Monthly Archives: March 2011

Cushing’s syndrome

Alternative Names: Itsenko-Cushing syndrome, hyperadrenocorticism or hypercorticism
Definition:
Cushing’s syndrome is a hormone disorder caused by high levels of cortisol in the blood. This can be caused by taking glucocorticoid drugs, or by tumors that produce cortisol or adrenocorticotropic hormone (ACTH) or CRH

You may click to see the pictures
Cushing’s disease refers to one specific cause of the syndrome, a tumor (adenoma) in the pituitary gland that produces large amounts of ACTH, which in turn elevates cortisol. It is the most common cause of Cushing’s syndrome, responsible for 70% of cases.

This pathology was described by Harvey Cushing in 1932.

Cushing’s syndrome is not confined to humans and is also a relatively common condition in domestic dogs and horses.

Treatments for Cushing’s syndrome can return your body’s cortisol production to normal and noticeably improve your symptoms. The earlier treatment begins, the better your chances for recovery.

Symptoms:
SymptomsMost people with Cushing syndrome will have:

•Upper body obesity (above the waist) and thin arms and legs
•Round, red, full face (moon face)
•Slow growth rate in children

Skin changes that are often seen:
•Acne or skin infections
•Purple marks (1/2 inch or more wide) called striae on the skin of the abdomen, thighs, and breasts
•Thin skin with easy bruising

Muscle and bone changes include:
•Backache, which occurs with routine activities
•Bone pain or tenderness
•Collection of fat between the shoulders (buffalo hump)
•Thinning of the bones, which leads to rib and spine fractures
•Weak muscles

Women with Cushing syndrome often have:


•Excess hair growth on the face, neck, chest, abdomen, and thighs
•Menstrual cycle becomes irregular or stops

Men may have:
•Decreased fertility
•Decreased or no desire for sex
•Impotence

Other symptoms that may occur with this disease:
*Mental changes, such as depression, anxiety and irritability or changes in behavior
*Fatigue
*Headache
*High blood pressure
*Increased thirst and urination
*Muscle weakness
*Loss of emotional control
*Cognitive difficulties
*New or worsened high blood pressure
*Glucose intolerance that may lead to diabetes
*Headache
*Bone loss, leading to fractures over time

Iatrogenic Cushing’s syndrome (caused by treatment with corticosteroids) is the most common form of Cushing’s syndrome. The incidence of pituitary tumors may be relatively high, as much as one in five people, but only a minute fraction are active and produce excessive hormones.

Adults with the disease may also have symptoms of extreme weight gain, excess hair growth in women, high blood pressure, and skin problems. In addition, they may show:

*muscle and bone weakness
*osteoporosis
*diabetes mellitus
*hypertension
*moodiness, irritability, or depression
*sleep disturbances
*menstrual disorders such as amenorrhea in women and decreased fertility in men
*baldness
*hypercholesterolemia

Cause:
There are several possible causes of Cushing’s syndrome.

Exogenous vs. endogenousHormones that come from outside the body are called exogenous; hormones that come from within the body are called endogenous.

The most common cause of Cushing’s syndrome is exogenous administration of glucocorticoids prescribed by a health care practitioner to treat other diseases (called iatrogenic Cushing’s syndrome). This can be an effect of steroid treatment of a variety of disorders such as asthma and rheumatoid arthritis, or in immunosuppression after an organ transplant. Administration of synthetic ACTH is also possible, but ACTH is less often prescribed due to cost and lesser utility. Although rare, Cushing’s syndrome can also be due to the use of medroxyprogesterone.

Endogenous Cushing’s syndrome results from some derangement of the body’s own system of secreting cortisol. Normally, ACTH is released from the pituitary gland when necessary to stimulate the release of cortisol from the adrenal glands.

*In pituitary Cushing’s, a benign pituitary adenoma secretes ACTH. This is also known as Cushing’s disease and is responsible for 70% of endogenous Cushing’s syndrome.

*In adrenal Cushing’s, excess cortisol is produced by adrenal gland tumors, hyperplastic adrenal glands, or adrenal glands with nodular adrenal hyperplasia.

*Finally, tumors outside the normal pituitary-adrenal system can produce ACTH that affects the adrenal glands. This final etiology is called ectopic or paraneoplastic Cushing’s syndrome and is seen in diseases like small cell lung cancer.

Pseudo-cushing’s syndrome:
Elevated levels of total cortisol can also be due to estrogen found in oral contraceptive pills that contain a mixture of estrogen and progesterone. Estrogen can cause an increase of cortisol-binding globulin and thereby cause the total cortisol level to be elevated. However, the total free cortisol, which is the active hormone in the body, as measured by a 24 hour urine collection for urinary free cortisol, is normal.

Pathophysiology:
The hypothalamus is in the brain and the pituitary gland sits just below it. The paraventricular nucleus (PVN) of the hypothalamus releases corticotropin-releasing hormone (CRH), which stimulates the pituitary gland to release adrenocorticotropin (ACTH). ACTH travels via the blood to the adrenal gland, where it stimulates the release of cortisol. Cortisol is secreted by the cortex of the adrenal gland from a region called the zona fasciculata in response to ACTH. Elevated levels of cortisol exert negative feedback on the pituitary, which decreases the amount of ACTH released from the pituitary gland. Strictly, Cushing’s syndrome refers to excess cortisol of any etiology. One of the causes of Cushing’s syndrome is a cortisol secreting adenoma in the cortex of the adrenal gland. The adenoma causes cortisol levels in the blood to be very high, and negative feedback on the pituitary from the high cortisol levels causes ACTH levels to be very low. Cushing’s disease refers only to hypercortisolism secondary to excess production of ACTH from a corticotrophic pituitary adenoma. This causes the blood ACTH levels to be elevated along with cortisol from the adrenal gland. The ACTH levels remain high because a tumor causes the pituitary to be unresponsive to negative feedback from high cortisol levels.

Cushing’s Syndrome was also the first autoimmune disease identified in humans.

Diagnosis:-
When Cushing’s syndrome is suspected, either a dexamethasone suppression test (administration of dexamethasone and frequent determination of cortisol and ACTH level), or a 24-hour urinary measurement for cortisol offer equal detection rates. Dexamethasone is a glucocorticoid and simulates the effects of cortisol, including negative feedback on the pituitary gland. When dexamethasone is administered and a blood sample is tested, high cortisol would be indicative of Cushing’s syndrome because there is an ectopic source of cortisol or ACTH (e.g.: adrenal adenoma) that is not inhibited by the dexamethasone. A novel approach, recently cleared by the US FDA, is sampling cortisol in saliva over 24 hours, which may be equally sensitive, as late night levels of salivary cortisol are high in Cushingoid patients. Other pituitary hormone levels may need to be ascertained. Performing a physical examination to determine any visual field defect may be necessary if a pituitary lesion is suspected, which may compress the optic chiasm causing typical bitemporal hemianopia.

When any of these tests are positive, CT scanning of the adrenal gland and MRI of the pituitary gland are performed to detect the presence of any adrenal or pituitary adenomas or incidentalomas (the incidental discovery of harmless lesions). Scintigraphy of the adrenal gland with iodocholesterol scan is occasionally necessary. Very rarely, determining the ACTH levels in various veins in the body by venous catheterization, working towards the pituitary (petrosal sinus sampling) is necessary.

Mnemonic:
C – Central obesity, Cervical fat pads, Collagen fibre weakness, Comedones (acne)
U – Urinary free cortisol and glucose increase
S – Striae, Suppressed immunity
H – Hypercortisolism, Hypertension, Hyperglycemia, Hypercholesterolemia, Hirsutism
I – Iatrogenic (Increased administration of corticosteroids)
N – Noniatrogenic (Neoplasms)
G – Glucose intolerance, Growth retardation

Treatment:-
Most Cushing’s syndrome cases are caused by steroid medications (iatrogenic). Consequently, most patients are effectively treated by carefully tapering off (and eventually stopping) the medication that causes the symptoms.

