Rapid and Effective Vitamin D Supplementation May Present Better Clinical Outcomes in COVID-19 (SARS-CoV-2) Patients by Altering Serum INOS1, IL1B,IFNg, Cathelicidin-LL37, and ICAM1

Background: We aimed to establish an acute treatment protocol to increase serum vitamin D, evaluate the effectiveness of vitamin D3 supplementation, and reveal the potential mechanisms in COVID-19. Methods: We retrospectively analyzed the data of 867 COVID-19 cases. Then, a prospective study was conducted, including 23 healthy individuals and 210 cases. A total of 163 cases had vitamin D supplementation, and 95 were followed for 14 days. Clinical outcomes, routine blood biomarkers, serum levels of vitamin D metabolism, and action mechanism-related parameters were evaluated. Results: Our treatment protocol increased the serum 25OHD levels significantly to above 30 ng/mL within two weeks. COVID-19 cases (no comorbidities, no vitamin D treatment, 25OHD <30 ng/mL) had 1.9-fold increased risk of having hospitalization longer than 8 days compared with the cases with comorbidities and vitamin D treatment. Having vitamin D treatment decreased the mortality rate by 2.14 times. The correlation analysis of specific serum biomarkers with 25OHD indicated that the vitamin D action in COVID-19 might involve regulation of INOS1, IL1B, IFNg, cathelicidin-LL37, and ICAM1. Conclusions: Vitamin D treatment shortened hospital stay and decreased mortality in COVID-19 cases, even in the existence of comorbidities. Vitamin D supplementation is effective on various target parameters; therefore, it is essential for COVID-19 treatment.     

Liver cyst with inflammatory hepatic duct polyp

This is a case report of a 50-year-old woman, who presented with upper abdominal pain, vomiting and two episodes of jaundice in five months. Computerised tomographic scan revealed a cyst in the 4th segment of the liver. Peroperatively it was found to be a simple liver cyst arising from the left hepatic duct. The cyst was excised. Peroperative cholangiogram revealed obstruction in the common hepatic duct. A polyp in the common hepatic duct, causing obstruction, was excised. The presence of liver cyst with hepatic duct polyp is a rare association.     

Spontaneous spinal epidural hemorrhage following disseminated intravascular coagulation resulting in paraplegia: a case report

Context: Spontaneous spinal epidural hemorrhage (SSEH) mostly presents as low back pain with or without a radiculopathy, and rarely with paraplegia or tetraplegia depending on the site and severity of spinal cord compression. We present here a case who had anemia and developed paraplegia following disseminated intravascular coagulation (DIC) due to a transfusion reaction.

Findings: A 65-year-old lady presented with sudden onset chest pain radiating to nape of the neck followed by loss of sensations and power in legs few hours after a blood transfusion. Her past history was negative for diabetes mellitus, hypertension, coronary artery disease, or a bleeding disorder. Her blood pressure was 90/57 mmHg and she had a normal pulse, respiratory rate, and temperature. On neurological examination, she had no motor power and unevokable muscle stretch reflexes in the lower limbs. The sensations were intact till T₃ dermatome. The laboratory evaluation was suggestive of DIC. The magnetic resonance imaging showed a non-enhancing abnormal signal intensity area in the posterior epidural space, extending from CV₄ to LV₄ causing cervico-dorsal cord compression associated with cord edema. Following diagnosis, urgent decompressive surgery was carried out due to deteriorating neurological status. The patient was transfused with five bags of red cell concentrate, two bags of platelets, and four bags of fresh frozen plasma during the operation. The patient regained consciousness following operation, however, the neurological status did not improve. She, unfortunately, died on the third post-op day due to cardiac arrest.

Conclusion: SSEH is a rare cause of paraplegia. Early radiological diagnosis is crucial for timely neurosurgical management and saving patient from permanent neurological deficit or a fatal outcome.     

