Preoperative Nomogram Incorporating Clinical Factors, Serological Markers and LI-RADS MRI Features to Predict Early Recurrence of Hepatocellular Carcinoma Treated with Transarterial Chemoembolization.

PURPOSE: To develop and validate a preoperative nomogram model that incorporates clinical factors, serological markers and liver imaging reporting and data system (LI-RADS v2018) MRI features for predicting early recurrence (ER) of hepatocellular carcinoma (HCC) treated with transarterial chemoembolization (TACE). METHODS: One hundred and fourteen patients with HCC who underwent MRI scanning before TACE were enrolled retrospectively and divided into a training cohort (n=80) and a test cohort (n=34). The clinical factors, serological markers and LI-RADS v2018 MRI features associated with ER were determined by univariable and multivariable analyses. A nomogram model predicting ER after TACE was developed, and its discriminatory ability, goodness-of-fit and clinical application were evaluated by receiver operating characteristic (ROC) curve, calibration curve and decision curve analysis (DCA), respectively. RESULTS: In total, 74 (64.9%) patients were diagnosed with ER according to the follow-up results. Increased alpha fetoprotein (AFP) levels, larger tumor size, nonsmooth margin, mosaic architecture satellite nodules and corona enhancement were independent predictors associated with ER (p < 0.05). For the established nomogram model that incorporated these six significant predictors, the AUC values were 0.94 (95% CI: 0.89-0.99) and 0.95 (95% CI: 0.88-1.00) for predicting ER after TACE in the training and test cohorts, respectively. The calibration curve and DCA results demonstrate the good goodness-of-fit and clinical benefits of this nomogram. CONCLUSION: A preoperative nomogram model based on serological markers and LI-RADS v2018 MRI features could adequately predict ER in HCC patients after TACE, which may provide personalized guidance for predicting prognosis.

Octreotide-induced acute life-threatening gallstones after vicarious contrast medium excretion: A case report.

BACKGROUND: Octreotide is widely used for the treatment of acromegaly, neuroendocrine tumors, and secretory diarrhea. However, long-term octreotide treatment can increase the incidence of gallstones. Vicarious contrast medium excretion (VCME) through the hepatobiliary system is well known. However, few studies have reported octreotide-induced acute gallstones following VCME. CASE SUMMARY: A 69-year-old man presented with left lower back pain and hematuria caused by a fall. The patient had a history of polycystic kidney disease. VCME occurred following renal artery embolization for a ruptured polycystic kidney. After 5 d of treatment with octreotide, the patient developed acute gallstones and intrahepatic cholestasis which further induced pancreatitis and cholangitis. He was discharged after hemodialysis, antibiotics, and supportive treatments. CONCLUSION: For patients with a high-risk of VCME, octreotide should be cautiously administered and carefully monitored.

Gut microbiota modulates the inflammatory response and cognitive impairment induced by sleep deprivation.

Sleep deprivation (SD) is increasingly common in modern society, which can lead to the dysregulation of inflammatory responses and cognitive impairment, but the mechanisms remain unclear. Emerging evidence suggests that gut microbiota plays a critical role in the pathogenesis and development of inflammatory and psychiatric diseases, possibly via gut microbiota-brain interactions and neuroinflammation. The present study investigated the impact of SD on gut microbiota composition and explored whether alterations of the gut microbiota play a causal role in chronic inflammatory states and cognitive impairment that are induced by SD. We found that SD-induced gut dysbiosis, inflammatory responses, and cognitive impairment in humans. Moreover, the absence of the gut microbiota suppressed inflammatory response and cognitive impairment induced by SD in germ-free (GF) mice. Transplantation of the "SD microbiota" into GF mice activated the Toll-like receptor 4/nuclear factor-κB signaling pathway and impaired cognitive function in the recipient mice. Mice that harbored "SD microbiota" also exhibited increases in neuroinflammation and microglial activity in the hippocampus and medial prefrontal cortex. These findings indicate that gut dysbiosis contributes to both peripheral and central inflammatory processes and cognitive deficits that are induced by SD, which may open avenues for potential interventions that can relieve the detrimental consequences of sleep loss.