If an adrenal adenoma is identified it may be removed by surgery. An ACTH-secreting corticotrophic pituitary adenoma should be removed after diagnosis. Regardless of the adenoma’s location, most patients will require steroid replacement postoperatively at least in the interim as long-term suppression of pituitary ACTH and normal adrenal tissue does not recover immediately. Clearly, if both adrenals are removed, replacement with hydrocortisone or prednisolone is imperative.

In those patients not suitable for or unwilling to undergo surgery, several drugs have been found to inhibit cortisol synthesis (e.g. ketoconazole, metyrapone) but they are of limited efficacy.

Removal of the adrenals in the absence of a known tumor is occasionally performed to eliminate the production of excess cortisol. In some occasions, this removes negative feedback from a previously occult pituitary adenoma, which starts growing rapidly and produces extreme levels of ACTH, leading to hyperpigmentation. This clinical situation is known as Nelson’s syndrome.

Lifestyle and home remedies:-

The length of your recovery from Cushing’s syndrome will depend on the severity and cause of your condition. Remember to be patient. You didn’t develop Cushing’s syndrome overnight and your symptoms won’t disappear overnight, either. In the meantime, these tips may help you on your journey back to health.

*Increase activities slowly. You may be in such a hurry to get your old self back that you push yourself too hard too fast, but your weakened muscles need a slower approach. Work up to a reasonable level of exercise or activity that feels comfortable without overdoing it. You’ll improve little by little, and your persistence will be rewarded.

*Eat sensibly. Nutritious, wholesome foods provide a good source of fuel for your recovering body and can help you lose the extra pounds that you gained from Cushing’s syndrome. Make sure you’re getting enough calcium and vitamin D. Taken together, they help your body absorb calcium, which can help strengthen your bones, counteracting the bone density loss that often occurs with Cushing’s syndrome.

*Monitor your mental health. Depression can be a side effect of Cushing’s syndrome, but it can also persist or develop after treatment begins. Don’t ignore your depression or wait it out. Seek help promptly from your doctor or a therapist if you’re depressed, overwhelmed or having difficulty coping during your recovery.

*Gently soothe aches and pains. Hot baths, massages and low-impact exercises, such as water aerobics and tai chi, can help alleviate some of the muscle and joint pain that accompanies Cushing’s syndrome recovery.

*Exercise your brain. If you’re recovering from any cognitive difficulties as a result of Cushing’s syndrome, mental exercises, such as math problems and crossword puzzles, may improve your brain function.

Coping and support:-
Support groups can be valuable in dealing with Cushing’s syndrome and recovery. They bring you together with other people who are coping with the same kinds of challenges, along with their families and friends, and offer a setting in which youe can share common problems.

Ask your doctor about support groups in your community. Your local health department, public library and telephone book and the Internet also may be good sources to find a support group in your area.

Prognosis:
Removing the tumor may lead to full recovery, but there is a chance that the condition will return.

Survival for people with ectopic tumors depends on the tumor type. Untreated, Cushing syndrome can be life-threatening.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://en.wikipedia.org/wiki/Cushing’s_syndrome

http://www.mayoclinic.com/health/cushings-syndrome/DS00470

http://www.nlm.nih.gov/medlineplus/ency/article/000410.htm

http://www.bbc.co.uk/health/physical_health/conditions/cushing1.shtml

http://nursingcrib.com/nursing-notes-reviewer/cushings-syndrome/

http://www.potbellysyndrome.com/documents/083EFB330BDDC27C6EEC8354AFFA139607633EB6.html

http://www.wrongdiagnosis.com/c/cushings_disease/book-diseases-7a.htm

http://www.nature.com/eye/journal/v20/n6/fig_tab/6701956f4.html

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Crouzon syndrome

Alternative Name :Branchial arch syndrome.

Definition:-
Crouzon syndrome is a genetic disorder of Chromosome 10.  Specifically, this syndrome affects the first branchial (or pharyngeal) arch, which is the precursor of the maxilla and mandible. Since the branchial arches are important developmental features in a growing embryo, disturbances in their development create lasting and widespread effects.

This syndrome is named after Octave Crouzon, a French physician who first described this disorder. He noted the affected patients were a mother and her daughter, implying a genetic basis. First called “craniofacial dysostosis”, the disorder was characterized by a number of clinical features. This syndrome is caused by a mutation in the fibroblast growth factor receptor II, located on chromosome 10.

Breaking down the name, “craniofacial” refers to the skull and face, and “dysostosis” refers to malformation of bone.

Now known as Crouzon syndrome, the disease can be described by the rudimentary meanings of its former name. What occurs in the disease is that an infant’s skull and facial bones, while in development, fuse early or are unable to expand. Thus, normal bone growth cannot occur. Fusion of different sutures leads to different patterns of growth of the skull. Examples include: trigonocephaly (fusion of the metopic suture), brachycephaly (fusion of the coronal suture), dolichocephaly (fusion of the sagittal suture), plagiocephaly (unilateral premature closure of lambdoid and coronal sutures), oxycephaly (fusion of coronal and lambdoidal sutures), Kleeblattschaedel (premature closure of all sutures).

In the United States it is estimated to affect 1 per 60,000 live births.It is responsible for approximately 4.8% of all cases of craniosynostosis. Crouzon syndrome affects individuals of all ethnic backgrounds. It may be inherited or it may occur spontaneously.

Incidence of Crouzon syndrome is currently estimated to occur in 1 out of every 25,000 people out of the general population. There is a greater frequency in families with a history of the disorder, but that doesn’t mean that everyone in the family is affected (as referred to above).

Symptoms:-
Crouzon syndrome is usually diagnosed in infancy because of its particular face and skull deformities, which are:

•Early fusion of the bones of the skull (craniosynostosis), causing a misshapen head
•The skull problems may push the brain down (tonsillar herniation), and may obstruct the flow of cerebrospinal fluid (hydrocephalus)
•The nose and upper jaw appear sunken in because of poor bone growth in the face (midface hypoplasia)
•The eyes may appear to pop out (exophthalmos or proptosis) for the same reason (midface hypoplasia)


There may be other internal problems with the face and head such as narrow or absent ear canals, problems with the teeth and palate, and problems with the nose and sinuses. In some individuals with Crouzon syndrome (about 18%), two or more bones of the neck may be fused together.

Some individuals with the syndrome (about 5%) may also have a skin disorder called acanthosis nigricans, in which lesions of darkened, thickened skin are present.

Causes:
Associations with mutations in the genes of FGFR2 and FGFR3 have been identified as cause  of Crouzon syndrome. This FGFR2 gene provides instructions for making a protein called fibroblast growth factor receptor 2. Among its multiple functions, this protein signals immature cells to become bone cells during embryonic development. Mutations in the FGFR2 gene probably overstimulate signaling by the FGFR2 protein, which causes the bones of the skull to fuse prematurely.

The condition is inherited in an autosomal dominant way, so that each child of a person with Crouzon syndrome has a 50 per cent chance of inheriting the condition. However, in about half of all cases the syndrome has resulted from a new mutation (that is, neither parents were affected).

Like Apert syndrome, Crouzon syndrome may be more common among children born to older fathers.

Diagnosis:-
Diagnosis of Crouzon syndrome usually can occur at birth by assessing the signs and symptoms of the baby. Further analysis, including radiographs, magnetic resonance imaging (MRI) scans, genetic testing, X-rays and CT scans can be used to confirm the diagnosis of Crouzon syndrome.

Treatment:-
Like other genetic conditions, Crouzon’s cannot be ‘cured’. But with the right help and care, most children lead a relatively normal life.

Surgery is typically used to prevent the closure of sutures of the skull from damaging the brain’s development. Without surgery, blindness and mental retardation are typical outcomes. Craniofacial surgery is a discipline of plastic surgery. To move the orbits forward, plastic surgeons work with neurosurgeons to expose the skull and orbits and reshape the bone. To treat the midface deficiency, plastic surgeons can move the lower orbit and midface bones forward (this does not need neurosurgical assistance). For jaw surgery, either plastic surgeons have experience to perform these operations. It is rare to wear a custom-fitted helmet (or cranial band) for several months after surgery as that is only for single-suture “strip craniectomy” repair. Crouzon patients tend to have multiple sutures involved, most specifically bilateral coronal craniosynostoses, therefore an open operation is used rather than the strip craniectomy with helmeting.

