Common Names: Figwort, Woodland figwort, and Common figwort, Knotted Figwort.
Habitat : Scrophularia nodosa is native to Europe, incl Britain, south and east from Norway to Spain and temperate Asia to the Yensei region. It grows on damp ground in woods, hedgebanks, by streams etc. An occasional garden weed.
Scrophularia nodosa is a perennial herbaceous plant. It grows upright, with thick, sharply square, succulent stems up to 150 cm tall from a horizontal rootstock. Its leaves are opposite, ovate at the base and lanceolate at the tip, all having toothed margins. It is in flower from Jun to September, and the seeds ripen from Jul to September. The flowers are in loose cymes in oblong or pyramidal panicles. The individual flowers are globular, with five green sepals encircling green or purple petals, giving way to an egg-shaped seed capsule.
Succeeds in most moist to wet soils in full sun or partial shade. Plants are hardy to at least -15°c
Seed – sow spring or autumn in a cold frame. When they are large enough to handle, prick the seedlings out into individual pots and plant them out in the summer. If you have sufficient seed then it can be sown outdoors in situ in the autumn or the spring. Division in spring. Larger divisions can be planted out direct into their permanent positions. We have found it best to pot up the smaller divisions and grow them on in a lightly shaded position in a cold frame, planting them out once they are well established in the summer.
Edible Uses: Root – cooked. It smells and tastes unpleasant, but has been used in times of famine. There must be some doubts about the edibility of this root.
Scrophularia nodosa is a plant that supports detoxification of the body and it may be used as a treatment for various kinds of skin disorders. The whole plant is alterative, anodyne, anti-inflammatory, diuretic, mildly purgative and stimulant. It is harvested as the plant comes into flower in the summer and can be dried for later use. A decoction is applied externally to sprains, swellings, burns, inflammations etc, and is said to be useful in treating chronic skin diseases, scrofulous sores and gangrene. The leaves can also be applied fresh or be made into an ointment. Internally, the plant is used in the treatment of chronic skin diseases (such as eczema, psoriasis and pruritis), mastitis, swollen lymph nodes and poor circulation. It should not be prescribed for patients with heart conditions. The root is anthelmintic
Powerful medicines whenever enlarged glands are present including nodosities in the breasts. Figwort is used to cleanse and purify the body. Figwort is used to treat skin diseases such as eczema, acne and psoriasis. It has been called the Scrofula Plant, on account of its value in all cutaneous eruptions, abscesses, wounds, etc., the name of the genus being derived from that of the disease for which it was formerly considered a specific (tuberculosis of the lymph glands in the neck). It has diuretic and anodyne properties. A decoction is made of it for external use and the fresh leaves are also made into an ointment. Of the different kinds of Figwort used, this species is most employed, principally as a fomentation for sprains, swellings, inflammations, wounds and diseased parts, especially in scrofulous sores and gangrene. The leaves simply bruised are employed as an application to burns and swellings. Figwort is used for lingering and congenital illnesses of the lymphatic system and the skin. It has a stimulating and strengthening effect on the bladder and kidneys. The glycosides it contains make it suitable for treating mild heart conditions that call for stimulating the metabolism and eliminating water retention in the body. For this purpose, use figwort as a tea or tincture.
The herb and root have been used to treat cancer of the fleshy parts. The powdered root in water has been used as a tea to treat condyloma. The juice of the root and leaf are applied externally to tumors and cancers. The ointment treats painful tumors, and the fresh poultice may be used for inflamed tumors and glandular indurations. When figwort is used externally, the tea is also given internally as further therapeutic support. In traditional Chinese medicine, Figwort (S. ningpoensis) is a standard remedy. Because of its ability to stimulate the pancreas, it is used in the treatment of diabetes Known as huyen sam or xuan shen, it is also a remedy for fever and sadness, swellings and pain of the throat, furuncles, and to aid digestion.
A decoction of the herb has been successfully used as a cure for the scab in swine. Cattle, as a rule, will refuse to eat the leaves, as they are bitter, acrid and nauseating, producing purging and vomiting if chewed.
The plant was thought, by the doctrine of signatures to be able to cure the throat disease scrofula because of the throat-like shape of its flowers.
Known Hazards: Avoid in patients with ventricular tachycardia (increased heart rate). Lack of toxicological data excludes use during pregnancy .
Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provider.
Pre-eclampsia, eclampsia or toxemia of pregnancy Definition:
Pre-eclampsia or preeclampsia (PE) is a disorder of pregnancy characterized by high blood pressure and a large amount of protein in the urine. The disorder usually occurs in the third trimester of pregnancy and gets worse over time. In severe disease there may be red blood cell breakdown, a low blood platelet count, impaired liver function, kidney dysfunction, swelling, shortness of breath due to fluid in the lungs, or visual disturbances. PE increases the risk of poor outcomes for both the mother and the baby. If left untreated, it may result in seizures at which point it is known as eclampsia.
