KOVID - Treatment more toxic than the disease!
In light of recent approvals of various drugs by DCGI, India without any clinical trials conducted in India. What if these drugs are behind the high mortality and complications? A peep into the documented adverse effects of the drugs being used reveal a lot.
It is shocking to observe that most of these drugs had failed miserably due to serious adverse reactions during clinical trials in the past in other countries. None of these drugs have any track record of treatment of pre-existing diseases in majority of population who have died due to comorbidity or suspected microorganism. As a concerned citizen, I am unable to understand rationale behind why such poisonous drugs with failed clinical trials or well known documented adverse reactions are getting approved for patients with pre-existing diseases.
"Since now, almost all deaths are taking place in hospitals and not in home isolation, it was felt that systems in each hospital need to be examined in detail. The CM has asked for the ratio of deaths to the total number of patients discharged in each hospital,” the CM’s office said.
"Remdesivir Phase II clinical trials were conducted in Ebola virus-infected patients. In clinical trials of anti-Ebola drugs, the fatality rate of patients in the experimental group using remdesivir was 53%, and the efficacy was significantly worse than that of the two monoclonal antibodies MAb114 (fatality rate 35%) and REGN-EB3 (fatality rate 33%) . The 53% fatality rate was not significantly different from the average 50% fatality rate of Ebola virus infection, and as a result, phase II clinical trials were stopped"
6.1 Clinical Trials
In a randomized, open-label clinical trial (Study GS-US-540-5773) of remdesivir
in 397 subjects with severe COVID-19 treated with remdesivir for 5 (n=200) or 10
days (n=197), adverse events were reported in 71% and 74% of subjects,
respectively, serious adverse events were reported in 21% and 35% of subjects,
respectively, and Grade ≥3 adverse events were reported in 31% and 43% of
subjects, respectively. Nine (5%) subjects in the 5-day group and 20 (10%)
subjects in the 10-day group discontinued treatment due to an adverse event. All-
cause mortality at Day 28 was 10% vs 13% in the 5- and 10-day treatment groups, respectively.
6.2 Hepatic Adverse Reactions
Clinical Trials Experience
Experience in Healthy Volunteers
Grade 1 and 2 transaminase elevations were observed in healthy volunteers in
Study GS-US-399-5505 (200 mg followed by 100 mg dosing for 5–10 days) and
Study GS-US-399-1954 (150 mg daily for 7 or 14 days), which resolved after
discontinuation of remdesivir.
*Experience in Patients with COVID-19* 👆
'Based on single-dose toxicity studies, the lethal dose for oral and intravenous favipiravir in mice is estimated to be >2000 mg/kg.18 In rats, the lethal dose for oral administration is >2000 mg/kg, while the lethal dose in dogs and monkeys is >1000 mg/kg.18 Symptoms of overdose appear to include but are not limited to reduced body weight, vomiting, and decreased locomotor activity.18
In repeat-dose toxicity studies involving dogs, rats, and monkeys, notable findings after administration of oral favipiravir included: adverse effects on hematopoietic tissues such as decreased red blood cell (RBC) production, and increases in liver function parameters such as aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine aminotransferase (ALT) and total bilirubin, and increased vacuolization in hepatocytes.18 Testis toxicity was also noted.18
Favipiravir is known to be teratogenic!"
1. Shock, anaphylaxis
3. Hepatitis fulminant, hepatic dysfunction, jaundice
4. Toxic epidermal necrolysis (TEN),
oculomucocutaneous syndrome (Stevens-Johnson
5. Acute kidney injury
6. White blood cell count decreased, neutrophil
count decreased, platelet count decreased
7. Neurological and psychiatric symptoms
(consciousness disturbed, abnormal behavior,
deliria, hallucination, delusion, convulsion, etc.)
8. Colitis haemorrhagic
👆Known adverse reactions caused by drugs with similar composition like favipiravir.
Prima facie, composition of these posionous drugs are similar to chemical fertilizers pesticides, insecticides etc. It kills everything, distroy gut Microbiome and cause long term gut disbiosys. It seem that liver damage is immediate impact but long term impact has potential to cause birth defects in next generation of human being.
Dexamethasone or DECADRON
The following adverse reactions have been reported with Dexamethasone or DECADRON or other corticosteroids:
*Allergic reactions:* Anaphylactoid reaction, anaphylaxis,
Cardiovascular: Bradycardia, cardiac arrest, cardiac arrhythmias, cardiac enlargement, circulatory collapse, congestive heart failure, fat embolism, hypertension, hypertrophic cardiomyopathy in premature infants,
myocardial rupture following recent myocardial infarction (see WARNINGS, Cardio-renal), edema, pulmonary
edema, syncope, tachycardia, thromboembolism, thrombophlebitis, vasculitis.
*Dermatologic* : Acne, allergic dermatitis, dry scaly skin,
ecchymoses and petechiae, erythema, impaired
wound healing, increased sweating, rash, striae, suppression of reactions to skin tests, thin fragile skin, thinning
scalp hair, urticaria.
Endocrine: Decreased carbohydrate and glucose tolerance, development of cushingoid state,
hyperglycemia, glycosuria, hirsutism, hypertrichosis, increased requirements for insulin or oral hypoglycemic
agents in diabetes, manifestations of latent diabetes mellitus, menstrual irregularities, secondary adrenocortical
and pituitary unresponsiveness (particularly in times of stress, as in trauma, surgery, or illness), suppression of
growth in pediatric patients.
*Fluid and electrolyte disturbances:* Congestive heart failure
in susceptible patients, fluid retention,
hypokalemic alkalosis, potassium loss, sodium retention.
*Gastrointestinal:* Abdominal distention, elevation in serum liver
enzyme levels (usually reversible upon
discontinuation), hepatomegaly, increased appetite, nausea, pancreatitis, peptic ulcer with possible perforation
and hemorrhage, perforation of the small and large intestine (particularly in patients with inflammatory bowel
disease), ulcerative esophagitis.
*Metabolic:* Negative nitrogen balance due to protein catabolism.
Clinical trials of Peginterferon alfa-2b - Approved by DCGI
Peginterferon alfa-2b is derived from the alfa-2b moeity of recombinant human interferon and acts by binding to human type 1 interferon receptors. Activation and dimerization of this receptor induces the body's innate antiviral response by activating the janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. Use of Peginterferon alfa-2b is associated with a wide range of severe adverse effects including the aggravation and development of endocrine and autoimmune disorders, retinopathies, cardiovascular and neuropsychiatric complications, and increased risk of hepatic decompensation in patients with cirrhosis. The use of Peginterferon alfa-2b has largely declined since newer interferon-free antiviral therapies have been developed.
In a joint recommendation published in 2016, the American Association for the Study of Liver Diseases (AASLD) and the Infectious Diseases Society of America (IDSA) no longer recommend Peginterferon alfa-2b for the treatment of Hepatitis C 2
- Compiled by Pritam Sinha.