Elopag 50 side effects

This drug has a boxed warning. This is the most serious warning from the Food and Drug Administration (FDA). A boxed warning alerts doctors and patients about drug effects that may be dangerous.

  • This drug may increase your liver enzymes. This can lead to liver damage. Your doctor will check your liver function when you first start taking this drug and during treatment. If your liver isn’t working well, your doctor may lower your dosage or stop your treatment with this drug.
Highlights for eltrombopag
  1. Eltrombopag oral tablet is available as a brand-name drug. It’s not available as a generic drug. Brand name: Promacta.
  2. Eltrombopag comes in two forms: oral tablet and oral suspension.
  3. Eltrombopag oral tablet is used to treat low platelet levels due to chronic immune thrombocytopenia (ITP) or chronic hepatitis C virus infection. It’s also used to treat severe aplastic anaemia.
What is eltrombopag?

Eltrombopag is a prescription drug. It comes as an oral tablet and an oral suspension.

Eltrombopag oral tablet is available as the brand-name drug Promacta. It’s not available as a generic drug.

This drug may be used as part of combination therapy. This means you may need to take it with other medications.

Why it’s used

Eltrombopag is used to treat:

  • Low platelet levels due to chronic immune thrombocytopenia (ITP). This is a bleeding disorder. Eltrombopag is given to people who haven’t responded well to other drugs or surgery.
  • Low platelet counts due to chronic hepatitis C virus infection. This drug is used before and during treatment with the drug pegylated interferon and ribavirin.
  • Severe aplastic anemia. Aplastic anaemia is when you have bone marrow failure, which results in low levels of platelets, red blood cells, and white blood cells. Eltrombopag is used in two ways for this condition:
    • First-line treatment of severe aplastic anaemia. This drug can be used as the first treatment option in some cases of severe aplastic anaemia. For this use, eltrombopag is given in combination with other initial treatments.
    • Treatment of refractory severe aplastic anaemia. Some cases of severe aplastic anaemia are refractory, which means the anaemia did not improve after treatment with other medications. Eltrombopag can be used alone for treating these cases of anaemia.

Eltrombopag is not used to treat myelodysplastic syndrome (MDS).

How it works

Eltrombopag belongs to a class of drugs called thrombopoietin (TPO) receptor agonists. A class of drugs is a group of medications that work similarly. These drugs are often used to treat similar conditions.

Eltrombopag works by increasing cells in your bone marrow. It causes these cells to make more platelets. This effect lowers your risk of bleeding.

Osicent 80 Uses

Presentation

Osicent 80: Each tablet contains Osimertinib Mesylate INN equivalent to Osimertinib 80 mg.

Description

Osimertinib is a kinase inhibitor of the epidermal growth factor receptor (EGFR), which binds irreversibly to certain mutant forms of EGFR (T790M, L858R, and exon 19 deletions) at approximately 9-fold lower concentrations than wild-type. In cultured cells and animal tumour implantation models, osimertinib exhibited anti-tumour activity against non-small cell lung cancer (NSCLC) lines harbouring EGFR-mutations (T790M/L858R, L858R, T790M/exon 19 deletion, and exon 19 deletions) and, to a lesser extent, wild-type EGFR amplifications.

Indications

Osimertinib is a kinase inhibitor indicated for the treatment of patients with metastatic epidermal growth factor receptor (EGFR) T790M mutation-positive non-small cell lung cancer (NSCLC), as detected by an FDA-approved test, who have progressed on or after EGFR tyrosine kinase inhibitor therapy.

Dosage & Administration

80 mg orally once daily, with or without food.

Side Effects

The most common (>20%) adverse reactions (all grades) observed in Osimertinib-treated patients were diarrhoea (42%), rash (41%), dry skin (31%), and nail toxicity (25%). The most frequent adverse reactions that led to dose reductions or interruptions were: electrocardiogram QTc prolonged (2.2%) and neutropenia (1.9%). Serious adverse reactions reported in 2% or more patients were pneumonia and pulmonary embolus.

Precautions

Interstitial Lung Disease (ILD)/Pneumonitis: Occurred in 3.3% of patients. Osimertinib should be permanently discontinued in patients diagnosed with ILD/Pneumonitis.
QTc Interval Prolongation: Electrocardiograms and electrolytes should be monitored in patients who have a history or predisposition for QTc prolongation, or those who are taking medications that are known to prolong the QTc interval. Osimertinib should be withheld then restarted at a reduced dose or permanently discontinued.
Cardiomyopathy: Occurred in 1.4% of patients. Left ventricular ejection fraction (LVEF) should be assessed before treatment and then every 3 months thereafter.

