Definition:
Infection with Group B Streptococcus (GBS), also known as ‘Streptococcus agalactiae’ and more colloquially as Strep B and group B Strep, can cause serious illness and sometimes death, especially in newborn infants, the elderly, and patients with compromised immune systems. Group B streptococci are also prominent veterinary pathogens, because they can cause bovine mastitis (inflammation of the udder) in dairy cows. The species name “agalactiae” meaning “no milk”, alludes to this.
Streptococcus is a genus of spherical, Gram-positive bacteria of the phylum Firmicutes. Streptococcus agalactiae is a gram-positive streptococcus characterized by the presence of Group B Lancefield antigen, and so takes the name Group B Streptococcus.
This type of bacteria (not to be confused with group A strep which causes “strep throat”) is commonly found in the human body, and it usually does not cause any symptoms. However, in certain cases it can be a dangerous cause of various infections that affect pregnant women & their newborns .
Group B streptococcal infections affect one in 2,000 babies born every year in the UK and Ireland. About 340 babies a year will develop group B streptococcal infection within seven days of birth (early group B streptococcus disease).
Causes:
The bacteria is found living harmlessly in the vaginal and gastrointestinal tracts of up to 50 per cent of healthy women (and in many men too). It may be passed on to a baby either while the baby is still in the womb or during delivery. Although about 50 per cent of babies born to mothers carrying group B streptococcus pick up the micro-organism, only about one to two per cent of these newborns then go on to develop severe group B streptococcal disease.
Group B streptococcal sepsis is most likely to develop when the baby is premature or if there has been prolonged rupture of the membranes, with many hours passing before the baby is born, or if the baby has no antibodies to group B streptococci.
In the last 30 years it’s been show to be a cause of serious infection in non-pregnant adults too. It’s extremely rare in healthy people and is almost always associated with underlying problems such as diabetes or cancer, or less often, problems with:
•Heart and blood vessels
•Genitourinary system
•Liver disease
•Kidney disease
About five per cent of affected adults will eventually experience a second episode of group B streptococcal disease.
How is group B strep transmitted?
In newborns, GBS infection is acquired through direct contact with the bacteria while in the uterus or during delivery; thus the infection is transmitted from the colonized mother to her newborn. However, not every baby born to a colonized mother will develop GBS infection. Statistics show that about one of every 100-200 babies born to a GBS-colonized mother will develop GBS infection.
There are maternal risk factors, however, that increase the chance of transmitting the disease to the newborn:
•labor or membrane rupture before 37 weeks
•membrane rupture more than 18 hours before delivery
•urinary tract infection with GBS during pregnancy
•previous baby with GBS infection
•fever during labor
•positive culture for GBS colonization at 35-37 weeks
.
Group B strep infection is not a sexually transmitted disease (STD).
Symptoms :
If a pregnant woman is carrying (or ‘colonised with’) group B streptococcus, there is a chance she could pass it to her unborn baby. Most babies will not be harmed and will simply carry the bacteria themselves, but it can cause:
•Early birth
•Stillbirth
•Late miscarriage and complications
Group B streptococcal disease in newborns is divided into early and late disease. Early group B streptococcal neonatal sepsis appears within 24 hours of delivery (and up to seven days afterwards) and accounts for over 80 per cent of cases. Typically it causes signs of pneumonia (breathing problems) or, less often, meningitis. Most of these babies will make a full recovery.
Late group B streptococcal neonatal sepsis appears between one week and three months after birth, and is more likely to cause meningitis. One in ten infected babies will die of blood poisoning, pneumonia or meningitis, while one in five will be affected permanently by cerebral palsy, blindness, deafness or serious learning difficulties.
Once a baby has reached three months of age, group B streptococcal infection is extremely rare.
In vulnerable adults, group B streptococcus can cause a range of different infections at different sites in the body.
Diagnosis:
In pregnant women, routine screening for colonization with GBS is recommended. This test is generally performed between 35-37 weeks of gestation. The test involves using a swab to collect a sample from both the vaginal and rectal area, and results are usually available within 24-72 hours.
In newborns, GBS infection can be diagnosed with blood tests and/or spinal-fluid analysis. Similar testing may be used to diagnose the disease in adults.
Treatment:
For women who test positive for GBS during pregnancy and for those with certain risk factors for developing or transmitting GBS infection during pregnancy, intravenous antibiotics are generally recommended at the time of labor (before delivery). The administration of antibiotics has been shown to significantly decrease GBS infection in newborns. If a pregnant carrier of GBS receives intravenous antibiotics prior to delivery, her baby has a one in 4,000 chance of developing GBS infection. Without antibiotics, her baby has a one in 200 chance of developing GBS infection.
