Diarrhoea of unknown cause: medical treatment in a stepwise mannerManagement of Idiopathic Diarrhoea Based on Experience of Step-Up Medical Treatment.

The basic principle for the treatment of idiopathic diarrhoea (functional diarrhoea K59.1) is to delay transit through the gut in order to promote the absorption of electrolytes and water. Under mild conditions, bulking agents may suffice. With increasing severity, antidiarrhoeal pharmaceuticals may be added in a stepwise manner. In diarrhoea of unknown aetiology, peripherally-acting opioid receptor agonists, such as loperamide, are first-line treatment and forms the pharmaceutical basis of antidiarrheal treatment. As second-line treatment opium drops have an approved indication for severe diarrhoea when other treatment options fail. Beyond this, various treatment options are built on experience with more advanced treatments using clonidine, octreotide, as well as GLP-1 and GLP-2 analogs which require specialist knowledge the field.

Chronic diarrhoea without an established cause is common.There are a small number of clinical trials, often with a limited number of patients or healthy volunteers.Treatment is often carried out on a trial-and-error basis, with considerable variation in the choice of treatment.There is a paucity of guidelines, and there is a gap in knowledge concerning treatment goals, such as the frequency, consistency and form of stool.The stepwise approach to the treatment of chronic idiopathic diarrhoea described in this article is based on clinical knowledge and experience.

[Pharmacological treatment of idiopathic diarrhea]. / Viktigt att stegvis öka insatser vid farmakologisk diarrébehandling.

The basic principle for treatment of idiopathic diarrhea is to delay transit through the gut in order to promote absorption of electrolytes and water. Under mild conditions bulking agents may suffice. With increasing severity, antidiarrheal pharmaceuticals may be added in a stepwise manner. Bile salt malabsorption is a clear indication for adsorptive resins, while in idiopathic diarrhea peripherally-acting opioid receptor agonists, such as loperamide, is the first-line treatment. Second-line treatment with approved indication for severe diarrhea when other treatment options fail includes opium drops. More advanced treatments are to be used by clinicians with specialist knowledge and experience in the field.

Elevated gaseous luminal nitric oxide and circulating IL-8 as features of Helicobacter pylori-induced gastric inflammation.

BACKGROUND: Gastric nitric oxide (NO) production in response to Helicobacter pylori via inducible nitric oxide synthase (iNOS) is suggested as a biomarker of inflammation and cytotoxicity. The aim of this study was to investigate relationships between gastric [NO], immunological biomarkers and histopathology. MATERIALS AND METHODS: Esophagogastroduodenoscopy was done in 96 dyspepsia patients. Luminal [NO] was measured by chemiluminescence. Biopsies were taken from gastric antrum and corpus for culture and histopathology. H. pylori IgG was detected by immunoblot assay. Biobanked plasma from 76 dyspepsia patients (11 H. pylori positives) was analyzed for 39 cytokines by multiplexed ELISA. RESULTS: H. pylori-positive patients had higher [NO] (336 ± 26 ppb, mean ± 95% CI, n = 77) than H. pylori-negative patients (128 ± 47 ppb, n = 19) (P < 0.0001). Histopathological changes were found in 99% of H. pylori-positive and 37% of H. pylori-negative patients. Histopathological concordance was 78-100% between corpus and antrum. Correlations were found between gastric [NO] and severity of acute, but not chronic, inflammation. Plasma IL-8 (increased in H. pylori positives) had greatest difference between positive and negative groups, with eotaxin, MIP-1ß, MCP-4, VEGF-A, and VEGF-C also higher (P < 0.004 to P < 0.032). Diagnostic odds ratios using 75% cut-off concentration were 7.53 for IL-8, 1.15 for CRP, and 2.88 for gastric NO. CONCLUSIONS: Of the parameters tested, increased gastric [NO] and circulating IL-8 align most consistently and selectively in H. pylori-infected patients. Severity of mucosal inflammatory changes is proportional to luminal [NO], which might be tied to IL-8 production. It is proposed that IL-8 be further investigated as a blood biomarker of treatment outcomes.

Helicobacter pylori causes gastrointestinal hemorrhage in patients with congenital bleeding disorders.

Helicobacter pylori (H. pylori) infection is associated with peptic ulcer disease and gastric cancer. The eradication of H. pylori is of special interest in patients with congenital bleeding disorders, for whom treatment of gastrointestinal hemorrhage with factor concentrates is costly. The prevalence of H. pylori varies between different populations and identification of high-risk subgroups may allow for more targeted screening and eradication of the infection. We performed a 5-year retrospective study of gastrointestinal bleeding, combined with screening and treatment for H. pylori and a long-term prospective follow-up in 168 Swedish and 23 Estonian patients with hemophilia or von Willebrand disease. The prevalence of seropositivity was lower in Sweden than in Estonia (28 versus 48%, p = 0.03), lower in native Swedes than in non-Nordic immigrants to Sweden (20 versus 76%, p = 0.0001) and lower in patients less than 40 years of age than older patients (16 versus 38%, p = 0.002). The incidence of gastrointestinal hemorrhages among the 35 Swedish patients with active H. pylori infection, confirmed by a urea breath test, was 6.0 per 100 patient-years before eradication therapy versus 1.7 during the prospective followup. A negative urea breath test one month after therapy always remained negative after one year. Screening, followed by treatment of all infected patients, yielded a reduction of direct costs over a 5-year period of 130 US-$ per screened patient. We conclude that screening and eradication therapy for infection with H. pylori in patients with congenital bleeding disorders is an effective and economic strategy.

Validated accuracy of a novel urea breath test for rapid Helicobacter pylori detection and in-office analysis.

BACKGROUND: A novel 14C-urea breath test (UBT) was developed to detect the presence of Helicobacter pylori by bench analysis in office, enabling the practitioner to readily reveal H. pylori infection. AIM: To validate the novel UBT (Heliprobe) versus conventional UBT. METHODS: Pretreatment (n = 203) and post-treatment (n = 147) detection of H. pylori. Additional tests with encapsulated 14C-urea (n = 37) were validated. After intake of liquid or encapsulated 14C-urea, exhaled 14CO2 in breath was trapped in benzethoniumhydroxide/ethanol, or adsorbed to LiOH-soaked pads on a dry cover surface (Heliprobe BreathCard). The amount of adsorbed 14C was detected using a beta-scintillator or two Geiger-Müller counters operating in parallel (Heliprobe Analyzer). RESULTS: For pretreatment detection, we found full concordance between the UBTs, with 100% sensitivity and specificity (CI 95-100% and 97-100%, respectively) and strong agreement (r = 0.80, CI 0.75-0.85; kappa = 1, CI 0.86-1.14; P < 0.0001). Similarly, for post-treatment follow-up detection, sensitivity and specificity were 100% (CI 85-100% and 97-100%, respectively) with significant agreement (r = 0.48, CI 0.34-0.59; kappa = 1, CI 0.84-1.16; P < 0.0001). The use of encapsulated 14C-urea did not change agreement between the tests. Sensitivity and specificity were 100% (CI 72-100% and 87-100%, respectively) with strong agreement between the tests (r = 0.71, CI 0.50-0.84; kappa = 1, CI 0.68-1.32; P < 0.0001). CONCLUSION: The novel Heliprobe UBT, with either liquid or encapsulated 14C-urea, seems equi-efficacious to conventional UBT in fulfilling its role as the non-invasive gold standard for detection of H. pylori.