Embryo-Fetal Toxicity: Osimertinib can cause fetal harm. Females should be advised of the potential risk to the fetus and to use effective contraception during treatment with Osimertinib and for 6 weeks after the final dose. Males should be advised to use effective contraception for 4 months, after the last dose of Osimertinib.

Use in Pregnancy & Lactation

Based on its mechanism of action and animal data, Osimertinib can cause fetal harm when administered to a pregnant woman. There are no available data on Osimertinib use in pregnant women. Pregnant women should be advised of the potential risk to a fetus.
There are no data on the presence of Osimertinib in human milk, the effects of Osimertinib on the breastfed infant or on milk production. A lactating woman should be advised not to breastfeed during treatment.

Pediatric Use
The safety and effectiveness of Osimertinib in pediatric patients have not been established.

Geriatric Use
No overall differences in safety were observed between patients 65 years and older and those younger than 65 years.

Drug Interaction

Strong CYP3A Inhibitors
Concomitant administration of Osimertinib should be avoided with strong CYP3A inhibitors, including macrolide antibiotics (e.g., telithromycin), antifungals (e.g., itraconazole), antivirals (e.g., ritonavir), nefazodone, as concomitant use of strong CYP3A inhibitors may increase Osimertinib plasma concentrations. If no other alternative exists, patients should be monitored more closely for adverse reactions.

Strong CYP3A Inducers
Concomitant administration of Osimertinib should be avoided with strong CYP3A inducers (e.g., phenytoin, rifampicin, carbamazepine, St. John’s Wort) as strong CYP3A inducers may decrease Osimertinib plasma concentrations.

Commercial Pack

Osicent 80 Container Pack: Each bottle contains 30 tablets.
Osicent 80: Each box contains 1 blister strip of 10 tablets.

PANOVIR TABLET

Presentation

Panovir: Each tablet contains Sofosbuvir INN 400 mg and Velpatasvir INN 100 mg.

Description

It is a fixed-dose combination tablet containing sofosbuvir and velpatasvir for oral administration. Sofosbuvir is a nucleotide analogue HCV NS5B polymerase inhibitor and velpatasvir is an NS5A inhibitor.

Indications

Sofosbuvir and Velpatasvir combination is indicated for the treatment of adult patients with chronic hepatitis C virus (HCV) genotype 1, 2, 3, 4, 5 or 6 infection

– without cirrhosis or with compensated cirrhosis

– with decompensated cirrhosis for use in combination with ribavirin

Dosage & Administration

The recommended dosage is one tablet (400 mg of Sofosbuvir and 100 mg of Velpatasvir) taken orally once daily. Recommended treatment regimen:
– Patients without cirrhosis and patients with compensated cirrhosis (Child-Pugh A) – one tablet once daily for 12 weeks
– Patients with decompensated cirrhosis (Child-Pugh B or C) – one tablet once daily and Ribavirin for 12 weeks. The recommended dosage of Ribavirin is based on body weight (1000 mg/day for patients < 75 kg and 1200 mg/day for ≥ 75 kg, in two divided doses/day)

No dosage recommendation can be given for patients with severe renal impairment (eGFR ≤ 30 mL/min/1.73 m2) or with ESRD, due to higher exposures of the predominant sofosbuvir metabolite.

Side Effects

The most common side effects of the Sofosbuvir and Velpatasvir combination include headache and tiredness. Treatment may result in slowing of the heart rate along with other symptoms when taken with amiodarone (a medicine used to treat certain heart problems).

Precautions

Serious symptomatic bradycardia may occur in patients taking amiodarone, particularly in patients also receiving beta-blockers, or those with underlying cardiac comorbidities and/or advanced liver disease. Coadministration of amiodarone with Sofosbuvir and Velpatasvir combination is not recommended. In patients without alternative viable treatment options, cardiac monitoring is recommended.

Use in Pregnancy & Lactation

No adequate human data are available to establish whether or not Sofosbuvir and Velpatasvir combination poses a risk to pregnancy outcomes. If Sofosbuvir and Velpatasvir combination administered with Ribavirin, the combination regimen is contraindicated in pregnant women and in men whose female partner is pregnant or going to be pregnant in the next six months.

Drug Interaction

Drugs may decrease the concentrations of sofosbuvir and/or velpatasvir: Antacids, H2-receptor antagonists, Proton-pump inhibitors etc.
Coadministration is not recommended with: topotecan, Carbamazepine, Phenytoin, Phenobarbital, Oxcarbazepine, Rifabutin, Rifampin, Rifapentine, efavirenz, Tipranavir, Ritonavir, Hypericum perforatum.
Coadministration of Sofosbuvir and Velpatasvir combination, with Rosuvastatin, Atorvastatin may significantly increase the concentration of Rosuvastatin, Atorvastatin.