Excessive fluid around the brain (hydrocephalus) may need to be drained by inserting a tube called a shunt. Other specialist help, for example, to treat dental, eye or ear, nose and throat problems, is often needed.

Long-term supportive treatments such as speech therapy, psychological and educational help, and genetic counselling for the family are also important in helping the child to reach their potential.

Once treated for the cranial vault symptoms, Crouzon patients generally go on to live a normal lifespan.

You may click to learn more  if you  have specific questions about Crouzon syndrome.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://www.bbc.co.uk/health/physical_health/conditions/crouzon2.shtml

http://en.wikipedia.org/wiki/Crouzon_syndrome

http://emedicine.medscape.com/article/942989-overview

http://rarediseases.about.com/cs/crouzonsyndrome/a/011804.htm

http://emedicine.medscape.com/article/1280034-overview

http://ufacts.blogspot.com/2007/12/real-egg-head-boy.html

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Knees Pain

We often take our knees for granted. They may be hidden under clothing and seem inconspicuous but are, in fact, most important as they balance the entire weight of the body. This makes them prone to injury and malfunction at all ages.

One of the commonest symptoms of any knee problem is pain. This may be acute following a fall. It may occur as a result of an unexpected unbalanced twisting movement in a game of basketball or football. Or the knee may be affected as a result of degenerative osteoarthritis. In autoimmune diseases such as rheumatoid arthritis, generally small joints of the hands and feet are affected. At times, one or both knees may also be swollen. Conditions like gout and pseudogout — which occur when crystals are deposited in the joint space — usually affect the big toe, but again the knee may be affected.

The bones of the knee joint are cushioned by cartilage. Bits of the latter can suddenly break away and form loose bodies inside the joint space. These can get wedged during movement of the knee. There is excruciating pain, and the joint gets “stuck”. It cannot be bent or straightened.

The cartilage may also become worn down and degenerate with constant wear and tear. This exposes the bones. They then tend to grind against each other and produce pain.

Problems in areas like the spine, hip and ankle can produce a change in gait. The person may not balance properly on both feet and may limp. This puts more pressure on one knee. This too can result in pain.

The patella is a triangular bone that sits on top of the knee. Degeneration of the patella or strain of the ligaments that attach it to the bone may cause pain. This is common in children, older people and particularly women athletes.

Bacterial infections which start in other parts of the body can spread via the bloodstream and localise in the knee. This causes an acute infection with redness, pain and fever.

Knee pain can usually be tackled at home. It often disappears with 48 hours of rest. Pain and swelling can be reduced with the application of an ice pack. The pack, however, should not be applied for more than 20 minutes. Ointments containing Capsicain are often effective. They should be applied on the affected joint, followed by an ice pack. Lidnocaine (a local anaesthetic) ointment may also provide relief. Ointments are particularly effective if combined with tablets of paracetamol, ibubrufen or nalidixic acid. Compression of the joint with an “elastocrepe” bandage or a “knee cap” prevents swelling. Elevation of the foot also helps.

Accupressure and acupuncture have been shown to be effective. The first involves application of pressure to specific points around the knee while in the second, needles are inserted into them.

A doctor needs to be consulted if the joint pain is accompanied by fever, there is obvious swelling, it is impossible to bear weight on that knee, or if it cannot be flexed or extended fully.

By examining the knee thoroughly and performing some diagnostic manoeuvres, it is usually possible for the doctor to arrive at a tentative diagnosis. Blood tests may be done to rule out gout or rheumatoid arthritis. X-rays, magnetic resonance imaging (MRI), computed tomography (CT) scans and ultrasound may be needed to clinch the diagnosis.

A combination of physical therapy and medication usually provides great relief. Injections of steroids and other chemicals into the joint space may reduce inflammation and pain. If the problem persists, surgery may be required. Arthroscopy may be done to remove loose bodies and repair tears to the ligaments inside the joint. Surgery for knee replacement — complete or partial — is now common and done in many centres. There are very few contraindications. More and more older people are opting for it and enjoying productive and pain-free lives.

Some knee problems — particularly those resulting from an injury or a systemic disease — may be inevitable and require long-term treatment. The painful arthritis of old age can, however, be prevented with a few lifestyle modifications.

Obesity increases the pressure on the knees. Many years of being overweight take their toll, resulting in degenerative changes. Try to remain as close to your ideal body weight as possible.

Physical activity maintains muscle tone and helps keep the knee joint aligned. Repetitive high impact activity can cause tears in ligaments and cause pain. Runners in particular can develop pain in the ligaments around the joint. This is particularly true if physical activity is not preceded and followed by stretching and strengthening exercises. Cross training helps balance joints and reduce strain and injury. A combination of cycling, swimming, jogging or walking, and yoga is ideal.

Source : The Telegraph ( Kolkata, India)

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Sweet Drag

T.V. Jayan on a new study that confirms that nicotine worsens diabetes-related complications

click to see
If you are diabetic and also enjoy your smoke, it’s a double whammy for you. Diabetic smokers will find it difficult to stave off complications associated with rising blood sugar levels, new research has shown.

The study — by Xian-Chuan Liu, a researcher at the California State Polytechnic University in the US — is the first to establish a strong link between smoking and diabetes-related complications. The work was presented at the 241st annual meeting of the American Chemical Society in Anaheim yesterday. “If you’re a smoker and have diabetes, you should be concerned and make every effort to quit smoking,” says Liu.

Though cigarette smoking is a major health risk factor that significantly increases your chances of heart disease, cancer, and acute and chronic respiratory tract infection, it was hardly implicated in the development of diabetes till very recently. One study in the recent past, however, showed that smokers may be nearly 50 per cent more vulnerable to developing type 2 diabetes than non-smokers. Similarly, children born to smoking mothers will have impaired production of insulin, the hormone required to regulate glucose uptake by cells, and thus may develop type 1 diabetes.

The new study has gone a step further to show that smoking worsens the complications associated with diabetes and how this really happens. Some of the complications linked to diabetes are heart attack, stroke, kidney failure and nerve damage.

According to the Brussels-based International Diabetes Federation, more than 300 million people around the world suffer from diabetes. The figure is expected to reach close to 500 million by 2030.

The study is particularly significant for India, where a large number of diabetics are also smokers. It is estimated that there are more than 50 million diabetics in the country. A study published in the New England Journal of Medicine in 2008 showed that India is home to more than 120 million smokers.

Though doctors have known for years that smoking increases the risk of developing diabetes-related complications, they haven’t been able to pinpoint the exact substance in cigarette smoke responsible for this. Liu and his colleagues suspected it may be nicotine, the chemical that makes smoking addictive.

As diabetes has no cure yet, the only way to ward off complications is to maintain the required blood sugar levels through medicine and lifestyle modification. The gold standard for monitoring long-term blood sugar levels in diabetics is a blood test called the haemoglobin A1c (HbA1c).

The premise for the HbA1c test is as follows. The haemoglobin in red blood cells reacts with glucose molecules to form what is called glycated haemoglobin. In individuals with poorly controlled diabetes, the quantities of these glycated haemoglobins are much higher than in healthy people. Hence, the number of glycated haemoglobins in one’s blood gives a fairly accurate measure of glucose levels in blood.

Used often in conjunction with regular blood sugar monitoring, the HbA1c test reveals the average amount of sugar in blood during a period of up to three months. High HbA1c test results mean that the condition is not well controlled and there is an increased risk of chronic complications.

To explore their theory that nicotine has a role, the scientists set out to check how the chemical influences HbA1c. Using human blood samples, they showed that concentrations of nicotine similar to those found in the blood of smokers did, indeed, raise levels of HbA1c.

Nicotine caused HbA1c levels to rise by as much as 34 per cent,” Liu told Knowhow. In moderate smokers, the increase was about 10 per cent.

“This looks like an important finding. We had so far thought that nicotine had no influence on diabetes-related complications,” says Balbir Singh, cardiologist at Medanta, a private hospital in Gurgaon.

High blood sugar or not, it doesn’t matter. Stub out that cigarette in any case.

Source: The Telegraph ( Kolkata, India)

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Is this Causing Your Chronic Cough?