Toxemia of pregnancy is a severe condition that sometimes occurs in the latter weeks of pregnancy. It is characterized by high blood pressure; swelling of the hands, feet, and face; and an excessive amount of protein in the urine. If the condition is allowed to worsen, the mother may experience convulsions and coma, and the baby may be stillborn.
The term toxemia is actually a misnomer from the days when it was thought that the condition was caused by toxic (poisonous) substances in the blood. The illness is more accurately called preeclampsia before the convulsive stage and eclampsia afterward.
Preeclampsia affects between 2–8% of pregnancies worldwide. Hypertensive disorders of pregnancy are one of the most common causes of death due to pregnancy. They resulted in 29,000 deaths in 2013 – down from 37,000 deaths in 1990. Preeclampsia usually occurs after 32 weeks; however, if it occurs earlier it is associated with worse outcomes. Women who have had PE are at increased risk of heart disease later in life. The word eclampsia is from the Greek term for lightning. The first known description of the condition was by Hippocrates in the 5th century BCE
Swelling (especially in the hands and face) was originally considered an important sign for a diagnosis of preeclampsia. However, because swelling is a common occurrence in pregnancy, its utility as a distinguishing factor in preeclampsia is not great. Pitting edema (unusual swelling, particularly of the hands, feet, or face, notable by leaving an indentation when pressed on) can be significant, and should be reported to a health care provider.
In general, none of the signs of preeclampsia are specific, and even convulsions in pregnancy are more likely to have causes other than eclampsia in modern practice. Further, a symptom such as epigastric pain may be misinterpreted as heartburn. Diagnosis, therefore, depends on finding a coincidence of several preeclamptic features, the final proof being their regression after delivery.
The symptoms of toxemia of pregnancy (which may lead to death if not treated) are divided into three stages, each progressively more serious:
Mild preeclampsia symptoms include edema (puffiness under the skin due to fluid accumulation in the body tissues, often noted around the ankles), mild elevation of blood pressure, and the presence of small amounts of protein in the urine.
Severe preeclampsia symptoms include extreme edema, extreme elevation of blood pressure, the presence of large amounts of protein in the urine, headache, dizziness, double vision, nausea, vomiting, and severe pain in the right upper portion of the abdomen.
Eclampsia symptoms include convulsions and coma.
It is also more frequent in a women’s first pregnancy and if she is carrying twins. The underlying mechanism involves abnormal formation of blood vessels in the placenta amongst other factors. Most cases are diagnosed before delivery. Rarely, preeclampsia may begin in the period after delivery. While historically both high blood pressure and protein in the urine were required to make the diagnosis, some definitions also include those with hypertension and any associated organ dysfunction. Blood pressure is defined as high when it is greater than 140 mmHg systolic or 90 mmHg diastolic at two separate times, more than four hours apart in a women after twenty weeks of pregnancy. PE is routinely screened for during prenatal care. Causes:
There is no definitive known cause of preeclampsia, though it is likely related to a number of factors. Some of these factors include:
*Abnormal placentation (formation and development of the placenta)
*Prior or existing maternal pathology – preeclampsia is seen more at a higher incidence in individuals with preexisting hypertension, obesity, antiphospholipid antibody syndrome, and those with history of preeclampsia
*Dietary factors, e.g. calcium supplementation in areas where dietary calcium intake is low has been shown to reduce the risk of preeclampsia.
*Environmental factors, e.g. air pollution
*Those with long term high blood pressure have a risk 7 to 8 times higher than those without.
Physiologically, research has linked preeclampsia to the following physiologic changes: alterations in the interaction between the maternal immune response and the placenta, placental injury, endothelial cell injury, altered vascular reactivity, oxidative stress, imbalance among vasoactive substances, decreased intravascular volume, and disseminated intravascular coagulation.
While the exact cause of preeclampsia remains unclear, there is strong evidence that a major cause predisposing a susceptible woman to preeclampsia is an abnormally implanted placenta. This abnormally implanted placenta is thought to result in poor uterine and placental perfusion, yielding a state of hypoxia and increased oxidative stress and the release of anti-angiogenic proteins into the maternal plasma along with inflammatory mediators. A major consequence of this sequence of events is generalized endothelial dysfunction. The abnormal implantation is thought to stem from the maternal immune system’s response to the placenta and refers to evidence suggesting a lack of established immunological tolerance in pregnancy. Endothelial dysfunction results in hypertension and many of the other symptoms and complications associated with preclampsia.
One theory proposes that certain dietary deficiencies may be the cause of some cases. Also, there is the possibility that some forms of preeclampsia and eclampsia are the result of deficiency of blood flow in the uterus.
Diagnosis: Pre-eclampsia is diagnosed when a pregnant woman develops:
*Blood pressure >_ 140 mm Hg systolic or >_90 mm Hg diastolic on two separate readings taken at least four to six hours apart after 20 weeks gestation in an individual with previously normal blood pressure.
*In a woman with essential hypertension beginning before 20 weeks gestational age, the diagnostic criteria are: an increase in systolic blood pressure (SBP) of >_ 30mmHg or an increase in diastolic blood pressure (DBP) of >_15mmHg.