OverDose

If an overdose occurs the patient must be monitored for evidence of toxicity. Treatment of overdose includes monitoring of vital signs as well as observation of the clinical status of the patient.

Storage

Store in a cool and dry place (preferably below 30°C). Keep out of reach of children.

Commercial Pack

Panovir Container Pack: Each bottle contains 28 tablets.
Hanover : Each box contains 1 blister strip of 6 tablets.

Tofacent 5

Tofacent 5: Each tablet contains Tofacitinib Citrate INN equivalent to Tofacitinib 5 mg

Tofacent XR 11: Each Extended-Release tablet contains Tofacitinib Citrate INN equivalent to Tofacitinib 11 mg

Description

Tofacitinib is a Janus kinase (JAK) inhibitor. JAKs are intracellular enzymes that transmit signals arising from cytokine or growth factor-receptor interactions on the cellular membrane to influence cellular processes of hematopoiesis and immune cell function. Within the signalling pathway, JAKs phosphorylate and activate Signal Transducers and Activators of Transcription (STATs) which modulate intracellular activity including gene expression. Tofacitinib modulates the signalling pathway at the point of JAKs, preventing the phosphorylation and activation of STATs. JAK enzymes transmit cytokine signalling through the pairing of JAKs (e.g., JAK1/JAK3, JAK1/JAK2, JAK1/TyK2 and JAK2/JAK2). Tofacitinib inhibited the in vitro activities of JAK1/JAK2, JAK1/JAK3, and JAK2/JAK2 combinations with IC50 of 406, 56, and 1377 nM, respectively. However, the relevance of specific JAK combinations to therapeutic effectiveness is not known.

Indications

Tofacitinib / Tofacitinib XR is a Janus kinase (JAK) inhibitor.

• Rheumatoid Arthritis: Tofacitinib / Tofacitinib XR is indicated for the treatment of adult patients with moderately to severely active

rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate. It may be used as monotherapy or in

combination with methotrexate or other nonbiologic disease-modifying antirheumatic drugs (DMARDs).

• Psoriatic Arthritis: Tofacitinib / Tofacitinib XR is indicated for the treatment of adult patients with active psoriatic arthritis who have

had an inadequate response or intolerance to methotrexate or other disease-modifying antirheumatic drugs (DMARDs).

• Ulcerative Colitis: Tofacitinib is indicated for the treatment of adult patients with moderately to severely active ulcerative colitis (UC).

• Limitations of Use: Use of Tofacitinib / Tofacitinib XR in combination with biologic DMARDs or potent immunosuppressants such as

azathioprine and cyclosporine are not recommended.

Dosage & Administration

Administration Instructions

Do not initiate Tofacitinib / Tofacitinib XR if absolute lymphocyte count <500 cells/mm3

, an absolute neutrophil count (ANC) <1000

cells/mm3

or hemoglobin <9 g/dL.

Recommended Dosage:

• Rheumatoid Arthritis: Tofacitinib 5 mg twice daily or Tofacitinib XR 11 mg once daily. Recommended dosage in patients with

moderate and severe renal impairment or moderate hepatic impairment is Tofacitinib 5 mg once daily.

• Psoriatic Arthritis (in combination with nonbiologic DMARDs): Tofacitinib 5 mg twice daily or Tofacitinib XR 11 mg once daily.

Recommended dosage in patients with moderate and severe renal impairment or moderate hepatic impairment is Tofacitinib 5 mg once daily.

• Ulcerative Colitis: • Induction: Tofacitinib 10 mg twice daily or Tofacitinib XR 22 mg once daily for 8 weeks; evaluate patients and

transition to maintenance therapy depending on therapeutic response. If needed, continue Tofacitinib 10 mg twice daily or Tofacitinib

XR 22 mg once daily for a maximum of 16 weeks. Discontinue Tofacitinib 10 mg twice daily or Tofacitinib XR 22 mg once daily after

16 weeks if the adequate therapeutic response is not achieved. • Maintenance: Tofacitinib 5 mg twice daily or Tofacitinib XR 11 mg once

daily. For patients with loss of response during maintenance treatment, Tofacitinib 10 mg twice daily or Tofacitinib XR 22 mg once

daily may be considered and limited to the shortest duration, with careful consideration of the benefits and risks for the individual

patient. Use the lowest effective dose needed to maintain response. • Dosage adjustment is needed in patients with moderate and

severe renal impairment or moderate hepatic impairment.

