Covid-19 and acute kidney injury: A new perspective.

The novel coronavirus disease 19 (nCoV19) is universally known as Covid-19, which is caused by severe acute respiratory coronavirus 2 (SARS-CoV-2), and affects diverse range of organs, presenting with pulmonary manifestations as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), and extra-pulmonary manifestations like acute kidney injury (AKI). AKI is regarded as a poor prognostic factor in patients with severe Covid-19, thus early detection and management of this critical status may reduce the risk of complications and mortality. We present the case of a 30 years old man with moderate Covid-19 presenting with haematuria and eventually diagnosed as AKI. The patient was managed compared with a Covid-19 patient as control. The patient recovered within three weeks of supportive and standard care therapy. Reversible AKI and associated haematuria can be the presenting features of Covid-19 and are linked with mild-moderate SARS-CoV-2 infection.

Osteocalcin serum levels in obese patients with type 2 diabetes mellitus: The virtual points observed in a case control study.

OBJECTIVE: To elucidate the effect of metformin alone or in combination with sitagliptin on osteocalcin serum levels in obese patients with type 2 diabetes mellitus (T2DM). METHODS: This case-control study was conducted at the Department of Clinical Pharmacology and Therapeutic, College of Medicine, Mustansiriyah University, Baghdad, Iraq, from February to April, 2019. This study comprised 62 obese T2DM patients compared with 28 healthy controls, they were divided into three groups; Group I: Obese patients with T2DM on metformin (n=36), Group II: Obese patients with T2DM on metformin plus sitagliptin (n=26), and Group III: healthy controls subjects (n=28). Body mass index (BMI), blood pressure profile, lipid profile, Glycaemic indices, and serum levels of human osteocalcin were measured. The data analysis was done by using SPSS 20. RESULTS: Osteocalcin serum level was lower in patients with T2DM compared with the control (P=0.001), also it was relatively low in metformin (MT) group (21.04±3.16 ng/mL) compared to sitagliptin (ST) group (25.65±7.30 ng/mL), (P=0.04). In relation to the HbA1c, osteocalcin serum level was reduced in patients with T2DM with high HbA1c (HbA1c-H) compared to the patients with T2DM with low HbA1c (HbA1c-L), (P=0.03) and was not significantly different when compared with moderate HbA1c (HbA1c-M), (P>0.05). However, osteocalcin was negatively correlated with HOMA-IR(r=-0.78, P=0.0001). CONCLUSIONS: Osteocalcin serum level was reduced in T2DM patients and negatively correlated with HOMA-IR and HbA1c and FBG. Combination of metformin with sitagliptin was more effective than metformin monotherapy in amelioration of osteocalcin serum level in patients with T2DM.

Intercellular adhesive molecule 1(ICAM-1) and acute ischaemic stroke: Role of statins.

OBJECTIVES: To demonstrate the differential effect of atorvastatin and rosuvastatin on the Intercellular adhesive molecule 1(ICAM-1) in acute ischaemic stroke (AIS) patients. METHODS: The case-control study was done in the Department of Clinical Pharmacology and Therapeutic, Mustansiriyah University, Baghdad, from May to July, 2020 and involved sixty-six patients with AIS compared with twenty-two healthy controls. They were divided into four groups; Group I: Patients with AIS on atorvastatin therapy (n=22). Group II: Patients with AIS on rosuvastatin therapy (n=22), Group III: Patients with AIS not on statin therapy (n=22), Group IV: Healthy controls (n=22). Anthropometric, lipid, and pressure profiles were evaluated. As well, ICAM-1 serum level was estimated in different treatment groups. SPSS version 20.00 was used for data analysis. RESULTS: ICAM-1 levels were increased in patients with AIS compared to the controls. ICAM-1 serum levels were higher in patients with AIS not on statins therapy compared to the controls (P=0.0001), and it was lower in patients with AIS on statins therapy (77.41±16.46) as compared with patients with AIS not on statin therapy (118.71±10.38), (P=0.001). Besides, there was differential effect of statin therapy on the ICAM-1 serum level, which was higher in patients with AIS on rosuvastatin (72.93±9.03) as compared with patients with AIS on atorvastatin (70.61±10.94), (P=0.44). Stroke risk score (SRS) was lower in patients with AIS on atorvastatin therapy (7.60±2.05) as compared with patients with AIS on rosuvastatin therapy (9.11±2.72), (P=0.04). CONCLUSIONS: ICAM-1 is regarded as a surrogate biomarker of AIS in patients with underlying poor cardio-metabolic profile. Both atorvastatin and rosuvastatin are effective in attenuation of AIS measured by lowering of ICAM-1 serum levels.

