2018年 · 第57卷第07期

Irritable bowel syndrome (IBS) is the most common functional gastrointestinal disease, with complex etiology and pathogenesis. It was previously thought to be related to mental stress, visceral hypersensitivity, abnormal intestinal motility, intestinal mucosal barrier dysfunction, etc. Recent studies have shown that intestinal microecological disturbance can lead to IBS by inducing local inflammatory reaction in the intestine, destroying the intestinal mucosal barrier function, affecting the enteral nervous system and even the function of the central nervous system. Therefore, targeting intestinal microecology may become a new and effective therapeutic modality. However, there are still many unknowns in the process from theory to clinical practice that need to be reliably evidenced through high-quality clinical research, such as: Which groups of IBS patients are effective for probiotic treatment? What probiotic strains, dosages, and dosage forms are better for IBS treatment? How to establish a fast, simple and accurate method to judge whether the structure of intestinal flora has changed? Which is the efficacy of a single probiotic strain versus a combination of multiple probiotic strains? How safe are probiotic preparations? In this issue, Professor Duan Liping of the Third Hospital of Peking University wrote an article "Attach importance to the clinical research on the use of intestinal microecological preparations in patients with irritable bowel syndrome". Welcome to Read.

irritable bowel syndrome (IBS) is the most common functional gastrointestinal disease, with a prevalence of up to 20% in western countries, and an average prevalence of about 6.5% in Chinese population^[1]。 The etiology and pathogenesis of IBS are complex, which are related to mental stress, visceral hypersensitivity, abnormal intestinal motility, intestinal mucosal barrier dysfunction and intestinal microecological disturbance^[2]。 The disturbance of intestinal microecology may lead to the occurrence of IBS by inducing local inflammatory reaction of intestine, destroying the function of intestinal mucosal barrier, affecting the function of enteral nervous system and even central nervous system. Therefore, targeting intestinal microecology may become a very effective therapeutic modality.

The patient was an 18-year-old male. He was admitted to hospital in January 2017 due to "numbness and weakness of his limbs for 4 months and unsteady walking for 2 months". Previous neurodermatitis for 5 years, denial of special drug, food contact history. The patient started taking nitrous oxide after studying abroad in August 2016 (N₂O, laughing gas), 500 tubes (8 g/tube) twice a week. In September 2016, I developed numbness in both toes, which lasted for half a month. I took "vitamin B" orally by myself.₁₂"1 month, during which smoking N₂O The frequency was the same as before, and the symptoms did not resolve. In October 2016, numbness worsened below both ankles, gradually rising to both thighs and fingers, accompanied by weakness in both lower limbs. At the beginning of November, the numbness of both fingers aggravated, and at the same time, there was weakness in both hands, labor in twisting the bottle cap, and unsteady walking. From mid-November to mid-December, the frequency of smoking decreased, and the patient's symptoms improved slightly during 2 to 3 smokes of 500 sticks each time. Physical examination of nervous system: clear consciousness, fluent speech, normal function of higher cortex; When both eyes were fixed to the left, they were accompanied by small horizontal nystagmus, and no obvious abnormality was found in the examination of remaining cranial nerves; Muscle volume and muscle tone of extremities were normal, and muscle strength of distal right lower extremity was 5^－Grade 5, body muscle strength of remaining limbs grade 5, superficial sensation of limbs and trunk normal, bilateral tuning fork vibration sensation, position sensation and figure sensation below anterior superior iliac spine decreased, Romberg sign (+), bilateral biceps reflex (+ + +), bilateral knee tendon reflex (+ + +), bilateral Achilles tendon reflex (+), abdominal wall reflex disappeared, bilateral Babinsky sign (+).

The patient was a 42-year-old female. He had a history of chronic hepatitis C for 2 years and was hospitalized on March 3, 2013. Hepatitis C virus (HCV) RNA was checked for 1.32×10⁵IU/ml, HCV genotype 1b, normal liver and kidney function, fasting blood glucose (FPG) 5.2 mmol/L, fasting insulin 12.70 mIU/L, glycosylated hemoglobin (HbA1c) 4.5%, anti-thyroglobulin antibody (TgAb), anti-thyroid peroxidase antibody (TPOAb) and other autoantibodies were negative. Antiviral therapy was started on March 4, and peginterferon α-2a (PEG-inf α-2a) 180 μ g was injected intramuscularly once a week, combined with ribavirin tablets 0.4 g, three times a day. After 1 week, HCV RNA was reexamined at 4.46×10⁴IU/ml.