Increasing peak expiratory flow time in amyotrophic lateral sclerosis

BACKGROUND: Serial measurements of pulmonary function to indicate decreasing respiratory muscle strength in patients with amyotrophic lateral sclerosis (ALS) is well documented. Quantitative outcome measures include declining FVC, FEV1, maximal inspired pressure, maximal expired pressure, and maximal voluntary ventilation. Increasing peak expiratory flow time (PEFT) may represent a further sensitive measure of declining respiratory muscle strength in ALS. METHODS: Fifty-five patients with ALS performed flow-volume loops serially after presentation. The percentage change from baseline values for FVC, peak expiratory flow (PEFR), and PEFT were compared using Spearman correlation coefficients. The prolongation of PEFT with serial tests was analyzed using a Kruskal-Wallis with a Dunn multiple comparison test. Bulbar-onset and limb-onset PEFT was compared using the Mann-Whitney test. RESULTS: PEFT was significantly increased from baseline values at all follow-up tests. However, PEFTs measured at the third, fourth, fifth, and sixth visits, although higher, were not significantly different. Significant negative correlations existed between the increase in PEFT and the decrease in PEFR and FVC. Significant positive correlations existed between the increase in PEFT and days from diagnosis and the decrease in PEFR and decrease in FVC. CONCLUSION: PEFT increases significantly and linearly with time in patients with ALS and may begin to plateau with bulbar symptoms. PEFT increases at a faster rate than the rate of decline in both FVC and PEFR. PEFT is a quantitative measure of decreasing pulmonary function in ALS that is easily measured.     

The relationship between plasma asymmetrical dimethyl-L-arginine and inflammation and adhesion molecule levels in subjects with normal, impaired, and diabetic glucose tolerance

Increasing evidence suggests that the postprandial state is a contributing factor to the development of atherosclerosis. To evaluate the effects of acute hyperglycemia on endothelial dysfunction and inflammation, plasma asymmetrical dimethyl-l-arginine (ADMA), intercellular adhesion molecule 1 (sICAM-1), vascular cell adhesion molecule 1, and C-reactive protein (CRP) levels and secretory phospholipase A(2) (sPLA(2)) activities were measured in subjects with normal (n = 35), impaired (IGT) (n = 25), and diabetic (DGT) (n = 20) glucose tolerance. At baseline, plasma ADMA, sICAM-1, and CRP concentrations and plasma sPLA(2) activities were higher in both the IGT and DGT groups than in the normal glucose tolerance group (for each comparison, each P < .001). Patients with DGT have higher plasma ADMA and sICAM-1 concentrations than patients with IGT (for each, P < .001).Two hours after glucose loading, plasma ADMA and CRP concentrations and sPLA(2) activities were significantly elevated in the 3 groups when compared with baseline levels (for each comparison, P < .001). Plasma vascular cell adhesion molecule 1 and sICAM-1 concentrations were found to be elevated from baseline levels after glucose loading in the IGT and DGT groups (for each comparison, P < .001). Correlation analysis at baseline suggested that there was a significant relationship between ADMA and inflammation and soluble adhesion markers in the studied groups. In conclusion, plasma concentrations of ADMA and of inflammation and adhesion molecules were elevated in the prediabetic state. A complex interrelation could exist between ADMA and inflammation, and mechanisms involved in endothelial dysfunction are multifactorial at the prediabetic and diabetic state.     

The susceptibility of red blood cells to autoxidation in type 2 diabetic patients with angiopathy

We examined the in vitro susceptibility of red blood cell (RBC) lipids to oxidation in type 2 diabetic patients with or without angiopathy. Lipid peroxidation was assessed by quantifying thiobarbituric acid (TBA) reactivity as malondialdehyde (MDA). We also examined the RBC antioxidant status by determining glutathione (GSH) levels. Before in vitro oxidation, RBC MDA levels were significantly higher in both diabetic groups than in the controls (P < .001), and a significant difference was found between the two diabetic groups (P < .05). After in vitro treatment of RBCs with hydrogen peroxide, the degree of lipid peroxidative damage was significantly higher in diabetic patients with angiopathy versus diabetics without angiopathy (P < .001). Diabetic patients have low RBC GSH levels compared with controls, and after in vitro oxidation, the levels were significantly decreased in diabetics (P < .001). There was not a significant correlation between RBC MDA levels and glycated hemoglobin (GHb), plasma cholesterol, and triglyceride. The correlation between RBC MDA and GSH was weak (P < .001). We suggest that the results of this study might help to clarify the role of oxidative mechanisms as an in vitro model of degenerative damage in type 2 diabetic angiopathic complications.