Beneficial effects of levothyroxine replacement therapy on leptin adiponectin ratio in patients with idiopathic primary hypothyroidism.

OBJECTIVE: To assess the metabolic effects of primary hypothyroidism (PHT) on the leptin (LP), adiponectin (ADP) level and leptin adiponectin ratio (LAR), with identification of the beneficial effects of L-thyroxine (LT4) therapy on these parameters. METHODS: This case-control study was conducted at the Department of Pharmacology, College of Medicine, Mustansiriyah University, Baghdad, Iraq, from July to October 2019. This study included 62 PHT patients, of whom 27 were newly diagnosed and 35 were on LT4 therapy. There were 28 healthy controls. Anthropometric, lipid and pressure profiles were evaluated along with estimation of TSH, T3, T4, LP and ADP serum levels. SPSS version 20.00 was used for data analysis. RESULTS: LP serum level did not significantly differ among the three groups (P=0.23), however, ADP serum level was higher in patients with PHT on LT4 therapy (77.48±9.97ng/dL) as compared to the newly diagnosed patients without LT4 (66.21±7.67ng/dL), and controls (71.40±10.72), (P=0.01). Moreover, LAR was higher in non-treated PHT (1.29±0.18) as compared to the controls (1.13±0.14), (95%CI=0.0568 to 0.2632, P=0.001) and treated PHT (1.04±0.16), (95%CI=-0.3480 to -0.1520, P=0.001). On the other hand, no significant difference was detected between healthy controls and treated PHT patients (95%CI=-0.1871 to 0.0071, P=0.07). CONCLUSIONS: PHT is associated with poor cardio-metabolic profile and high LAR. ADP but not LP, mainly affected in patients with PHT. However LAR is better than ADP and LP in reflecting the underlying PHT-induced cardio-metabolic derangements. LT4 replacement therapy improves cardio-metabolic profile, ADP and LP serum levels with significant amelioration of LAR in PHT patients.

Neuropeptide Y-Agouti related peptide ratio (NAR) in patients with idiopathic primary hypothyroidism: Nudge and Risk.

OBJECTIVE: To illustrate the role of neuropeptide Y (NPY), agouti-related-peptide (AgRp) and their ratio in patients with primary hypothyroidism (PHT) regarding the effect of levothyroxine (LT4) replacement therapy. METHODS: The case-control study was conducted at the Department of Pharmacology, College of Medicine, Mustansiriya University, Baghdad, Iraq, from March to June, 2020 and involved 40 patients with primary hypothyroidism (PHT), including 20 newly diagnosed patients and 20 patients on levothyroxine (LT4) replacement therapy compared to 20 healthy controls. Anthropometric, lipid and pressure profiles were evaluated. Also T3, T4, TSH, NPY and AgRp serum level were estimated in different treated groups. SPSS version 20.00 was used for data analysis. RESULTS: Body mass index (BMI) was higher in the newly diagnosed patients without thyroxine therapy as compared to patients on thyroxine therapy (P=0.03). Blood pressure profile was higher in patients with PHT compared to the controls (P=0.0001). NPY serum level was lower in patients with PHT without thyroxine therapy (27.32±10.30ng/dL) as compared to patients with PHT on thyroxine therapy (61.10±22.78ng/dL), (P=0.04). AgRP serum level was lower in patients with PHT (9.81±4.86ng/dL) as compared to the patients on the thyroxine therapy (28.99±2.16ng/dL), (P=0.03). Besides, NPY-AgRP ratio (NAR) was higher in patients with PHT (2.78±0.14) as compared to patients with PHT on thyroxine therapy (2.10±0.19), (P=0.0001). CONCLUSION: Both of NPY and AgRP serum levels are reduced in the newly diagnosed patients with PHT and ameliorated following LT4 replacement therapy. Also NPY/AgRP ratio is linked with early PHT and regarded as a prognostic value for the outcomes of patients with PHT.

Differential effects of statins on matrix metalloproteinase-9 (MMP-9) in patients with acute ischaemic stroke: A potential for salutary.