Treatment Effects of Short-Term Continuous Positive Airway Pressure on Blood Glucose Control in Type 2 Diabetic Patients with Obstructive Sleep Apnea Syndrome.

PURPOSE: The study aimed at assessing glucose control measured with a continuous glucose monitoring system (CGMS) before and after short-term continuous positive airway pressure (CPAP). MATERIALS AND METHODS: Twenty-four type 2 diabetic patients (T2DM) with Obstructive sleep apnea syndrome (OSAS) (mean age 55.0 ± 9.0 years; BMI 29.5 ± 5.2 kg/m2) were admitted and kept under diet control for 2 days, then underwent 2 overnight polysomnographies: a diagnostic study and one with CPAP titration. Then they were treated by CPAP during sleep for the following three nights. Participants were divided into subgroup D (only diet control) and subgroup M (with DM medication). CGMS was utilized over the last five days. Glucose control was also assessed with plasma insulin and a clinical measure of insulin resistance (HOMA-IR) index. RESULTS: The mean (±SD) apnea-hypopnea index (AHI) at diagnostic polysomnography was 51.2 ± 22.4 (range 10-88) events/h. CPAP treatment in the subjects with OSAS resulted in the index of oxygenation desaturations being reduced from 33.3 ± 20.1 to 1.1 ± 1.6 (P =0.00). CGMS showed mean 24-hours glucose values significantly lower after CPAP treatment than at baseline in both subgroups (7.97±1.31 vs 7.52±0.94, P=0.033 in subgroup D; and 7.72±1.51 vs 7.17±1.21, P=0.05 in subgroup M), as the fasting plasma insulin levels and HOMA-IR were also decreased significantly after CPAP treatment (13.0 ± 7.5µU/mL vs 10.8 ± 5.4µU/mL, P=0.044; and 4.2 ± 2.2 vs 3.1±1.7, P=0.003, respectively). Standard deviation (SD) and mean amplitude of glucose excursions (MAGE) were also decreased in the subgroup D (1.91 ± 1.10 vs 1.61 ± 1.20, P=0.014; 1.26 ± 1.13 vs 1.01 ± 0.98, P=0.008, respectively) only. CONCLUSION: Short-term CPAP treatment in OSAS with type 2 diabetic patients is accompanied by a decrease in blood glucose level and improved insulin sensitivity. Glucose variability was reduced but only in the patients with diet control.

[Effect of acute hypoxia and hypercapnia on arterial stiffness and blood pressure in patients with obstructive sleep apnea hypopnea syndrome].

OBJECTIVE: To investigate the effect of acute hypoxia and/or hypercapnia on cardio-ankle vascular index (CAVI) and blood pressure (BP) in patients with obstructive sleep apnea hypopnea syndrome (OSAHS). METHOD: CAVI and blood pressure were measured before and after isocapnic hypoxic, hyperoxia hypercapnic, and hypoxic and hypercapnic challenge in 28 non-hypertensive patients with OSAHS (AHI > 10/h) and 26 healthy controls (AHI < 5/h), respectively. They were matched for age and sex. Hypoxia and hypercapnia were induced by re-breathing technique. RESULTS: The 2 groups had no differences in regard to systolic (SBP) and diastolic BP(DBP) and CAVI. After hypercapnic challenge, SBP increased significantly in both groups. CAVI decreased significantly in controls, but not in OSAHS. Hypoxia induced significant increase of CAVI, but not in OSAHS. SBP and DBP maintained to the pre-challenge levels in both group. Hypercapnia and hypoxia together caused increase of SBP in both groups, and CAVI increased significantly in controls, but not in OSAHS. CONCLUSIONS: Acute hypoxia and hypercapnia exposure caused change of arterial stiffness and BP in both control and patients with sleep apnea hypopnea syndrome. However, CAVI responses to hypoxic and/or hypercapnic challenge were blunted in patients with OSAHS.