Vitamin B-12 deficiency is a known cause of central and peripheral nervous system damage. It has been implicated in sensory neuropathy and autonomic nervous system dysfunction — which can in turn have a role in chronic, unexplained coughs.

A recent study showed that vitamin B-12 deficiency patients had a higher prevalence of laryngeal hyperresponsiveness. After being given B-12 supplements, their symptoms and laryngeal, bronchial, and cough thresholds significantly improved.

According to the study in the American Journal of Clinical Nutrition:

“This study suggests that [vitamin B-12 deficiency] may contribute to chronic cough by favoring sensory neuropathy as indicated by laryngeal hyperresponsiveness and increased NGF expression in pharyngeal biopsies of [vitamin B-12 deficiency] patients. [Vitamin B-12 deficiency] should be considered among factors that sustain chronic cough, particularly when cough triggers cannot be identified.”

Source: American Journal of Clinical Nutrition January 19, 2001; 93(3): 542-548

Posted By Dr. Mercola | March 12 2011

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Croup

Alternative Names: Viral croup; Laryngotracheobronchitis – acute; Spasmodic croup

Definition:
Croup  is a respiratory condition that is usually triggered by an acute viral infection of the upper airway. The infection leads to swelling inside the throat, which interferes with normal breathing and produces the classical symptoms of a “barking” cough, stridor, and hoarseness. It may produce mild, moderate, or severe symptoms, which often worsen at night.

..

The barking cough of croup is the result of inflammation around the vocal cords (larynx) and windpipe (trachea). When the cough reflex forces air through this narrowed passage, the vocal cords vibrate with a barking noise. Because children have small airways to begin with, those younger than age 5 are most susceptible to having more-marked symptoms with croup.

Croup typically occurs between the ages of six months and six years, but the peak age is two and it’s less common after three. Children with asthma may get repeated episodes.

Croup usually isn’t serious. Most cases of croup can be treated at home. Sometimes, your child will need prescription medication.

Once due primarily to diphtheria, this cause is now primarily of historical significance in the Western world due to the success of vaccination.

 

Croup affects about 15% of children, and usually presents between the ages of 6 months and 5–6 years. It accounts for about 5% of hospital admissions in this population. In rare cases, it may occur in children as young as 3 months and as old as 15 years. Males are affected 50% more frequently than are females, and there is an increased prevalence in autumn (fall).

History:
The word croup comes from the Early Modern English verb croup, meaning “to cry hoarsely”; the name was first applied to the disease in Scotland and popularized in the 18th century. Diphtheritic croup has been known since the time of Homer’s Ancient Greece and it was not until 1826 that viral croup was differentiated from croup due to diphtheria by Bretonneau. Viral croup was thus called “faux-croup” by the French, as “croup” then referred to a disease caused by the diphtheria bacteria. Croup due to diphtheria has become nearly unknown due to the advent of effective immunization

Symptoms:
Croup is characterized by a “barking” cough, stridor, hoarseness, and difficult breathing which usually worsens at night. The “barking” cough is often described as resembling the call of a seal or sea lion.


As the cough gets more frequent, the child may have labored breathing or stridor (a harsh, crowing noise made during inspiration).The stridor is worsened by agitation or crying, and if it can be heard at rest, it may indicate critical narrowing of the airways. As croup worsens, stridor may decrease considerably.

Other symptoms include fever, coryza (symptoms typical of the common cold), and chest wall indrawing. Drooling or a very sick appearance indicate other medical conditions

Rarely, croup can last for weeks. Croup that lasts longer than a week or recurs frequently should be discussed with your doctor to determine the cause.

Causes:
Viral croup is the most common. Other possible causes include bacteria, allergies, and inhaled irritants. Acid reflux from the stomach can trigger croup.

Croup is usually (75% of the time) caused by parainfluenza viruses, but RSV, measles, adenovirus, and influenza can all cause croup.

Before the era of immunizations and antibiotics, croup was a dreaded and deadly disease, usually caused by the diphtheria bacteria. Today, most cases of croup are mild. Nevertheless, it can still be dangerous.

Croup tends to appear in children between 3 months and 5 years old, but it can happen at any age. Some children are prone to croup and may get it several times.

In the northern hemisphere, it is most common between October and March, but can occur at any time of the year.

In severe cases of croup, there may also be a bacterial superinfection of the upper airway. This condition is called bacterial tracheitis and requires hospitalization and intravenous antibiotics. If the epiglottis becomes infected, the entire windpipe can swell shut, a potentially fatal condition called epiglottitis.

Diagnosis:
Croup is a clinical diagnosis. The first step is to exclude other obstructive conditions of the upper airway, especially epiglottitis, an airway foreign body, subglottic stenosis, angioedema, retropharyngeal abscess, and bacterial tracheitis.

A frontal X-ray of the neck is not routinely performed, but if it is done, it may show a characteristic narrowing of the trachea, called the steeple sign. The steeple sign is suggestive of the diagnosis, but is absent in half of cases.

Other investigations (such as blood tests and viral culture) are discouraged as they may cause unnecessary agitation and thus worsen the stress on the compromised airway. While viral cultures, obtained via nasopharyngeal aspiration, can be used to confirm the exact cause, these are usually restricted to research settings. Bacterial infection should be considered if a person does not improve with standard treatment, at which point further investigations may be indicated

Severity:
The most commonly used system for classifying the severity of croup is the Westley score. It is primarily used for research purposes rather than in clinical practice. It is the sum of points assigned for five factors: level of consciousness, cyanosis, stridor, air entry, and retractions.The points given for each factor is listed in the table to the right, and the final score ranges from 0 to 17.

*A total score of ? 2 indicates mild croup. The characteristic barking cough and hoarseness may be present, but there is no stridor at rest.
*A total score of 3–5 is classified as moderate croup. It presents with easily heard stridor, but with few other signs.
*A total score of 6–11 is severe croup. It also presents with obvious stridor, but also features marked chest wall indrawing.
*A total score of ? 12 indicates impending respiratory failure. The barking cough and stridor may no longer be prominent at this stage.
85% of children presenting to the emergency department have mild disease; severe croup is rare (<1%).

Treatment :-
Most cases of croup can be safely managed at home, but call your health care provider for guidance, even in the middle of the night.

Cool or moist air might bring relief. You might first try bringing the child into a steamy bathroom or outside into the cool night air. If you have a cool air vaporizer, set it up in the child’s bedroom and use it for the next few nights.

Acetaminophen can make the child more comfortable and lower a fever, lessening his or her breathing needs. Avoid cough medicines unless you discuss them with your doctor first.

You may want your child to be seen. Steroid medicines can be very effective at promptly relieving the symptoms of croup. Medicated aerosol treatments, if necessary, are also powerful.

Serious illness requires hospitalization. Increasing or persistent breathing difficulty, fatigue, bluish coloration of the skin, or dehydration indicates the need for medical attention or hospitalization.

Medications are used to help reduce upper airway swelling. This may include aerosolized racemic epinephrine, corticosteroids taken by mouth, such as dexamethasone and prednisone, and inhaled or injected forms of other corticosteroids. Oxygen and humidity may be provided in an oxygen tent placed over a crib. A bacterial infection requires antibiotic therapy.

Increasing obstruction of the airway requires intubation (placing a tube through the nose or mouth through the larynx into the main air passage to the lungs). Intravenous fluids are given for dehydration. In some cases, corticosteroids are prescribed.

Alternative Treatments :-
Since most croup cases are mild in severity, over the counter treatments are often used. These treatments include ointments such as Vick’s or other menthol creams. These often are used to open up the airways. Other over the counter treatments include humidifiers to keep the humidity up in a room and lessen the chances of the airways becoming further inflamed or irritated.

Other methods of breaking croup attacks include hot shower exposure and cold air exposure. In the hot shower method, the shower is used as a sauna, in that the shower is running but people sit outside of it, taking in the warm, humid air. This method can be very effective when used in ten minute increments. Cuddling or reading to the child can limit the stress that is on the child during such a treatment. Cold or cool air exposure is another very effective alternative treatment. This method of treatment relies on the idea that the inflamed tissues will cool and shrink when exposed to cool air. Since most croup cases occur during the fall or winter seasons, this is often achieved simply by going outside or driving with the windows rolled down.