*Proteinuria >_ 0.3 grams (300 mg) or more of protein in a 24-hour urine sample or a SPOT urinary protein to creatinine ratio >_ 0.3 or a urine dipstick reading of 1+ or greater (dipstick reading should only be used if other quantitative methods are not available)
Suspicion for preeclampsia should be maintained in any pregnancy complicated by elevated blood pressure, even in the absence of proteinuria. Ten percent of individuals with other signs and symptoms of preeclampsia and 20% of individuals diagnosed with eclampsia show no evidence of proteinuria. In the absence of proteinuria, the presence of new-onset hypertension (elevated blood pressure) and the new onset of one or more of the following is suggestive of the diagnosis of preeclampsia:
*Evidence of kidney dysfunction (oliguria, elevated creatinine levels)
*Impaired liver function (impaired liver function tests)
*Thrombocytopenia (platelet count <100,000/microliter)
*Ankle edema pitting type
*Cerebral or visual disturbances
*Preeclampsia is a progressive disorder and these signs of organ dysfunction are indicative of severe preeclampsia. A systolic blood pressure ?160 or diastolic blood pressure ?110 and/or proteinuria >5g in a 24-hour period is also indicative of severe preeclampsia. Clinically, individuals with severe preeclampsia may also present epigastric/right upper quadrant abdominal pain, headaches, and vomiting. Severe preeclampsia is a significant risk factor for intrauterine fetal death.
Of note, a rise in baseline blood pressure (BP) of 30 mmHg systolic or 15 mmHg diastolic, while not meeting the absolute criteria of 140/90, is still considered important to note, but is not considered diagnostic.
There have been many assessments of tests aimed at predicting preeclampsia, though no single biomarker is likely to be sufficiently predictive of the disorder. Predictive tests that have been assessed include those related to placental perfusion, vascular resistance, kidney dysfunction, endothelial dysfunction, and oxidative stress. Examples of notable tests include:
*Doppler ultrasonography of the uterine arteries to investigate for signs of inadequate placental perfusion. This test has a high negative predictive value among those individuals with a history of prior preeclampsia.
*Elevations in serum uric acid (hyperuricemia) is used by some to “define” preeclampsia, though it has been found to be a poor predictor of the disorder. Elevated levels in the blood (hyperuricemia) are likely due to reduced uric acid clearance secondary to impaired kidney function.
*Angiogenic proteins such as vascular endothelial growth factor (VEGF) and placental growth factor (PIGF) and anti-angiogenic proteins such as soluble fms-like tyrosine kinase-1 (sFlt-1) have shown promise for potential clinical use in diagnosing preeclampsia, though evidence is sufficient to recommend a clinical use for these markers.
*Recent studies have shown that looking for podocytes, specialized cells of the kidney, in the urine has the potential to aid in the prediction of preeclampsia. Studies have demonstrated that finding podocytes in the urine may serve as an early marker of and diagnostic test for preeclampsia. Research is ongoing.
Pre-eclampsia can mimic and be confused with many other diseases, including chronic hypertension, chronic renal disease, primary seizure disorders, gallbladder and pancreatic disease, immune or thrombotic thrombocytopenic purpura, antiphospholipid syndrome and hemolytic-uremic syndrome. It must be considered a possibility in any pregnant woman beyond 20 weeks of gestation. It is particularly difficult to diagnose when preexisting disease such as hypertension is present. Women with acute fatty liver of pregnancy may also present with elevated blood pressure and protein in the urine, but differs by the extent of liver damage. Other disorders that can cause high blood pressure include thyrotoxicosis, pheochromocytoma, and drug misuse Treatment:
Preeclampsia and eclampsia cannot be completely cured until the pregnancy is over. Until that time, treatment includes the control of high blood pressure and the intravenous administration of drugs to prevent convulsions. Drugs may also be given to stimulate the production of urine. In some severe cases, early delivery of the baby is needed to ensure the survival of the mother.
Recommendations for prevention include: aspirin in those at high risk, calcium supplementation in areas with low intake, and treatment of prior hypertension with medications. In those with PE delivery of the fetus and placenta is an effective treatment. When delivery becomes recommended depends on how severe the PE and how far along in pregnancy a person is. Blood pressure medication, such as labetalol and methyldopa, may be used to improve the mother’s condition before delivery. Magnesium sulfate may be used to prevent eclampsia in those with severe disease. Bedrest and salt intake have not been found to be useful for either treatment or prevention.
Protein or calorie supplementation have no effect on preeclampsia rates, and dietary protein restriction does not appear to increase preeclampsia rates. Further, there is no evidence that changing salt intake has an effect.
Supplementation with antioxidants such as vitamin C and E has no effect on preeclampsia incidence, nor does supplementation with vitamin D. Therefore, supplementation with vitamins C, E, and D is not recommended for reducing the risk of pre-eclampsia.
Calcium supplementation of at least 1 gram per day is recommended during pregnancy as it prevents preeclampsia where dietary calcium intake is low, especially for those at high risk. Low selenium status is associated with higher incidence of preeclampsia.