In adults who develop GBS infection, whether they are pregnant women or individuals with chronic medical conditions, intravenous(IV) antibiotics are also recommended.
At this point in time, the best treatment for GBS infection is prevention through routine screening during pregnancy. This testing has served to decrease the overall number of GBS infections in newborns, and there is currently research underway to develop a GBS vaccine.
Should all at-risk women be treated?
Some women prefer not to receive antibiotics if their risk is only slightly increased. Experts advise that the risk of infection in the baby must be balanced against the wishes and beliefs of the woman in labour and against her risk of an adverse reaction to the antibiotics. If a group B streptococcus carrying woman had a healthy baby in a previous pregnancy, she is unlikely to be at greater risk with following pregnancies.
Scientists are trying to develop a vaccine for group B streptococcus, but technical problems mean that it’s likely to be some years before one is available.
Prevention:
Through collaborative efforts clinicians, researchers, professional organizations, parent advocacy groups, and the public health community developed recommendations for intrapartum prophylaxis to prevent perinatal GBS disease. Many organizations have developed perinatal GBS disease prevention and education programs to reduce the incidence of the disease. Information about the recommendations and the prevention programs can be found in medical journals and on the internet. Simple anti-septic wipes do not prevent mother-to-child transmission
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.
Habitat : Native to the Eastern United States.Common greenbriar grows in roadsides, landscapes, clearings and woods. When it is growing around a clearing, it often forms dense and impassable thickets . It grows throughout the Eastern United States, as far north as Illinois, south to Florida and as far west as Texas .
Description:
Common Greenbriar is a common woody vine. Common greenbriar climbs other plants using green tendrils growing out of the petioles
click to see…>…….(01)..…..(1)..…(2).…….(3).….(4)..…..(5).... Leaf: Alternate, simple, rounded to cordate, 2 to 5 inches long, parallel veined, entire margins, shiny green above, paler below.
Flower: Monoecious; small light yellow-green, borne in small round clusters in late spring.
Fruit: Dark blue to black berries, borne in clusters, often covered with a powdery, waxy bloom; maturing in late summer and persist over winter.
Twig: Stout, green, usually sharply 4-angled with many scattered, stiff prickles, climbs with tendrils; very tough and stiff but new spring sprouts are tender and edible.
Bark: Remaining green for a long period of time, turning brown on old stems.
Form: Most often a climbing vine, but may also form a small, tangled bush.
Edible Uses:
The young shoots of common greenbriar are reported to be excellent when cooked like asparagus . The young leaves and tendrils can be prepared like spinach or added directly to salads . The roots have natural gelling agent in them that can be extracted and used as a thickening agent
Medicinal Uses:
The stem prickles have been rubbed on the skin as a counter-irritant to relieve localized pains, muscle cramps and twitching. A tea made from the leaves and stems has been used in the treatment of rheumatism and stomach problems. The parched and powdered leaves have been used as a dressing on burns and scalds. The wilted leaves have been used as a poultice on boils. A tea made from the roots is used to help the expelling of afterbirth
Alternative Names :Toxic diffuse goiter, thyrotoxicosis,diffuse thyrotoxic goiter
Definition:
Graves’ disease is the most common cause of hyperthyroidism . Hyperthyroidism is an autoimmune disorder that occurs when the thyroid gland makes more thyroid hormone than the body needs.
The thyroid is a small, butterfly-shaped gland in the front of the neck below the larynx, or voice box. The thyroid gland makes two thyroid hormones, triiodothyronine (T3) and thyroxine (T4). Thyroid hormones affect metabolism, brain development, breathing, heart and nervous system functions, body temperature, muscle strength, skin dryness, menstrual cycles, weight, and cholesterol levels.
Thyroid hormone production is regulated by another hormone called thyroid-stimulating hormone (TSH), which is made by the pituitary gland located in the brain.
Graves’ disease is an autoimmune disorder, meaning the body’s immune system acts against its own healthy cells and tissues. In Graves’ disease, the immune system makes antibodies called thyroid-stimulating immunoglobulin (TSI) that attach to thyroid cells. TSI mimics the action of TSH and stimulates the thyroid to make too much thyroid hormone. Sometimes the antibodies can instead block thyroid hormone production, leading to a confusing clinical picture. The diagnosis and treatment of Graves’ disease is often performed by an endocrinologist—a doctor who specializes in the body’s hormone-secreting glands.
Graves’ disease is rarely life-threatening. Although it may develop at any age and in either men or women, Graves’ disease is more common in women and usually begins after age 20.
