Precancerous Disease Systemic Lupus Erythematosus–The Role of BAFF in Corticosteroids Treatment | Chapter 11 | Medical Research and Its Applications Vol. 6

Background: The B cell Activating Factor (BAFF) is implicated as a key cytokine in autoimmune precancerous disease Systemic Lupus Erythematosus, SLE. The objective of the work was to determine how glucocorticoids (GCs) treatment applied in SLE patients affects serum BAFF levels. The described study is the first one to consider this therapeutical internship.                                                                        

Methodology: The study was performed in two groups: 1 - GCs treatment (21 patients); 2 - conventional treatment (8 patients). The first group was divided into three subgroups, according to the dose of GCs: <10.0 mg/day, 10.0-49.0 mg/day and ≥50.0 mg/day). The BAFF measurement in blood was done using the ELISA method. Data were analyzed with descriptive statistical techniques, depending on the type of variable, and the Mann-Whitney inference test.

Results: BAFF values were higher in patients with GCs ≥ 50.0 mg/day, with a mean of 2,844 pg/ml ± 1,495. In patients receiving GCs <50.0 mg/day, the mean was 2,422 ± 1,280. The mean BAFF in patients receiving GCs was 2,482 pg/ml and in the control group 0.990 pg/ml. The difference between these two averages is statistically significant, using the non-parametric Mann-Whitney test, with p <0.001. GCs therapy is associated with an increase in serum BAFF levels using higher doses of GCs. 

Conclusion: The evaluation of serum BAFF level in SLE treatment has become the potential new biomarker of GCs therapy. The presented results constitute a novel contribution to the diagnosis and therapy of SLE.

 

Author(s)details:-

 

Jerzy Trojan
CEDEA / ICGT – Oncological & Autoimmune Diseases Center, Bogota D.C., Colombia and Cancer Center - INSERM & Paris / Saclay University, Villejuif, France.

 

Maryam Raja
CEDEA / ICGT – Oncological & Autoimmune Diseases Center, Bogota D.C., Colombia and  Department of Biotechnology, Isfahan University, Isfahan, Iran.

 

Jose J. Siachoque
CEDEA / ICGT – Oncological & Autoimmune Diseases Center, Bogota D.C., Colombia.

 

Gabriela Quintero
CEDEA / ICGT – Oncological & Autoimmune Diseases Center, Bogota D.C., Colombia and Faculty of Medicine, UNAB University, Floridablanca, Colombia.

 

Alvaro Alvarez
Faculty of Medicine, University of Cartagena, Cartagena de Indias, Colombia.

 

Heber O. Siachoque
CEDEA / ICGT – Oncological & Autoimmune Diseases Center, Bogota D.C., Colombia and Faculty of Science, National University, Bogota D.C., Colombia.

 

Please See the book here :- https://doi.org/10.9734/bpi/mria/v6/7520C

Understanding the Symptoms and Signs of Endogenous Cushing Syndrome: A Spectrum of Cases | Chapter 2 | New Visions in Medicine and Medical Science Vol. 5

Introduction: Cushing’s syndrome (CS) is a rare disorder characterised by symptoms and signs of chronic excessive tissue exposure to glucocorticoids, and is associated with high morbidity and mortality if untreated. A few common features of CS include truncal obesity, moon facies, increased fat in dorsocervical area, ecchymoses, plethora, striae, proximal muscle weakness, thin skin, pigmentation of the skin, osteopenia/ osteoporosis with fractures, avascular necrosis of bone, mood changes, hypertension, impairment of glucose tolerance or worsening of glycemic control, susceptibility to infections, edema, deep vein thrombosis/ pulmonary thromboembolism. The excess cortisol state can result from a number of etiologies- both exogenous and endogenous. It can present with varied and non-specific clinical features. Hence, having a high clinical suspicion is important and it can be challenging to arrive at an exact diagnosis, which is very important to initiate appropriate treatment. Here, we present a spectrum of endogenous Cushing’s syndrome of different etiologies, which are presented to us at different age groups and with different clinical features.

 

Description of Cases: The main aim of this article is to understand the different symptoms and signs with which the patients with Endogenous Cushing’s syndrome present, the knowledge required to suspect it even in a non-typical presentation, the extensive and laborious work-up done at arriving the diagnosis and localizing the cause, and then finally initiating appropriate treatment. We randomly chose 8 cases of Endogenous Cushing’s syndrome of different presentation and etiology, who presented to our Hospital. We had patients whose ages ranged from 13 years to 60 years; patients presenting with typical features of Cushing’s syndrome to non-specific features and even being asymptomatic. All the cases underwent appropriate and elaborate work-up to arrive at a diagnosis and also to localize the exact lesion. They then underwent appropriate treatment either in the form of surgery (excision of the lesion responsible for the cortisol excess) or medical therapy. The outcome of the patients was good in 6 of these patients, they achieved remission during follow-up. However, 2 patients, one with Adrenocortical carcinoma and another with Ectopic adreno-cortical tropic hormone (ACTH) syndrome due to Poorly differentiated adenocarcinoma of the left lung, died due to the severity of underlying diseases.

 

Conclusion: Endogenous Cushing’s syndrome, though rare, is associated with high morbidity and mortality if untreated. A high degree of suspicion and a good clinical examination are required to diagnose Cushing’s syndrome, especially in non-florid cases and those with nonspecific features. A systematic, orderly evaluation is required to establish the correct diagnosis and to localize the cause, which will help in the planning of appropriate treatment.