[Effects of short-term continuous positive airway pressure treatment on arterial stiffness in patients with obstructive sleep apnea hypopnea syndrome].

OBJECTIVE: To investigate the effect of short-term continuous positive airway pressure (CPAP) treatment on the arterial stiffness in patients with obstructive sleep apnea hypopnea syndrome (OSAHS). METHODS: Cardio ankle vascular index (CAVI) and blood pressure (BP) were measured before and after sleep in 60 non-hypertensive patients with OSAHS and gender and 60 age-matched healthy controls. CPAP was administrated in 22 of the 60 OSAHS patients. And on the first and third days of the CPAP treatment CAVI and BP were measured in the morning, i. e., after sleep. RESULTS: In the morning, the CAVI of the OSAHS patients was 8.0 +/- 1.2 m/s, significantly higher than that before sleep (7.3 +/- 1.0, P = 0.000), the diastolic BP (DBP) was (86 +/- 12) mm Hg, significantly higher than that before sleep (83 +/- 13 mmHg, P = 0.001), and the mean BP (MBP) was (101 +/- 12) mm Hg, significantly higher than that before sleep (98 +/- 14, P = 0.00116). However, there were no significant differences in these parameters among the controls The systolic BP (SBP) of the OSAHS patients did not changed significantly after sleep, however, there was a tendency to decrease in the controls [(123 +/- 14) vs (121 +/- 13) mm Hg, P = 0.074). After the first night treatment, the CAVI, SBP, DBP, and mean BP of the 22 severe OSAHS patients decreased significantly (all P < 0.05), and after three nights treatment, only the CAVI showed further significant decrease (P < 0.05). CONCLUSION: Sleep induces increase of artery stiffness in OSAHS patients, but not in the normal controls. Short-term CPAP may decrease CAVI without affecting the blood pressures. Early atherosclerosis in the patients with OSAHS may be reversed by CPAP therapy.

[Respiration control dysfunction and the relationship to sleep-disordered breathing in patients with chronic obstructive pulmonary disease].

OBJECTIVE: To analyze the polysomnographic (PSG) features of sleep apnea hypopnea syndrome (SAHS) in patients with chronic obstructive pulmonary disease (COPD), and to define the association between SAHS and respiratory control disorder. METHODS: Three hundred patients with stable COPD were screened for SAHS using questionnaire, Epworth sleep scale (ESS) and home pulse oximeter testing. Those with ESS > or = 10 or oxygen desaturation over 3% more than 5 times per hour sleep were under further PSG testing. The PSG features were compared between COPD patients with apnea hypopnea index (AHI) > 10 and 118 SAHS patients with normal lung function. The two groups were matched for age, body mass index (BMI) and AHI. Among them 22 with COPD and AHI > or = 10 were tested for the chemo-responsiveness to isocapnic hypoxia and hypercapnia. RESULTS: Among the 300 patients with stable COPD, 79 had AHI over 10, meeting the diagnostic criteria of overlap syndrome (OS). Analysis of the polysomnography found that 32 cases (40%) with OS had more hypoventilation lasting over 1 min during sleep. Compared to patients with SAHS only, OS patients had higher percentage of hypopnea index over AHI [(69 +/- 30)% vs (52 +/- 31)%] and a higher percentage of total hypopnea time over total time of sleep apnea and hypopnea [(15 +/- 12)% vs (12 +/- 10)%]. OS patients also had lower hypoxic [(-0.11 +/- 0.05) vs (-0.35 +/- 0.24) L.min(-1).%(-1)] and hypercapnic responses [(1.1 +/- 0.8) vs (1.6 +/- 0.8) L.min(-1).mm Hg(-1) (1 mm Hg = 0.133 kPa)]. CONCLUSION: Patients with both COPD and SAHS had more episodes of hypopnea and hypoventilation during sleep, and had depressed chemo-responsiveness to hypoxia during wakefulness.

[Effect of noninvasive ventilation on chemoresponsiveness in patients with sleep apnea and chronic obstructive pulmonary disease].