Lifestyle and home remedies:
Croup often runs its course within three to seven days. In the meantime, keep your child comfortable with a few simple measures.

*Stay calm. Comfort or distract your child — cuddle, read a book or play a quiet game. Crying makes breathing more difficult.

*Moisten the air. Use a cool-air humidifier in your child’s bedroom or have your child breathe the warm, moist air in a steamy bathroom. Although researchers have questioned the benefits of humidity as part of emergency treatment for croup, moist air seems to help children breathe easier — especially when croup is mild.

*Get cool. Sometimes breathing fresh, cool air helps. If it’s cool outdoors, wrap your child in a blanket and walk outside for a few minutes.

*Hold your child in an upright position. Sitting upright can make breathing easier. Hold your child on your lap, or place your child in a favorite chair or infant seat.

*Offer fluids. For babies, water, breast milk or formula is fine. For older children, soup or frozen fruit pops may be soothing.

*Encourage resting. Sleep can help your child fight the infection.

*Try an over-the-counter pain reliever. If your child has a fever, acetaminophen (Tylenol, others) may help. Cough syrup, which doesn’t affect the larynx or trachea, isn’t likely to relieve your child’s cough. Over-the-counter cold preparations are not recommended for children younger than age 5.

Your child’s cough may improve during the day, but don’t be surprised if it returns at night. You may want to sleep near your child or even in the same room so that you can take quick action if your child’s symptoms become severe.

Prognosis:
Viral croup is usually a self-limited disease, but can very rarely result in death from respiratory failure and/or cardiac arrest. Symptoms usually improve within two days, but may last for up to seven days. Other uncommon complications include bacterial tracheitis, pneumonia, and pulmonary edema

Prevention:
To prevent croup, take the same steps you use to prevent colds and flu. Frequent hand washing is most important. Also keep your child away from anyone who’s sick, and encourage your child to cough or sneeze into his or her elbow.

To stave off more-serious infections, keep your child’s immunizations current. The diphtheria, Haemophilus influenzae type b (Hib) and measles vaccines offer protection from some of the rarest — but most dangerous — forms of upper airway infection.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://www.bbc.co.uk/health/physical_health/conditions/croup2.shtml

http://www.mayoclinic.com/health/croup/DS00312

http://en.wikipedia.org/wiki/Croup

http://www.nlm.nih.gov/medlineplus/ency/article/003215.htm

http://modernmedicalguide.com/croup-acute-spasmodic-laryngitis/

http://savingmommymoney.com/croup-symptoms-and-cure

http://www.methodsofhealing.com/Healing_Conditions/croup/

http://www.sciencephoto.com/images/download_lo_res.html?id=770500647

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Creutzfeldt-Jakob Disease (CJD)

Definition:
Creutzfeldt–Jakob disease or CJD  is a degenerative neurological disorder (brain disease) that is incurable and invariably fatal. The disease is at times called a human form of Mad Cow disease given the fact that Bovine spongiform encephalopathy is the cause of variant Creutzfeldt-Jakob disease in humans.

click to see the picture

It is the most common among the types of transmissible spongiform encephalopathy found in humans. This means that the brain develops holes and takes on a sponge-like texture. This is caused by a type of infectious protein called a prion, prions are misfolded proteins which replicate by converting their properly folded counterparts.t is usually transmitted by eating contaminated beef. The disease is always fatal. There is no cure, and all treatments are experimental.

Creutzfeldt-Jakob disease captured public attention in the 1990s when individuals in the United Kingdom developed a form of the disease — variant CJD (vCJD) — after eating meat from diseased cattle. However, “classic” Creutzfeldt-Jakob disease has not been linked to contaminated beef.

Although serious, CJD is rare, and vCJD is the least common form. Worldwide, there is an estimated one case of Creutzfeldt-Jakob disease diagnosed per million people each year. In the United States there are about 200 cases per year. CJD usually appears in later life and runs a rapid course.

There are three major categories of CJD:

•Sporadic CJD: In sporadic CJD, the disease appears even though the person has no known risk factors for the disease. This is by far the most common type of CJD and accounts for at least 85% of cases.

•Hereditary CJD: In hereditary CJD, the person has a family history of the disease and/or tests positive for a genetic mutation associated with CJD. About 5 to 10% of cases of CJD in the United States are hereditary.

•Acquired CJD: In acquired CJD, the disease is transmitted by exposure to brain or nervous system tissue, usually through certain medical procedures. There is no evidence that CJD is contagious through casual contact with a CJD patient. Since CJD was first described in 1920, fewer than 1% of cases have been acquired CJD.

click to see the pictures

CJD belongs to a family of human and animal diseases known as the transmissible spongiform encephalopathies (TSEs). Spongiform refers to the characteristic appearance of infected brains, which become filled with holes until they resemble sponges under a microscope. CJD is the most common of the known human TSEs. Other human TSEs include kuru, fatal familial insomnia (FFI), and Gerstmann-Straussler-Scheinker disease (GSS). Kuru was identified in people of an isolated tribe in Papua New Guinea and has now almost disappeared. Fatal familial insomnia and GSS are extremely rare hereditary diseases, found in just a few families around the world. Other TSEs are found in specific kinds of animals. These include bovine spongiform encephalopathy (BSE), which is found in cows and often referred to as “mad cow” disease, scrapie, which affects sheep and goats, mink encephalopathy, and feline encephalopathy. Similar diseases including chronic wasting disease (CWD) occur in elk, deer, and exotic zoo animals.

Symptoms:-
Early symptoms are as follows:-

*Memory loss
*Personality changes
*Loss of interest in life
*Anxiety
*Depression
*Impaired thinking
*Blurred vision
*Insomnia
*Difficulty speaking
*Difficulty swallowing
*Sudden jerky movements

As the disease progresses, mental symptoms worsen. Most people eventually lapse into a coma. Heart failure, respiratory failure, pneumonia or other infections are generally the cause of death. The disease usually runs its course in about seven months, although a few people may live up to one or two years after diagnosis

The symptoms of CJD are caused by the progressive death of the brain’s nerve cells, which is associated with the build-up of abnormal prion proteins forming amyloids. When brain tissue from a CJD patient is examined under a microscope, many tiny holes can be seen where whole areas of nerve cells have died. The word “spongiform” in “transmissible spongiform encephalopathies” refers to the sponge-like appearance of the brain tissue.

Cause:-

Transmissible spongiform encephalopathy diseases are caused by prions. The diseases are thus sometimes called prion diseases. Other prion diseases include Gerstmann–Sträussler–Scheinker syndrome (GSS), fatal familial insomnia (FFI) and kuru in humans, as well as bovine spongiform encephalopathy (BSE, commonly known as mad cow disease) in cattle, chronic wasting disease (CWD) in elk and deer, and scrapie in sheep. Alpers’ syndrome in infants is also thought to be a transmissible spongiform encephalopathy caused by a prion.

The prion that is believed to cause Creutzfeldt–Jakob exhibits at least two stable conformations. One, the native state, is water-soluble and present in healthy cells. As of 2007[update], its biological function is presumably in transmembrane transport or signaling. The other conformational state is very poorly water-soluble and readily forms protein aggregates.

People can also acquire CJD genetically through a mutation of the gene that codes for the prion protein (PRNP). This occurs in only 5–10% of all CJD cases.

The CJD prion is dangerous because it promotes refolding of native proteins into the diseased state,[citation needed]. The number of misfolded protein molecules will increase exponentially and the process leads to a large quantity of insoluble prions in affected cells. This mass of misfolded proteins disrupts cell function and causes cell death. Mutations in the gene for the prion protein can cause a misfolding of the dominantly alpha helical regions into beta pleated sheets. This change in conformation disables the ability of the protein to undergo digestion. Once the prion is transmitted, the defective proteins invade the brain and are produced in a self-sustaining feedback loop, causing exponential spread of the prion, leading to death within a few months, although a few patients have lived as long as two years.

