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The modern Gastroenterology have witnessed an essential stride since Helicobacter pylori was first found in the stomach and then its pathogenic effect was discovered. According to the researches conducted during the nearly 40 years, it has been found that this bacterium is associated with a natural history of many upper gastrointestinal diseases. Epidemiological data show an increased incidence of autoimmune disorders with or after infection with specific microorganisms. The researches have revealed that H. pylori is a potential trigger of gastric autoimmunity, and it may be associated with other autoimmune diseases, both innate and acquired. This paper reviews the current support or opposition about H. pylori as the role of potential triggers of autoimmune diseases, including inflammatory bowel disease, autoimmune thyroiditis, type 1 diabetes mellitus, autoimmune liver diseases, rheumatoid arthritis, idiopathic thrombocytopenic purpura, systemic lupus erythematosus, as well as Sjogren’s syndrome, chronic urticaria and psoriasis, and tried to explain the possible mechanisms.

Thrombocytopenia in Pregnant WomenPlatelet counts often fall during pregnancy; decreases below 50×103 per cubic millimeter may be due to an autoimmune cause. Detection and management of immune thrombocytopenia may be lifesaving.

To the Editor: In their review article on the management of immune thrombocytopenia (ITP) during pregnancy, Bussel et al. (Aug. 10 issue) 1 state that “anesthesiologists generally do not perform neuraxial anesthesia in patients with a platelet count below 70×10 3 to 80×10 3 per cubic millimeter.” However, the risks associated with epidural placement may be overstated. To our knowledge, no cases of neuraxial hematoma related to epidural placement have been reported in patients with ITP. Epidurals have been safely placed in patients with ITP who have a platelet count as low as 2×10 3 per cubic millimeter. 2 Moreover, an epidural is not the . . .

Herein, we detail our experience with a unique patient with concomitant multiple sclerosis (MS) and idiopathic thrombocytopenic purpura (ITP) treated with ofatumumab, which resulted in stable disease activity and platelet count normalization. A 21-year-old Japanese woman presented with medial longitudinal fasciculus syndrome and was subsequently diagnosed with MS. She was treated with methylprednisolone pulse therapy (1,000 mg/day for 5 days). During her first hospitalization, her platelet count was low (40 × 10 /L). Based on investigations, serologic findings, and bone marrow aspiration, she was diagnosed with ITP. Following methylprednisolone treatment, oral prednisolone was initiated and gradually tapered. Glatiramer acetate was used as a disease-modifying drug (DMD). As prednisolone was tapered off, the platelet count decreased correspondingly. The clinical course included two MS relapses, each of which was treated with a methylprednisolone pulse and DMD adjustments (the DMT was sequentially switched from glatiramer acetate to dimethyl fumarate, then fingolimod, and finally natalizumab). Despite an initial recovery of the platelet count following these interventions, the platelet count declined correspondingly with the prednisolone dose reduction. Finally, the DMD was switched to ofatumumab, an anti-CD20 monoclonal antibody with pharmacological similarities to rituximab, a second-line treatment for ITP. After the initiation of ofatumumab, the patient remained clinically stable with no further MS relapses, and her platelet count stabilized over 2 years. Herein, we report our experience with a novel case of MS concomitant with ITP that was safely treated with ofatumumab. Considering the pharmacological similarities of ofatumumab to rituximab (a second-line treatment for ITP), anti-CD20 monoclonal antibodies such as ofatumumab could be a promising treatment option for cases of MS concomitant with ITP.

Patients with immune thrombocytopenia (ITP) usually present with minor mucocutaneous bleeding. Corpus luteum hemorrhage (CLH) is generally asymptomatic but may, rarely, lead to severe intraperitoneal bleeding, mostly in patients with coagulation disorders. CLH causing intraperitoneal bleeding has only been described in few individuals with ITP. The objective of this retrospective observational study was to assess the clinical course and incidence of symptomatic CLH in adolescent females with newly diagnosed or chronic ITP. Additionally, a comprehensive literature review was conducted to scrutinize cases of pediatric female patients with ITP, complicated by CLH. We identified three patients with ITP and hemoperitoneum secondary to CLH. They presented with acute abdominal pain, had severe thrombocytopenia (platelet counts below 20 × 10 9 /L), and required blood transfusions as well as ITP-directed therapy. All the patients were hemodynamically stable and did not require emergency surgical intervention.   Conclusion : CLH could potentially pose a significant complication in the context of adolescent females with ITP, requiring a strong index of suspicion to direct expedient therapy. What is Known: • Immune thrombocytopenia is typically associated with minor bleeding tendency. • Corpus luteum hemorrhage is generally asymptomatic; however, in women with bleeding disorders, it has the potential to result in substantial intra-abdominal bleeding. What is New: • Corpus luteum hemorrhage leading to intra-abdominal bleeding is a potential severe complication of immune thrombocytopenia in adolescent females.