Recent studies in England put the incidence of Graves’ disease at 1 to 2 cases per 1,000 population per year (in England). It occurs much more frequently in women than in men. The disease frequently presents itself during early adolescence or begins gradually in adult women, often after childbirth, and is progressive until treatment. It has a powerful hereditary component.
Graves’ disease tends to be more severe in men, even though it is rarer. It appears less likely to go into permanent remission and the eye disease tends to be more severe, but men are less likely to have large goitres. In a statistical study of symptoms and signs of 184 thyrotoxic patients (52 men, 132 women), the male patients were somewhat older than the females, and there were more severe cases among men than among women. Cardiac symptoms were more common in women, even though the men were older and more often had a severe form of the disease; palpitations and dyspnea were more common and severe in women.
Cigarette smoking, which is associated with many autoimmune diseases, raises the incidence of Graves’ ophthalmopathy 7.7-fold.
There’s no way to stop your immune system from attacking your thyroid gland, but treatments for Graves’ disease can ease symptoms and decrease the production of thyroxine.
Symptoms: Graves’ disease symptoms may include:
*Anxiety
*Difficulty sleeping
*Fatigue
*A rapid or irregular heartbeat
*A fine tremor of your hands or fingers
*An increase in perspiration
*Sensitivity to heat
*Weight loss, despite normal food intake
*Brittle hair
*Enlargement of your thyroid gland (goiter)
*Change in menstrual cycles
*Frequent bowel movements
*Increased appetite
*Diarrhoea
*Tremor and shaking
*Irritability and emotional upsets
*Profuse sweating
*Dislike of hot weather
*Itching, reddening and thickening of the skin, typically over the shins
Graves’ ophthalmopathy
It’s also fairly common for your eyes to exhibit mild signs of a condition known as Graves’ ophthalmopathy. In Graves’ ophthalmopathy, your eyeballs bulge out past their protective orbit (exophthalmos). This occurs as tissues and muscles behind your eyes swell and cause your eyeballs to move forward. Because your eyes may be pushed so far forward, the front surface of your eyes can become dry. Cigarette smokers with Graves’ disease are five times more likely than nonsmokers to develop Graves’ ophthalmopathy. This is possibly because smoking inhibits the absorption of anti-thyroid medication that is used to treat Graves’ disease.
Graves’ ophthalmopathy may cause these mild signs and symptoms:
*Excess tearing and sensation of grit or sand in either or both eyes
*Reddened or inflamed eyes
*Widening of the space between your eyelids
*Swelling of the lids and tissues around the eyes
*Light sensitivity
. Less often, Graves’ ophthalmopathy can produce these serious signs and symptoms:
*Ulcers on the cornea
*Double vision
*Limited eye movements
*Blurred or reduced vision
There may also be a goitre (or swelling of the thyroid gland in the neck) and swelling of the tissues over the front of the shins.
Cause:
The trigger for autoantibody production is unknown.
Since Graves’ disease is an autoimmune disease which appears suddenly, often quite late in life, it is thought that a viral or bacterial infection may trigger antibodies which cross-react with the human TSH receptor (a phenomenon known as antigenic mimicry, also seen in some cases of type I diabetes)[citation needed]. One possible culprit is the bacterium Yersinia enterocolitica (not the same as Yersinia pestis, the agent of bubonic plague). However, although there is indirect evidence for the structural similarity between the bacterium and the human thyrotropin receptor, direct causative evidence is limited. Yersinia seems not to be a major cause of this disease, although it may contribute to the development of thyroid autoimmunity arising for other reasons in genetically susceptible individuals. It has also been suggested that Y. enterocolitica infection is not the cause of auto-immune thyroid disease, but rather is only an associated condition; with both having a shared inherited susceptibility. More recently the role for Y. enterocolitica has been disputed.
Some of the eye symptoms of hyperthyroidism are believed to result from heightened sensitivity of receptors to sympathetic nervous system activity, possibly mediated by increased alpha-adrenergic receptors in some tissues.
Like most auto-immune conditions, women seem to be far more susceptible. Graves is up to eight times more common in women than men.
Some people may have a genetic predisposition to develop TSH receptor autoantibodies. HLADR (especially DR3) appears to play a significant role.
Risk Factors:
It’s known there are links between autoimmune conditions, so Graves’ disease is linked to insulin-dependent diabetes and pernicious anaemia (which are classed as autoimmune conditions). So when a person has one of these, they or members of their family may be at increased risk of developing another.
There’s also a genetic influence contributing to Graves’ disease and it can run in families.