Taking aspirin is associated with a 1% to 5% reduction in preeclampsia and a 1% to 5% reduction in premature births in women at high risk. The WHO recommends low-dose aspirin for the prevention of preeclampsia in women at high risk and recommend it be started before 20 weeks of pregnancy. The United States Preventive Services Task Force recommends a low-dose regimen for women at high risk beginning in the 12th week.
There is insufficient evidence to recommend either exercise or strict bedrest as preventative measures of pre-eclampsia.
In low-risk pregnancies the association between cigarette smoking and a reduced risk of preeclampsia has been consistent and reproducible across epidemiologic studies. High-risk pregnancies (those with pregestational diabetes, chronic hypertension, history of preeclampsia in a previous pregnancy, or multifetal gestation) showed no significant protective effect. The reason for this discrepancy is not definitively known; research supports speculation that the underlying pathology increases the risk of preeclampsia to such a degree that any measurable reduction of risk due to smoking is masked. However, the damaging effects of smoking on overall health and pregnancy outcomes outweighs the benefits in decreasing the incidence of preeclampsia. It is recommended that smoking be stopped prior to, during and after pregnancy
Restriction of salt in the diet may help reduce swelling, it does not prevent the onset of high blood pressure or the appearance of protein in the urine. During prenatal visits, the doctor routinely checks the woman’s weight, blood pressure, and urine. If toxemia is detected early, complications may be reduced.
It is best known as the cause of infectious mononucleosis (glandular fever). It is also associated with particular forms of cancer, such as Hodgkin’s lymphoma, Burkitt’s lymphoma, nasopharyngeal carcinoma, and conditions associated with human immunodeficiency virus (HIV), such as hairy leukoplakia and central nervous system lymphomas. There is evidence that infection with the virus is associated with a higher risk of certain autoimmune diseases, especially dermatomyositis, systemic lupus erythematosus, rheumatoid arthritis, Sjögren’s syndrome, and multiple sclerosis.
Infection with EBV occurs by the oral transfer of saliva and genital secretions.
Most people become infected with EBV and gain adaptive immunity. In the United States, about half of all five-year-old children and 90 to 95 percent of adults have evidence of previous infection. Infants become susceptible to EBV as soon as maternal antibody protection disappears. Many children become infected with EBV, and these infections usually cause no symptoms or are indistinguishable from the other mild, brief illnesses of childhood. In the United States and other developed countries, many people are not infected with EBV in their childhood years. When infection with EBV occurs during adolescence, it causes infectious mononucleosis 35 to 50 percent of the time.
EBV infects B cells of the immune system and epithelial cells. Once the virus’s initial lytic infection is brought under control, EBV latently persists in the individual’s B cells for the rest of the individual’s life.
Symptoms: Epstein-Barr virus infection generally causes a minor cold-like or flu-like illness, but, in some cases, there may be no symptoms of infection.Initial symptoms of infectious mononucleosis are fever, sore throat, and swollen lymph glands. Sometimes, a swollen spleen or liver involvement may develop. Heart problems or involvement of the central nervous system occurs only rarely, and infectious mononucleosis is almost never fatal. There are no known associations between active EBV infection and problems during pregnancy, such as miscarriages or birth defects. Although the symptoms of infectious mononucleosis usually resolve in 1 or 2 months, EBV remains dormant or latent in a few cells in the throat and blood for the rest of the person’s life. Periodically, the virus can reactivate and is commonly found in the saliva of infected persons. Reactivated and post-latent virus may pass the placental barrier in (also seropositive) pregnant women via macrophages and therefore can infect the fetus. Also re-infection of prior seropositive individuals may occur. In contrast, reactivation in adults usually occurs without symptoms of illness.
EBV also establishes a lifelong dormant infection in some cells of the body’s immune system. A late event in a very few carriers of this virus is the emergence of Burkitt’s lymphoma and nasopharyngeal carcinoma, two rare cancers. EBV appears to play an important role in these malignancies, but is probably not the sole cause of disease.
Most individuals exposed to people with infectious mononucleosis have previously been infected with EBV and are not at risk for infectious mononucleosis. In addition, transmission of EBV requires intimate contact with the saliva (found in the mouth) of an infected person. Transmission of this virus through the air or blood does not normally occur. The incubation period, or the time from infection to appearance of symptoms, ranges from 4 to 6 weeks. Persons with infectious mononucleosis may be able to spread the infection to others for a period of weeks. However, no special precautions or isolation procedures are recommended, since the virus is also found frequently in the saliva of healthy people. In fact, many healthy people can carry and spread the virus intermittently for life. These people are usually the primary reservoir for person-to-person transmission. For this reason, transmission of the virus is almost impossible to prevent.
