximab , Púrpura Trombocitopênica Idiopática/fisiopatologia , Indução de Remissão , Resultado do TratamentoRESUMO
Patients often complain about food intolerances and accuse them of causing diarrhea, constipation, meteorism, flatulence and abdominal pain. With alarm symptoms, patients usually suffer from structural diseases, which have to be clarified immediately by extensive diagnostic steps. With no alarm symptoms present, patients usually suffer from functional disorders. Their workup should be done stepwise. Therapy is dependent on the underlying disorder and often symptom-adapted. General measures of prevention for food-preparation and nutrition are important.
Assuntos
Hipersensibilidade Alimentar/terapia , Alimentos/efeitos adversos , Hipersensibilidade Alimentar/diagnóstico , Hipersensibilidade Alimentar/etiologia , HumanosRESUMO
OBJECTIVES: Serum immunoglobulin E (IgE) was investigated in patients with chronic pancreatitis in order to elucidate possible disease mechanisms linking pancreatitis, adverse reaction to foods and allergy. DESIGN AND METHODS: Serum IgE was analysed in 86 non-atopic patients with advanced chronic pancreatitis and 54 non-atopic controls. IgE detection was performed by enzyme-linked immunofluorescence. RESULTS: Mean IgE levels (+/- standard error of mean) in chronic pancreatitis patients (286.1+/-49 kU/l) were found to be significantly elevated compared to controls (67.7+/-11 kU/l; P<0.0001). Normal IgE levels (<100 kU/l) were present in 40/54 control patients (74.1%), but only 39/86 pancreatitis patients (45.3%). Of the patients with chronic pancreatitis, 47/86 (54.6%) had clearly elevated IgE levels of >100 kU/l and their IgE values did not show a Gaussian distribution. However, nine-fold higher IgE levels were found in chronic pancreatitis patients with alcohol consumption of >25 g/day and exocrine insufficiency (915.5+/-240 kU/l) than in pancreatitis patients with normal exocrine function and no alcohol consumption (103.4+/-43 kU/l; P<0.001). Moreover, acute episodes of chronic pancreatitis were found to increase serum IgE levels. CONCLUSIONS: In patients with chronic pancreatitis, serum IgE production is markedly enhanced, especially during acute inflammatory episodes or when alcohol is consumed. Since abstinence from alcohol and pancreatic enzyme substitution are associated with clearly lower IgE levels, it may be concluded that pancreatic insufficiency with reduced nutrient digestion and alcohol consumption stimulate IgE production. This finding gives rise to the speculation that, apart from pancreatic inflammation, cross-linking of IgE with alimentary or other antigens might be involved in the pathophysiology of a sub-population of patients with chronic pancreatitis and manifest pancreatic insufficiency.