Mycoplasma pneumoniae (M. pneumoniae), as one of the susceptible pathogens during childhood, may lead to severe mycoplasmal pneumonia and affect platelet fluctuations. We prospectively collected data on persistent/chronic ITP children who were infected with M. pneumoniae infection from August 2023 to December 2023. There were 64 patients (40 males) with a median age of 7.08 years (range 4.30 to 9.76) enrolled in this study. Overall, 33 (51.6%) children received TPO-RAs therapy and 31 (48.4%) received other treatments. The impact of M. pneumoniae infection on platelet count is bidirectional, but thrombocytopenia remains predominant. During M. pneumoniae infection, platelet changes in the TPO-RA group were higher than in the non-TPO-RA group. Thrombocytosis was observed in 6 patients (5 in the TPO-RA group vs. 1 in the non-TPO-RA group). Rescue treatment was implemented in 18 patients (7 in the TPO-RA group vs. 11 in the non-TPO-RA group). Monitoring platelets should be strengthened during M. pneumoniae infection.

Background Brain abscesses caused by Nocardia farcinica are rare, and mostly occur in immunocompromised individuals. Rapid and accurate diagnosis of nocardiosis is challenging. Due to the inadequate performance of conventional diagnostic methods for Nocardia infection, metagenomics next-generation sequencing (mNGS) of cerebrospinal fluid (CSF) has the potential to improve the diagnosis intracranial nocardiosis. Case presentation We report a case of 50-year-old man with brain abscess caused by Nocardia farcinica . The patient had a idiopathic thrombocytopenic purpura complication that required long-term methylprednisolone administration. His chest image showed multiple lesions, which had been misdiagnosed as lung cancer, and his head image showed multiple intracranial metastases. No pathogen was detected in routine examinations including blood culture, sputum culture and traditional culture methods of cerebrospinal fluid. In order to accurately identify the pathogen, mNGS was used to detect Nocardia in CSF. Although the patient’s condition improved after using sensitive antibiotics, he transferred to the local hospital for treatment because of many complicated diseases and family financial limitations. Conclusion This case highlights the value of mNGS in the diagnosis of Nocardia brain abscess, and emphasizes the inadequate sensitivity of conventional diagnostic methods for Nocardia infection. Using mNGS can facilitate early and accurate detection of Norcadia-associated of meningitis in immunocompromised patients, thereby reducing unnecessary use of antibiotics and reducing mortality of the disease.

BackgroundChronic Granulomatous Disease (CGD) is a rare immunodeficiency disorder characterized by impaired phagocytic function, leading to recurrent infections and granuloma formation. Genetic mutations in NADPH oxidase complex components, such as CYBB, NCF1, NCF2, and CYBA genes, contribute to the pathogenesis. This case report explores the possible ocular and hematologic complications associated with CGD.Case PresentationA 6-year-old girl with a history of vitrectomy, membranotomy, and laser therapy due to congenital blindness (diagnosed with chorioretinopathy) was referred to the hospital with generalized ecchymosis and thrombocytopenia. Diagnostic workup initially suggested chronic immune thrombocytopenic purpura (ITP). Subsequent admissions revealed necrotic wounds, urinary tract infections, and recurrent thrombocytopenia. Suspecting immunodeficiency, tests for CGD, Nitroblue tetrazolium (NBT) and dihydrorhodamine (DHR) were performed. She had a low DHR (6.7), and her NBT test was negative (0.0%). Her whole exome sequencing results confirmed autosomal recessive CGD with a homozygous NCF1 mutation.ConclusionThis case underscores the diverse clinical manifestations of CGD, including recurrent thrombocytopenia and possible early-onset ocular involvement. The diagnostic challenges highlight the importance of a multidisciplinary approach involving hematologists, immunologists, and ophthalmologists for accurate diagnosis and management. The rare coexistence of ITP in CGD emphasizes the intricate link between immunodeficiency and autoimmunity, requiring tailored therapeutic strategies.