Stanley B. Prusiner of the University of California, San Francisco (UCSF) was awarded the Nobel Prize in physiology or medicine in 1997 for his discovery of prions. For more than a decade, Yale University neuropathologist Laura Manuelidis has been challenging this explanation for the disease. In January 2007, she and her colleagues published an article in the Proceedings of the National Academy of Science and reported that they have found a virus-like particle (but without finding nucleic acids so far) in less than 10% of the cells a scrapie-infected cell line and in a mouse cell line infected by a human CJD agent.

Transmission:-
The risk of CJD is low. The disease can’t be transmitted through coughing or sneezing,  touching or sexual contact. The three ways it develops are:

*Spontaneously. Most people with classic CJD develop the disease for no apparent reason. CJD that occurs without explanation is termed spontaneous CJD or sporadic CJD and accounts for the majority of cases.

*By genetic mutation. In the United States, about 5 to 10 percent of people with CJD have a family history of the disease or test positive for a genetic mutation associated with CJD. This type is referred to as familial CJD.

*By contamination. A small number of people have developed CJD after being exposed to infected human tissue during a medical procedure, such as a cornea or skin transplant. Also, because standard sterilization methods do not destroy abnormal prions, a few people have developed CJD after undergoing brain surgery with contaminated instruments. Cases of CJD related to medical procedures are referred to as iatrogenic CJD. Variant CJD is linked primarily to eating beef infected with bovine spongiform encephalopathy (BSE), the medical term for mad cow disease.

Blood donor restrictions:
In 2004 a new report published in the Lancet medical journal showed that vCJD can be transmitted by blood transfusions. The finding alarmed healthcare officials because a large epidemic of the disease might arise in the near future. There is no test to determine if a blood donor is infected while in the latent phase of vCJD. In reaction to this report, the UK government banned anyone who had received a blood transfusion since January 1980 from donating blood. From 1999 there has been a ban in the UK for using UK blood to manufacture fractional products such as albumin.

Sperm donor restrictions:
In the U.S., the FDA has banned import of any donor sperm, motivated by a risk of Creutzfeldt–Jakob disease, inhibiting the once popular import of, for example, Scandinavian sperm. The risk, however, is not known, since artificial insemination has not been studied as a route of transmission. It is also not known whether prions cross the blood-testis barrier.

Diagnosis:-
At present  there is no single diagnostic test for CJD. When CJD is suspected, the first concern is to rule out treatable forms of dementia such as encephalitis (inflammation of the brain) or chronic meningitis. A neurological examination and spinal tap are often performed to rule out more common causes of dementia. An electroencephalogram (EEG) to record the brain’s electrical pattern can be particularly valuable because it shows a specific type of abnormality in CJD. Computerized tomography (CT) of the brain can help rule out the possibility that the symptoms result from other problems such as stroke or a brain tumor. Magnetic resonance imaging (MRI) brain scans also can reveal characteristic patterns of brain degeneration that can help diagnose CJD.

At present, the only sure way to confirm a diagnosis of CJD is by brain biopsy or autopsy. In a brain biopsy, a neurosurgeon removes a small piece of tissue from the patient’s brain so that it can be examined by a neuropathologist. This procedure may be dangerous for the patient, and the operation does not always obtain tissue from the affected part of the brain. Because a correct diagnosis of CJD does not help the patient, a brain biopsy is discouraged unless it is needed to rule out a treatable disorder. In an autopsy, the whole brain is examined after death. More tests for CJD are under development.

Risk Factors:
Most cases of Creutzfeldt-Jakob disease occur for unknown reasons, and no risk factors can be identified. However, a few factors seem to be associated with different kinds of CJD.

*Age. Sporadic CJD tends to develop later in life, usually around the age of 60. Onset of familial CJD occurs only slightly earlier. On the other hand, vCJD has affected people at a much younger age, usually in their late 20s.

*Genetics. People with familial CJD have a genetic mutation that causes the disease. The disease is inherited in an autosomal dominant fashion, which means you need to inherit only one copy of the mutated gene, from either parent, to develop the disease. If you have the mutation, the chance of passing it on to your children is 50 percent. Genetic analysis in people with iatrogenic and variant CJD suggest that inheriting identical copies of certain variants of the prion gene may predispose a person to developing CJD if exposed to contaminated tissue.

*Exposure to contaminated tissue. People who’ve received human growth hormone derived from human pituitary glands or who’ve had dura mater grafts may be at risk of iatrogenic CJD. The risk of contracting vCJD from eating contaminated beef is difficult to determine. In general, if countries are effectively implementing public health measures, the risk is very low. For example, in the United Kingdom the current estimated risk of acquiring vCJD from beef and beef products appears to be about 1 case in 10 billion servings. The risk from beef in other high-incidence countries is estimated to be very low, as well

Complications:
As with other causes of dementia, Creutzfeldt-Jakob disease profoundly affects the mind as well as the body, although CJD and its variants usually progress much more rapidly. People with CJD usually withdraw from friends and family and eventually lose the ability to recognize or relate to them in any meaningful way. They also lose the ability to care for themselves, and many eventually slip into a coma. The disease ultimately is fatal.

Physical complications, all of which may become life-threatening, include:

*Infection
*Heart failure
*Respiratory failure

Treatment:-
There is no treatment that can cure or control CJD. Researchers have tested many drugs, including amantadine, steroids, interferon, acyclovir, antiviral agents, and antibiotics. However, none of these treatments has shown any consistent benefit. Current treatment for CJD is aimed at alleviating symptoms and making the patient as comfortable as possible.

Prevention:-

There is no known way to prevent sporadic CJD from developing. If you have a family history of neurological disease, you may benefit from talking with a genetics counselor, who can help you sort through the risks associated with your particular situation.

Caregivers
If you’re caring for someone with CJD or vCJD, the National Institutes of Health recommend the following basic precautions:

*Wash your hands and exposed skin before eating, drinking or smoking.
*Protect your hands and face from exposure to the person’s blood or fluids.
*Cover cuts or wounds with waterproof bandages.

Preventing iatrogenic CJD:-
Hospitals and other medical institutions follow explicit policies to prevent iatrogenic CJD. These measures have included:

*Exclusive use of synthetic human growth hormone, rather than the kind derived from human pituitary glands
*Destruction of surgical instruments used on the brain or nervous tissue of someone with known or suspected CJD
*Single-use kits for spinal taps (lumbar punctures)

You could contract CJD from an organ transplant if the donor was in the incubation stage of the disease and not yet showing signs and symptoms. However, this scenario is very unlikely. The benefits obtained from an organ transplant are generally much greater than the risk of contracting CJD.

To help ensure the safety of the blood supply, people with a risk of exposure to CJD or vCJD aren’t eligible to donate blood. This includes people who:

*Have a biological relative who has been diagnosed with CJD
*Have received a dura mater brain graft
*Have received human growth hormone
*Spent a total of at least three months in the U.K. from 1980 to 1996
*Spent five years or more in France from 1980 to the present
*Received a blood transfusion in the U.K. between 1980 and the present
*Have injected bovine insulin at any time since 1980

Preventing vCJD :
The risk of contracting vCJD in the United States remains extremely low. So far, a total of three cases have been reported in the U.S. According to the Centers for Disease Control and Prevention, strong evidence suggests that these cases were acquired abroad — two in the United Kingdom and one in Saudi Arabia.

In the United Kingdom, where the majority of vCJD cases have occurred, fewer than 200 cases have been reported. After its first appearance in 1995, CJD incidence peaked between 1999 and 2000, and has been declining since.

Regulating potential sources of vCJD :
Most countries have taken steps to prevent BSE-infected tissue from entering the food supply, including tight restrictions on importation of cattle from countries where BSE is common; restrictions on animal feed; strict procedures for dealing with sick animals; surveillance and testing methods for tracking cattle health; and restrictions on which parts of cattle can be processed for food.

The risk of vCJD from the following sources is estimated to be extremely low:

*Vaccines. Some parts of cows, including blood, enzymes and amino acids, are used to grow the bacteria and viruses needed to make certain vaccines. Not all vaccines are grown in cattle parts, however, and the Food and Drug Administration (FDA) recommends that companies producing such vaccines use cattle parts only from low-risk countries. These recommendations apply to cosmetics as well. The FDA keeps a listing on its Web site of companies that use cattle from countries that aren’t classified as low-risk.