OBJECTIVE: To illustrate the differential outcome of atorvastatin versus rosuvastatin on matrix metalloproteinases (MMP-9) in patients with acute ischaemic stroke (AIS). METHODS: The case-control study was done in the Department of Clinical Pharmacology and Therapeutic, Mustansiriyah University, Baghdad, Iraq, from March to June, 2020 and involved 66 AIS patients and 22 healthy controls. They sub-grouped into Group A: AIS patient on statins therapy (n=44), with 22 on atorvastatin and 22 on rosuvastatin. Group B: AIS patients not on statins therapy (n=22). Anthropometric, lipid, and pressure profiles were evaluated. As well, MMP-9 level was estimated in different treated groups. SPSS version 20.00 was used for data analysis. RESULTS: MMP-9 level was greater in patients with AIS (19.69±7.49 ng/dL) mainly those not on statin therapy (28.24±12.14 ng/dL) compared to the controls (10.54±1.92 ng/dL), (P=0.003). Regarding the differential effect of statins therapy on MMP-9 serum level in patients with AIS, it was (20.63±5.67 ng/dL) in patients on atorvastatin therapy and (19.69±5.41 ng/dL) in patients on rosuvastatin therapy, (P=0.57). MMP-9 serum level was highly correlated with stroke risk score (SRS) in patients with AIS not on statins therapy (P<0.001, r=0.89) as compared with SRS in patients with AIS on statins therapy (P=0.03, r=0.42). CONCLUSIONS: MMP-9 is regarded as a surrogate biomarker of AIS in patients with underlying poor cardio-metabolic profile. Both atorvastatin and rosuvastatin are operative in attenuation of AIS measured by lowering of MMP-9 serum levels.

Pregnancy and risk of vertical transmission in Covid-19.

OBJECTIVE: The current systematic review was planned to illustrate severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections during pregnancy and to explore pregnancy outcomes, vertical and perinatal transmission as well as management of coronavirus disease-2019 (Covid-19) during pregnancy. METHODS: The multidisciplinary systematic review was conducted at the Department of Clinical Pharmacology and Therapeutic Medicine, Al-Mustansiriyah University, Bagdad, Iraq. The literature search was conducted in September 2021 and included databases as Medline, PubMed, Scopus, Web of Science, Cochrane Central Register of Controlled Trials and Science Direct databases related to articles on pregnancy and SARS-CoV-2 infections, published between December 2019 and July 2021. RESULTS: Of the 30 articles reviewed, 12(40%) were included. Major reasons for including a small number of studies in systematic review were that majority of the studies had insufficient description of study; analysis was duplicate across various publications, and inadequate explanation of impact of SARA-CoV-2 infection on the pregnancy outcomes. This review included 12 studies based on the assessment and estimation of risk of bias and quality of the eligible studies. CONCLUSIONS: Findings revealed that pregnant women were predominantly susceptible to the respiratory viral infection and severe pneumonia due to physiological immune-suppression, immune adaptation and pregnancy-induced changes. The clinical presentation and management of pregnant women with Covid-19 is similar to that of non-pregnant women and there is no strong clinical evidence of vertical transmission. Also, only chloroquine and remdesivir have been found to be effective in the treatment of Covid-19 during pregnancy.

Colchicine in the management of Covid-19: With or lieu of evidence.

Coronavirus disease 2019 (Covid-19), leads to global calamitous effects. Covid-19 is caused by a novel coronavirus named as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Covid-19 is associated with development of hyper-inflammation and/or cytokine storm that together with high viral load trigger tissue damage and multi-organ failures (MOF). Colchicine (CN) is a lipophilic tricyclic alkaloid used for treatment of gout since ancient time. In Covid-19 era, CN is repurposed for treatment of SARS-CoV-2 infection depending on its anti-inflammatory and broad-spectrum antiviral effects. Therefore, a recent clinical trial recommends use of CN in treating Covid-19 patients. It has been confirmed that inhibition of neutrophil chemotaxis, lysosomal degranulation, and release of pro-inflammatory cytokines is the main mechanism by which CN produces anti-inflammatory effects. CN attenuates generation of free radicals and reactive oxygen species (ROS) with consequent inhibition release of pro-inflammatory cytokines. Different studies illustrate that microtubule network is necessary and important for replication of different viruses including SARS-CoV-2 since; intracellular transport of viral particles is mediated through cytosolic microtubules. Therefore, CN therapy is effective in the management of Covid-19 patients when timely administrated through reduction of tissue damage and hyper-inflammations. Thus, the anti-inflammatory, antiviral, and immunomodulatory properties of CN might be the potential mechanisms of CN therapy against Covid-19. The review concludes that CN is a potent anti-inflammatory agent for the management of Covid-19; it inhibits SARS-CoV-2-induced-acute lung injury(ALI) due to its anti-inflammatory and anti-viral effects.