Background evidence indicates that the macrolide-resistant EC2 mutant of Mycoplasma pneumoniae (MP) emerged as the predominant strain during the 2023–2024 epidemic, being associated with immune-mediated complications (e.g., severe immune thrombocytopenia [ITP]), whose clinical characteristics and prognosis remain undefined. This study aimed to compare the severity of bleeding, treatment response and long-term prognosis in children with newly diagnosed severe ITP and non-MP-associated ITP with MP-related mutations during the epidemic of EC2 mutant strains. A cohort of children with MP-ITP or non-MP ITP admitted to Beijing Children’s Hospital from October 2023 to February 2024 was enrolled. Twelve-month outcomes included baseline platelet counts, bleeding severity, short-term responses (at 1 week/1 month/3 months), and sustained remission rates at 6/12 months. The MP group ( n  = 20, median age 6.4 years) showed lower baseline platelet counts (12.0 × 10⁹/L) and higher proportions of severe bleeding (grade 3/4: 30%) compared with non-MP controls ( n  = 46, median age 5.5 years; platelets 21.0 × 10⁹/L; grade 3/4: 13%). Following monotherapy/combination therapy, A one-way analysis of covariance(ANCOVA) revealed significantly higher platelet counts in MP-ITP at 3–12 months ( p  ≤ 0.008), with consistently higher complete response rates in MP-ITP (100% at 1 month, 90% at 12 months) than in non-MP controls (87% at 1 month, 78% at 12 months). In conclusion, MP-related ITP was characterized by severe bleeding but demonstrated favorable treatment responses and long-term outcomes, warranting further investigation of its immunopathogenic mechanisms.

Eltrombopag is an oral, non-peptide, thrombopoietin-receptor agonist that stimulates thrombopoiesis, leading to increased platelet production. This study assessed the efficacy, safety, and tolerability of once daily eltrombopag 50 mg, and explored the efficacy of a dose increase to 75 mg. In this phase III, randomised, double-blind, placebo-controlled study, adults from 63 sites in 23 countries with chronic idiopathic thrombocytopenic purpura (ITP), platelet counts less than 30 000 per μL of blood, and one or more previous ITP treatment received standard care plus once-daily eltrombopag 50 mg (n=76) or placebo (n=38) for up to 6 weeks. Patients were randomly assigned in a 2:1 ratio of eltrombopag:placebo by a validated randomisation system. After 3 weeks, patients with platelet counts less than 50 000 per μL could increase study drug to 75 mg. The primary endpoint was the proportion of patients achieving platelet counts 50 000 per μL or more at day 43. All participants who received at least one dose of their allocated treatment were included in the analysis. This study is registered with ClinicalTrials.gov, number NCT00102739. 73 patients in the eltrombopag group and 37 in the placebo group were included in the efficacy population and were evaluable for day-43 analyses. 43 (59%) eltrombopag patients and six (16%) placebo patients responded (ie, achieved platelet counts ≥50 000 per μL; odds ratio [OR] 9·61 [95% CI 3·31–27·86]; p<0·0001). Response to eltrombopag compared with placebo was not affected by predefined study stratification variables (baseline platelet counts, concomitant ITP drugs, and splenectomy status) or by the number of previous ITP treatments. Of the 34 patients in the efficacy analysis who increased their dose of eltrombopag, ten (29%) responded. Platelet counts generally returned to baseline values within 2 weeks after the end of treatment. Patients receiving eltrombopag had less bleeding at any time during the study than did those receiving placebo (OR 0·49 [95% CI 0·26–0·89]; p=0·021). The frequency of grade 3–4 adverse events during treatment (eltrombopag, two [3%]; placebo, one [3%]) and adverse events leading to study discontinuation (eltrombopag, three [4%]; placebo, two [5%]), were similar in both groups. Eltrombopag is an effective treatment for managment of thrombocytopenia in chronic ITP. GlaxoSmithKline.