Diagnosis:-
The onset of Graves’ disease symptoms is often insidious: the intensity of symptoms can increase gradually for a long time before the patient is correctly diagnosed with Graves’ disease, which may take months or years. (Not only Graves’ disease, but most endocrinological diseases have an insidious, subclinical onset.) One study puts the average time for diagnosis at 2.9 years, having observed a range from 3 months to 20 years in their sample population. A 1996 study offers a partial explanation for this generally late diagnosis, suggesting that the psychiatric symptoms (due to the hyperthyroidism) appeared to result in delays in seeking treatment as well as delays in receiving appropriate diagnosis. Also, earlier symptoms of nervousness, hyperactivity, and a decline in school performance, may easily be attributed to other causes.[citation needed] Many symptoms may occasionally be noted, at times, in otherwise healthy individuals who do not have thyroid disease (e.g., everyone feels anxiety and tension to some degree), and many thyroid symptoms are similar to those of other diseases. Thus, clinical findings may be full blown and unmistakable or insidious and easily confused with other disorders. The results of overlooking the thyroid can however be very serious. Also noteworthy and problematic, is that in a 1996 survey study respondents reported a significant decline in memory, attention, planning, and overall productivity from the period 2 years prior to Graves’ symptoms onset to the period when hyperthyroid.[28] Also, hypersensitivity of the central nervous system to low-grade hyperthyroidism can result in an anxiety disorder before other Graves’ disease symptoms emerge. E.g., panic disorder has been reported to precede Graves’ hyperthyroidism by 4 to 5 years in some cases, although it is not known how frequently this occurs.
English: Photograph showing a classic finding of Graves’ Disease, proptosis and lid retraction. (Photo credit: Wikipedia)
The resulting hyperthyroidism in Graves’ disease causes a wide variety of symptoms. The two signs that are truly ‘diagnostic’ of Graves’ disease (i.e., not seen in other hyperthyroid conditions) are exophthalmos (protuberance of one or both eyes) and pretibial myxedema, a rare skin disorder with an occurrence rate of 1-4%, that causes lumpy, reddish skin on the lower legs. Graves’ disease also causes goitre (an enlargement of the thyroid gland) that is of the diffuse type (i.e., spread throughout the gland). This phenomenon also occurs with other causes of hyperthyroidism, though Graves’ disease is the most common cause of diffuse goitre. A large goitre will be visible to the naked eye, but a smaller goitre (very mild enlargement of the gland) may be detectable only by physical exam. Occasionally, goitre is not clinically detectable but may be seen only with CT or ultrasound examination of the thyroid.
A highly suggestive symptom of hyperthyroidism, is a change in reaction to external temperature. A hyperthyroid person will usually develop a preference for cold weather, a desire for less clothing and less bed covering, and a decreased ability to tolerate hot weather. When thyroid disease runs in the family, the physician should be particularly wary: studies of twins suggest that the genetic factors account for 79% of the liability to the development of Graves’ disease (whereas environmental factors account presumably for the remainder). Other nearly pathognomonic signs of hyperthyroidism are excessive sweating, high pulse during sleep, and a pattern of weight loss with increased appetite (although this may also occur in diabetes mellitus and malabsorption or intestinal parasitism).
Hyperthyroidism in Graves’ disease is confirmed, as with any other cause of hyperthyroidism, by a blood test. Elevated blood levels of the principal thyroid hormones (i.e. free T3 and T4), and a suppressed thyroid-stimulating hormone (low due to negative feedback from the elevated T3 and T4), point to hyperthyroidism
However, a 2007 study makes clear that diagnosis depends to a considerable extent on the position of the patient’s unique set point for T4 and T3 within the laboratory reference range (an important issue which is further elaborated below).
Differentiating Graves’ hyperthyroidism from the other causes of hyperthyroidism (thyroiditis, toxic multinodular goiter, toxic thyroid nodule, and excess thyroid hormone supplementation) is important to determine proper treatment. Thus, when hyperthyroidism is confirmed, or when blood results are inconclusive, thyroid antibodies should be measured. Measurement of thyroid stimulating immunoglobulin (TSI) is the most accurate measure of thyroid antibodies. They will be positive in 60 to 90% of children with Graves’ disease. If TSI is not elevated, then a radioactive iodine uptake should be performed; an elevated result with a diffuse pattern is typical of Graves’ disease. Biopsy to obtain histological testing is not normally required but may be obtained if thyroidectomy is performed.
Treatment : Treatment aims to:
•Keep thyroid hormone levels in the normal range
•Prevent eye problems (which can result from exposure of the delicate eye tissues in Graves’ opthalmopathy) – this can be very difficult and eye symptoms may persist even when treatments work well to keep thyroid hormone levels within the normal range.
. Treatment for the raised hormone levels can include:
•Drugs for immediate and then long-term control
•Surgery to remove part of the thyroid gland
•Radioactive iodine treatment (RAI)
.