The clinical diagnosis of infectious mononucleosis is suggested on the basis of the symptoms of fever, sore throat, swollen lymph glands, and the age of the patient. Usually, laboratory tests are needed for confirmation. Serologic results for persons with infectious mononucleosis include an elevated white blood cell count, an increased percentage of certain atypical white blood cells, and a positive reaction to a “mono spot” test. Causes:
Epstein–Barr can cause infectious mononucleosis, also known as ‘glandular fever’, ‘Mono‘ and ‘Pfeiffer’s disease’. Infectious mononucleosis is caused when a person is first exposed to the virus during or after adolescence. Though once deemed “The Kissing Disease,” recent research has shown that transmission of EBV not only occurs from exchanging saliva, but also from contact with the airborne virus. It is predominantly found in the developing world, and most children in the developing world are found to have already been infected by around 18 months of age. Infection of children can occur when adults mouth feed or pre-chew food before giving it to the child. EBV antibody tests turn up almost universally positive.
There is no specific treatment for infectious mononucleosis, other than treating the symptoms. No antiviral drugs or vaccines are available. Some physicians have prescribed a 5-day course of steroids to control the swelling of the throat and tonsils. The use of steroids has also been reported to decrease the overall length and severity of illness, but these reports have not been published.
It is important to note that symptoms related to infectious mononucleosis caused by EBV infection seldom last for more than 4 months. When such an illness lasts more than 6 months, it is frequently called chronic EBV infection. However, valid laboratory evidence for continued active EBV infection is seldom found in these patients. The illness should be investigated further to determine if it meets the criteria for chronic fatigue syndrome, or CFS. This process includes ruling out other causes of chronic illness or fatigue.
There is currently no specific cure for an Epstein-Barr virus infection. Treatment includes measures to help relieve symptoms and keep the body as strong as possible until the disease runs its course. This includes rest, medications to ease body aches and fever, and drinking plenty of fluids. People who are in good health can generally recover from an Epstein-Barr virus infection at home with supportive care, such as rest, fluids and pain relievers.
Treatment of most viral diseases begins with preventing the spread of the disease with basic hygiene measures. However, controlling the spread of the Epstein-Barr virus is extremely difficult because it is so common and because it is possible to spread the Epstein-Barr virus even when a person does not appear sick. Many healthy people who have had an Epstein-Barr virus infection continue to carry the virus in their saliva, which means they can spread it to others throughout their lifetimes. However, avoiding contact with another person’s saliva by not sharing drinking glasses or toothbrushes is still a good general disease prevention measure.
Regular exercise with healthy food habits and healthy life style is the best way of prevention.
As a relatively complex virus, EBV is not yet fully understood. Laboratories around the world continue to study the virus and develop new ways to treat the diseases it causes. One popular way of studying EBV in vitro is to use bacterial artificial chromosomes. Epstein–Barr virus and its sister virus KSHV can be maintained and manipulated in the laboratory in continual latency. Although many viruses are assumed to have this property during infection of their natural host, they do not have an easily managed system for studying this part of the viral lifecycle. Genomic studies of EBV have been able to explore lytic reactivation and regulation of the latent viral episome.
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:
Alternative Names: Mikulicz disease” and “Sicca syndrome
Sjögren’s syndrome (SHOW-grins)is a systemic autoimmune disease in which immune cells attack and destroy the exocrine glands that produce tears and saliva.In some cases, other organs of the body are also affected, including the:
It is named after Swedish ophthalmologist Henrik Sjögren (1899–1986), who first described it.
Nine out of ten Sjögren’s patients are women and the average age of onset is late 40s, although Sjögren’s occurs in all age groups in both women and men. It is estimated to strike as many as 4 million people in the United States alone, making it the second most common autoimmune rheumatic disease.
Sjogren’s syndrome may be classified as primary or secondary. Primary Sjogren’s syndrome occurs alone; secondary Sjogren’s syndrome is seen alongside another disease, such as rheumatoid arthritis and systemic lupus erythematosis (SLE).
The disorder should not be confused with the Sjögren–Larsson syndrome, which was also denoted T. Sjögren syndrome in early studies.
There are many different symptoms of Sjogren’s. However, not everyone experiences the same ones or to the same degree.
The characteristic dryness of Sjogren’s means the eyes often feel very uncomfortable and may burn, itch or feel gritty. Mouth dryness makes talking, chewing and swallowing difficult.
•A sore or cracked tongue
•Dry nose and skin
•Dental problems are more likely (because of the lack of saliva)
As is often the case with any long-term condition, a person’s quality of life may be adversely affected. This may result in depression and make social life, work and relationships more difficult to maintain and enjoy.
Sjogren’s is also associated with an increased risk of miscarriage, Raynauds phenomenom and adverse reactions to medication such as antibiotics.
Sjogren’s syndrome is an autoimmune disorder. This means that your immune system mistakenly attacks your body’s own cells and tissues.
Scientists aren’t certain why some people develop Sjogren’s syndrome and others don’t. Certain genes put people at higher risk for the disorder, but it appears that a triggering mechanism — such as infection with a particular virus or strain of bacteria — is also necessary.
In Sjogren’s syndrome, your immune system first targets the moisture-secreting glands of your eyes and mouth. But it can also damage other parts of your body, such as your:
*Nerves Risk Factors:
Although anyone can develop Sjogren’s syndrome, it typically occurs in people with one or more known risk factors. These include:
*Age. Sjogren’s syndrome is usually diagnosed in people older than 40. *Sex. Women are much more likely to have Sjogren’s syndrome. *Rheumatic disease. It’s common for people who have Sjogren’s syndrome to also have a rheumatic disease — such as rheumatoid arthritis or lupus.