Side Effects

The most common adverse reactions are:

• Rheumatoid and Psoriatic Arthritis: Reported during the first 3 months in rheumatoid arthritis controlled clinical trials and occurring in

≥2% of patients treated with Tofacitinib monotherapy or in combination with DMARDs: upper respiratory tract infection,

nasopharyngitis, diarrhoea, and headache.

• Ulcerative Colitis: Reported in ≥5% of patients treated with either 5 mg or 10 mg twice daily of Tofacitinib and ≥1% greater than

reported in patients receiving placebo in either the induction or maintenance clinical trials: nasopharyngitis elevated cholesterol

levels, headache, upper respiratory tract infection, increased blood creatine phosphokinase, rash, diarrhoea, and herpes zoster.

Precautions

• Serious Infections: Use of Tofacitinib / Tofacitinib XR should be avoided during an active serious infection, including localized infections.

• Gastrointestinal Perforations: Caution should be used in patients that may be at increased risk.

• Laboratory Monitoring: Laboratory Monitoring should be recommended due to potential changes in lymphocytes, neutrophils,

haemoglobin, liver enzymes and lipids.

• Immunizations: Live vaccines: Use with Tofacitinib / Tofacitinib XR should be avoided.

Use in Pregnancy & Lactation

Pregnancy Category C. There are no adequate and well-controlled studies in pregnant women. Tofacitinib should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. It is not known whether Tofacitinib is excreted in human milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from Tofacitinib, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug for the mother. Pediatric Use: The safety and effectiveness of Tofacitinib in pediatric patients have not been established. Geriatric Use: The frequency of serious infection among Tofacitinib-treated subjects 65 years of age and older was higher than among those under the age of 65. As there is a higher incidence of infections in the elderly population in general, caution should be used when treating the elderly.

Drug Interaction

Strong CP3A4 Inhibitors (e.g., ketoconazole): Dosage adjustment of Tofacitinib / Tofacitinib XR is recommended.

Moderate CYP3A4 Inhibitors Coadministered with Strong CYP2C19 Inhibitors (e.g., fluconazole): Dosage adjustment of Tofacitinib /

Tofacitinib XR is recommended.

Strong CYP3A4 Inducers (e.g., rifampin): Coadministration with Tofacitinib / Tofacitinib XR is not recommended.

Immunosuppressive drugs (e.g., azathioprine, tacrolimus, and cyclosporine): Coadministration with Tofacitinib / Tofacitinib XR is not

recommended.

Storage

Do not store above 30 0C. Keep away from light and out of the reach of children.

Commercial Pack

Tofacent 5: Each box contains 2 blister strips of 10 tablets.

Tofacent XR 11 Container Pack: Each bottle contains 10 tablets.

Heart Disease

Heart Disease Narrowing for Women Younger Than 65

THURSDAY, Feb. 25, 2021 (HealthDay News) — For women aged younger than 65 years, the mortality gap between cancer and heart disease is narrowing, according to a study published online Feb. 8 in the European Heart Journal: Quality of Care & Clinical Outcomes.

 

Safi U. Khan, M.B.B.S., from West Virginia University in Morgantown, and colleagues compared premature heart disease- and cancer-related deaths in women aged younger than 65 years in the United States. The annual percentage changes (APCs) in age-adjusted mortality rates (AAMRs) and years of potential life lost per 100,000 persons were compared.

 

The researchers found that cancer was a more prevalent cause of premature death than heart disease overall. Between 1999 and 2018, there were decreases in the AAMRs for both cancer (61.9 to 45.6 per 100,000) and heart disease (29.2 to 22.6 per 100,000). The APC in AAMR for cancer decreased consistently over time, while for heart disease, the APC in AAMR declined initially but increased between 2010 and 2018 (0.53), with significant increases in the Midwest, medium/small metros, and rural areas after 2008. The APC in AAMR for heart disease increased in women aged 25 to 34 years (2.24) and 55 to 64 years (0.46) compared with cancer. There was a narrowing in the mortality gap observed between cancer and heart disease, from 32.7 to 23.0 per 100,000.

