Extrapontine myelinolysis caused by rapid correction of pituitrin-induced severe hyponatremia: A case report.

BACKGROUND: Severe hyponatremia is considered a rare complication of pituitrin, which is widely used for the treatment of pulmonary hemorrhage. However, the management of pituitrin-associated hyponatremia can be challenging because a rapid correction of hyponatremia may cause the development of osmotic demyelination syndrome, resulting in life-threatening neurological injuries. CASE SUMMARY: A 20-year-old Chinese man with massive hemoptysis developed symptomatic hyponatremia (116 mmol/L) after therapy by a continuous intravenous drip of pituitrin. To normalize his serum sodium, a hypertonic saline infusion was applied for 3 d, and the pituitrin administration was stopped concurrently. Then, an overly rapid increase in serum sodium level (18 mmol/L in 24 h) was detected after treatment. One day later, the patient experienced a sudden onset of generalized tonic-clonic seizures, as well as subsequent dysarthria and dystonia. Magnetic resonance imaging revealed increased signal intensity in the bilateral symmetric basal ganglia on the T2-weighted images, compatible with a diagnosis of extrapontine myelinolysis. The patient received an intravenous administration of high-dose corticosteroids, rehabilitation, and neurotrophic therapy. Finally, his clinical abnormalities were vastly improved, and he was discharged with few residual symptoms. CONCLUSION: Physicians should be fully aware that pituitrin can cause profound hyponatremia and its correction must be performed at a controlled rate to prevent the development of osmotic demyelination syndrome.

Autonomic nervous infiltration positively correlates with pathological risk grading and poor prognosis in patients with lung adenocarcinoma.

BACKGROUND: Perineural invasion has been found in several types of human tumors, and is associated with poor prognosis; however, few studies have examined perineural invasion in lung cancer. We evaluated the relationship between autonomic nervous densities, pathological risk grading, and prognosis in patients with lung adenocarcinoma (LADC). METHODS: Neural fiber expression was examined by immunofluorescence in resected lung specimens in control patients (n = 30), and low-risk (n = 22), and high-risk LADC patients (n = 43). The nerve densities of normal lung tissue and abnormal lung tissues in the tumor and surrounding tissues were evaluated by a semi-quantitative score method. RESULTS: Increased sympathetic fibers mainly infiltrated the paratumoral area, while increased parasympathetic fibers were largely restricted to the tumor (paratumor vs. tumor, P = 0.000 in high, P = 0.034 in low; each). In addition, high-risk patients presented the highest density of neural fibers, followed by low-risk and control patients ( P = 0.000; each). In Kaplan-Meier survival analysis, the densities of sympathetic fibers in paratumoral tissue and parasympathetic fibers in the tumor, respectively, correlated with poor recurrence-free survival in patients who were not treated with adjuvant therapy ( P < 0.001; each). Further multivariate analysis showed that these two factors were associated with poor prognosis in all LADC patients ( P = 0.024 sympathetic fibers; P = 0.037 parasympathetic fibers). CONCLUSION: These findings reveal a positive correlation between nervous infiltration and risk of poor prognosis in patients with LADC.

Determination of antioxidant capacity and phenolic content of chocolate by attenuated total reflectance-Fourier transformed-infrared spectroscopy.

Antioxidant capacity and phenolic content of chocolate, containing different amounts of cacao (35-100%), were determined using attenuated total reflectance (ATR)-Fourier transformed-infrared (FT-IR) spectroscopy (4000-550cm(-1)). Antioxidant capacities were first characterized using DPPH (2,2-diphenyl-1-picrylhydrazyl) and ORAC (oxygen radical absorbance capacity) assays. Phenolic contents, including total phenol and procyanidins monomers, were quantified using the Folin-Ciocalteu assay and high performance liquid chromatography coupled with photodiode array detector (HPLC-DAD), respectively. Five partial least-squares regression (PLSR) models were constructed and cross-validated using FT-IR spectra from 18 types of chocolate and corresponding reference values determined using DPPH, ORAC, Folin-Ciocalteu, and HPLC assays. The models were validated using seven unknown samples of chocolate. PLSR models showed good prediction capability for DPPH [R(2)-P (prediction)=0.88, RMSEP (root mean squares error of prediction)=12.62µmol Trolox/g DFW], ORAC (R(2)-P=0.90, RMSEP=37.92), Folin-Ciocalteu (R(2)-P=0.88, RMSEP=5.08), and (+)-catechin (R(2)-P=0.86, RMSEP=0.10), but lacked accuracy in the prediction of (-)-epicatechin (R(2)-P=0.72, RMSEP=0.57). ATR-FT-IR spectroscopy can be used for rapid prediction of antioxidant capacity, total phenolic content, and (+)-catechin in chocolate.

[Event-related potentials P(300) with memory function in obstructive sleep apnea syndrome].

OBJECTIVE: To explore the variability of event-related potentials P(300) and memory function in patients with obstructive sleep apnea syndrome(OSAS). METHODS: Polysomnography (PSG) event-related potentials (ERPs) P(300) and Wechsler Memory Scale (WMS) were detected in 30 subjects with OSAS and 20 normal controls. RESULTS: The memory quotient [(86 ± 13) scores] in the OSAS group was significantly lower than that in the control group (P < 0.01). The latency of P(300) [(410 ± 80) ms at Cz and (409 ± 80) ms at Pz] in the OSAS group was significantly longer than that in the control group (P < 0.01). In the OSAS group, the latency of P(300) was correlated negatively with the memory quotient and nocturnal hypoxemia, but positively with apea/hypopnea index (AHI, P < 0.01). CONCLUSION: OSAS has memory deficit, which can be evaluated comprehensively by P(300) and WMS. The longer latency of P(300) might be regarded as one of the electrophysiological markers to indicate the severity of cognition in OSAS. Recurrent attacks of nocturnal intermittent hypoxemia may cause the regional brain damage related to cognition defect.