The most common complications of Sjogren’s syndrome involve your eyes and mouth.
*Dental cavities. Because saliva helps protect the teeth from the bacteria that cause cavities, you’re more prone to developing cavities if your mouth is dry.
*Yeast infections. People with Sjogren’s syndrome are much more likely to develop oral thrush, a yeast infection in the mouth.
*Vision problems. Dry eyes can lead to light sensitivity, blurred vision and corneal ulcers.
Less common complications may affect your:
*Lungs, kidneys or liver. Inflammation may cause pneumonia, bronchitis or other problems in your lungs; may lead to problems with kidney function; and may cause hepatitis or cirrhosis in your liver.
*Unborn baby. If you’re a woman with Sjogren’s syndrome and you plan to become pregnant, talk with your doctor about being tested for certain autoantibodies that may be present in your blood. In rare cases, these antibodies have been associated with heart problems in newborns
*Lymph nodes. A small percentage of people with Sjogren’s syndrome develop cancer of the lymph nodes (lymphoma).
*Nerves. You may develop numbness, tingling and burning in your hands and feet (peripheral neuropathy).
Diagnosing Sjögren’s syndrome is complicated by the range of symptoms a patient may manifest, and the similarity between symptoms of Sjögren’s syndrome and those of other conditions. Nevertheless, the combination of several tests can lead to a diagnosis of Sjögren’s syndrome.
Blood tests can be done to determine if a patient has high levels of antibodies that are indicative of the condition, such as anti-nuclear antibody (ANA) and rheumatoid factor (because SS frequently occurs secondary to rheumatoid arthritis), which are associated with autoimmune diseases. Typical Sjögren’s syndrome ANA patterns are SSA/Ro and SSB/La, of which SSB/La is far more specific; SSA/Ro is associated with numerous other autoimmune conditions but are often present in Sjögren’s.
Schirmer’s test measures the production of tears: a strip of filter paper is held inside the lower eyelid for five minutes, and its wetness is then measured with a ruler. Producing less than five millimeters of liquid is usually indicative of Sjögren’s syndrome. However, lacrimal function declines with age or may be impaired from other medical conditions. An alternative test is nonstimulated whole saliva flow collection, in which the patient spits into a test tube every minute for 15 minutes. A resultant collection of less than 1.5 mL is considered a positive result. It takes longer to perform than Schirmer’s test, but does not require special equipment.
A slit-lamp examination can reveal dryness on the surface of the eye. Salivary gland function can be tested by collecting saliva and determining the amount produced in a five minute period. A lip biopsy can reveal lymphocytes clustered around salivary glands, and damage to these glands due to inflammation.
Ultrasound examination of the salivary glands is the simplest confirmatory test and has the added advantage of being non-invasive with no complications. The parenchyma of the gland demonstrates multiple, small-2-6 mm hypoechoic lesions which are representations of the lymphocytic infiltrates. Often sialectasis with calculi are demonstrated if the disease is advanced. The sonographic findings have excellent symptom correlation. The other advantage of ultrasound is that complications of the disease such as extra-nodal lymphomas can often be detected as larger 1–4 cm hypoechoic intra-parenchymal masses.
There is also a radiological procedure which is a reliable and accurate test for Sjögren’s syndrome. A contrast agent is injected into the parotid duct, which opens from the cheek into the vestibule of the mouth opposite the neck of the upper second molar tooth. Widespread puddling of the injected contrast scattered throughout the gland indicates Sjögren’s syndrome.
The Revised Classification Criteria for Sjögren’s Syndrome requires the presence of signs, symptoms, and lab findings.
Patient-reported symptoms must include both ocular symptoms, such as daily, persistent, troublesome dry eyes for more than three months, and oral symptoms, such as needing to drink water to swallow food.
Objective evidence of eye involvement relies on Schirmer’s test and the Rose bengal score (or similar). Histopathology studies should show focal lymphocytic sialadenitis. Objective evidence of salivary gland involvement is tested through ultrasound examinations, the level of unstimulated whole salivary flow, a parotid sialography, or salivary scintigraphy. Autoantibodies against Ro (SSA) and/or La (SSB) antigens are also expected.
SS can be excluded from people with past head and neck radiation therapy, hepatitis C infection, Acquired immunodeficiency syndrome (AIDS), pre-existing lymphoma, sarcoidosis, graft-versus-host disease, and use of anticholinergic drugs (since a time shorter than four times the life of the drug).
It’s not possible to prevent Sjogren’s syndrome and there’s no cure, but treatments can help to relieve many of the symptoms. Treatment varies depending on which parts of the body are affected and may include:
•Artificial tears to help with dry eyes
•Saliva stimulants and mouth lubricants for dry mouth
•Anti-inflammatory medication for joint or muscle pain
•Corticosteroids or immunosuppressive drugs for lung, kidney, blood vessel or nervous system problems
Lifestyle and home remedies:
Many symptoms of Sjogren’s syndrome respond well to self-care measures.
To relieve dry eyes:
*Use artificial tears, an eye lubricant or both. Artificial tears (in eyedrop form) and eye lubricants (in eyedrop, gel or ointment form) help relieve the discomfort of dry eyes. Both types of product are available over-the-counter. You don’t have to apply eye lubricants as often as artificial tears. Because of their thicker consistency, though, eye lubricants can blur your vision and collect on your eyelashes. Your doctor may recommend artificial tears without preservatives because the preservatives can be irritating for people with dry eye syndrome.
* Increase humidity. Increasing the indoor humidity and reducing your exposure to blowing air may help keep your eyes from getting uncomfortably dry. For example, avoid sitting in front of a fan or air-conditioning vent, and wear goggles or protective eyewear when you go outdoors.
To help with dry mouth:
*Increase fluid intake. Drinking lots of fluids, particularly water, helps to reduce dry mouth.
*Stimulate saliva flow. Sugarless gum or hard candies can boost saliva flow. Because Sjogren’s syndrome increases your risk of dental cavities, limit sweets, especially between meals. Lemon juice in water can also help stimulate saliva flow.
*Try artificial saliva. Saliva replacement products often work better than plain water because they contain a lubricant that helps your mouth stay moist longer. These products may come as a spray or lozenge.
*Use nasal saline spray. A nasal saline spray can help moisturize and clear nasal passages so you can breathe freely through your nose. A dry, stuffy nose can increase mouth breathing.
Dry mouth increases your risk of dental cavities and tooth loss. The following precautions may help prevent those types of problems.
*Brush your teeth and floss after every meal.
*Schedule regular dental appointments, at least every six months.
*Use daily topical fluoride treatments and antimicrobial mouthwashes.
Other areas of dryness:
If dry skin is a problem, avoid hot water when you bathe and shower. Pat your skin — don’t rub — with a towel and apply moisturizer when your skin is still damp. Use rubber gloves when doing dishes or housecleaning. Vaginal moisturizers and lubricants help women who experience vaginal dryness.
Sjögren’s can damage vital organs of the body with symptoms that may plateau or worsen, but the disease does not go into remission as with other autoimmune diseases. Some people may experience only the mild symptoms of dry eyes and mouth, while others have symptoms of severe disease. Many patients are able to treat problems symptomatically. Others are forced to cope with blurred vision, constant eye discomfort, recurrent mouth infections, swollen parotid glands, hoarseness, and difficulty in swallowing and eating. Debilitating fatigue and joint pain can seriously impair quality of life. Some patients can develop renal involvement (autoimmune tubulointerstitial nephritis) leading to proteinuria, urinary concentrating defect and distal renal tubular acidosis.
Patients with Sjögren’s syndrome have a higher rate of non-Hodgkin lymphoma compared to both patients with other autoimmune diseases and healthy people. About 5% of patients with Sjögren’s syndrome will develop some form of lymphoid malignancy. Patients with severe cases are much more likely to develop lymphomas than patients with mild or moderate cases. The most common lymphomas are salivary extranodal marginal zone B cell lymphomas (MALT lymphomas in the salivary glands) and diffuse large B-cell lymphoma.
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.
A kidney transplant is an operation that places a healthy kidney in your body. The transplanted kidney takes over the work of the two kidneys that failed, and you no longer need dialysis.
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During a transplant, the surgeon places the new kidney in your lower abdomen and connects the artery and vein of the new kidney to your artery and vein. Often, the new kidney will start making urine as soon as your blood starts flowing through it. But sometimes it takes a few weeks to start working.
If you have advanced and permanent kidney failure, kidney transplantation may be the treatment option that allows you to live much like you lived before your kidneys failed. Since the 1950s, when the first kidney transplants were performed, much has been learned about how to prevent rejection and minimize the side effects of medicines.
But transplantation is not a cure; it’s an ongoing treatment that requires you to take medicines for the rest of your life. And the wait for a donated kidney can be years long.
Many transplanted kidneys come from donors who have died. Some come from a living family member. The wait for a new kidney can be long. People who have transplants must take drugs to keep their body from rejecting the new kidney for the rest of their lives.
A successful transplant takes a coordinated effort from your whole health care team, including your nephrologist, transplant surgeon, transplant coordinator, pharmacist, dietitian, and social worker. But the most important members of your health care team are you and your family. By learning about your treatment, you can work with your health care team to give yourself the best possible results, and you can lead a full, active life.
Around 40 per cent of patients with end-stage renal failure (ESRF) need a transplant which frees people from the need for dialysis treatments.
A successful kidney transplant has ten times the function of dialysis (for example ten times the ability to remove toxins and extra water from the blood). It means that transplant patients have a better quality of life, with more energy than they did on dialysis.
How transplants work:-
An assessment is necessary to determine whether your body will accept an available kidney. This may require several visits over four to six months, and all potential recipients must be healthy enough for surgery.
Although there is no age limit, few units will transplant patients over 70 years – unless very fit.
If a family member, partner or friend wants to donate a kidney, they will need to be evaluated for general health too.
If there is no potential living donor, you will need to register with hospital and be put on a national waiting list to receive a kidney from a deceased donor. but this varies considerably around the country. Kidneys can also be donated by strangers.
If there is a suitable living donor, the operation can be scheduled in advance, when it suits both sides. If you’re on a waiting list for a deceased donor kidney, as soon as it becomes available, you must go to the hospital quickly – where a test is carried out to check the kidney won’t be rejected. If it’s suitable, the transplant can proceed. The operation usually takes three to four hours.
A surgeon places the new kidney inside your lower abdomen and connects the artery and vein of the new kidney to your artery and vein. Your blood flows through the new kidney, which makes urine, just like your own kidneys did when they were healthy. Unless they are causing infection or high blood pressure, your own kidneys are left in place.
During the operation, the transplant kidney is inserted into the lower abdomen and connected to an artery and vein (to the leg). The blood flows through the new kidney, which makes urine, just like the old kidneys did when they were healthy. The old kidneys are usually left in place.
Often the new kidney will start making urine as soon as blood starts flowing through it, but about one third of patients will require dialysis for around a week. Most patients leave hospital two weeks after the operation.
To prevent the immune system from seeing the new kidney as foreign and rejecting it, you’ll have to take drugs that turn off (or suppress) your immune response (immunosupressants). It’s important to understand the instructions for taking these medicines before leaving hospital, as missing the tablets for just 24 hours can cause rejection and the loss of the kidney.
Recovery From Surgery:-
As after any major surgery, you’ll probably feel sore and groggy when you wake up. However, many transplant recipients report feeling much better immediately after surgery. Even if you wake up feeling great, you’ll need to stay in the hospital for about a week to recover from surgery, and longer if you have any complications.
Your body’s immune system is designed to keep you healthy by sensing “foreign invaders,” such as bacteria, and rejecting them. But your immune system will also sense that your new kidney is foreign. To keep your body from rejecting it, you’ll have to take drugs that turn off, or suppress, your immune response. You may have to take two or more of these immunosuppressant medicines, as well as medications to treat other health problems. Your health care team will help you learn what each pill is for and when to take it. Be sure that you understand the instructions for taking your medicines before you leave the hospital.
If you’ve been on hemodialysis, you’ll find that your posttransplant diet is much less restrictive. You can drink more fluids and eat many of the fruits and vegetables you were previously told to avoid. You may even need to gain a little weight, but be careful not to gain weight too quickly and avoid salty foods that can lead to high blood pressure
You can help prevent rejection by taking your medicines and following your diet, but watching for signs of rejection—like fever or soreness in the area of the new kidney or a change in the amount of urine you make—is important. Report any such changes to your health care team.
Even if you do everything you’re supposed to do, your body may still reject the new kidney and you may need to go back on dialysis. Unless your health care team determines that you’re no longer a good candidate for transplantation, you can go back on the waiting list for another kidney.
Side Effects of Immunosuppressants:
Immunosuppressants can weaken your immune system, which can lead to infections. Some drugs may also change your appearance. Your face may get fuller; you may gain weight or develop acne or facial hair. Not all patients have these problems, though, and diet and makeup can help.
Immunosuppressants work by diminishing the ability of immune cells to function. In some patients, over long periods of time, this diminished immunity can increase the risk of developing cancer. Some immunosuppressants cause cataracts, diabetes, extra stomach acid, high blood pressure, and bone disease. When used over time, these drugs may also cause liver or kidney damage in a few patients.
Hope through Research:-
The NIDDK, through its Division of Kidney, Urologic, and Hematologic Diseases, supports several programs and studies devoted to improving treatment for patients with progressive kidney disease and permanent kidney failure, including patients who receive a transplanted kidney.
•The End-Stage Renal Disease Program promotes research to reduce medical problems from bone, blood, nervous system, metabolic, gastrointestinal, cardiovascular, and endocrine abnormalities in kidney failure and to improve the effectiveness of dialysis and transplantation. The program seeks to increase kidney graft and patient survival and to maximize quality of life.
•The NIH Organ/Tissue Transplant Center, located at the NIH Clinical Center in Bethesda, MD, is a collaborative project of NIH, the Walter Reed Army Medical Center, the Naval Medical Research Center, and the Diabetes Research Institute at the University of Miami. The site includes a state-of-the-art clinical transplant ward, operating facility, and outpatient clinic designed for the study of new drugs or techniques that may improve the success of organ and tissue transplants.
•The U.S. Renal Data System (USRDS) collects, analyzes, and distributes information about the use of dialysis and transplantation to treat kidney failure in the United States. The USRDS is funded directly by NIDDK in conjunction with the Centers for Medicare & Medicaid Services. The USRDS publishes an Annual Data Report, which characterizes the total population of people being treated for kidney failure; reports on incidence, prevalence, mortality rates, and trends over time; and develops data on the effects of various treatment modalities. The report also helps identify problems and opportunities for more focused special studies of renal research issues.
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