Statins and Covid-19: The Neglected Front of bidirectional effects.

Covid-19 is caused by a novel coronavirus named as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 binds angiotensin converting enzyme 2 (ACE2), which is greatly expressed in different tissues including lung alveolar type II cells. Infection with SARS-CoV-2 triggers acute host immune response, inflammatory reactions and cytokine storm leading to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Different studies reported the pleiotropic effects of statins such as the anti-inflammatory and immune-modulatory effects via modulation of antigen presentation and adhesion of inflammatory molecules since; statins have potential anti-oxidant and redox balance effects that improve endothelial dysfunction and cardiovascular integrity. Objective of the present study is to verify the beneficial and harmful effects of statins in Covid-19. Statins upregulates ACE2 receptors and attenuates the down-regulation effect of SARS-CoV-2 on the ACE2 receptors. Consequently, reduction of ACE2 receptors augment the deleterious effect of angiotensin II (AngII) which causes vasoconstriction and initiation of ALI. On the other hand, statins therapy may increase risk of viral infections such as SARS-CoV-2 via lowering of low density lipoprotein (LDL) since; circulating LDL adhere and inactivates SARS-CoV-2. Statin therapy improves the outcomes of Covid-19 pneumonia through anti-inflammatory, immune-modulation, and in vitro anti-SARS-CoV-2 effects. The antiplatelet and antithrombotic effects may reduce Covid-19 induced-coagulopathy and progression of ARDS.

Anti-histamines and Covid-19: Hype or Hope.

ABSTRACT: Histamine is a biogenic amine distributed extensively in the human cells. Histamine is linked with different inflammatory and allergic disorders through promoting of chemoatractant activity and endothelial changes. Antihistamine drugs are effective in the treatment and prevention of infection of influenza H7N9 through inhibition of viral entry to the host cells. A multiplicity of search strategies including experimental, preclinical and clinical studies were taken on and assumed to review the potential role of H1, H2 or their combination in the management of Coronavirus disease 2019 (Covid-19). Histamine release is associated with early and late pathology of Covid-19 and clinical presentation. Despite the potential effect of famotidine in attenuating the pathogenesis of Covid-19, famotidine has no direct effect on the replication of SARS-CoV-2. However, azelastine (H1receptor blocker) used for allergic rhinitis as nasal spray has potential anti-SARS-CoV-2 activity comparable to that of remdesivir, lopinavir and chloroquine. Azelastine is more effective than other agents that are used in the management of Covid-19 due to significant inhibition of endosomal acidification at respiratory epithelial cells. However, famotidine and cetirizine combination improve clinical outcome and reduce intubation and duration of hospitalization in Covid-19 patients. Taken together, hospitalised Covid-19 patients treated with famotidine only showed more complications as compared with those treated with combination of famotidine and cetirizine. CONCLUSIONS: Both H1 and H2 blockade are effective in the management of Covid-19 patients through antiviral and anti-inflammatory properties, which together reduce the risk of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).

Misfortune and spy story in the neurological manifestations of Covid-19.

Covid-19 is associated with different neurological manifestations. About one third of Covid-19 patients have some neurological disorders as paresthesia, headache, cold extremities and disturbances of consciousness, which are more evident in severely affected patients. These neurological manifestations may coexist or precede the onset of respiratory manifestations by about 2-3 weeks. Acute ischaemic stroke (AIS) and associated brain damage may develop due to acute respiratory distress syndrome (ARDS) induced-hypoxia. Prolonged hypoxia in late-stage Covid-19 leads to vasodilatation, intracranial hypertension, brain oedema, and AIS. In view of substantial evidence, this perspective explores the potentially direct or indirect effect of SARS-CoV-2 on the Central Nervous System of patients with COVID-19 pneumonia. The AIS is the end of most Covid-19-induced neurological complications. Covid-19 can lead to various neurological manifestations due to involvement of CNS directly through olfactory neurons or indirectly through induction of cytokine storm.