OBJECTIVE: To investigate the effect of noninvasive ventilation on respiratory control in patients with chronic obstructive pulmonary disease (COPD) combined with sleep a apnea-hypopnea syndrome (SAHS)-overlap syndrome (OS). METHODS: Ten body mass index, apnea-hypopnea index, and age-matched OSAHS patients, 5 being hypercapnic (PaCO(2) > 45 mm Hg) OSAHS patients with normal FEV(1)/FVC, and 5 being OSAHS patients with COPD and the mean FEV(1)/FVC of 59% +/- 6% underwent bi-level positive airway pressure (BiPAP) treatment. Hypoxic responses, including the ratio of the change in minute ventilation (DeltaVE) to the change in arterial oxygen saturation (DeltaSaO(2)), and hypercapnic responses (DeltaVE/DeltaPaCO(2) ratio) were tested during wakefulness before treatment and 6 weeks after the treatment. RESULTS: Before treatment, the DeltaVE/DeltaSaO(2) ratios of the OS and OSAHS patients were (-0.023 +/- 0.049) L.min(-1).%(-1) and (-0.16 +/- 0.06) L.min(-1).%(-1) respectively, both lower than the laboratory normal value [(-0.35 +/- 0.21) L.min(-1).%(-1)]. The DeltaVE/DeltaPaCO(2) ratio of the OS patients was (0.54 +/- 0.16) L.mm Hg(-1), significantly lower than the normal value [(1.26 +/- 0.54) L.mm.Hg(-1), P < 0.05]. After receiving 6 weeks of noninvasive ventilation treatment, the hypoxic response of OSAHS patients were (-0.16 +/- 0.06) L.min(-1).%(-1), significantly higher than that before treatment [(-0.36 +/- 0.14) L.min(-1).%(-1)], and hypercapnic response of the OSAHS patients was (1.30 +/- 0.62) L.min(-1).mm Hg(-1), significantly lower than that before treatment [(1.78 +/- 0.93) L.min(-1).mm Hg(-1)], both bring within the normal ranges. In the patients with OS, the hypercapnic response was unchanged [(0.54 +/- 0.16) vs (0.51 +/- 0.23) L.min(-1).mm Hg(-1)], and the hypoxic responses increased significantly but still remained at a very low level [(-0.023 +/- 0.049) vs (-0.09 +/- 0.007) L.min(-1).%(-1)] after treatment. CONCLUSION: Hypercapnic and hypoxic responses in patients with OS and in patients with OSAHS respond differently after pressure support ventilation. This indicates that depressed chemoresponsiveness in patients with OS may not be only a response to sleep-disordered breathing.

[Changes of sleep architecture in patients with narcolepsy].

OBJECTIVE: To investigate the sleep architectures of patients with narcolepsy. METHODS: 38 drug-naive narcoleptic patients, 25 males and 13 females, aged 21 +/- 6.5, and 44 age-, sex ratio-, and BMI-matched normal persons underwent polysomnography (PSG) and multiple sleep latency test (MSLT) during one night sleep. Conventional visual scoring of the polysomnograms was performed according to the international. RESULTS: The sleep latency of the patients was 5.6 min, however, 30 patients (79%) complained of fragmented nocturnal sleep and difficulty to fall asleep again. The sleep efficiency of the narcoleptics was 81.7% +/- 12.5%, significantly lower than that of the normal persons (87.1% +/- 7.9%, P = 0.029). The non-rapid eye movement (NREM) I sleep accounted for (21.5 +/- 12.2)% in the patients, a proportion significantly higher than that of the normal persons [(10.3 +/- 6.3)%, P = 0.000]). The AHI of the patients was 0.6 +/- 1.3 times/h, not significantly different from that of the normal persons (0.5 +/- 1.1 times/h). Although the rapid eye movement (REM) period and eye movement density of the narcoleptics were significantly increased, their REM period duration was not significantly different from that of the normal subjects (17.7% +/- 6.9% vs 18.9% +/- 5.5%, P = 0.23), probably due to the interruption of REM sleep by more frequent arousals in narcoleptics. PSG did not show significant periodic leg movements in these 2 groups. CONCLUSION: One of the important symptoms of narcolepsy, night sleep disturbance may contribute to the pathological sleepiness of narcolepsy during daytime.

