{"title":"[Community acquired bacterial meningitis in adults].","authors":"Marie Madlener, Insa Joost","doi":"10.1007/s00108-025-01851-2","DOIUrl":"10.1007/s00108-025-01851-2","url":null,"abstract":"<p><p>Bacterial meningitis is a rare but severe disease with a high mortality. The most frequent pathogens in adults are pneumococcus, meningococcus and Listeria. The most important key symptoms are headache, meningism and fever; however, the absence of individual cardinal symptoms does not exclude the diagnosis. The empirical treatment consists of ceftriaxone and ampicillin, supplemented with dexamethasone as needed. It should be initiated without delay if bacterial meningitis is suspected. Before this, two pairs of blood cultures should be obtained followed by a lumbar puncture. An elevated intracranial pressure must be excluded via cerebral computed tomography before performing a lumbar puncture only in patients with confirmation of impaired consciousness, focal neurological deficits or epileptic seizures. In such cases treatment is initiated immediately after obtaining blood cultures but before the lumbar puncture. The identification and management of a focus are essential and should be conducted on the day of admission.</p>","PeriodicalId":73385,"journal":{"name":"Innere Medizin (Heidelberg, Germany)","volume":" ","pages":"190-198"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Celiac disease: an update].","authors":"Helga Paula Török, Sibylle Koletzko","doi":"10.1007/s00108-024-01842-9","DOIUrl":"10.1007/s00108-024-01842-9","url":null,"abstract":"<p><p>Celiac disease is one of the most common lifelong autoimmune disorders and is currently understood as a genetically determined immune intolerance to gluten. In genetically predisposed individuals, the consumption of gluten, along with additional environmental factors, triggers an immunological reaction in the small intestinal epithelium, leading to the destruction of the mucosal architecture with villous atrophy. This can be asymptomatic, but may also cause a wide range of symptoms and lead to systemic complications, such as osteoporosis or infertility. The only treatment is a lifelong, strictly gluten-free diet. Despite advances in diagnostics, many cases remain unrecognized. Diagnosis is based on the serological detection of autoantibodies against tissue transglutaminase 2 (tTG-IgA) and, if necessary, a small intestinal biopsy. Population-wide screening during childhood or adolescence, as legally introduced in Italy in September 2023, could promote early detection and prevent long-term complications. For the monitoring of diagnosed patients, regular clinical check-ups and serological testing are standard practice. In cases of persistent symptoms or risk factors for ongoing villous atrophy, a follow-up duodenal histology examination is recommended. Persistent symptoms despite adherence to a gluten-free diet are often due to continued gluten exposure; however, alternative causes must also be ruled out. In cases of severe malabsorptive symptoms, the rare condition of refractory celiac disease should be considered, with management carried out in specialized centers.</p>","PeriodicalId":73385,"journal":{"name":"Innere Medizin (Heidelberg, Germany)","volume":" ","pages":"165-173"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Christoph Werner, Sebastian Schmidt, Christiane Kellner, Katharina Burghardt, Philipp A Reuken, Christof Kloos, Gunter Wolf
{"title":"[Striking manifestation and unexpected therapeutic course of diabetes mellitus in a 22-year-old male patient].","authors":"Christoph Werner, Sebastian Schmidt, Christiane Kellner, Katharina Burghardt, Philipp A Reuken, Christof Kloos, Gunter Wolf","doi":"10.1007/s00108-024-01797-x","DOIUrl":"10.1007/s00108-024-01797-x","url":null,"abstract":"<p><p>The case of a 22-year-old male patient who presented with acute on chronic hyperglycemia in known MODY (\"maturity onset diabetes of the young\") 12 (ABCC8 gene) after 11 months of treatment cessation is reported. To emphasize the importance of the awareness of this therapeutically important entity of diabetes, the essential facts of this inherited disease are summarized.</p>","PeriodicalId":73385,"journal":{"name":"Innere Medizin (Heidelberg, Germany)","volume":" ","pages":"236-240"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11799017/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142333872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[The intestinal microbiota in inflammatory bowel diseases].","authors":"Benjamin Misselwitz, Dirk Haller","doi":"10.1007/s00108-024-01845-6","DOIUrl":"10.1007/s00108-024-01845-6","url":null,"abstract":"<p><strong>Background: </strong>The intestinal microbiota comprises all living microorganisms in the gastrointestinal tract and is crucial for its function. Clinical observations and laboratory findings confirm a central role of the microbiota in chronic inflammatory bowel diseases (IBD). However, many mechanistic details remain unclear.</p><p><strong>Objectives: </strong>Changes in the microbiota and the causal relationship with the pathogenesis of IBD are described and current and future diagnostic and therapeutic options are discussed.