Reno-protective effect of berberine.

OBJECTIVE: To assess the reno-protective effect of berberine on diclofenac-induced acute kidney injury in rats. METHODS: The experimental study was conducted at the College of Medicine, Mustansiriya University, Baghdad, Iraq, from January to March 2018, and comprised Sprague Dawley male rats which were divided into 3 equal groups. Group1 rats were treated with distilled water plus normal saline for 14 days, Group2 rats were treated with distilled water plus diclofenac for 14 days and Group3 rats were treated with berberine plus diclofenac for 14 days. Parameters measured were blood urea, serum creatinine, serum malondialdehyde, superoxide dismutase, glutathione reductase, neutrophil gelatinase associated lipocalin, kidney injury molecules-1, Interleukin-18and cystatin-c. Anthropometric measurements and estimated glomerular filtration rate were also noted. SPSS 20 was used for data analysis. RESULTS: Of the 30 rats, the three groups had 10(33.3%) each. Berberine reduced blood urea, serum creatinine, malondialdehyde, neutrophil gelatinase associated lipocalin, kidney injury molecules-1 and Interleukin-18 significantly compared to diclofenac-induced acute kidney injury (p<0.01 each). Berberine improved anti-oxidant capacity through significant elevation of superoxide dismutase and glutathione reductase sera levels (p<0.01 each). CONCLUSIONS: Berberine was found to be an effective agent in the attenuation of diclofenac-induced acute kidney injury through the modulation of pro-inflammatory and oxidative stress biomarkers.

Rosuvastatin Attenuates acute nephrotoxicity through modulation of oxidative stress in Sprague Dawley rats.

OBJECTIVE: To assess the reno-protective effect of rosuvastatin on gentamicin-induced nephrotoxicity in rats. METHODS: The prospective experimental study was conducted at the College of Medicine, Mustansiriya University, Baghdad, Iraq, from March to July, 2018, and comprised Sprague Dawley male rats aged 3-4 months and weighing 200-400g each. The rats were divided into 3 equal groups which were treated for 14 days. Group1 was treated with distilled water plus normal saline, Group2 with distilled water plus gentamicin, and Group3 with rosuvastatin plus gentamicin. Parameters measured were blood urea, serum creatinine, serum malondialdehyde, superoxide dismutase, glutathione reductase, neutrophil gelatinase associated lipocalin, kidney injury molecule-1, interleukin- 18 and Cystatin-c. SPSS 20 was used for data analysis. RESULTS: Of the 30 rats, there were 10(33.3%) in each of the three groups. Rosuvastatin produced significant renoprotective effect through reduction of blood urea, kidney injury molecule-1 and interleukin-18 (p<0.01) compared to the gentamicin group. CONCLUSIONS: Rosuvastatin was found to be a reno-protective against gentamicin-induced nephrotoxicity through modulation of pro-inflammatory and oxidative/anti-oxidant pathways.

Berberine and Pentoxifylline: A novel combination in amelioration of acute kidney injury.

OBJECTIVE: To evaluate the nephro-protective effects of berberine and/or pentoxifylline on the reduction of diclofenac-induced acute kidney injury in rats. METHODS: The experimental study was conducted at the Department of Pharmacology, College of Medicine, Mustansiriya University, Baghdad, Iraq, from February to April, 2018, and comprised fifty male Sprague-Dawley rats aged 3-4 months and weighing 250-400 grams each. They were divided into five equal groups and were treated for 12 days. Group 1 rats were treated with distilled water plus normal saline, Group 2 with distilled water plus diclofenac, Group 3 with berberine plus diclofenac, Group 4 with pentoxifylline plus diclofenac, and Group 5 rats were treated with berberine, pentoxifylline and diclofenac. Blood urea, creatinine, Neutrophil Gelatinase Associated Lipocalin (NGAL), kidney injury molecules (KIM-1) and cystatin-C were used to measure the severity of AKI. RESULTS: Diclofenac led to significant AKI by significant elevation of blood urea, serum creatinine level, KIM-1, NGAL. Treatment with berberine showed no significant effect on all biomarkers level compared to diclofenac group except on serum KIM-1 level which was also seen in pentoxifylline group. Whereas, combination of berberine and pentoxifylline led to more significant effect in reduction of all renal biomarkers. CONCLUSIONS: Combination of berberine with pentoxifylline led to more significant reno-protective than either berberine or pentoxifylline when used alone on diclofenac induced-AKI.