In recent years, efforts have been made to find a dose of RAI that will give a good cure rate for thyrotoxicosis without leading to underactivity (known as hypothyroidism). However, this has proved difficult and hypothyroidism remains a side-effect of the treatment, affecting as many as 20 per cent of those treated within the first couple of years after treatment, and three to five per cent more each year after that.
Those affected may need lifelong supplements of thyroid hormones.
Treatment for the eye problems includes:
•Drug treatments and eye drops to reduce swelling and close lids
•Steroids, especially if the eye muscles are paralysed or the swelling is very bad
•Surgery to reduce swelling or closed lids
•Radiotherapy is sometimes used in difficult cases.
.
Neuropsychiatric symptoms:
A substantial proportion of patients have an altered mental state, even after successful treatment of hyperthyroidism. When psychiatric disorders remain after restoration of euthyroidism and after treatment with beta blockers, specific treatment for the psychiatric symptoms, especially psychotropic drugs, may be needed.[10] A literature study concluded in 2006, found that, after being diagnosed with Graves’ hyperthyroidism, approximately one-third of patients are prescribed psychotropic drugs. Sometimes these drugs are given to treat mental symptoms of hyperthyroidism, sometimes to treat mental symptoms remaining after amelioration of hyperthyroidism, and sometimes when the diagnosis of Graves’ hyperthyroidism has been missed and the patient is treated as having a primary psychiatric disorder. There are no systematic data on the general efficacy of psychotropic drugs in the treatment of mental symptoms in patients with hyperthyroidism, although many reports describe the use of individual agents. De Groot mentions that a mild sedative or tranquilizer is often helpful. German research of 2004 reported that 35 percent of treated Graves’ disease patients (with normal thyroid tests for at least six months after treatment), suffered from psychological distress, and had high levels of anxiety. Almost all these patients had clear-cut depression
General measurements:
Graves’ disease patients are nutritionally depleted in proportion to the duration and severity of their illness. Until metabolism is restored to normal, and for some time afterward, caloric and protein requirements may be well above normal. Specific deficiencies may exist, and multivitamin supplementation is indicated. The intake of calcium should be above normal. All in all, the physician should pay heed to the patient’s emotional needs, as well as to his or her requirements for rest, nutrition, and specific (anti)thyroid medication
Prognosis:
The disease typically begins gradually, and is progressive unless treated. If left untreated, more serious complications could result, including bone loss and fractures, inanition, birth defects in pregnancy, increased risk of a miscarriage. Graves disease is often accompanied by an increase in heart rate, which may lead to cardiovascular damage and further heart complications including loss of the normal heart rhythm (atrial fibrillation), which may lead to stroke. If the eyes are bulging severely enough that the lids do not close completely at night, severe dryness will occur with a very high risk of a secondary corneal infection which could lead to blindness. Pressure on the optic nerve behind the globe can lead to visual field defects and vision loss as well. In severe thyrotoxicosis, a condition frequently referred to as thyroid storm, the neurologic presentations are more fulminant, progressing if untreated through an agitated delirium to somnolence and ultimately to coma. All in all, untreated Graves’ disease can lead to significant morbidity, disability and even death. However, the long-term history also includes spontaneous remission in some cases and eventual spontaneous development of hypothyroidism if autoimmune thyroiditis coexists and destroys the thyroid gland.
When effective thyroid treatment is begun, the general response is quite favorable: physical symptoms resolve, vitality returns and the mental processes become efficient again. However, symptom relief is usually not immediate and is achieved over time as the treatments take effect and thyroid levels reach stability. In addition, not all symptoms may resolve at the same time. Prognosis also depends on the duration and severity of the disease before treatment. Swedish research of 2005 reports a lower quality of life for 14 to 21 years after treatment of Graves’ disease, with lower mood and lower vitality, regardless of the choice of treatment.
Remission and relapses:
A literature study in 2006 found that patients who have residual mental symptoms have a significantly higher chance of relapse of hyperthyroidism. Patients with recurrent Graves’ hyperthyroidism, compared with patients in remission and healthy subjects, had significantly higher scores on scales related to depression and anxiety, as well as less tolerance of stress. According to a 2010 publication, a total thyroidectomy offers the best chance of preventing recurrent hyperthyroidism.
Mental impairment:
A literature review in 2006, whilst noting methodology issues in the consistency of Graves’ disease diagnostic criteria, found many reports about residual complaints in patients who were euthyroid after treatment with a high prevalence of anxiety disorders and bipolar disorder, as well as elevated scores on scales of anxiety, depression and psychological distress. Bunevicius et al. point out that this “substantial mental disability” is more severe in patients with residual hyperthyroidism but is present even in euthyroid patients. Delay in therapy markedly worsens the prognosis for recovery, but complications can be prevented by early treatment. In rare cases, patients will experience psychosis-like symptoms only after they have been treated for hypo- or hyperthyroidism, due to a rapid normalisation of thyroid hormone levels in a patient who has partly adapted to abnormal values.