[Effects of uvulopalatopharyngoplasty surgery on subsequent continuous positive airway pressure in patients with obstructive sleep apnea-hypopnea syndrome].

OBJECTIVE: To determine the effect of uvulopalatopharyngoplasty (UPPP) therapy on post-surgery continuous positive airway pressure (CPAP) treatment during non-rapid eye movement (NREM) and rapid eye movement (REM) sleep in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), and to evaluate the use of Bi-level positive airway pressure (BiPAP) in whom CPAP therapy failed. METHODS: Thirty-four OSAHS patients after UPPP surgery were tested more than 3 months after the procedure. Among them 25 patients were treated with classical UPPP (cUPPP), in which all of the uvula and part of the soft palate were removed. Nine underwent modified UPPP (mUPPP), keeping part of the uvula. The control group consisted of 34 age, body mass index (BMI) and apnea hypopnea index (AHI) matched, newly diagnosed OSAHS patients without prior treatment. Four patients receiving both pre- and post-surgery tests were included in both groups. A manual titration of CPAP to determine the optimal CPAP pressure (oCPAP) and the highest CPAP pressure (hCPAP) the patient can tolerate was performed during both NREM and REM sleep in all 68 patients. RESULTS: 72% of the UPPP patients had less than 50% decrease in AHI, and 82% of the 34 patients still had AHI > 15 during post-operation PSG test. Hence, most of them needed further therapy. All of the untreated OSAHS patients could tolerate 17-20 cm H2O of CPAP during NREM and REM sleep. None had severe mouth air leak before an oCPAP was reached. In contrast, five in the surgery group failed to respond to CPAP treatment during both NREM and REM sleep, and one more during REM sleep. All of the nine patients who had a mUPPP could tolerate CPAP. One of the four tested both before and after surgery failed to respond to CPAP treatment after surgery during REM sleep and one during both NREM and REM sleep. However, the six patients failed to respond to CPAP treatment tolerated BiPAP therapy well. CONCLUSIONS: In a considerable number of patients with OSAHS, UPPP may compromise the applicability of nasal CPAP as a subsequent therapy, and BiPAP might be a treatment option for patients who could not tolerate CPAP treatment.

[Clinical features of early-onset narcolepsy].

OBJECTIVE: To investigate the clinical features of early onset narcolepsy. METHODS: The clinical data of 105 consecutive patients with narcolepsy, 63 of which with an onset age of 9.7 +/- 3.1 on average and 42 with an onset age of 22.8 +/- 9.3 on average. Interrogation, physical examination, CT, and MRI were carried out. Polysomnography was conducted. Then the data were compared between these 2 groups. RESULTS: All 105 patients showed daytime sleepiness. The incidence rate of cataplexy was 92% in the early onset group, significantly higher than that of the late onset group (P = 0.023). There were no significant differences in the rates of sleep paralysis, hypnagogic hallucination, and disturbed nocturnal sleep. Multiple sleep latency test showed that the mean sleep latency of the early-onset group was 4.5 +/- 4.0 min, significantly shorter than that of the late onset group (7.0 +/- 5.7 min, P = 0.018); the REM sleep latency of the early onset group was 3.4 +/- 3.2 min, significantly shorter than that of the late onset group (4.8 +/- 2.2 min, P = 0.02). The number of REM sleep of the early onset group was 3.4 +/- 2.0, significantly more than that of the late onset group (2.5 +/- 1.9, P = 0.09). The apnea and hypopnea index of the late onset group was 9.2 +/- 16.5, significantly higher than that of the early onset group (1.9 +/- 6.3, P = 0.009). The 3 cases of narcolepsy with family history were all cases of early onset narcolepsy. CONCLUSION: Early onset narcolepsy patients have more severe daytime sleepiness and higher rate of cataplexy. The pathogenesis of early onset narcolepsy may be more closely associated with genetic factors.