Gingko Biloba protects cardiomyocytes against acute doxorubicin induced cardiotoxicity by suppressing oxidative stress.

OBJECTIVE: To evaluate the cardio-protective effect of Ginkgo Biloba (GB) on doxorubicin induced-cardiotoxicity. METHODS: The experimental study was conducted at the College of Medicine, Mustansiriya University, Baghdad, Iraq, from January to March, 2016, and comprised thirty Wistar Sprague male rats aged 3-4 months and weighing 200-400 g. The rats were divided into three equal groups (n=10); Group І (control): rats were treated with distilled water, Group ІІ (doxorubicin): rats were treated with distilled water and doxorubicin 20 mg/kg, and Group ІІІ (GB): rats were treated with GB and doxorubicin 20mg/kg. Serum malondialdehyde (MDA), glutathione reductase (GSH), lipid peroxidise (LPO), tumour necrosis factor-alpha (TNF-α), cardiac troponin (cTnI), brain natriuretic peptide (BNP) and caspase-3 (Cas-3) were measured using enzyme-linked immunosorbent assay kits. SPSS 20 was used to compare the effect GB with doxorubicin on the biomarkers of doxorubicin induced-cardiotoxicity. RESULTS: Doxorubicin led to cardiotoxicity through elevation of cTnI, BNP, Cas-3 and LPO compared with controls (p<0.01).Also, MDA and TNF-α were elevated while; GSH was decreased significantly (p<0.01) compared with controls. Co-administration of GB with doxorubicin led to significant reduction in cTnI, Cas-3 sera levels with elevation in GSH serum level significantly (p<0.05). The effect of GB on BNP, LPO, MDA and TNF-α was insignificant (p>0.05) compared with the doxorubicin. CONCLUSIONS: GB has significant cardio-protective effect through attenuation of oxidative stress during doxorubicin induced-cardiotoxicity in rats.

Proton pump inhibitors regulate metabolic profile and glycaemic indices in patients with type 2 diabetes mellitus: A rising dawn of a new therapeutic concept.

OBJECTIVE: To evaluate the effect of proton pump inhibitors on glycaemic indices in patients with type 2 diabetes mellitus. METHODS: The case-control study was conducted at the National Diabetes Centre, Mustansiriyah University, Baghdad, Iraq, from January to April 2018, and comprised type 2 diabetes patients and non-diabetic healthy controls. The subjects were divided into three groups: Group A had controls on proton pump inhibitors; Group B had patients treated with metformin 850 g/day; and Group C had patients treated with metformin 850 g/day plus proton pump inhibitors. Gastrin serum levels, lipid profile, glycaemic indices and blood pressure changes were measured in the groups. Data was analysed using SPSS 20. RESULTS: Of the 100 subjects, 60(60%) were patients with a mean age of 54.98}4.22 years, while40(40%) were controls with a mean age of 50.69}4.34 years. Group A had 40(40%) subjects, while Group B and Group C had 30(30%) each. Proton pump inhibitors improved glycaemic indices and lipid profile in the patients 9p<0.05) while increasing gastrin serum levels which were significantly correlated with reduction in glycated haemoglobin, fasting blood glucose and augmentation of ß-cell function (p<0.05 each). CONCLUSIONS: Proton pump inhibitors improved glycemic indices and metabolic profile in type 2 diabetes patients via augmentation of gastrin serum levels.

Statins an oft-prescribed drug is implicated in peripheral neuropathy: The time to know more.

Statins are hydroxymethylglutaryl-coenzyme A reductase inhibitors inhibit denovo cholesterol synthesis leading to reduction of serum cholesterol and low density lipoprotein as well as elevation of high density lipoprotein level. Statins are used in the treatment of dyslipidaemia, prevention of major cardiovascular events and complications. The potential role of statins in the induction of peripheral neuropathy has not been verified as most of statins induced-peripheral neuropathy had been reported as case reports. Also, statins therapy leads to noteworthy reduction of Coenzyme Q10, causing impairment of neuronal energy. The incidence of polyneuropathy was high with atorvastatin (65%) which is lipophilic, and relatively less with fluvastatin (54%) which is hydrophilic. Long-term statins therapy, mainly with atorvastatin and simvastatin, is linked with thedevelopment of peripheral neuropathy.