 

“If extreme public health measures are not taken to mitigate cardiovascular risk factors, focusing on high-risk groups, heart disease mortality may supersede cancer to become the leading cause of death in young women,” the authors write

Eight Skin Cancer Myths You Need To Stop Believing Skin cancer is the most common type of cancer in the U.S.—with current estimates suggesting that one in five Americans develop skin cancer by the time they hit 70. But with so much contradictory information out there on the subject, skin cancer is often misunderstood and sometimes, not taken seriously enough. In order to help you better protect yourself against the potentially fatal disease, I spoke with a board-certified dermatologist to get the facts behind some of the biggest misconceptions about skin cancer: MYTH #1 I'm not at risk of developing skin cancer in the winter months or when it’s cloudy because the sun isn’t as strong. One of the most prevalent myths when it comes to sun protection is that you don't need to apply sunscreen or sunblock on cold or cloudy days. "The harmful UV rays emitted by the sun—that are largely responsible for all of the major types of skin cancer, including melanoma—are present year-round. Also, they can penetrate through clouds and even glass windows," tells Dr. Julie Karen, a board-certified dermatologist who specializes in Mohs micrographic surgery, laser surgery and skin cancer. Bottom line: No matter what the forecast is, don't skip sunscreen. MYTH #2 The damage is already done. I was careless in my youth, it's too late now to make any significant impact on my skin cancer risk. "While we used to estimate that the vast majority of a person's sun damage in a lifetime occurred during childhood, we now know that by age 22, only about 20% of your lifetime damage has been accrued," says Dr. Karen. "Each decade thereafter, you acquire an additional 10% of your lifetime damage. So, it's not too late to make a difference at any age. Introducing sun-smart behaviors, even after years of carelessness, will help to reduce additional UV damage from occurring and thus reduce your cumulative risk of developing all forms of skin cancer," she notes. MYTH #3 I used SPF 50 this morning, so I can safely sunbathe now. "Often patients will present to my office with tan lines or worse yet, sunburns and declare that they 'wore SPF 50.' So, I spend a ton of time educating them about what true 'sun smart behavior' is," says Dr. Karen. "First of all, there is no such thing as a safe tan. Your skin thickens and darkens (i.e. tans) to protect itself from further damage caused by UV exposure. So even though a tan is less harmful than a blistering sunburn, once you see a tan, the damage is done," tells the dermatologist. Secondly, "most people apply far less than 50% of the recommended amount of sunscreen required for adequate protection. So, the SPF on the label of your bottle is rarely achieved in daily practice," Dr. Karen points out. "You should apply at least one ounce (a shot glass full or golf ball-sized) of sunscreen from head to toe, twenty minutes before going into the sun. And reapply an equally generous amount every two hours or sooner after swimming or perspiring," she suggests. Though wearing sunscreen is a critical component of skin protection, it's by no means a license to lie in the sun. Rather, sunscreen should be used in conjunction with a hat, sunglasses and sun-protective clothing, adds the skin specialist. MYTH #4 I shouldn't wear sunscreen because sun exposure on my bare skin is essential to boost my Vitamin D levels. "Indeed, exposure of the skin to ultraviolet B (UVB) radiation is responsible for cutaneous production of vitamin D precursors," says Dr. Karen. However, it's important to note that the beneficial effects of exposure to UVB radiation cannot be separated from its harmful effects. "UV radiation from the sun is a known carcinogen that is responsible for DNA damage that results in skin cancer," tells the dermatologist. Besides, photodamage also contributes to other skin concerns such as wrinkles, dark spots and redness. This is why intentional UV exposure to increase Vitamin D levels is ill-advised, says the skincare expert. The safest way to prevent Vitamin D deficiency is to eat a balanced diet that includes whole foods rich in Vitamin D (such as fatty fish, egg yolks, mushrooms, spinach, etc.) and take a daily oral supplement, suggests Dr. Karen. MYTH #5 Dark-skinned people aren't at risk of developing skin cancer. "Although fair skin, light eyes, light hair, the tendency to freckle or burn are risk factors for developing melanoma (one of the most aggressive forms of skin cancer), no ethnicity is completely immune," says Dr. Karen. Therefore, people of all colors, including those who have black or brown skin, need to integrate safe-sun practices into their daily routine. MYTH #6 Tanning beds are safer than sunbathing. Tanning booths and beds expose you to ultraviolet rays that can cause serious DNA damage, increasing your risk of developing skin cancer. "The amount of UV radiation emitted by these indoor lamps exceeds ten times that emitted by the sun during peak hours," says Dr. Karen. According to the American Academy of Dermatology (AAD), just one indoor tanning session can increase the risk of developing melanoma by 20%, squamous cell carcinoma by 67% and basal cell carcinoma by 29%. MYTH #7 Makeup with sunscreen provides suitable protection against skin cancer. "No. A dedicated sunscreen should be applied before putting on makeup, even if there is SPF within a makeup product—this is because often it's not applied in adequate amounts to achieve the stated SPF on the product and therefore, won't offer sufficient protection," Dr. Karen explains. MYTH #8 If I want to get a mole checked out, I have to get surgery. Having a suspicious mole or skin lesion observed by a dermatologist can be a scary thought. "While the traditional method of melanoma diagnosis involves a scalpel, that’s not the only option available. Dermatologists can use genomic assays like DermTech, which uses a smart sticker to painlessly and noninvasively diagnose atypical moles at an earlier stage. This option obviates a biopsy for every mole and can even be administered at home, once prescribed by your dermatologist," notes Dr. Karen. "Research what your dermatologist can provide and know that you’re not solely bound to surgical cutting and consequent scarring in order to have peace of mind," adds the skin specialist. Besides slathering on sunscreen before stepping outdoors, it is also important to follow other critical measures including seeking the shade—especially when the sun is at its strongest (between 10 a.m. and 4 a.m.) and wearing sunglasses and sun-protective clothing—which, unlike sunscreen, don't lose their efficacy over the course of a day, says Dr. Karen. It's also important to examine your skin (and that of your partner/loved ones) for lesions that may be new or changing or appear to be distinct from all others. And lastly, get your skin examined by a dermatologist annually, suggests Dr. Karen. "When caught in the earliest stage, skin cancer is completely curable. If however, it is not caught early, it can be deadly," adds the skincare expert.

Eight Skin Cancer Myths You Need To Stop Believing

Eight Skin Cancer Myths You Need To Stop Believing

Skin cancer is the most common type of cancer in the U.S.—with current estimates suggesting that one in five Americans develop skin cancer by the time they hit 70. But with so much contradictory information out there on the subject, skin cancer is often misunderstood and sometimes, not taken seriously enough. 

 

To help you better protect yourself against the potentially fatal disease, I spoke with a board-certified dermatologist to get the facts behind some of the biggest misconceptions about skin cancer:

 

MYTH #1 I’m not at risk of developing skin cancer in the winter months or when it’s cloudy because the sun isn’t as strong.

 

One of the most prevalent myths when it comes to sun protection is that you don’t need to apply sunscreen or sunblock on cold or cloudy days. “The harmful UV rays emitted by the sun—that are largely responsible for all of the major types of skin cancer, including melanoma—are present year-round. Also, they can penetrate through clouds and even glass windows,” tells Dr Julie Karen, a board-certified dermatologist who specializes in Mohs micrographic surgery, laser surgery and skin cancer. Bottom line: No matter what the forecast is, don’t skip sunscreen.

 

MYTH #2 The damage is already done. I was careless in my youth, it’s too late now to make any significant impact on my skin cancer risk.

 

“While we used to estimate that the vast majority of a person’s sun damage in a lifetime occurred during childhood, we now know that by age 22, only about 20% of your lifetime damage has been accrued,” says Dr Karen. “Each decade thereafter, you acquire an additional 10% of your lifetime damage. So, it’s not too late to make a difference at any age. Introducing sun-smart behaviours, even after years of carelessness, will help to reduce additional UV damage from occurring and thus reduce your cumulative risk of developing all forms of skin cancer,” she notes.

 

MYTH #3 I used SPF 50 this morning, so I can safely sunbathe now.

 

“Often patients will present to my office with tan lines or worse yet, sunburns and declare that they ‘wore SPF 50.’ So, I spend a ton of time educating them about what true ‘sun smart behaviour’ is,” says Dr Karen. “First of all, there is no such thing as a safe tan. Your skin thickens and darkens (i.e. tans) to protect itself from further damage caused by UV exposure. So even though a tan is less harmful than a blistering sunburn, once you see a tan, the damage is done,” tells the dermatologist. Secondly, “most people apply far less than 50% of the recommended amount of sunscreen required for adequate protection. So, the SPF on the label of your bottle is rarely achieved in daily practice,” Dr Karen points out. “You should apply at least one ounce (a shot glass full or golf ball-sized) of sunscreen from head to toe, twenty minutes before going into the sun. And reapply an equally generous amount every two hours or sooner after swimming or perspiring,” she suggests. Though wearing sunscreen is a critical component of skin protection, it’s by no means a license to lie in the sun. Rather, sunscreen should be used in conjunction with a hat, sunglasses and sun-protective clothing, adds the skin specialist.  

 

MYTH #4 I shouldn’t wear sunscreen because sun exposure on my bare skin is essential to boost my Vitamin D levels.

 

“Indeed, exposure of the skin to ultraviolet B (UVB) radiation is responsible for cutaneous production of vitamin D precursors,” says Dr Karen. However, it’s important to note that the beneficial effects of exposure to UVB radiation cannot be separated from its harmful effects. “UV radiation from the sun is a known carcinogen that is responsible for DNA damage that results in skin cancer,” tells the dermatologist. Besides, photodamage also contributes to other skin concerns such as wrinkles, dark spots and redness. This is why intentional UV exposure to increase Vitamin D levels is ill-advised, says the skincare expert. The safest way to prevent Vitamin D deficiency is to eat a balanced diet that includes whole foods rich in Vitamin D (such as fatty fish, egg yolks, mushrooms, spinach, etc.) and takes a daily oral supplement, suggests Dr Karen. 

 

MYTH #5 Dark-skinned people aren’t at risk of developing skin cancer.

 

“Although fair skin, light eyes, light hair, the tendency to freckle or burn are risk factors for developing melanoma (one of the most aggressive forms of skin cancer), no ethnicity is completely immune,” says Dr Karen. Therefore, people of all colours, including those who have black or brown skin, need to integrate safe-sun practices into their daily routine. 

 

MYTH #6 Tanning beds are safer than sunbathing.

 

Tanning booths and beds expose you to ultraviolet rays that can cause serious DNA damage, increasing your risk of developing skin cancer. “The amount of UV radiation emitted by these indoor lamps exceeds ten times that emitted by the sun during peak hours,” says Dr Karen. According to the American Academy of Dermatology (AAD), just one indoor tanning session can increase the risk of developing melanoma by 20%, squamous cell carcinoma by 67% and basal cell carcinoma by 29%. 

 

MYTH #7 Makeup with sunscreen provides suitable protection against skin cancer.

 

“No. A dedicated sunscreen should be applied before putting on makeup, even if there is SPF within a makeup product—this is because often it’s not applied in adequate amounts to achieve the stated SPF on the product and therefore, won’t offer sufficient protection,” Dr Karen explains. 

 

MYTH #8 If I want to get a mole checked out, I have to get surgery.

 

 Having a suspicious mole or skin lesion observed by a dermatologist can be a scary thought. “While the traditional method of melanoma diagnosis involves a scalpel, that’s not the only option available. Dermatologists can use genomic assays like DermTech, which uses a smart sticker to painlessly and noninvasively diagnose atypical moles at an earlier stage. This option obviates a biopsy for every mole and can even be administered at home, once prescribed by your dermatologist,” notes Dr Karen. “Research what your dermatologist can provide and know that you’re not solely bound to surgical cutting and consequent scarring to have peace of mind,” adds the skin specialist. 

 

Besides slathering on sunscreen before stepping outdoors, it is also important to follow other critical measures including seeking the shade—especially when the sun is at its strongest (between 10 a.m. and 4 a.m.) and wearing sunglasses and sun-protective clothing—which, unlike sunscreen, don’t lose their efficacy for a day, says Dr Karen.

 

It’s also important to examine your skin (and that of your partner/loved ones) for lesions that may be new or changing or appear to be distinct from all others. And lastly, get your skin examined by a dermatologist annually, suggests Dr Karen. “When caught in the earliest stage, skin cancer is completely curable. If however, it is not caught early, it can be deadly,” adds the skincare expert.

7 Rarest Cancers in the World

Type of 7 rarest cancer 

 

1. Head And Neck Cancer

Cancers are known as head and neck cancers usually begin in the squamous cells that line the mucosal surfaces inside the head and neck (e.g. mouth, nose and throat). Cancers of the head and neck can be categorised by the area where they begin, e.g. the oral cavity, pharynx, larynx, paranasal sinuses and nasal cavity and salivary glands. 

 

2. Sarcoma

Sarcoma arises in the connective tissue of the body, i.e. fat, blood vessels, nerves, bones, muscles, deep skin tissues and cartilage. This type of cancer is divided into either bone sarcomas or soft tissue sarcomas – all share certain microscopic characteristics and have similar symptoms. 

 

3. Thyroid Cancer

Thyroid cancer is a rare type of cancer that affects the thyroid gland, a small gland at the base of the neck that produces hormones. Symptoms include a painless lump or swelling in the front of the neck, swollen glands in the neck, unexplained hoarseness, a lingering sore throat and difficulty swallowing. 

 

4.Neuroendocrine Cancer

A neuroendocrine tumour begins in the hormone-producing cells of the body’s neuroendocrine system. Neuroendocrine cells are found in organs like the lungs and gastrointestinal tract, including the stomach and intestines. 

 

5. Brain Tumours

Cancerous brain tumours are high-grade tumours that either start in the brain (primary tumours) or spread into the brain from elsewhere (secondary tumours). Symptoms include severe, persistent headaches, seizures, persistent nausea, vomiting and drowsiness, mental or behavioural changes, vision or speech problems, progressive weakness or paralysis on one side of the body. 

 

6. Lymphoma

Lymphoma occurs when lymphocytes (white blood cells) get out of control. They divide abnormally or don’t die when they should. Abnormal lymphocytes can collect in your lymph nodes, often in your armpits, neck or groin, but they can collect in almost any part of your body. Symptoms will depend on where the lymphoma starts and what parts of your body are affected. 

 

7. Paediatric (Childhood) Cancer

The most common cancers in children include leukaemia, lymphoma and brain cancer. Things that cause cancer in adults (e.g. smoking or exposure to environmental toxins) are usually not the same as in children. In most cases, childhood cancers come from random mutations in the genes of growing cells, which means that there’s often no effective way to prevent them.

What is Thyroid Cancer

What is Thyroid Cancer?

Thyroid cancer is a disease in which the cells of cancer are found in thyroid glands. The thyroid glands are the lower part of the throat. This is a rare type of cancer. People in their 30s and those over the age of 60 may be infected by this disease. Women are 2 to 3 times more likely to develop it than men.

Types of Thyroid Cancer:

Generally, there are mainly four main types of thyroid cancer which are based on how the cancer cells look under a microscope. They are:

  • Papillary
  • Follicular 
  • Medullary
  • Anaplastic

Symptoms of Thyroid Cancer:

If you have the symptoms which are given below please talk to your doctor right away. The symptoms are:

  • Pain in the front of the neck and sometimes it travels upward to the ears.
  • A lump in the neck, sometimes growing quickly.
  • Swelling in the neck.
  • Hoarseness or other voice changes that do not go away.
  • A constant cough that does not contain due to cold
  • Trouble swallowing.
  • Trouble breathing.

Many of these symptoms can also be caused by non-cancerous conditions or even other cancer of the neck area. 

Remedy of Thyroid Cancer:

Different tests and procedures are used to diagnose thyroid cancer. Which is as follows:

  • Physical exam
  • Blood tests
  • Ultrasound imaging 
  • Removing a sample of thyroid tissue
  • Other imaging tests
  • Genetic testing

Most of thyroid cancer can be cured by treatment. Very small thyroid cancer that has a low risk of spreading in the body might not need treatment right away. If the risk risks of thyroid cancer grow then treatment should be initiated. Those are:

  • Surgery
  • Removing a portion of the thyroid (thyroid lobectomy)
  • Removing all or most of the thyroid (thyroidectomy)
  • Removing lymph nodes in the neck (lymph node dissection)
  • Thyroid hormone therapy
  • Radioactive iodine
  • External radiation therapy
  • Chemotherapy
  • Targeted drug therapy
  • Injecting alcohol into cancer
  • Supportive care

Mortality Gap Between Cancer

Heart Disease Narrowing for Women Younger Than 65

THURSDAY, Feb. 25, 2021 (HealthDay News) — For women aged younger than 65 years, the mortality gap between cancer and heart disease is narrowing, according to a study published online Feb. 8 in the European Heart Journal: Quality of Care & Clinical Outcomes.

 

Safi U. Khan, M.B.B.S., from West Virginia University in Morgantown, and colleagues compared premature heart disease- and cancer-related deaths in women aged younger than 65 years in the United States. The annual percentage changes (APCs) in age-adjusted mortality rates (AAMRs) and years of potential life lost per 100,000 persons were compared.

 

The researchers found that cancer was a more prevalent cause of premature death than heart disease overall. Between 1999 and 2018, there were decreases in the AAMRs for both cancer (61.9 to 45.6 per 100,000) and heart disease (29.2 to 22.6 per 100,000). The APC in AAMR for cancer decreased consistently over time, while for heart disease, the APC in AAMR declined initially but increased between 2010 and 2018 (0.53), with significant increases in the Midwest, medium/small metros, and rural areas after 2008. The APC in AAMR for heart disease increased in women aged 25 to 34 years (2.24) and 55 to 64 years (0.46) compared with cancer. There was a narrowing in the mortality gap observed between cancer and heart disease, from 32.7 to 23.0 per 100,000.

 

“If extreme public health measures are not taken to mitigate cardiovascular risk factors, focusing on high-risk groups, heart disease mortality may supersede cancer to become the leading cause of death in young women,” the authors write