Thyroid replacement treatment after thyroidectomy or radioiodine:
Several studies find a high frequency of TSH level abnormalities in patients who take thyroid hormone supplemenation for long periods of time, and stress the importance of periodic assessment of serum TSH.
Possible Complications:-
*Complications from surgery, including:
*Hoarseness from damage to the nerve leading to the voice box
*Low calcium levels from damage to the parathyroid glands (located near the thyroid gland)
*Scarring of the neck
*Eye problems (called Graves ophthalmopathy or exophthalmos)
•Heart-related complications, including:
*Rapid heart rate
*Congestive heart failure (especially in the elderly)
*Atrial fibrillation
*Thyroid crisis (thyrotoxic storm), a severe worsening of overactive thyroid gland symptoms
*Increased risk for osteoporosis, if hyperthyroidism is present for a long time
•Complications related to thyroid hormone replacement
*If too little hormone is given, fatigue, weight gain, high cholesterol, depression, physical sluggishness, and other symptoms of hypothyroidism can occur
*If too much hormone is given, symptoms of hyperthyroidism will return
Lifestyle and Home Remedies:
For Graves’ ophthalmopathy
These steps may make your eyes feel better if you have Graves’ ophthalmopathy:
*Apply cool compresses to your eyes. The added moisture may soothe your eyes.
*Wear sunglasses. When your eyes protrude, they’re more vulnerable to ultraviolet rays and more sensitive to bright light. Wearing sunglasses that wrap around the sides of your head will lessen the irritation of your eyes from the wind.
*Use lubricating eyedrops. Eyedrops may relieve the dry, scratchy sensation on the surface of your eyes. At night, a paraffin-based gel such as Lacri-Lube can be applied.
*Elevate the head of your bed. Keeping your head higher than the rest of your body lessens fluid accumulation in the head and may relieve the pressure on your eyes.
For Graves’ dermopathy
If the disease affects your skin (Graves’ dermopathy), use over-the-counter creams or ointments containing hydrocortisone to relieve swelling and reddening. In addition, using compression wraps on your legs may help.
Coping and support:
If you have Graves’ disease, make your mental and physical well-being a priority. Eating well and exercising can enhance the improvement in some symptoms while being treated and help you feel better in general. For example, because your thyroid controls your metabolism, you may have a tendency to gain weight when the hyperthyroidism corrects. Brittle bones can also occur with Graves’ disease and weight-bearing exercises can help maintain bone density.
Try to ease stress as much as you can, as stress possibly contributes to the development of Graves’ disease. Listening to music, taking a warm bath or walking can help relax you and put you in a better frame of mind. Partner with your doctor to construct a plan that incorporates good nutrition, exercise and relaxation into your daily routine.
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.
Botanical Name :Platycodon grandiflorum Family: Campanulaceae Genus: Platycodon Species: P. grandiflorus Kingdom: Plantae Order: Asterales
Synonyms:Platycodon chinensis Lindl, P. autumnalis Decne., P. sinensis Lem., P. stellatum, Campanula grandiflora Jacq., Campanula glauca Thunb., Campanula gentianoides Lam.
Common Names : platycodon, Chinese bellflower. Depending upon the region, it is also referred to as the Japanese bellflower, common balloon flower, or balloon flower.
Parts Used : dried root
Local names
Balloon-flower, chieh keng, Chinese bell flower, gil gyeong, Japanese bellflower, jiegeng, jieseng, kikiyou, kikyo, kikyokon, kikyou, platycodon radix
Habitat : It is native to East Asia (such as China, Korea, Japan, and East Siberia) and bears big blue flowers, although varieties with white and pink flowers are in cultivation. In Korea, white flowers are more common.