</p><p><strong>Materials and methods: </strong>Narrative review.</p><p><strong>Results: </strong>The intestinal microbiota is altered in composition, diversity, and function in IBD patients, but specific (universal) IBD-defining bacteria have not been identified. The healthy microbiota has numerous anti-inflammatory functions such as the production of short-chain fatty acids or competition with pathogens. In contrast, the IBD microbiota promotes inflammation through the destruction of the intestinal barrier and direct interaction with the immune system. The balance between pro- and anti-inflammatory effects of the microbiota appears to be crucial for the development of intestinal inflammation. Microbiota-based IBD diagnostics show promise but are not yet ready for clinical use. Probiotics and fecal microbiota transplantation have clinical effects, especially in ulcerative colitis, but the potential of microbiota-based therapies is far from being fully realized.</p><p><strong>Conclusion: </strong>IBD dysbiosis remains undefined so far. It is unclear how the many parallel pro- and anti-inflammatory mechanisms contribute to IBD pathogenesis. An inadequate mechanistic understanding hinders the development of microbiota-based diagnostics and therapies.</p>","PeriodicalId":73385,"journal":{"name":"Innere Medizin (Heidelberg, Germany)","volume":" ","pages":"146-155"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stefan Begré, Mark Fox, Sebastian Bruno Ulrich Jordi, Benjamin Misselwitz
{"title":"[Functional disorders in chronic inflammatory bowel disease: the gut-brain axis].","authors":"Stefan Begré, Mark Fox, Sebastian Bruno Ulrich Jordi, Benjamin Misselwitz","doi":"10.1007/s00108-024-01832-x","DOIUrl":"10.1007/s00108-024-01832-x","url":null,"abstract":"<p><strong>Background: </strong>In patients with inflammatory bowel diseases (IBD), functional complaints frequently persist after the clearing of inflammation and are clinically difficult to distinguish from symptoms of inflammation. In recent years, the influence of bidirectional communication between the gut and brain on gut physiology, emotions, and behavior has been demonstrated.</p><p><strong>Research questions: </strong>What mechanisms underlie the development of functional gastrointestinal complaints in patients with irritable bowel syndrome (IBS) and IBD? What therapeutic approaches arise from this?</p><p><strong>Materials and methods: </strong>Narrative review.</p><p><strong>Results: </strong>The pathogenesis of IBS involves interactions between psychosocial factors, genetics, and microbiota as well as the central and peripheral nervous systems. The interplay between stress and visceral hypersensitivity is of central importance. Therapeutically, lifestyle changes with stress reduction and exercise alongside dietary, pharmacological, and psychotherapeutic options are useful.</p><p><strong>Discussion: </strong>The treatment of functional gastrointestinal disorders remains challenging, as pharmacological therapies are often ineffective and gut-directed psychotherapies are rarely available.</p>","PeriodicalId":73385,"journal":{"name":"Innere Medizin (Heidelberg, Germany)","volume":" ","pages":"181-189"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Eosinophilic esophagitis].","authors":"Thomas Greuter","doi":"10.1007/s00108-024-01828-7","DOIUrl":"10.1007/s00108-024-01828-7","url":null,"abstract":"<p><p>Eosinophilic esophagitis (EoE) was first described in the early 1990s. Initially a rarity, it is now the most common cause of dysphagia for solid foods in young adults. Its prevalence is estimated to be 1:2000. Mechanistically, EoE is characterized by a chronic type‑2 T‑helper cell (Th2) inflammation of the esophagus which is triggered by food allergens. It often occurs in association with other Th2-mediated diseases, such as asthma, atopic dermatitis, and chronic rhinosinusitis with nasal polyps. EoE is diagnosed based on an esophagogastroduodenoscopy with biopsies of the esophageal epithelium. The diagnosis can be established when both symptoms of esophageal dysfunction (usually dysphagia) and an eosinophilic infiltration of at least 15 eosinophils per high-power field (HPF) are present. EoE can be treated with drugs, diet, and endoscopic dilatation. In terms of diet, milk elimination appears most reasonable, particularly as first choice. Drug treatment includes proton pump inhibitors (PPI), topical steroids, and the biologic agent dupilumab. Endoscopic dilatation is effective but does not treat the underlying inflammation. Therefore, it should never be used alone, but rather as an add-on therapy. In cases where clinical suspicion of EoE is strong but no or only few eosinophils are detected in esophageal biopsies, the diagnosis of an EoE variant should be considered. This review article provides a detailed discussion of the epidemiology, clinical features, diagnosis, treatment, and variants of EoE.</p>","PeriodicalId":73385,"journal":{"name":"Innere Medizin (Heidelberg, Germany)","volume":" ","pages":"156-164"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142959778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}