Neurocysticercosis: A new concept and insight into basic and future pharmacotherapy.

Neurocysticercosis is a neurological infection caused by the larva of taenia solium. The larva infection may affect different parts of the human brain and spinal cord, leading to focal neurological deficit with/without inflammatory reactions. Neurocysticercosis is one of the major causes of epilepsy in the developing countries. It is of two types. One is extra-parenchymal neurocysticercosis in which cysticerci cysts at subarachinoid space and ventricles lead to obstructive hydrocephalus and increase in the intracranial pressure. The other type is intra-parenchymal neurocysticercosis in which the cysticerci cyst grows inside the brain parenchyma, causing the feature of space-occupying lesion. The common presentation of intra-parenchymal neurocysticercosis is secondary epilepsy which is due to focal lesion and/or local inflammatory reactions. Cysticidal therapy increases the risk of seizure due to the induction of host inflammatory reactions. Therefore, coadministration of corticosteroids reduces the risk of seizure through attenuation of inflammatory reactions and brain oedema. Praziquantel alone or in combination with albendazole is regarded as the basic cysticidal therapy against neurocysticercosis. Newer drugs and agents are recommended to overcome the partial failure of standard cysticidal therapy.

COVID-19 and Diabetes: will Novel Drugs for Diabetes Help in COVID-19?

COVID-19 is caused by the SARS-CoV-2 virus, which has afflicted more than 245.37 million individuals worldwide and resulted in more than 4.9 million deaths as of today, with a mortality rate of 2.1%. Diabetes mellitus (DM) and its secondary complications are the major serious global health concerns today due to its growth rate, and it is the fastest-growing non-communicable disease. According to International Diabetes Federation (IDF) data, one out of 11 adults is diabetic, and the projection says that the figure will reach 642 million by 2040 globally. The occurrence of DM and its secondary complications is also associated with the severity of COVID-19 and high mortality. People with DM have a weakened immune system owing to innate immunity defects affecting phagocytosis, neutrophil chemotaxis, and cellmediated immunity; however, the high prevalence of diabetes in serious cases of COVID-19 may reflect the higher prevalence of type 2 DM (T2DM) in older people. Moreover, DM is linked to cardiovascular illness in older people, which could underlie the correlation between COVID-19 and fatal outcomes. SARS-CoV-2 infects via the angiotensin-converting enzyme 2 (ACE2), which is found in pancreatic islets, and infection with SARS-CoV-1 has been linked to hyperglycemia in individuals who do not have DM. And hence diabetic patients need to take more precautions and maintain their blood glucose levels. Many pieces of research say that COVID-19 and DM, especially its secondary complications are interlinked. But it also needs more elaborative evidence on whether the anti-diabetic drugs can manage only blood glucose or SARS-CoV-2.

Effects of ß-Blockers on the Sympathetic and Cytokines Storms in Covid-19.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a causative virus in the development of coronavirus disease 2019 (Covid-19) pandemic. Respiratory manifestations of SARS-CoV-2 infection such as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) leads to hypoxia, oxidative stress, and sympatho-activation and in severe cases leads to sympathetic storm (SS). On the other hand, an exaggerated immune response to the SARS-CoV-2 invasion may lead to uncontrolled release of pro-inflammatory cytokine development of cytokine storm (CS). In Covid-19, there are interactive interactions between CS and SS in the development of multi-organ failure (MOF). Interestingly, cutting the bridge between CS and SS by anti-inflammatory and anti-adrenergic agents may mitigate complications that are induced by SARS-CoV-2 infection in severely affected Covid-19 patients. The potential mechanisms of SS in Covid-19 are through different pathways such as hypoxia, which activate the central sympathetic center through carotid bodies chemosensory input and induced pro-inflammatory cytokines, which cross the blood-brain barrier and activation of the sympathetic center. ß2-receptors signaling pathway play a crucial role in the production of pro-inflammatory cytokines, macrophage activation, and B-cells for the production of antibodies with inflammation exacerbation. ß-blockers have anti-inflammatory effects through reduction release of pro-inflammatory cytokines with inhibition of NF-κB. In conclusion, ß-blockers interrupt this interaction through inhibition of several mediators of CS and SS with prevention development of neural-cytokine loop in SARS-CoV-2 infection. Evidence from this study triggers an idea for future prospective studies to confirm the potential role of ß-blockers in the management of Covid-19.