Description:
Balloon Flower is a Perennial herb wholly glabrous, slightly glaucescent; root white, fleshy, radishshaped, finger-thick, with abundant milky juice; stems ascending from base or straight, simple, 40–50 cm, herbaceous, glabrous or smooth, longitudinally striate in lower part; radical leaves alternate or sometimes nearly opposite, arranged along the lower half of stem or even higher, ovate-lanceolate, sessile, tapering at base, 2.5–3.4 cm long, 2–3 cm wide, rather large-toothed, pale beneath, glaucescent, upper leaves reduced. Flowers usually 1, sometimes 2, large, lengthily pedunculate, broadly campanulate or deeply saucer-shaped; calyx in 5 segments; corolla 5-lobed, violet-blue, 4 cm long; stamens 5; ovary many-celled. Fruit an ovoid capsule dehiscent at the top; seeds ovoid, compressed, obtuse, first violet then brown; albumen fleshy
Chemical assays:
Triterpene saponins, not less than 2%. Saponin content of the root can be evaluated by thin-layer chromatography–densitometry
Major chemical constituents: The major chemical constituents of Radix Platycodi root are triterpene saponins based on the sapogenins platycodigenin and polygalacic acid; examples are platycodins A–I and polygalacins D and D2
Medicinal Uses:
The root of this species (radix platycodi) is used extensively as an anti-inflammatory in the treatment of coughs and colds; in Korea the plant is known as doraji and its root, either dried or fresh, is a popular ingredient in salads and traditional cuisine. However, doraji (Chinese bellflower) should not be confused with Korean bellflower. Chinese bellflower is used in traditional Chinese medicine.
It loosens phlegm, stops cough in both hot and cold conditions, aids the elimination of pus in the upper parts of the body, is effective for sore throat, lung abscess, and loss of voice. It has an ascending energy and is sometimes added in small amounts to formulas to direct the therapeutic action of other herbs to the upper parts of the body.
Other Uses:
The plant is also a popular garden ornamental. It is hardy to USDA plant hardiness zone 3 and requires little care.
Popular culture:-
In Taiwan
In the Taiwanese drama Autumn’s Concerto, “Hua Tuo Ye” refers to the woman of his affection, “Liang Mu Cheng” as a Chinese Bellflower.
In Japan
Rumiko Takahashi named her character Kikyo (??, Kikyou) from her manga Inuyasha after the flower. The Cloud Real Six Funeral Wreath leader, Kikyo, from Katekyo Hitman Reborn! is also named after this flower, following the “one thousand flowers” naming of the Millefiore family. Kikyou (aka Reverse Sia) from the Shuffle! series is named after this flower, but her name is written in katakana rather than the actual kanji. Mahoro from Mahoromatic leaves theres flowers at the Grave of Commander Morisato every year and was known to Shugura as the “Bell Flower” person until late in the anime.
In Japan, the pentagram is sometimes called the “Bellflower seal”, and the flower was the symbol of the Onmyoryo (Bureau of Taoist Geomancy), because of its associations with Abe no Seimei and the Five Chinese Elements.
In the manga and anime series Bleach, the insignia for the Fourth Division is the Bellflower; the meaning behind it is Those who grieve are loved.
In Korea
Main article: Doraji (folk song)
In Korea, the white Chinese bellflower is called Doraji and is sung in the traditional folk song, Doraji.
Disclaimer:
The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.
Alternative Names:Nevoid basal cell carcinoma syndrome (NBCCS),basal cell nevus syndrome, multiple basal cell carcinoma syndrome and Gorlin–Goltz syndrome
Definition:–
Gorlin syndrome is an inherited medical condition involving defects within multiple body systems such as the skin, nervous system, eyes, endocrine system, and bones. People with this syndrome are particularly prone to developing a common and usually non-life-threatening form of non-melanoma skin cancers.
People with the syndrome have a predisposition to multiple basal cell carcinomas (a form of skin cancer), jaw cysts and other generally harmless abnormalities in the bone. The severity of the disease can be wide-ranging.
About 10% of people with the condition do not develop basal cell carcinomas (BCCs). the name Gorlin syndrome refers to researcher Robert J. Gorlin (1923–2006).
First described in 1960, NBCCS is an autosomal dominant condition that can cause unusual facial appearances and a predisposition for basal cell carcinoma, a malignant type of skin cancer. The prevalence is reported to be 1 case per 56,000-164,000 population. Recent work in molecular genetics has shown NBCCS to be caused by mutations in the PTCH (Patched) gene found on chromosome arm 9q. If a child inherits the defective gene from either parent, he or she will have the disorder
Incidence:–
About 750,000 new cases of sporadic basal cell carcinomas (BCCs) occur each year in the United States. Ultraviolet (UV) radiation from the sun is the main trigger of these cancers, and people with fair skin are especially at risk. Most sporadic BCCs arise in small numbers on sun-exposed skin of people over age 50, although younger people may also be affected. By comparison, NBCCS has an incidence of 1 in 50,000 to 150,000 with higher incidence in Australia. One aspect of NBCCS is that basal cell carcinomas will occur on areas of the body which are not generally exposed to sunlight, such as the palms and soles of the feet and lesions may develop at the base of palmer and plantar pits. One of the prime features of NBCCS is development of multiple BCCs at an early age, often in the teen years. Each person who has this syndrome is affected to a different degree, some having many more characteristics of the condition than others.
Components:- Some or all of the following may be seen in someone with Gorlin Syndrome:
1.Multiple basal cell carcinomas of the skin
2.Odontogenic keratocyst: Seen in 75% of patients and is the most common finding. There are usually multiple lesions found in the mandible. They occur at a young age (19 yrs average).
3.Rib and vertebrae anomalies
4.Intracranial calcification
5.Skeletal abnormalities: bifid ribs, kyphoscoliosis, early calcification of falx cerebri (diagnosed with AP radiograph)
6.Distinct faces: frontal and temporopariental bossing, hypertelorism, and mandibular prognathism
What genes are related to Gorlin syndrome?
Mutations in the PTCH1 gene cause Gorlin syndrome. This gene provides instructions for making a protein called Patched-1, which functions as a receptor. Receptor proteins have specific sites into which certain other proteins, called ligands, fit like keys into locks. Together, ligands and their receptors trigger signals that affect cell development and function. A protein called Sonic Hedgehog is the ligand for the Patched-1 receptor. Patched-1 prevents cell growth and division (proliferation) until Sonic Hedgehog is attached.
The PTCH1 gene is a tumor suppressor gene, which means it keeps cells from proliferating too rapidly or in an uncontrolled way. Mutations in this gene prevent the production of Patched-1 or lead to the production of an abnormal version of the receptor. An altered or missing Patched-1 receptor cannot effectively suppress cell growth and division. As a result, cells proliferate uncontrollably to form the tumors that are characteristic of Gorlin syndrome.
How do people inherit Gorlin syndrome?
Gorlin syndrome is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the features that are present from birth, such as large head size and skeletal abnormalities. An affected person often inherits a PTCH1 mutation from one affected parent. Other cases may result from new mutations in the gene. These cases occur in people with no history of the disorder in their family. For tumors to develop, a mutation in the other copy of the PTCH1 gene must occur in certain cells during the person’s lifetime. Most people who are born with one PTCH1 mutation eventually acquire a second mutation in certain cells and develop basal cell carcinomas and other tumors.
Causes:-
Gorlin syndrome is an autosomal dominant condition. The abnormal gene is found on chromosome 9. New mutations (where neither parent carries the gene) are common.
Diagnosis:–
Diagnosis of NBCCS is made by having 2 major criteria or 1 major and 2 minor criteria.
The major criteria consist of the following:
1.more than 2 BCCs or 1 BCC in a person younger than 20 years;
2.odontogenic keratocysts of the jaw
3.3 or more palmar or plantar pits
4.ectopic calcification or early (<20 years) calcification of the falx cerebri
5.bifid, fused, or splayed ribs
6.first-degree relative with NBCCS.
. The minor criteria include the following:
1.macrocephaly.
2.congenital malformations, such as cleft lip or palate, frontal bossing, eye anomaly (cataract, colobma, microphtalmia, nystagmus).
3.other skeletal abnormalities, such as Sprengel deformity, pectus deformity, polydactyly, syndactyly or hypertelorism.
4.radiologic abnormalities, such as bridging of the sella turcica, vertebral anomalies, modeling defects or flame-shaped lucencies of hands and feet.
5.ovarian and cardio fibroma or medulloblastoma (the latter is generally found in children below the age of two).
People with NBCCS need education about the syndrome, and may need counseling and support, as coping with the multiple BCCs and multiple surgeries is often difficult. They should reduce UV light exposure, to minimize the risk of BCCs. They should also be advised that receiving Radiation therapy for their skin cancers may be contraindicated. They should look for symptoms referable to other potentially involved systems: the CNS, the genitourinary system, the cardiovascular system, and dentition.
Genetic counseling is advised for prospective parents, since one parent with NBCCS causes a 50% chance that their child will also be affected.
Treatment:–
Although there’s no cure, the carcinomas can be treated by surgery, lasers or photodynamic therapy, which reduces scarring.
If there’s a family history of the syndrome, it’s possible for family members to be tested to see if they carry the faulty gene.
Those with Gorlin syndrome are now advised to avoid – or to take advice before undergoing – any radiation treatment, as it’s thought it may exacerbate the condition.
Treatment is usually supportive treatment, that is, treatment to reduce any symptoms rather than to cure the condition.
*Enucleation of the odontogenic cysts can help but new lesions, infections and jaw deformity are usually a result.
*The severity of the basal cell carcinoma determines the prognosis for most patients. BCCs rarely cause gross disfigurement, disability or death .
*Genetic counseling
Advice and support:-
•Gorlin Syndrome Group
•Tel: 01772 496849
•Email: info@gorlingroup.org
•Website: www.gorlingroup.org
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.