Author(s) Details:

Santosh B,
Department of Endocrinology, Yashoda Hospital, Secunderabad, Telangana, India.

Raman Boddula,
Department of Endocrinology, Yashoda Hospital, Secunderabad, Telangana, India.

Ashok Venkatanarasu,
Department of Endocrinology, Yashoda Hospital, Secunderabad, Telangana, India.

Aditya Hegde,
Department of Endocrinology, Yashoda Hospital, Secunderabad, Telangana, India.

Chimutai Chinte,
Department of Endocrinology, Yashoda Hospital, Secunderabad, Telangana, India.

Vidya Tickoo,
Department of Endocrinology, Yashoda Hospital, Secunderabad, Telangana, India.

Please see the link here: https://stm.bookpi.org/NVMMS-V5/article/view/14151

Recent Development and Validation of a RP-HPLC Analytical Method for the Simultaneous Determination of Luliconazole and Clobetasol Propionate in Synthetic Mixture | Chapter 6 | Current Aspects in Pharmaceutical Research and Development Vol. 5

 Aim: The goal of this study is to establish an analytical method for determining drug concentrations or analyses in synthetic mixes including both antifungal drug Luliconazole and corticosteroid medicine Clobetasol Propionate, regardless of their composition.

The approach was validated to meet the requirements of the International Conference on Harmonization (ICH). On a reversed-phase Inertsil C18 column (5 m, 250mm x 4.6mm i.d) with a mixture of Acetonitrile: Water pH adjusted with H3PO4 (60: 40) and UV detection at 264 nm, chromatographic separation was performed using an isocratic approach. With a 20L injection volume, the compounds were eluted at a flow rate of 1.0 mL/min.

The calibration curves for Luliconazole and Clobetasol Propionate were linear (r2 > 0.999) for the concentration ranges of 10-200 g/mL and 5-100 g/mL, respectively. Luliconazole and Clobetasol Propionate had average retention durations of 3.16 and 6.94 minutes, respectively. The proposed method's percent RSD was determined to be less than 2 percent. The devised method's percent recovery was determined to be between 99.22 and 99.48 percent.

Conclusion: Because the devised approach is simple, quick, precise, and accurate, it was successfully used to determine Luliconazole and Clobetasol Propionate in a synthetic mixture.

Author(S) Details

Binal Solanki
Nootan Pharmacy College, Sankalchand Patel University, Visnagar, Laxminarayan Dev College of Pharmacy, Bharuch, India.

Hirak Joshi
Faculty of Pharmacy, Nootan Pharmacy College, Sankalchand Patel University, Visnagar, India.

View Book:- https://stm.bookpi.org/CAPRD-V5/article/view/4938

Insight into Drugs Induce Liver Toxicity | Book Publisher International

 In the human body, the liver is a vital organ. It has a variety of activities, including metabolism, immunity, digestion, detoxification, and vitamin storage, among others.

Non-reactive chemicals are thought to be biotransformed in two phases: functionalization, which involves the use of oxygen to create a reactive site, and conjugation, which involves the addition of a water-soluble group to the reactive site. Phase I and phase II detoxification refer to the two phases of functionalization and conjugation, respectively. As a result, a lipophilic chemical that cannot be expelled in urine is biotransformed into a water-soluble compound that can be eliminated in urine.

The liver is the primary organ engaged in drug and xenobiotic metabolism and detoxification.

There are three stages of drug metabolism. The superfamily of CYP monooxygenases is involved in phase I drug oxidation. Phase I reactions can convert prodrugs to active forms and xenobiotics to benign molecules, but they can also increase the toxicity of the metabolites in some cases. Phase II processes include sulfation, methylation, and glucuronidation to improve the solubility of oxidised metabolites, which are released by phase III drug transporters found in the membranes of hepatocytes, intestinal cells, kidneys, and other organs for excretion.

A drug-induced liver injury (DILI) is a liver injury caused by exposure to a medication or a non-infectious toxic substance that causes organ dysfunction in varying degrees.

From a pharmacological standpoint, two types of DILI can be distinguished: dose-dependent and dose-independent or idiosyncratic. Direct toxicity, also known as dose-dependent DILI, is predictable, repeatable, and develops quickly after consuming a dose that exceeds a recognised hazardous threshold. The damage entity is proportional to the dose given. DILI that is idiosyncratic, on the other hand, is unpredictable and frequently occurs at therapeutic levels. The quantity of damage is not necessarily proportionate to the injected dose, and the time it takes for harm to appear varies greatly.

DILI can cause mitochondrial impairment, biliary efflux inhibition, lysosomal impairment, endoplasmic reticulum stress, production of reactive metabolites leading to chemical stress, oxidative stress, and protein modification, as well as triggering innate and adaptive immune responses and causing cytokine activation. All of these manifestations have the potential to harm the liver.

Acute hepatic necrosis, elevated enzymes, acute hepatitis, cholestatic hepatitis, mixed hepatitis, chronic hepatitis, bland cholestasis, acute fatty liver disease, lactic acidosis, hepatic failure, nonalcoholic fatty liver disease, sinusoidal obstruction syndrome, and nodular regenerative hyperplasia are all phenotypes of DILI.

Author(s) Details

Dheaa Shamikh Zageer
Forensic DNA Center For Research and Training/ Al-Nahrain University, Baghdad, Iraq.

Sundus Fadhil Hantoosh
Forensic DNA Center For Research and Training/ Al-Nahrain University, Baghdad, Iraq.

View Book:- https://stm.bookpi.org/IDILT/article/view/2098