In September 2017, Nature Communications Magazine, an important international journal, published a clinical-basic comprehensive study led by Professor Fan Dongsheng of the Department of Neurology, Peking University Third Hospital, and jointly completed by Chinese, Australian and 25 international scientific research institutions: "Cross-ethnic meta-analysis clarifies the association between GPX3-TNIP1 gene and amyotrophic lateral sclerosis" [Benyamin B, He J, Zhao Q, et al. Cross-ethnic meta-analysis identifies association of the GPX3-TNIP1 locus with amyotrophic lateral sclerosis. Nat Commun, 2017, 8 (1): 611.].

Sepsis is the most common cause of death in patients in critical care medicine, and the rational use of antibacterial drugs is an important treatment for sepsis^[1]。 However, due to the complexity and lack of specificity of sepsis itself, overuse of antimicrobial drugs is very common. Procalcitonin (PCT), as a commonly used clinical biomarker of sepsis, has been shown to guide the basis for antimicrobial reduction and discontinuation through dynamic monitoring^[2]。 It is worth noting that the level of PCT is influenced by various clinical factors. Only by fully understanding the various clinical factors affecting the level of PCT can the dynamic change of PCT be better used to rationalize the withdrawal of antimicrobial drugs. Combined with clinical examples, the implementation of PCT-guided antibacterial drug reduction in the treatment of sepsis is discussed.

Charcot-Marie-Tooth disease (CMT) is a group of monogenic hereditary motor and sensory neuropathies (HMSN) with high clinical and genetic heterogeneity. This group of diseases onset more than in children and adolescents, and clinically is typical of slowly progressing symmetrical distal limb muscle weakness and atrophy, mild to moderate peripheral sensory impairment, attenuation or disappearance of tendon reflexes, and high arched foot. According to the characteristics of neuroelectrophysiology and neuropathology, CMT is mainly divided into demyelinating type (CMT1) and axonal type (CMT2). In recent years, CMT intermediate type (DI-CMT) is gradually being recognized.

portal vein thrombosis (PVT) is attracting more and more attention as one of the common complications of liver cirrhosis. The pathogenesis of PVT is complex, and anticoagulant therapy is challenging for patients with liver cirrhosis. Some existing studies suggest that treatment of PVT may improve the prognosis of patients with liver cirrhosis^[1]However, due to the lack of clear guidelines, there are still many problems to be solved urgently in clinical work. It is intended to review and review the current research on PVT anticoagulant therapy for liver cirrhosis, so as to provide help for formulating more standardized and rational treatment strategies in clinic.

Azathioprine is a commonly used immunosuppressive agent in clinic, which is commonly used in the treatment of various autoimmune diseases and acute lymphocytic leukemia and anti-rejection of transplanted organs. Common adverse drug reactions include bone marrow suppression, liver injury, drug fever, arthritis, rash, gastrointestinal symptoms, etc. Among them, azathioprine-associated leukopenia is defined as leukocyte<3.0×10⁹/L, is one of the important adverse reactions of azathioprine, which often leads to clinical discontinuation. In severe cases, it can cause bone marrow hematopoietic arrest, secondary infection and even life-threatening. Among Caucasians, the incidence of leukopenia is about 3.7%^[1]； Among Asians, the incidence rate is as high as 25.7% to 39.6%^[2,3,4]。 Understanding the mechanism of azathioprine-related leukopenia has important clinical significance for rational drug selection, improving therapeutic efficiency and reducing side effects. In the past, the knowledge of azathioprine-related leukopenia was relatively limited, but recent studies have found that multiple genetic/molecular pathways affect the production and role of azathioprine metabolites. The recent progress on the mechanism of azathioprine-related leukopenia in recent years is summarized as follows.