*Insulin. Insulin sold in the United States isn’t derived from cattle, but you’re allowed to import beef insulin from other countries if you follow specific guidelines. Because there’s no way to guarantee the safety of imported insulin, talk to your doctor about the best way to obtain insulin from sources outside the United States.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://www.bbc.co.uk/health/physical_health/conditions/cjd1.shtml

http://en.wikipedia.org/wiki/Creutzfeldt%E2%80%93Jakob_disease

http://www.medterms.com/script/main/art.asp?articlekey=2863

http://www.mayoclinic.com/health/creutzfeldt-jakob-disease/DS00531

http://health.allrefer.com/health/creutzfeldt-jacob-disease-creuztfeldt-jakob-disease.html

http://stanford.edu/~drm1987/cjdclassic.html

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Cradle Cap

Alternative Names:  Seborrheic eczema; Cradle cap,infantile or neonatal seborrhoeic dermatitis,
crusta lactea, milk crust, honeycomb disease.

Definition:
Cradle cap  is a yellowish, patchy, greasy, scaly and crusty skin rash that occurs on the scalp of recently born babies. It is usually not itchy, and does not bother the baby. Cradle cap most commonly begins sometime in the first 3 months. Similar symptoms in older children are more likely to be dandruff than cradle cap. The rash is often prominent around the ear, the eyebrows or the eyelids. It may appear in other locations as well, where it is called seborrhoeic dermatitis rather than cradle cap. Some countries use the term pityriasis capitis for cradle cap. It is extremely common, with about half of all babies affected. Most of them have a mild version of the disorder. Severe cradle cap is rare.
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It’s not due to poor hygiene and isn’t contagious or an allergy. Cradle cap tends to run in families, so there may be a genetic predisposition.

Cradle cap usually resolves on its own within a few months. Self-care measures, such as washing your baby’s scalp daily with a mild shampoo, can help loosen and remove the cradle cap scales. If cradle cap persists or seems severe, your doctor may suggest a medicated shampoo, lotion or other treatment.

Symptoms:-
Common signs of cradle cap include:
*Skin lesions
*Plaques over large area
*Greasy, oily areas of skin
*Skin scales — white and flaking, or yellowish, oily, and adherent — “dandruff”
*Itching — may become more itchy if infected
*Mild redness
*Hair loss
*Patchy scaling or thick crusts on the scalp
*Greasy skin covered with flaky white or yellow scales
*Skin flakes or dandruff
*Possibly mild redness

Similar scales may also be present on the ears, eyelids, nose and groin.

Cradle cap is most common in newborns. It isn’t contagious and probably won’t bother your baby. In most cases, the condition isn’t itchy for infants.

Causes:
Cradle cap is not caused by a bacterial infection, allergy, nor from poor hygiene. Doctors are not in agreement as to the causes, but the two most common hypotheses include fungal infection and overactive sebaceous glands.

In many cases, what is commonly called cradle cap is actually a fungal infection. This infection may be related to antibiotics given to the mother just before the infant’s birth, or the infection could be related to antibiotics routinely given to infants during the first week of life. Antibiotics kill both harmful bacteria as well as the helpful bacteria that prevent the growth of yeast, which is why people who are prone to fungal infections will often discover a fungal infection after taking a round of antibiotics. In infants, the fungus is mostly likely to appear on the scalp (cradle cap), diaper area (fungal diaper rash, jock itch), ear (fungal ear infection, or an ear infection that does not respond to antibiotics),or in the mouth (thrush).

Another common cause of cradle cap appears to be a common manifestation of biotin insufficiency. This may be due, in part, to the influence of biotin on fatty acid biosynthesis. Possibly it has to do with overactive sebaceous glands in the skin of newborn babies, due to the mother’s hormones still in the baby’s circulation. The glands release a greasy substance that makes old skin cells attach to the scalp instead of falling off as they dry. There may be a relationship with skin yeasts (Pityrosporum ovale, newly renamed Malassezia furfur). Seborrheic dermatitis is the adult version of cradle cap

SOME SIGNS OF WARNING:-
If the condition thickens, turns red and irritated, starts spreading, appears on other body parts, or if the baby develops thrush (fungal mouth infection), fungal ear infection (an ear infection that does not respond to antibiotics) or a persistent diaper rash, medical intervention is recommended.

Severe cases of cradle cap, especially with cracked or bleeding skin, can provide a place for bacteria to grow. If the cradle cap is caused by a fungal infection which has worsened significantly over days or weeks to allow bacterial growth (impetigo, most commonly), a combination treatment of antibiotics and antifungals may be necessary. Since it is difficult for a layperson to distinguish the difference between sebaceous gland cradle cap, fungal cradle cap, or either of these combined with a bacterial infection, medical advice should be sought if the condition appears to worsen.

Cradle cap is occasionally linked to immune disorders. If the baby is not thriving and has other problems (e.g. diarrhoea), a doctor should be consulted.

Possible Complications:
•Psychological distress, low self esteem, embarrassment
•Secondary bacterial or fungal infections

Treatment:
Treatment other than gentle washing is not necessary in most mild cases (flaking, with or without small patches of yellow crusting), as the problem often resolves itself whether the cause is sebaceous-gland-related or fungal, but since many patients (and/or parents) are concerned about cosmetic issues, the following options are often considered:

-For all ages: Home remedies include the application of various oils, lotions, or petroleum jelly. There is little adequate or controlled research to support or negate the usefulness of most common home remedies at any age, but there is anecdotal evidence to support either position. When cradle cap is related to fungal infection, treatment for other fungal infections can also work. Tinea capitis is one example of a fungal cause. Doctors may prescribe a seven-day daily application of clotrim (commonly prescribed for jock itch or athlete’s foot) or miconazol nitrate (commonly prescribed for vaginal yeast infections).

-For infants: in cases that are related to fungal infection, doctors may recommend once-daily application of clotrim (1%) or miconozal nitrate (2%) for seven to fourteen days.

-Application of  lavender oil may be helpful for fungal infection.

-For toddlers: doctors may recommend a treatment with a mild dandruff shampoo such as Selsun Blue or Neutrogena T-gel, even though the treatment may cause initial additional scalp irritation. A doctor may instead prescribe an antifungal soap such as ketoconazole (2%) shampoo, which can work in a single treatment and shows significantly less irritation than over-the-counter shampoos such as selenium sulfide shampoos, but no adequate and controlled study has been conducted for pediatric use as of 2010.

-For adults: Seborrheic dermatitis (the adult version of cradle cap) usually requires the use of an antifungal shampoo, possibly along with the nightly application of an antifungal cream or an anti-itch cream/gel like Scalpicin. Some doctors also recommend the supplementation of a B-vitamin complex to improve fatty acid metabolism.

..

Scalp, behind ears, eyebrows:
The common home remedy of applying oil (vegetable, particularly olive oil, or mineral oil) liberally to the scalp and letting it soak in overnight or for lesser periods of time seems to conflict with the fact that Malassezia yeasts thrive in oily environments preferring saturated fats, although anecdotal reports suggest it may be effective. This may be because olive oil is primarily unsaturated fat and does not promote fungal growth. If the cradle cap is not severe, you may try to comb it out gently after bathing. The softened scales can then be brushed away with a soft brush, comb or cloth, but if not done very gently, this can worsen the condition and bring about temporary hair loss. There has been no studies done on these recommendations. Applying petroleum jelly (e.g., Vaseline) liberally overnight is another popular treatment. The softened scales either fall off during the night, or can be brushed off in the morning. Making a paste from sodium bicarbonate (baking soda) and leaving it on the affected area for 10 minutes can also help lift the scales.

There is broad disagreement regarding the role of shampoos. Some sources warn against frequent shampooing, others recommend it. Mild baby shampoo is often recommended, while never specifying what “mild” actually means. Baby shampoos often contain detergent surfactants, perfumes, quaternium-15 and other eczemagenic irritants. Again, no studies have been performed on non-prescription shampoos.

Keratolytic (dandruff) shampoos (e.g. with sulfur, selenium, zinc pyrithione, or salicylic acid) are generally not recommended as they sting eyes and may worsen the dermatitis. In stubborn cases some doctors do recommend them while others warn against the use of medicated shampoos in newborns due to systemic absorption. Dandruff shampoos often contain sodium dodecyl sulfate, a noted skin irritant.

Steroid and tar preparations have also been used but have significant drawbacks. Immunomodulators (tacrolimus/Protopic, pimecrolimus/Elidel) have not been approved for babies under two years.

Ketoconazole shampoos and creams are taking first place in medical treatment of moderate to serious cradle cap. Research so far indicates that this anti-fungal medication is not absorbed into the bloodstream. Ketoconazole shampoo is currently made with a number of problematic irritants and allergens.

A Swedish study   found good results from massaging the scalp with small amounts of borage oil twice a day.

Other home remedies recommended in various alternative sources and parent forums are herbal washes (e.g. burdock or chamomile), aloe gel, and tea tree oil (Melaleuca oil) shampoo. Tea tree oil and aloe can be sensitizers; any worsening should be an occasion to discontinue the remedy in question. Both remedies have been tested in medical trials and found useful.

Eyelids:
Typical medical advice is to use diluted baby shampoo on a cotton swab to cleanse the eyelid. There is no agreement on the dilution, which ranges from a few drops to a half cup warm water, to a 50/50 mix. No studies have been performed on the efficacy or safety of this treatment. (Please note the problems with baby shampoo noted above.) In adults, a study comparing soap and baby shampoo to commercial eyelid scrubs found that patients strongly preferred not to put soap or shampoo on their eyelids. Baking soda has also been recommended (a teaspoonful in a cup of boiled water) and is well accepted by adults. Boiled warm water wash may help.

Prognosis:
As the baby matures this conditions will be cleared.However, studies have shown that the condition occasionally persists into the toddler years, and less commonly into later childhood. It tends to recur in adolescence and persists into adulthood. In an Australian study, about 15 percent of previously diagnosed children still had eczema 10 years later. Sometimes, cradle cap turns into atopic dermatitis. Rarely, it turns out to be misdiagnosed psoriasis.

Prevention:
Shampooing your baby’s hair every few days can help prevent cradle cap. Stick with a mild baby shampoo unless your baby’s doctor recommends something stronger.

The severity of cardle cap can be lessened by controlling the risk factors and by paying careful attention to skin care.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://www.bbc.co.uk/health/physical_health/conditions/cradlecap2.shtml

http://www.nlm.nih.gov/medlineplus/ency/article/000963.htm

http://www.mayoclinic.com/health/cradle-cap/DS01074

http://en.wikipedia.org/wiki/Cradle_cap

http://www.livestrong.com/article/294548-itchy-scalp-behind-my-ears/

http://www.dermis.net/dermisroot/en/39521/image.htm

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Costochondritis

Alternative Names:Chest wall pain,costosternal syndrome and costosternal chondrodynia.

Definition:
Costochondritis is a benign inflammation of the costal cartilage, which is a length of cartilage which connects each rib, except the eleventh and twelfth, to the sternum. It causes sharp pain in the costosternal joint — where your ribs and breastbone are joined by rubbery cartilage. Pain caused by costochondritis may mimic that of a heart attack or other heart conditions.

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This pain can be quite excruciating, especially after rigorous exercise. When the pain of costochondritis is accompanied by swelling, it’s referred to as Tietze syndrome.

 

Most cases of costochondritis have no apparent cause. In these cases, treatment focuses on easing your pain while you wait for costochondritis to improve on its own. While it can be extremely painful, it is considered to be a benign condition that generally resolves in 6–8 weeks.

Costochondritis occurs most often in women and in people older than 40. However, costochondritis can affect anyone, including infants and children.

Symptoms:
Costochondritis symptoms can be similar to the chest pain associated with a heart attack.It is the most common cause of chest pain originating in the chest wall.

Costochondritis usually develops gradually with increasing tenderness over the breastplate and pain if you put pressure on the ribs in this area. The pain is made worse by anything that moves the ribs and pulls on the cartilage connecting them to the sternum.

Symptoms include:

*Pain and tenderness in the locations where your ribs attach to your breastbone (costosternal joints)
*Often sharp pain, though also dull and gnawing pain
*Location often on left side of breastbone, but possible on either side of chest

Other costochondritis symptoms may include:
*Pain when taking deep breaths
*Pain when coughing
*Difficulty breathing

Causes:
Costochondritis often results from a physical strain or minor injury, but the true causes are not well understood. . It was at one time thought to be associated with, or caused by, a viral infection acquired during surgery, but this is now known not to be the case. Most sufferers have not had recent surgery. Only some cases of costochondritis have a clear cause. Those causes include:

*Injury.•Mechanical pressure or stress on the sternum or A blow to the chest could cause costochondritis.

*Physical strain. Heavy lifting and strenuous exercise have been linked to costochondritis.

*Upper respiratory illness. An infection that produces sneezing or a cough may produce costochondritis.

*Infection. Infection can develop in the costosternal joint, causing pain.

*Fibromyalgia. Recurring costochondritis could be a symptom of fibromyalgia. People with fibromyalgia often have several tender spots. The upper part of the breastbone is a common tender spot.

*Pain from other areas of your body. Pain signals can sometimes be misinterpreted by your brain, causing pain in places far away from where the problem occurs. Your doctor might refer to this as “referred pain.” Pain in your chest can sometimes be caused by problems with the bones in your spine compressing the nerves.

Diagnosis:
Doctor can diagnose costochondritis by pressing on the area where the ribs meet the chest bone (sternum). If this area is tender and sore, costochondritis is the most likely cause of your chest pain. He or she will ask you to describe your pain and what influences it. The pain of costochondritis can be very similar to the pain associated with heart disease, lung disease, gastrointestinal problems and osteoarthritis. Your doctor will feel along your breastbone for areas of tenderness or swelling.

Costochondritis generally can’t be seen on chest X-rays or other imaging tests used to see inside your body. Sometimes your doctor may orders these tests or others to rule out other conditions.

Treatment:
Treatment mostly consists of finding pain relief that works for you while waiting for the body to heal.

Start with simple analgesics such as paracetamol, which must be taken at regular intervals and not just when the pain is bothering you. Pain killers which also reduce inflammation such as ibuprofen (these are known as non-steroidal anti-inflammatory drugs or NSAIDs) may be particularly helpful. Local heat (such as from a warm pack) can also be soothing.

Vigorous exercise might not be a good idea. When you exercise, you need to increase your breathing depth and rate, increasing the movement of your ribs. This is more likely to aggravate any inflammation. Gentle exercise, however, is fine and some research suggests that gentle stretching of the pectoral muscles 2-3 times a day may help.

Although most people find that the pain soon settles, a significant number still have some discomfort and tenderness several months later. In persistent cases local injections of anaesthetic and steroids to the rib area may be recommended.

Prognosis :With treatment, the condition usually goes away in a few days.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://www.bbc.co.uk/health/physical_health/conditions/costochondritis.shtml

http://www.mayoclinic.com/health/costochondritis/DS00626

http://en.wikipedia.org/wiki/Costochondritis

http://www.nlm.nih.gov/medlineplus/ency/article/000164.htm

http://www.graphicshunt.com/health/images/costochondritis-1030.htm

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Lavender Oil has Potent Antifungal Effect

Lavender oil could be used to combat the increasing incidence of antifungal-resistant infections, according to a study published in the Journal of Medical Microbiology. The essential oil shows a potent antifungal effect against strains of fungi responsible for common skin and nail infections.


Scientists tested lavender oil and found it to be lethal to a range of skin-pathogenic strains known as dermatophytes, as well as various species of Candida. Dermatophytes cause infections of the skin, hair and nails, and Candida species can cause mucocutaneous candidosis, also known as thrush.

Science Daily reports:
“Currently, there are relatively few types of antifungal drugs to treat infections and those that are available often have side effects … Essential oils distilled from the Lavandula genus of lavender plants are already used widely, particularly in the food, perfume and cosmetic industries. Studies of the biological activities of these oils suggest Lavandula oils have sedative and antispasmodic properties as well being potent antimicrobials and antioxidants.”

Resources:
Science Daily February 16, 2011
Journal of Medical Microbiology February 14, 2011

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