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Herbs & Plants

Gossypium herbaceum

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Botanical Name : Gossypium herbaceum
Family: Malvaceae
Genus: Gossypium
Species: G. herbaceum
Kingdom: Plantae
Order: Malvales

Common Name:  Levant cotton
Habitat: Gossypium herbaceum is native to Asia Minor, and cultivated in U.S.A. and Egypt, India, Mediterranean.

Description:
Gossypium herbaceum is a biennial or triennial plant with branching stems 2 to 6 feet high, palmate hairy leaves, lobes lanceolate and acute flowers with yellow petals, and a purple spot in centre, leaves of involucre serrate, capsule when ripe splits open and shows a loose white tuft surrounding the seeds and adhering firmly to outer coating; it requires warm weather to ripen its seeds, which they do not do north of Virginia.
Their flowers are small and yellow with a purple center. When ripe and in warm weather, the flower capsule will burst and expose the cotton surrounding the seeds firmly. The cotton produced by this plant is short, about 2 inches (5.1 cm) long and is firmly attached to the seed, which is covered in hairy down. An acre of cotton can be expected to produce about 300 pounds (140 kg)……..CLICK & SEE THE PICTURES

The flowering time ends in September, and a month or so earlier the tops are cut off in order to ripen and send the sap back to the capsules. The pods are about the size of a walnut, and are collected by hand as they ripen;the cotton is also separated by hand and packed in bales. In the Levant the seeds are often used as food. An acre may be expected to produce 240 to 300 lb. of cotton.

The herbaceous part of the plant contains much mucilage and has been utilized as a demulcent. Cotton seeds have been used in the Southern States for intermittent fever with great success. The root and stem-bark deteriorates with age, so only newly harvested material should be used. The root-bark of commerce consists of thin flexible bands of quilled pieces covered with a browny yellow periderm, odour not strong, taste slightly acid.

Part Used in medicines: Bark of root and of other cultivated species.
Constituents: A peculiar acid resin, odourless and insoluble in water, absorbing oxygen when exposed, then changes to a red colour. The bark also contains sugar, gum, tannin, fixed oil, chlorophyll.

Medicinal Uses:
Orally administered ethyl ether and ethanol extracts of Gossypium herbaceum significantly decreased the blood glucose level. Gossypium herbaceum is not only lowered TC, TG, LDL, VLDL levels but also increased level of cardioprotective lipid HDL Therefore, Gossypium herbaceum has potential role to prevent formation of atherosclerosis and coronary heart disease. The study demonstrated that both above given extracts of Gossypium herbaceum could be useful in management of diabetes associated with abnormalities in lipid profiles.

Mainly used as an abortifacient in place of ergot, being not so powerful but safer; it was used largely in this way by the slaves in the south. It not only increases the contractions of the uterus in labour, but also is useful in the treatment of metrorrhagia, specially when dependent on fibroids; useful also as an ecbolic; of value in sexual lassitude. A preparation of cotton seed increases milk of nursing mothers.

Click to see  :  Homeopathic remedies    
Other Uses:
Cotton is usually used as a textile while making clothing and can be made into yarns and sheets of fabric. In the Levant seeds are often used for food. It is utilized so often because of its comfortable, breathable properties. It has been cultivated for women’s menstrual cycle pains and irregular bleeding, and it also has been used after birth to expel placenta afterbirth and to increase lactation. Cotton has been used for gastrointestinal issues also, such as hemorrhages, nausea, and diarrhea, as well as fevers and headaches, especially in the southern United States. Levant cotton seed extract, gossypol, also has a potential use as a male contraceptive but can cause infertility after discontinuing. In lab rat studies, it has been able to stop pregnancies early.
The crushed seeds give a fixed, semi-drying oil used in making soap, etc.
Click & see : Gossypium Herbaceum (Cotton) Seed Oil 

Resources:
https://en.wikipedia.org/wiki/Gossypium_herbaceum
http://www.botanical.com/botanical/mgmh/c/cotto109.html

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Pediatric Pregnancy & Child birth

Complications In Pregnancy

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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.

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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

Symptoms:
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.

Risk Factors:
Known risk factors for preeclampsia include:

*Nulliparity (never given birth)
*Older age, and diabetes mellitus
*Kidney disease
*Chronic hypertension
*Prior history of preeclampsia
*Family history of preeclampsia
*Advanced maternal age (>35 years)
*Obesity
*Antiphospholipid antibody syndrome
*Multiple gestation
*Having donated a kidney.
*Having sub-clinical hypothyroidism or thyroid antibodies

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)
*Immunologic factors
*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)
*Pulmonary edema
*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.

Predictive tests:
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,[14] 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.

Differential diagnosis:
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.

Prevention:
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.

Diet:
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.

Aspirin:
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.

Physical activity:
There is insufficient evidence to recommend either exercise or strict bedrest as preventative measures of pre-eclampsia.

Smoking cessation:
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.

Resources:
http://health.howstuffworks.com/pregnancy-and-parenting/pregnancy/complications/a-guide-to-pregnancy-complications-ga13.htm
http://en.wikipedia.org/wiki/Pre-eclampsia

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Ailmemts & Remedies

Pheochromocytomas

Definition:
Pheochromocytomas are a type of tumor of the adrenal glands that can release high levels of epinephrine and norepinephrine. As the name implies, the “ad-renal” glands are located near the “renal” area. In other words, the adrenal glands are small glands that are located near the top of the kidneys. One adrenal gland sits on top of each of the two kidneys.

Despite their small size, the adrenal glands have many functions. They are complex endocrine (hormone secreting) glands. Cells in different regions of the adrenal glands have different functions in the endocrine system. There is an area (zona fasciculata) where the cells secrete cortisol, a hormone similar to cortisone. There is another area (zona glomerulosa) where cells secrete a hormone called aldosterone which helps in water regulation.

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There is yet another area, referred to as the adrenal medulla, where the cells secrete substances called catecholamines — epinephrine, norepinephrine and dopamine. These are “flight or fight” hormones. They are responsible in part for that feeling of an “adrenaline” rush people feel when they are afraid. It is these cells that are involved in a pheochromocytoma. Basically, a pheochromocytoma is a tumor of these catecholamine-secreting cells, and that causes the clinical signs and symptoms we will discuss below. The catecholamine-secreting cells are sometimes referred to as chromaffin cells, and they are found in other areas of the body as well as in the adrenal medulla.

Sometimes, pheochromocytomas arise from chromaffin cells that are located outside of the adrenal gland. In this case, they are termed extra-adrenal pheochromocytomas or paragangliomas and are usually located in the abdomen.

Pheochromocytomas may occur in persons of any age. The peak incidence is between the third and the fifth decades of life, but approximately 10% occur in children. Pheochromocytomas are, fortunately, quite rare (only about 800 new cases are diagnosed per year in the US) and the majority of them are entirely benign. Only about 10% of pheochromocytomas are malignant.

Signs and symptoms:
The signs and symptoms of a pheochromocytoma are those of sympathetic nervous system hyperactivity, including:

*Skin sensations
*Flank pain
*Elevated heart rate
*Elevated blood pressure, including paroxysmal (sporadic, episodic) high blood pressure, which sometimes can be more difficult to detect; another clue to the presence of pheochromocytoma is orthostatic hypotension (a fall in systolic blood pressure greater than 20 mmHg or a fall in diastolic blood pressure greater than 10 mmHg upon standing)

*Palpitations
*Anxiety often resembling that of a panic attack
*Diaphoresis (excessive sweating)
*Headaches
*Pallor
*Weight loss
*Localized amyloid deposits found microscopically
*Elevated blood glucose level (due primarily to catecholamine stimulation of lipolysis (breakdown of stored fat) leading to high levels of free fatty acids and the subsequent inhibition of glucose uptake by muscle cells. Further, stimulation of beta-adrenergic receptors leads to glycogenolysis and gluconeogenesis and thus elevation of blood glucose levels).

A pheochromocytoma can also cause resistant arterial hypertension. A pheochromocytoma can be fatal if it causes malignant hypertension, or severely high blood pressure. This hypertension is not well controlled with standard blood pressure medications.

Not all patients experience all of the signs and symptoms listed. The most common presentation is headache, excessive sweating, and increased heart rate, with the attack subsiding in less than one hour.

Tumors may grow very large, but most are smaller than 10 cm.

Causes:
Conditions that are associated with Pheochromocytomas can be a component of certain familial or genetic syndromes. The most common familial condition is called multiple endocrine neoplasia, or MEN for short. Two types of MEN — MEN 2A and 2B — are associated with pheochromocytomas. Both are genetic syndromes that run in families and are transmitted from parent to child in an autosomal dominant manner.

Pheochromocytomas are not the only tumors that occur in MEN 2A and 2B. MEN 2A carries an increased risk of tumors of the parathyroids, glands near the thyroid that help to regulate calcium levels in the body. And both MEN 2A and 2B elevate the risk of thyroid cancer. In families where MEN is suspected, genetic testing can be done to help identify family members at risk.

Pheochromocytomas are a feature of other genetic disorders, including von Hippel-Lindau syndrome and neurofibromatosis. Both of these disorders are associated with the development of numerous benign and malignant tumors.

There are also many individuals who have pheochromocytomas with no known family history of them. These cases are termed sporadic. In general, if these patients have bilateral disease (pheochromocytomas in both adrenal glands) or are diagnosed before the age of 21, genetic screening is recommended.

Statistics:
*About 10% of adrenal cases are bilateral (suggesting hereditary disease)
*About 10% of adrenal cases occur in children (also suggesting hereditary disease)
*About 15% are extra-adrenal (located in any orthosympathetic tissue): of these 9% are in the abdomen and 1% are located elsewhere. Some extra-adrenal pheochromocytomas are probably actually paragangliomas, but the distinction is only possible after surgical resection.

*About 11.1% of adrenal cases are malignant, but this rises to 30% for extra-adrenal cases
*About 26% are hereditary (earlier opinion had 10%)
*About 3% recur after being resected
*About 14% of affected individuals do not have arterial hypertension (Campbell’s Urology)

Other Causes:
Basically, anything that can cause over activity of the sympathetic nervous system can be on the list of diagnoses to rule out when suspecting a pheochromocytoma. The sympathetic system is the main control panel governing the release of the “flight or fight” response in response to stress or fear, as mentioned above. Things that can stimulate this include drugs (even excessive use of decongestants should be considered); withdrawal from drugs (such as suddenly stopping certain blood pressure medications); panic attacks, and spinal cord injuries are among the many conditions that can also lead to some of the symptoms seen in pheochromocytomas.

Up to 25% of pheochromocytomas may be familial. Mutations of the genes VHL, RET, NF1(Gene 17 Neurofibromatosis type 1), SDHB and SDHD are all known to cause familial pheochromocytoma/extra-adrenal paraganglioma.

Pheochromocytoma is a tumor of the multiple endocrine neoplasia syndrome, type IIA and type IIB (also known as MEN IIA and MEN IIB, respectively). The other component neoplasms of that syndrome include parathyroid adenomas, and medullary thyroid cancer. Mutations in the autosomal RET proto-oncogene drives these malignancies . Common mutations in the RET oncogene may also account for medullary sponge kidney as well.

Pheochromocytoma linked to MEN II can be caused by RET oncogene mutations. Both syndromes are characterized by pheochromocytoma as well as thyroid cancer (thyroid medullary carcinoma). MEN IIA also presents with hyperparathyroidism, while MEN IIB also presents with mucosal neuroma. It is now postulated that Lincoln suffered from MEN IIB, rather than Marfan’s syndrome as previously thought, though this is uncertain.

Pheochromocytoma is also associated with neurofibromatosis.

Diagnosis:
The diagnosis can be established by measuring catecholamines and metanephrines in plasma (blood) or through a 24-hour urine collection. Care should be taken to rule out other causes of adrenergic (adrenalin-like) excess like hypoglycemia, stress, exercise, and drugs affecting the catecholamines like stimulants, methyldopa, dopamine agonists, or ganglion blocking antihypertensives. Various foodstuffs (e.g. vanilla ice cream) can also affect the levels of urinary metanephrine and VMA (vanillylmandelic acid). Imaging by computed tomography or a T2 weighted MRI of the head, neck, and chest, and abdomen can help localize the tumor. Tumors can also be located using an MIBG scan, which is scintigraphy using iodine-123-marked metaiodobenzylguanidine.

Pheochromocytomas occur most often during young-adult to mid-adult life.

These tumors can form a pattern with other endocrine gland cancers which is labeled multiple endocrine neoplasia (MEN). Pheochromocytoma may occur in patients with MEN 2 and MEN 3 (MEN 2B). Von Hippel Lindau patients may also develop these tumors.

Patients experiencing symptoms associated with pheochromocytoma should be aware that it is rare. However, it often goes undiagnosed until autopsy; therefore patients might wisely choose to take steps to provide a physician with important clues, such as recording whether blood pressure changes significantly during episodes of apparent anxiety.

Testing:
*Blood Tests: analysis of free metanephrine in blood plasma. High levels are indicative of pheochromocytoma

*Urine Tests: Although this test is slightly less effective than plasma testing it is still considered highly effective in diagnosis. Usually the metabolites of norepinephrine and epinephrine, vanillylmandelic acid (VMA) and homovanillic acid (HVA) are found in relatively small amounts in normal humans. The increased intermittent excretion of these metabolites is indicative of the disease, but does not completely rule out other diseases which may cause the same excretion values.

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*Other Tests:
….#One diagnostic test used in the past for a pheochromocytoma is to administer clonidine, a centrally-acting alpha-2 agonist used to treat high blood pressure. Clonidine mimics catecholamines in the brain, causing it to reduce the activity of the sympathetic nerves controlling the adrenal medulla. A healthy adrenal medulla will respond to the clonidine suppression test by reducing catecholamine production; the lack of a response is evidence of pheochromocytoma.

….#Chromogranin A is elevated in case of pheochromocytoma.

….#Another test is for the clinician to press gently on the adrenal gland. A pheochromocytoma will often release a burst of catecholamines, with the associated signs and symptoms quickly following. This method is NOT recommended because of possible complications arising from a potentially massive release of catecholamines.

….#Warning: Testing via histamine and tyramine is dangerous and should not be used.

Tumor location:
In adults, approximately 80% of pheochromocytomas are unilateral and solitary, 10% are bilateral, and 10% are extra-adrenal. In children, a fourth of tumors are bilateral, and an additional fourth are extra-adrenal. Solitary lesions inexplicably favor the right side. Although pheochromocytomas may grow to large size (>3 kg), most weigh <100 g and are <10 cm in diameter. Pheochromocytomas are highly vascular.

The tumors are made up of large, polyhedral, pleomorphic chromaffin cells. Fewer than 10% of these are malignant. As with several other endocrine tumors, malignancy cannot be determined from the histologic appearance; tumors that contain large number of aneuploid or tetraploid cells, as determined by flow cytometry, are more likely to recur. Local invasion of surrounding tissues or distant metastases indicate malignancy.

Extra-adrenal Pheochromocytomas: Extra-adrenal pheochromocytomas usually weigh 20 to 40 g and are <5 cm in diameter. Most are located within the abdomen in association with the celiac, superior mesenteric, inferior mesenteric ganglia and Organ of Zuckerkandl. Approximately 10% are in the thorax, 1% are within the urinary bladder, and less than 3% are in the neck, usually in association with the sympathetic ganglia or the extracranial branches of the ninth cranial nerves....CLICK  & SEE
Differential diagnosis
The differential diagnoses of pheochromocytoma include:

*Anxiety disorders

*Paragangliomas
*Essential hypertension
*Hyperthyroidism
*Insulinoma
*Mercury poisoning
*Paroxysmal supraventricular tachycardia
*Renovascular hypertension
*Carcinoid

Treatment and recovery
Treatment involves drugs to bring blood pressure to normal levels, followed by surgery to remove the tumour. Blood pressure and adrenaline/noradrenaline levels must be checked for some time afterwards to ensure that removal of the tumour was complete. If the tumour was benign then survival rates are high, but in people affected by malignant pheochromocytomas, less than 50 per cent survive longer than five years.

Prevention;
Since the cause of phaeochromocytoma is unknown, it isn’t possible to prevent it.

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

Resources:
http://en.wikipedia.org/wiki/Pheochromocytoma
http://www.bbc.co.uk/health/physical_health/conditions/phaeochromocytoma1.shtml
http://www.lexic.us/definition-of/pheochromocytoma

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Lower Your BP, Live Longer

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In western countries, the number of people affected by high blood pressure (BP) or hypertension is decreasing. In India, however, the figure is creeping up, albeit marginally (2-3 per cent). This is worrying because, untreated, hypertension may result in complications like a heart attack, heart or kidney failure, tearing of the blood vessels and loss of vision. It can also cause subtle loss of memory and the ability to think clearly.
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BP indicates the force with which the heart pumps blood against the blood vessel. It has two values — an upper or systolic and a lower or diastolic. Values of 120/80 are normal, while 139/89 indicates pre-hypertension and 140/90 or above hypertension. With age, the blood vessels tend to harden, decreasing their pliability. This causes a peculiar type of hypertension where only the upper value is high. About 70 per cent of the population over the age of 60 has this type of systolic hypertension. BP should be measured every two years after the age of 20 and yearly after 40.

Normal BP:->..
The risk of hypertension increases with age, obesity, a family history of high BP, kidney diseases, diabetes, endocrine diseases, smoking, alcohol consumption, medications like corticosteroids, birth control pills or those for losing weight. Narrow abnormally placed blood vessels present from birth can also lead to high BP. If no cause can be detected, it’s called “essential hypertension” and requires medication to prevent complications. Even isolated systolic hypertension requires treatment.

BP is linked to salt intake. A high salt intake results in elevated BP. The effect is even more pronounced in people (around 20 per cent of the population) who are “salt sensitive”.

The recommended salt intake for a normal person is 5gm or 1 teaspoon a day. But the “hidden salt” must also be considered. All food and even drinking water contains varying amounts of natural salt. Sodium (a component of salt) is added to food products in the form of monosodium glutamate, sodium nitrite, sodium saccharin, baking soda (sodium bicarbonate) or sodium benzoate. These are ingredients in condiments and seasonings like tomato sauce, soy sauce and pickles. Processed meats such as bacon, sausage and ham, and fast foods like burgers and pizzas are high in sodium content.

Medications belonging to groups such as diuretics, alpha blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta blockers, calcium channel blockers and rennin inhibitors are available to control blood pressure. The pharmaceutical industry also introduces “new and improved” drugs in the market with monotonous regularity. Control remains unsatisfactory in many patients who are then dosed with two or more anti hypertensives. The older, long-acting diuretics, surprisingly, remain one of the most effective medications, either as an adjuvant to existing medicine or alone.

Better control of BP with lower doses of medication can often be achieved if the person is willing to make certain lifestyle changes. Weight needs to be ideal. As weight increases, so does the pressure on your artery walls. To calculate your ideal body weight, multiply your height in meter squared by 23.

Inactive people have a faster heart rate, forcing the heart to work harder for longer periods of time. Aerobic exercise like walking, jogging, swimming or running needs to be done daily. It should be started at the age of around six with 20 minutes of running. