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EOSINOPHILIA-Origin,Definition,Causes,Diagnosis,Symptoms,Treatment…Ect..!

Eosinophilia – Definition, Causes, and Treatment.

Definition
Eosinophilia indicates elevated levels of eosinophils in the peripheral blood, usually related to an infectious, neoplastic, or allergic process. Often, high numbers of eosinophils may be present in other body fluids or tissues, but the term typically refers to peripheral blood eosinophilia. It is often defined as an absolute eosinophil count of ≥500 eosinophils/microliter (cells/microL) of blood. 500-1500cell/microL is considered mild, 1500-5000 cells moderate, and >5000 severe.

Pathophysiology
Allergic reactions are associated with a raised eosinophil count, slight at first but increasing with each exposure. Mast cells and basophils associated with a hypersensitivity reaction produce and release a number of cytokines, which evoke IgE production. IgE, elevated levels, stimulates eosinophil production. IL-5 is a chemokine that is extremely important in the final differentiation of mature eosinophils, as well as their recruitment into sites of inflammation, and their prolonged survival.

In addition, eosinophils produce growth factors which are responsible for the fibrotic response to inflammatory injury in affected tissues. This is because the eosinophils release cytokines which not only induce inflammation, but also attract more eosinophils and other immune cells of various types to the organ site. The release of various chemicals and reactive oxygen species by the eosinophils and other cells creates more tissue damage.

Types
Eosinophilia is classified as primary or secondary, in addition to the hypereosinophilic syndromes.

Primary Eosinophilia

Primary eosinophilia is a rise in the peripheral eosinophil count without any underlying condition to account for it. It is subclassified into clonal and idiopathic types.
Clonalprimary eosinophilia is the type of eosinophilia that is due to the proliferation of a clone of eosinophils in the bone marrow and is found in leukemias or other myeloproliferative disorders. Idiopathic primary eosinophilia is a term used to refer to peripheral blood eosinophilia without any detectable cause.
Secondary Eosinophilia

Secondary eosinophilia is the result of other disorders not associated with bone marrow proliferation, such as atopy, asthma, and most commonly helminthic infestations.

Hypereosinophilic Syndromes

Hypereosinophilic syndromes are disorders which are characterized by eosinophilia above 1500/µL persisting for at least 6 months, with no underlying disease condition, but associated with organ dysfunction due to eosinophil recruitment into tissues which suffer resulting damage. These include the syndromes of pulmonary eosinophilic infiltrate with eosinophilia, such as:

Churg-Strauss syndrome
Tropical pulmonary eosinophilia
Causes and Risk factors        
There are numerous reasons your eosinophil count may be elevated. Some of the causes are benign and require little treatment. It is not uncommon for the elevated count to be transient and resolve without treatment. Let’s review some of the causes now.

Parasite infections: The most common cause of eosinophilia is a parasite infection include schistosomiasis, trichinosis, strongyloidiasis, and ascariasis. 

Drug reactions:  Medications can trigger eosinophilia, sometimes without any obvious signs or symptoms. The most common medications associated with eosinophilia include antibiotics (penicillin, cephalosporins), non-steroidal anti-inflammatory medications (aspirin, ibuprofen), ranitidine (for gastroesophageal reflux), phenytoin (anti-seizure) and allopurinol (used to treat gout). The most severe form is called drug reaction with eosinophilia and systemic symptoms (DRESS). Fortunately, most people will not have these reactions when they receive these medications.

Atopy: Atopy is a particular reaction that occurs in the body. Typically, atopy refers to asthma, seasonal allergies (also called allergic rhinitis), and eczema. It is not uncommon for someone to have more than one of these medical conditions as they are related. These are some of the most common causes of mild to moderate eosinophilia, particularly in children. Similarly, food allergies can also cause elevated eosinophil counts.

Eosinophilia esophagitis (EoE):  This is a disorder characterized by eosinophils spreading to esophagus which normally does not contain eosinophils. About 50% of people with EoE will also have elevated eosinophil counts in the blood.

Cancers:  There are several cancers, particularly blood cancers that are known for increasing the eosinophil count. These include a rare type of acute myeloid leukemia (AML) called eosinophilic leukemia. Other causes include several of the myeloproliferative neoplasms (such as, essential thrombocythemia, polycythemia vera) B-cell and T-cell lymphoma, as well as adenocarcinomas of the gastrointestinal tract, lung, and cervix.

Clinical Manifestations
Symptoms of eosinophilia vary based on the underlying conditions.

Frequent wheezing and breathlessness are symptoms typical to eosinophilia caused due to asthma.
In case of eosinophilia due to parasitic infections symptoms may include

Abdominal pain
Diarrhea
Fever
Cough
Rashes
Frequent infections
Abscesses
Pneumonia
Mouth sores
Few other symptoms of eosinophilia include

Weight loss
Night sweats
Enlargement of lymph nodes
Skin rashes
Tingling and numbness due to nerve damage, these symptoms however occur rarely.
Complications arises during Eosinophilia
Weight loss
Night sweats
Lymph node enlargement
Skin rashes
Numbness and tingling due to nerve damage
Wheezing
Breathlessness
In case of eosinophilia types following complications arise

Myocardial fibrosis
Chronic heart failure
Death
Diagnosis and Test
History

First, a careful history is taken, to elicit travel to places where helminthiasis is rife; exposure to drugs; ingestion of possibly helminth-infected food; family history of myeloproliferative disorders, allergies, and drug hypersensitivity.

Symptoms which should be inquired about include:

Those of helminth infestation
Symptoms of organ involvement such as lung infiltration, inflammatory bowel disease, or vasculitis of various organs
Symptoms of allergies of the skin or respiratory system in particular
Systemic symptoms such as fever, joint pain and swelling, or lymphadenopathy
Drug exposure should be classified based on the association between the drug and the chances of eosinophilia. For instance, anticonvulsants, allopurinol (a drug used in gout), and semisynthetic penicillins have a higher chance of causing eosinophilia.

Specific findings may also point to the culprit drug, such as:

Anticonvulsants, if hepatitis or DRESS is present
NSAIDs or semisynthetic penicillins in pneumonitis
Immunevasculitis with phenytoin or allopurinol
Nephritis with cephalosporins
Physical Examination

The patient should have a detailed examination of the cardiovascular, renal, respiratory, gastrointestinal, and neurologic systems. Such findings as a skin rash, asthma or lung congestion, or generalized lymphadenopathy are suspicious of underlying conditions such as pulmonary syndromes with eosinophilia, myeloproliferative disorders, and vasculitis or atopic disease. This examination will also help to pick up complications due to hypereosinophilia, the most important of which include pulmonary, neurologic, and cardiac dysfunction.

Screening and Testing

In addition to the basic blood counts which revealed the eosinophilia, other tests may include:

Peripheral blood smear for abnormal eosinophils or blast cells suggestive of myeloproliferative disorders
Stool ova and parasite tests on three consecutive specimens
Parasite tests such as thin and thick blood smears
Specific serological tests for parasites
Anti-neutrophil cytoplasmic antibodies which are raised in some types of immune disease
Organ-specific tests such as renal or hepatic function tests as clinically indicated
Chest radiograph
Electrocardiogram,cardiac troponin
IgE levels and other immunoglobulins
Urinalysis
Serologic tests for vasculitis and other connective tissue disorders
Specialized tests such as bone marrow aspirate examination and cytogenetic tests for myeloproliferative disorders
Echocardiography if other tests are normal, or if cardiac symptoms are present
Pulmonary function tests
Tissue biopsies for parasites such as Trichinella, filariasis, and visceral larva migrans
Imaging tests based on symptoms or signs of organ involvement, such as CT scan of the chest or abdomen
Treatment and Medications
Treatment tackles the underlying cause of the condition, whether it is caused due to allergens, medical reaction or a parasitic reaction. Treatments such as intake of oral Corticosteroid drugs which are steroid hormones produced from the adrenal cortex of the vertebrates. Corticosteroid drugs such as Prednisolone are preferred at single doses of 30–60mg. These treatments are effective and non-toxic.

Natural Home Remedies foreosinophilia

Ginger, it is a very good herb in lowering down the increase count of eosinophils. It is taken by preparing its juice by mashing it properly and put this in a tea drink this tea one to two times daily for few days which gives better results.
Turmeric powder is a very good remedy to treat patients who have higher values of eosinophils. It is prepared by putting a pinch of turmeric powder in one glass of water and makes it boil and drink.
Ginseng is a very good home remedy in reducing the inflammation in airways and thus lowers down the count of high eosinophils.
Eucalyptus its oil is used in reducing the various symptoms in eosinophilia.
Fenugreekits seeds are used in combating the infections that are related to increasing eosinophilia. The seeds of fenugreek are boiled in one glass of water the two tablespoons of seeds are added in a glass of water drink this mixture every day morning and evening.
HolyBasil (Tulsi leaves) it is a very effective home remedy known for treating high eosinophilic count. The chewing of two to three leaves is recommended for better results.
Malabar Nut It is the very useful home remedy in reducing the symptoms of eosinophilia. Drink its juice daily for better results.
Neem(Azadirachta indica) It is used as medicine since many years it has a property of anti-bacterial, antifungal, antiviral, sedative, anti-diabetic so it is useful for various purposes it helps in removing unwanted harmful toxins from the body. Thus it is helpful in controlling various types of allergies related to food, in the skin like eczema, psoriasis etc.
Prevention of Eosinophilia
Cause of eosinophilia is not always clear. As a result, there are no specific steps to prevent eosinophilia.

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Sarcopenia- Origin,Definition,Causes,Diagnosis,Symptoms,Treatment…Ect..!

Definition
Sarcopenia is a disease associated with the aging process. Loss of muscle mass and strength, which in turn affects balance, gait and overall ability to perform tasks of daily living, are hallmark signs of this disease. Most people begin to lose modest amounts of muscle mass after age 30, but the resulting loss of strength increases exponentially with age.

Possible effects of sarcopenia include decreased muscle strength, problems with mobility, frailty, weak bones (osteoporosis), falls and fractures, decreased activity levels, diabetes, middle‐age weight gain and a loss of physical function and independence.

Stages of Sarcopenia
Different stages of sarcopenia may be used to help identify the severity of the condition, such as:

Pre-sarcopenia: Characterized by reduced muscle mass. No reduction in muscle strength or physical performance
Sarcopenia: Characterized by the presence of low muscle mass and low muscle function (strength OR performance)
Severe sarcopenia: Characterized by reduced muscle mass and reduction in muscle strength.
Pathophysiology
Immobility and malnutrition, especially low protein intake, could deteriorate sarcopenia, and the influence of multiple factors leading to aging-related sarcopenia. Skeletal muscle consists of two types of fibers: Type I and Type II. Type II fast fibers have a higher glycolytic potential, lower oxidative capacity, and faster response as compared to type I slow fibers. Type I fibers are known as fatigue-resistant fibers due to their characteristics that include greater density of mitochondria, capillaries and myoglobin content. With age, atrophy almost only affects type II fibers. Molecular mechanisms of sarcopenia are not fully understood. Some factors have been suggested to be involved as described below.

Changes in Hormones and Metabolism: GH is released from the pituitary gland and promotes IGF-1 secretion. IGF-1 binds to the IGF-1 receptor and activates its downstream Akt/ mammalian target of rapamycin (mTOR) pathway. mTOR induces muscle hypertrophy by promoting protein synthesis. Akt inhibits FOXO transcriptional factors and blocks the upregulation of E3 ubiquitin ligases, or muscle RING-finger protein-1 (MuRF1) and Muscle Atrophy F-Box (MAFbx), which stimulate protein degradation. Therefore, the decrease of GH and IGF-1 might be involved in sarcopenia. Insulin is also an anabolic hormone and activates Akt/mTOR pathway. Skeletal muscle protein synthesis is resistant to the anabolic action of insulin in older subjects, and this could be involved in the development of sarcopenia.

Neuromuscular Aging: Neuron loss is a progressive, irreversible process that increases with age. Multiple levels of the nervous system are affected by age, including the motor cortex, the spinal cord, peripheral neurons, and the neuromuscular junction. As age goes these leads to degeneration and could be the cause of sarcopenia.

Systemic Inflammation: As humans age, the serum level of tumor necrosis factor-a (TNF-α), interleukin-6 (IL-6), interleukin-1 (IL-1) and C-reactive protein (CRP) elevate. Adipose tissues are supposed to secrete these cytokines. A theory called inflamm-aging (inflammation +aging) proposes that, as humans age, systemic low-grade inflammation is one of the causes of various diseases such as atherosclerosis, dementia, type 2 diabetes, and osteoporosis. The high-sensitivity CRP levels are significantly and independently associated with sarcopenic obesity. Inflamm-aging might be involved in sarcopenia.

Causes and Risk factors
A common cause of sarcopenia is decreased physical activity throughout the day. However, although less frequent, some people with active lifestyles may also be diagnosed with sarcopenia. This suggests that there could be other reasons for the development of the disease.

Researchers currently believe that other causes of sarcopenia could include:

A reduction in the nerve cells that send signals from your brain to tell your muscles to move
A lowering of your hormone levels
A decline in your body’s ability to convert protein to energy
Not consuming enough daily calories and protein in order to maintain your muscle mass
Symptoms
Symptoms of sarcopenia may vary depending on how much muscle mass a person has lost. Symptoms include:

A decrease in muscle size
Weakness
Loss of endurance
Poor balance
Trouble climbing stairs
A decline in muscle mass may not seem like a big concern for most people. However, muscle loss can be significant enough to cause weakness, increase fall risk, and limit a person’s independence.

Sarcopenia may also cause a person to reduce their participation in physical activities. This decrease in activity causes even further muscle loss, which can adversely affect a person’s quality of life.

Complications
Sarcopenia has been linked to metabolic problems like type 2 diabetes, high blood pressure, and obesity. These conditions put you at greater risk of developing coronary heart disease, stroke, and other conditions that affect the blood vessels.

Sarcopenia has a pervasive, negative impact on patients’ quality of life and often leads to:

Increased inpatient length of stay
A decline in daily activities and ambulatory function
Reduced day-to-day activities
Increased risk of illness and infection
Reduced recovery from surgery, illness, and injury
Poor wound healing
Increased mortality
Diagnosis and Test
Sarcopenia should be diagnosed in three criteria:

i) Muscle mass:

Computed Tomography scan (CT scan).
Magnetic Resonance Imagery (MRI).
Dual Energy X-ray Absorptiometry (DXA).
Bioimpedance analysis (BIA).
ii) Muscle strength:

Handgrip strength.
iii) Physical performance:

Short Physical Performance Battery (SPPB).
Gait speed.
Grip strength.
Thigh muscle thickness ratio.
Treatment and Medications
Hormone replacement therapy (HRT)
HRT can help to raise lean body mass, decrease abdominal fat, and prevent bone deterioration in women whose hormone levels decrease with menopause. However, the use of HRT is debated because of an increased risk of some cancers and other severe health conditions.

Some other treatments that are under investigation include:
Growth hormone supplements
Testosterone supplements
hydroxymethyl butyrate
Angiotensin-converting enzyme inhibitors
Vitamin D
Medications for the treatment of metabolic syndromes
Although drug therapy is not the preferred treatment for sarcopenia, a few medications are under investigation. They include:

Urocortin II. This has been shown to stimulate the release of a hormone called adrenocorticotropic hormone (ACTH) from your pituitary gland. Given through an IV, this can prevent muscle atrophy that can happen when you’re in a cast or taking certain medicines. Its use for building muscle mass in humans has not been studied and isn’t recommended.

Other treatments under investigation for sarcopenia include:

Testosterone supplements
Growth hormone supplements
Medication for the treatment of metabolic syndrome includes insulin resistance, obesity, and hypertension).
Home remedies
Instead of medication or hormone therapy, management of sarcopenia focuses on lifestyle changes to prevent muscle loss. These usually include:

Exercise
Strength training or resistance training can improve muscle size, strength, and tone. It can also strengthen bones, ligaments, and tendons, which is good for a person’s overall health. Strength training involves using resistance to cause muscle contraction. The muscle contraction builds muscle size and increases strength. Strength training may involve using weights, resistance bands, or exercise machines. A person’s own body weight can also be used for resistance.

Nutrition
Proper nutrition is essential to treat sarcopenia, and may even prevent or delay the condition. Healthy protein. Healthy sources of protein, such as fish, nuts, lentils, and quinoa, can help to build up and sustain normal muscle mass levels.

Eating enough protein is an important dietary consideration in preventing sarcopenia. The IOF recommend that adults eat 1.0-1.2 grams of protein per kilogram of body weight daily.

Dietary supplements
Taking certain dietary supplements may be another way to improve sarcopenia or help prevent the condition. For example, taking creatine supplements may increase strength and lean muscle mass in adults of any age. Similarly, maintaining adequate levels of vitamin D, either through diet or supplements, may help older adults maintain muscle strength.

Prevention
Lack of activity is the most common reason behind this condition. Therefore, being physically active may lessen your chances of getting sarcopenia. Just half an hour of moderate exercise each day, like walking or jogging, will help keep your system working and fit.

In order for exercise to be effective, proper nutrition is also important. Research has shown that consuming more protein may help older adults reduce their chance of sarcopenia. Supplements have also proven useful in the prevention of sarcopenia. Some include:

Creatine, for increasing and maintaining muscle mass
Vitamin D, for maintaining bone and muscle tissues
Whey protein, to help preserve body mass
 

Acne vulgaris

What is Acne vulgaris?

vulgaris is an inflammatory disorder of the pilosebaceous unit, which runs a chronic course and it is self-limiting.

Acne vulgaris is triggered by Propionibacterium acne in adolescence, under the influence of normal circulating dehydroepiandrosterone (DHEA). It is a very common skin disorder which can present with inflammatory and non-inflammatory lesions chiefly on the face but can also occur on the upper arms, trunk, and back.

Acne vulgaris
Epidemiology
Acne may appear in adolescence, and it persists through the early thirties. Acne is more common in males than in females. Urban populations are more affected than rural populations. About 20% of the affected individuals develop severe acne which results in scarring. Some races appear to be more affected than others. Asians and Africans tend to develop severe acne, but mild acne is more common in the white population. In general, populations with darker skin also tend to develop hyperpigmentation. Acne can also develop in neonates but in most cases resolves spontaneously.

Types of acne vulgaris
Four main types are recognized:

Pyoderma faciale is seen usually in an older woman with existing acne who is subjected to stress when a localized but explosive pattern of the disease appears.

Acne conglobata is a severe form of the disease which affects the face, back, and limbs. Cystic and pustular lesions occur and scarring may be marked. It occurs mainly in men.

Acne fulminans is an immunologically induced severe systemic variant of acne conglobata. The clinical features are those of acne conglobata plus the classic delayed hypersensitivity systemic reaction with splenomegaly, arthropathy, and rashes.

Gram-negative folliculitis is associated with the long-term antibiotic treatment of acne. Acne which was well controlled suddenly appears to “escape” from control. This condition takes the form of a sudden eruption of small follicular pustules.

Acne vulgaris risk factors
Risk factors increase with:

Exposure to extremely hot or cold temperatures
Stress
Oily skin
Endocrine disorders
Use of drugs, such as cortisone, male hormones, or oral contraceptives
Family history of acne
Some cosmetics
Acne vulgaris pathogenesis
Acne vulgaris is a multifactorial condition that ultimately results in inflammatory changes of the pilosebaceous unit.

Although no specific genetic factor has been correlated with acne vulgaris, epidemiologic studies have demonstrated a family history of acne is associated with increased incidence.
Diet has traditionally been associated with a causal or influential factor in acne vulgaris, but this remains controversial. However, recent data is suggestive of an association with a high glycemic index diet.
The instigating step in an acne lesion is keratinocyte proliferation and adhesion

Androgen production controls this effect and simultaneously increases sebum production.
These changes create an obstruction of the pilosebaceous duct and the formation of a microcomedone.
In the setting of elevated androgens, sebum collection continues, and closed and open comedones appear.
Bacteria, in particular, Propionibacterium acnes, proliferate within this environment and contribute to local inflammation.
With worsening inflammatory mediators, the comedones progress to erythematous papules, pustules, cysts, and nodules.
In the setting of unremitting disease, the cysts and nodules can rupture, incite further inflammation, and create deep sinus tracts with severe scarring
Causes of Acne vulgaris
Hormones: At around 8 years of age, the adrenal glands start to produce androgens (male hormone) and the amount produced gradually increases during puberty. The sebaceous glands respond to androgens by producing more sebum and sometimes whiteheads (closed comedones) may develop in young children.

Sebaceous gland blockage: The skin cells lining the upper part of the hair follicle duct are not shed as normal but accumulate and form a plug (comedone). The oil is trapped behind it.

Bacteria and inflammation: Increased numbers of acne bacteria (Propionibacterium acnes) accumulate in the duct and contribute to the inflammation that develops in the pimples.

Genetics: Hereditary factors contribute, however it is not known exactly how this works.

Stress: Adrenal glands produce more androgens when an individual is stressed. This can make acne worse.

Diet: Certain diets may contribute to the development of acne, however good scientific data is lacking.

Occupation: In rare cases, people working in certain industries may develop occupational acne where strict Work Health and Safety regulations have not been observed.

Symptoms of Acne vulgaris
Skin lesions and scarring can be a source of significant emotional distress. Nodules and cysts can be painful. Lesion types frequently coexist at different stages.
Comedones appear as whiteheads or blackheads. Whiteheads (closed comedones) are flesh-colored or whitish palpable lesions 1 to 3 mm in diameter; blackheads (open comedones) are similar in appearance but with a dark center.
Papules and pustules are red lesions 2 to 5 mm in diameter. Papules are relatively deep. Pustules are more superficial.
Nodules are larger, deeper, and more solid than papules. Such lesions resemble inflamed epidermoid cysts, although they lack true cystic structure.
Cysts are suppurative nodules. Rarely, cysts form deep abscesses. Long-term cystic acne can cause scarring that manifests as tiny and deep pits (icepick scars), larger pits, shallow depressions, or hypertrophic scarring or keloids.

Acne vulgaris symptoms
Acne vulgaris complications
Scars
Depression
Anxiety
Socially withdrawn
Poor facial aesthetics
Lack of self-esteem
Diagnosis and test
A doctor or dermatologist will diagnose acne following a skin examination, taking note of where the acne is located and its severity. These factors are important in determining how the condition should be treated.

Professionals typically use a grading system to categorize acne:

Grade 1: Mild acne, probably limited to blackheads and whiteheads.

Grade 2: Moderate acne with papules and pustules, mostly confined to the face.

Grade 3: Moderately severe acne affecting the face, back and chest. Papules and pustules will be present, and inflamed nodules are possible.

Grade 4: Severe acne, with a large number of painful papules, pustules, and nodules.

Treatment and medications

Topical therapy
Topical retinoids like retinoic acid, adapalene, and tretinoin are used alone or with other topical antibiotics or benzoyl peroxide. Retinoic acid is the best comedolytic agent, available as 0.025%, 0.05%, 0.1% cream, and gel.
Topical clindamycin 1% to 2%, nadifloxacin 1%, and azithromycin 1% gel and lotion are available. Estrogen is used for Grade 2 to Grade 4 acne.
Topical benzoyl peroxide is now available in combination with adapalene which serves as comedolytic as well as antibiotic preparation. It is used as 2.5%, 4%,and 5% concentration in gel base.
Azelaic acid is antimicrobial and comedolytic available 15% or 20% gel. It can also be used in postinflammatory pigmentation of acne.
Beta hydroxy acids like salicylic acid are used as topical gel 2% or chemical peel from 10% to 20% for seborrhoea and comedonal acne, as well as, pigmentation after healing of acne.
Topical dapsone is used for both comedonal and papular acne, though there are some concerns with G6PD deficient individuals.

Before and after treatment
Systemic therapy
Doxycycline 100 mg twice a day as an antibiotic and anti-inflammatory drug as it affects free fatty acids secretion and thus controls inflammation.
Minocycline 50 mg and 100 mg capsules are used as once a day dose.
Other antibiotics such as amoxicillin, erythromycin and Bactrim are sometimes used, and if bacterial overgrowth or infection is masquerading as acne, other antibiotics such as ciprofloxacin may be used in pseudomonas related ‘acne.’
Isotretinoin is used as 0.5 mg/kg to 1 mg/kg body weight in daily or weekly pulse regimen. It controls sebum production, regulates pilosebaceous epidermal hyperproliferation, and reduces inflammation by controlling P. acnes. It may give rise to dryness, hairless, and cheilitis.
An oral contraceptive containing low dose estrogen 20 mcg along with cyproterone acetate as anti-androgens are used for severe recurrent acne.
Spironolactone (25 mg per day) can also be used in males. It decreases the production of androgens and blocks the actions of testosterone. If given to females, then pregnancy should be avoided because the drug can cause feminization of the fetus.
Scars are treated with submission, trichloroacetic acid, derma roller, micro needling, or fractional CO2 laser.
Prevention of Acne vulgaris
There are several ways to help prevent the development of acne. Not all preventive measures will work for all people, however, and no technique is guaranteed to be effective.

Techniques for helping to prevent acne include:

Keeping the face clean: The face should be cleaned roughly twice daily using warm water and mild soap in order to remove impurities and dead skin cells from the surface. Avoid washing the face too often, however, and do not use harsh soap or cleanser.

Moisturize: Moisturizing can help to keep the skin moist and prevent it from peeling. Products with “non-comedogenic” on the label should not block the pores and thus also not contribute to acne.

Diet and exercise: Eating a diet rich in fruits and vegetables, and low in fats and sugars may help to control acne. Similarly, getting plenty of exercises may also help to prevent acne outbreaks, as well as promoting general good health. After exercising, be sure to wash away any residual sweat, as this can contribute to acne.

Avoid makeup: Limiting makeup use may help to prevent an acne outbreak. Any makeup that is used should be oil-free and non-comedogenic.

Shampoo often: Wash the hair regularly with shampoo. If the hair is particularly oily, use shampoo daily.

Don’t touch: Avoid the temptation to touch the face throughout the day and be sure not to squeeze, pick or pop pimples; this will allow the acne to heal naturally.

Avoid excessive sunlight and tanning beds: Too much exposure to the sun and the use of tanning beds may damage the skin and is therefore not recommended.

Over-the-counter medication: Many anti-acne products are available over the counter from pharmacists and general stores. As well as controlling outbreaks after they have occurred, these products may help to prevent an outbreak from happening in the first place.

Acoustic Neuroma- Origin, Signs,Diagnosis,Treatment,Symptoms and Prevention

Description – Acoustic Neuroma

Acoustic Neuroma is also known as vestibular schwannoma. An acoustic neuroma is a benign tumor that develops when the specialized (Schwann) cells surrounding the vestibular division of the auditory nerve, grow at an abnormal rate in the internal auditory canal. The tumor if left untreated, can grow into the auditory canal and all the way through to the brain.

Acoustic neuromas generally grow slowly, so symptoms develop gradually. The main ones – dizziness, hearing loss and ringing in the ears (tinnitus) – are due to the effects of the tumor pressing on the auditory nerve. If the tumor grows large enough, it also may press on the nearby facial nerve and cause facial paralysis or tingling. Although the tumors are not cancerous, they can become life-threatening if they grow so large that they press on brain structures that control vital body functions.

People with a hereditary disease called neurofibromatosis have a higher risk of developing acoustic neuromas and can develop tumors on both sides of the head.

Types of Acoustic Neuroma
There are two main types of acoustic neuroma:

Unilateral
A tumor affects only one ear. This variant is by far the more common, accounting for 95% of all instances of acoustic neuroma. It is also known as the ‘sporadic’ type and the causes behind its appearance are not well understood.

Bilateral
Tumors arise on both sides affecting both ears. Acoustic neuroma of this kind accounts for only 5% of reported cases, is clearly linked with a rare genetic disorder known as neurofibromatosis type II (NF2).

Pathophysiology of acoustic neuroma
As the acoustic neuroma grows, it compresses the hearing and balance nerves, usually causing unilateral (one-sided) hearing loss, tinnitus (ringing in the ear), and dizziness or loss of balance. As it grows, it can also interfere with the facial sensation nerve (the trigeminal nerve), causing facial numbness.

It can also exert pressure on nerves controlling the muscles of the face, causing facial weakness or paralysis on the side of the tumor.

Vital life-sustaining functions can be threatened when large tumors cause severe pressure on the brainstem and cerebellum.

What causes acoustic neuroma?
The cause of acoustic neuromas is largely unknown. No environmental factor (such as cell phones or diet) has been scientifically proven to cause these tumors. Acoustic neuromas can be sporadic or caused by an inherited condition called neurofibromatosis type 2 (NF-2). Sporadic tumors occur 95% of the time, while 5% of acoustic neuromas occur with NF-2.

Neurofibromatosis is a rare disease that occurs in two forms. Type 1 causes tumors to grow on nerves throughout the body, especially the skin. Type 2 can cause acoustic neuromas on both the left and right sides, creating the possibility of complete deafness if the tumors grow unchecked. The presence of bilateral acoustic tumors affects the choice of treatment, as hearing preservation is a prime objective.

Who is at risk?
The only known risk factor for acoustic neuroma is having a parent with the genetic disorder neurofibromatosis 2 (NF2). Most of these tumors appear spontaneously. They occur in people with no family history of the disease.

Scientists still don’t understand why some people get these tumors. Some risk factors might include:

Loud noises
A parathyroid neuroma, which is a benign tumor of the thyroid
Exposure to low levels of radiation during childhood
How to find if you have acoustic neuroma?
Signs and symptoms of acoustic neuroma are often subtle and may take many years to develop. They usually arise from the tumor’s effects on the hearing and balance nerves. Pressure from the tumor on adjacent nerves controlling facial muscles and sensation (facial and trigeminal nerves), nearby blood vessels, or brain structures may also cause problems.

As the tumor grows, it may be more likely to cause more noticeable or severe signs and symptoms.

Common signs and symptoms of acoustic neuroma include:

Hearing loss, usually gradual – although in some cases sudden – and occurring on only one side or more pronounced on one side
Ringing (tinnitus) in the affected ear
Unsteadiness, loss of balance
Dizziness (vertigo)
Facial numbness and very rarely, weakness or loss of muscle movement
In rare cases, an acoustic neuroma may grow large enough to compress the brainstem and become life-threatening.

Complications of acoustic neuroma
Several complications can arise, including:

Hearing loss: This may persist even after treatment.
Dizziness and loss of balance: If this occurs, it can make daily activities difficult to do.
Facial palsy: If surgery, or rarely, the tumor itself, affects the facial nerve, which is close to the acoustic nerve, the face may droop on one side, and swallowing and speaking clearly may be difficult. This is facial palsy, also known as Bell’s palsy.
Hydrocephalus: If a large tumor presses against the brainstem, this can affect the flow of fluid between the spinal cord and the brain. If fluid accumulates in the head, it can lead to hydrocephalus.
How is acoustic neuroma (vestibular schwannoma) diagnosed?
Because symptoms of these tumors resemble other middle and inner ear conditions, they may be difficult to diagnose. Preliminary diagnostic procedures include ear examination and hearing test. Computerized tomography (CT) and magnetic resonance imaging (MRI) scans help to determine the location and size of the tumor. Early diagnosis offers the best opportunity for successful treatment.

Diagnosis involves:
A hearing test (audiometry): A test of hearing function, which measures how well the patient hears sounds and speech, is usually the first test performed to diagnose acoustic neuroma. The patient listens to sounds and speech while wearing earphones attached to a machine that records responses and measures hearing function. The audiogram may show increased “pure tone average” (PTA), increased “speech reception threshold” (SRT) and decreased “speech discrimination” (SD).

Brainstem auditory evoked response (BAER): This test is performed in some patients to provide information on brain wave activity as a response to clicks or tones. The patient listens to these sounds while wearing electrodes on the scalp and earlobes and earphones. The electrodes pick up and record the brain’s response to these sounds.

Scans of the head: If other tests show that the patient may have an acoustic neuroma, magnetic resonance imaging (MRI) is used to confirm the diagnosis. MRI uses magnetic fields and radio waves, rather than x-rays, and computers to create detailed pictures of the brain. It shows visual “slices” of the brain that can be combined to create a three-dimensional picture of the tumor. A contrast dye is injected into the patient. If an acoustic neuroma is present, the tumor will soak up more dye than normal brain tissue and appear clearly on the scan. The MRI commonly shows a densely “enhancing” (bright) tumor in the internal auditory canal.

Acoustic Neuroma Treatments
There are three main courses of treatment for acoustic neuroma:

Observation
Surgery
Radiation therapy
Observation
Observation is also called watchful waiting. Because acoustic neuromas are not cancerous and grow slowly, immediate treatment may not be necessary. Often doctors monitor the tumor with periodic MRI scans and will suggest other treatment if the tumor grows a lot or causes serious symptoms.

Surgery
Surgery for acoustic neuromas may involve removing all or part of the tumor.

There are three main surgical approaches for removing an acoustic neuroma:

Translabyrinthine, which involves making an incision behind the ear and removing the bone behind the ear and some of the middle ear. This procedure is used for tumors larger than 3 centimeters. The upside of this approach is that it allows the surgeon to see an important cranial nerve (the facial nerve) clearly before removing the tumor. The downside of this technique is that it results in permanent hearing loss.

Retrosigmoid/sub-occipital, which involves exposing the back of the tumor by opening the skull near the back of the head. This approach can be used for removing tumors of any size and offers the possibility of preserving hearing.

Middle fossa, which involves removing a small piece of bone above the ear canal to access and remove small tumors confined to the internal auditory canal, the narrow passageway from the brain to the middle and inner ear. Using this approach may enable surgeons to preserve a patient’s hearing.

Radiation therapy
Radiation therapy is recommended in some cases for acoustic neuromas. State-of-the-art delivery techniques make it possible to send high doses of radiation to the tumor while limiting expose and damage to surrounding tissue.

Radiation therapy for this condition is usually delivered in one of two ways:

Single fraction stereotactic radiosurgery (SRS), in which many hundreds of small beams of radiation are aimed at the tumor in a single session.

Multi-session fractionated stereotactic radiotherapy (FRS), which delivers smaller doses of radiation daily, generally over several weeks. Early studies suggest multi-session therapy may preserve hearing better than SRS.

Both of these are outpatient procedures, which means they don’t require a hospital stay. They work by causing tumor cells to die. The tumor’s growth may slow or stop or it may even shrink, but radiation doesn’t completely remove the tumor.

Prevention
Early diagnosis of a vestibular schwannoma is key to preventing its serious consequences.

ANAPHYLAXIS- Origins,Signs,Diagnose,Treatment,Symptoms and Prevention.

Overview – Anaphylaxis
Anaphylaxis is a serious, life-threatening allergic reaction.

The most common anaphylactic reactions are to foods, insect stings, medications, and latex.

If you are allergic to a substance, your immune system overreacts to this allergen by releasing chemicals that cause allergy symptoms. Typically, these bothersome symptoms occur in one location of the body. However, some people are susceptible to a much more serious anaphylactic reaction. This reaction typically affects more than one part of the body at the same time.

Anaphylaxis requires immediate medical treatment, including a prompt injection of epinephrine and a trip to a hospital emergency room. If it isn’t treated properly it can be fatal.

Pathophysiology of anaphylaxis
Interaction of antigen with IgE on basophils and mast cells triggers the release of histamine, leukotrienes, and other mediators that cause diffuse smooth muscle contraction (eg, resulting in bronchoconstriction, vomiting, or diarrhea) and vasodilation with plasma leakage (eg, resulting in urticaria or angioedema).

Anaphylactoid reactions
Anaphylactoid reactions are clinically indistinguishable from anaphylaxis but do not involve IgE and do not require prior sensitization. They occur via direct stimulation of mast cells or via immune complexes that activate complement.

The most common triggers of anaphylactic reactions are

Iodinated radiopaque contrast agents
Aspirin and other NSAIDs
Opioids
Monoclonal antibodies
Exercise
What causes the anaphylaxis?
Anaphylaxis is a severe, whole-body allergic reaction to a chemical that has become an allergen. An allergen is a substance that can cause an allergic reaction.

After being exposed to a substance such as a bee sting venom, the person’s immune system becomes sensitized to it. When the person is exposed to that allergen again, an allergic reaction may occur. It happens quickly after the exposure. The condition is severe and involves the whole body.

Tissues in different parts of the body release histamine and other substances. This causes the airways to tighten and leads to other symptoms.

Some drugs (morphine, x-ray dye, aspirin, and others) may cause an anaphylactic-like reaction (anaphylactoid reaction) when people are first exposed to them. These reactions are not the same as the immune system response that occurs with true anaphylaxis. But, the symptoms, risk of complications, and treatment are the same for both types of reactions.

Anaphylaxis can occur in response to an allergen. Common causes include:

Drug allergies
Food allergies
Insect bites/stings
Pollen and other inhaled allergens rarely cause anaphylaxis. Some people have an anaphylactic reaction with no known cause. It is life-threatening and can occur at any time. Risks include a history of any type of allergic reaction.

Risk factors
There aren’t many known risk factors, but some things that might increase your risk include:

Previous history. If you’ve had anaphylaxis once, your risk of having this serious reaction increases. Future reactions might be more severe than the first reaction.
Allergies or asthma. People who have either condition are at increased risk.
Certain other conditions. These include heart disease and an abnormal accumulation of a certain type of white blood cell (mastocytosis).
Signs and Symptoms of anaphylaxis
Anaphylaxis symptoms occur suddenly and can progress quickly. The early symptoms may be mild, such as a runny nose, a skin rash or a “strange feeling.” These symptoms can quickly lead to more serious problems, including:

Trouble breathing
Hives or swelling
The tightness of the throat
Hoarse voice
Nausea
Vomiting
Abdominal pain
Diarrhea
Dizziness
Fainting
Low blood pressure
Rapid heartbeat
Feeling of doom
Cardiac arrest

People who have had a severe allergic reaction are at risk for future reactions. Even if your first reaction is mild, future reactions might be more severe. That’s why it’s important to carry self-injectable epinephrine if you are at risk.

A patient would not necessarily experience all of these symptoms in the same episode.

There are several different types of reaction which could occur:

Uniphasic – these come on quickly and symptoms get rapidly worse, but once treated, the symptoms go and don’t return.
Bi-phasic – these are reactions which may be mild or severe to start with, followed by a period of time when there are no symptoms, and then increasing symptoms with breathing and blood-pressure problems.
Protracted anaphylaxis – this can last for several days and may need treatment in hospital for some time.
Complications of anaphylaxis
Complications from anaphylaxis are rare, and most patients completely recover. Myocardial ischemia may result from hypotension and hypoxia, particularly when underlying coronary artery disease exists. Ischemia or arrhythmias may result from treatment with pressors. Prolonged hypoxia also may cause brain injury. At times, a fall or other injury may occur when anaphylaxis leads to syncope.

Respiratory failure from severe bronchospasm or laryngeal edema can cause hypoxia, which could lead to brain injury if prolonged.

Diagnosis
Tests used in the diagnosis of anaphylaxis may include:

Medical history
Physical examination of symptoms and signs
Detailed questioning about what led up to the event
Blood tests to check for the presence of particular antibodies
Skin prick tests to confirm or rule out suspected triggers
Tests to exclude other medical conditions that can mimic certain symptoms of anaphylaxis – for example, unconsciousness is also a symptom of epilepsy.
Some ‘allergy tests’ are not proven
Some ‘tests’ that claim to diagnose allergies are not scientifically or medically proven. The test may have no value and is not proven to provide accurate information on your anaphylaxis trigger or triggers. This can be dangerous if it means you don’t get the medical attention you require.

Some alternative testing methods that may lead to inappropriate or inadequate treatment include:

Alcat testing
Allergen elimination techniques
Cytotoxic food testing
Kinesiology
Hair analysis
IgG food antibody testing
Iridology
Pulse testing
Reflexology
Rinkel’s intradermal testing
Vega testing.
Always seek advice from your doctor before consulting a complementary or alternative therapist about your allergies.

Treatment for anaphylaxis
Anaphylaxis is a medical emergency that requires immediate recognition and intervention. Patient management and disposition are dependent on the severity of the initial reaction and the treatment response. Measures beyond basic life support are not necessary for patients with purely local reactions. Patients with refractory or very severe anaphylaxis (with cardiovascular and/or severe respiratory symptoms) should be admitted or treated and observed for a longer period in the emergency department or an observation area.

Non-pharmacotherapy
Supportive care for patients with suspected anaphylaxis includes the following:

Airway management (eg, ventilator support with bag/valve/mask, endotracheal intubation)
High-flow oxygen
Cardiac monitoring and/or pulse oximetry
Intravenous access (large bore)
Fluid resuscitation with isotonic crystalloid solution
Supine position (or position of comfort if dyspneic or vomiting) with legs elevated
Pharmacotherapy
The primary drug treatments for acute anaphylactic reactions are epinephrine and H1 antihistamines. Medications used in patients with anaphylaxis include the following:

Adrenergic agonists (eg, epinephrine)
Antihistamines (eg, diphenhydramine, hydroxyzine)
H2 receptor antagonists (eg, cimetidine, ranitidine, famotidine)
Bronchodilators (eg, albuterol)
Corticosteroids (eg, methylprednisolone, prednisone)
Positive inotropic agents (eg, glucagon)
Vasopressors (eg, dopamine)

Surgical option
In extreme circumstances, cricothyrotomy or catheter jet ventilation may be lifesaving when orotracheal intubation or bag/valve/mask ventilation is not effective. Cricothyrotomy is easier to perform than emergency tracheostomy.

How to prevent anaphylaxis?
Agents causing anaphylaxis should be identified when possible and avoided. Patients should be instructed how to minimize exposure.

Beta-adrenergic antagonists, including those used to treat glaucoma, may exacerbate anaphylaxis and should be avoided, where possible. Angiotensin-converting enzyme (ACE) inhibitors may also increase susceptibility to anaphylaxis, particularly with insect venom-induced anaphylaxis.

Epinephrine is the drug of choice to treat anaphylaxis. Individuals at high risk for anaphylaxis should be issued epinephrine syringes for self-administration and instructed in their use. Intramuscular injection into the anterolateral thigh is recommended since it results in prompt elevation of plasma concentrations and has prompt physiological effects. Subcutaneous injection results in delayed epinephrine absorption.

Patients must be alerted to the clinical signs of impending anaphylaxis and the need to carry epinephrine syringes at all times and to use it at the earliest onset of symptoms.

Unused syringes should be replaced when they reach their use-by/expiration date, as epinephrine content and bioavailability of the drug decreases in proportion to the number of months past the expiration date.

Pre-treatment with glucocorticosteroids and H1 and H2 antihistamines is recommended to prevent or reduce the severity of a reaction where it is medically necessary to administer an agent known to cause anaphylaxis, for example, radio-contrast media.

Other important patient instructions include:

Personalized written anaphylaxis emergency action plan
Medical Identification (e.g., bracelet, wallet card)
Medical record electronic flag or chart sticker, and emphasis on the importance of follow-up investigations by an allergy/immunology specialist

HOW TO TEST LIVER FUNCTION

Expert Reviewed
How to Test Liver Function
Testing your liver function may be a good idea if you have a history of liver issues in your family, as some liver conditions can be hereditary. Your doctor may also suggest you get your liver function tested if you have abdominal pain, have a history of hepatitis C, use alcohol regularly, have suspected liver issues, or may be suffering side effects from certain medications, such as cholesterol medicine. This test can be done by drawing a blood sample from a vein in your arms. Your doctor can then help you understand your test results and provide information on how to treat your liver function issues.

Part One of Three:
Getting the Blood Test

1
Do not eat the night before the test unless your doctor approves it. Fast for at least 8 hours before the test to ensure the results are accurate. You can drink water, but have no food. Your doctor should discuss the importance of fasting before you take the test.[1]
Even if your doctor approves eating, you should not drink alcohol the night before the test.
The blood test should not be too taxing and you should be able to drive yourself home after the test. However, if you’d prefer not to drive after the test, ask someone to drop you off for the test and pick you up.

2
Discuss any medications you are taking with your doctor. Let your doctor know about any prescription or over-the-counter medication you are taking. You should also tell your doctor if you are taking any supplements or herbs.[2]
Medication like oral corticosteroids and ones made to lower your cholesterol can affect the results of the test. Iron supplements and herbal supplements can also skew the results.
Your doctor may suggest that you abstain from taking medication 1-2 days before the test to avoid skewing the results. Do not stop taking medication unless your doctor suggests that you do this.

3
Wear loose clothing to your appointment. Make it easy for you to expose your arms to your doctor or nurse by wearing a short-sleeved shirt or a long sleeved top with arms that can be rolled up.
4
Let your doctor or nurse remove a sample of blood from a vein in your arm. Your doctor or nurse will sterilize the injection area with cleaning solution on a piece of gauze. Then, they will inject you with a syringe and draw a small amount of blood into a collection tube attached to the syringe. You may feel a slight sting when the needle is inserted and soreness in the area once the needle is removed.[3]
If you are uncomfortable with needles, try distracting yourself by chatting with the doctor or nurse. You can also avoid looking at the needle directly so you are less nervous.
5
Put pressure on the injection site and let it heal. Your doctor or nurse will provide gauze you can apply on the site to stop any bleeding. Your arm may be sore for a few days but the soreness should fade.
The needle will leave a small wound at the injection site that should scab over within a few days. If the wound becomes very red, inflamed, or is not scabbing over, go see your doctor.
Part Two of Three:
Discussing the Test Results with Your Doctor
1
Meet with your doctor to find out the results within a few hours or days. The test results from your blood sample are usually processed fairly quickly. Your doctor will then contact you to inform you of your test results. They may also set up an office appointment for you to discuss your test results in detail, if necessary.[4]
2
Find out if you have any signs of acute or chronic liver damage. Your doctor will run a series of panels on your blood sample to see if you have a high amount of certain enzymes in your blood. High levels of enzymes like Alanine Transaminase (ALT), Aspartate Transaminase (AST), Alkaline Phosphatase (ALP), Alkaline Phosphatase (ALP) may be a sign that you have liver damage.[5]
They will also run a panel on your blood sample to determine if you have a low amount of protein in your blood, such as globulin and albumin. Low levels of these proteins can indicate you have liver damage or your liver is not functioning properly.
High levels of these enzymes and low protein levels may also indicate you have a liver issue like hepatitis or cirrhosis. These conditions are often caused by chronic alcohol consumption.
3
Check if your results indicate you have bile duct issue. Your doctor will also run a panel to determine how much bilirubin is in your blood, which is a yellow fluid your body produces in your liver. If you test very high for bilirubin, you may have a malfunctioning bile duct or a blockage in your liver that is causing bilirubin to leak into your blood.[6]
Bile duct issues can also cause your skin and eyes to appear yellow or jaundiced. In some cases, your urine may appear very dark.
4
Do follow up tests with your doctor. Your doctor will evaluate your blood test results as a whole. Depending on your results, they may also order follow up tests like a hepatitis virus test and ultrasound imaging of your liver and gallbladder.[7]
Your doctor may also monitor your liver function over a period of several weeks and do another blood test to confirm your diagnosis.
5
Allow your doctor to take a biopsy of your liver, if needed. In some cases, your doctor may need to take a very small sample of your liver to confirm your diagnosis. A biopsy of your liver is done while you under sedation. The doctor will insert a small biopsy needle into your abdomen or neck to extract a sample of your liver. The sample will be very small and will not affect the functioning of your liver.[8]
The biopsy is then sent to the lab for analysis. The results of the biopsy will help your doctor determine your diagnosis in more detail.
Part Three of Three:
Treating Liver Function Issues
1
Make lifestyle and diet changes to treat hepatitis or cirrhosis. Your doctor will recommend you switch to eating a nutritious, balanced diet and if you have cirrhosis, to quit drinking alcohol. They may also suggest you have vitamin and mineral supplements to help your liver recover.[9]
If you are overweight, your doctor may suggest you lose weight by doing daily exercise and maintain a healthy weight as part of your recovery plan.
People who have central obesity, meaning they mostly gain weight around their abdomen, also gain weight around their internal organs, including the liver. This can lead to “fatty liver” disease and abnormal liver blood tests. Weight loss will alleviate your symptoms.
Keep in mind cirrhosis is a progressive disease that will only get worse if you do not make lifestyle and diet changes. You will need to maintain these changes for the remainder of your life to prevent further damage to your liver.
2
Take medication to treat liver damage. If your test results show you have acute or chronic liver damage, your doctor may prescribe medication to help your liver function properly. Discuss dosage for these medications with your doctor and never take more than prescribed.[10]
The type of medication you receive will depend on whether you have acute or chronic liver disease and if you also have bile duct issues.
You will likely need to take medication along with making lifestyle and diet changes to treat your liver issue effectively.
3
Discuss a liver transplant with your doctor if your condition is severe. If your liver is damaged beyond repair, your doctor may suggest a liver transplant. During a liver transplant, your damaged liver is replaced with a functioning liver from a deceased or living donor. You may need to be put on a donor wait list or find out if any family members or friends are a good match and can donate a part of their liver for the procedure.[11]
Your doctor should outline this procedure in detail for you so you are aware of the risks and possible side effects.
You will need to take medication to help your new liver regenerate and function well. You will also need to spend 4-6 weeks recovering and check in regularly with your doctor to ensure your new liver is working properly.
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Tips
Avoiding the usage of food and alcohol can give you better results.
Liver transplants are lengthy, and could not always work. Doctors would have to get a liver donor that matches your blood type, and something that your body will accept.
Warnings
Avoid alcohol while your liver is strengthening. Alcohol can affect the functions of your new liver.
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Expert Review By:
JL
Janice Litza, M.D.
Family Medicine Physician
Co-authors: 6
Updated: January 31, 2018
Views: 7,161
Article Rating: 88% – 8 votes
Categories: Featured Articles | Liver Health
Sources and Attribution
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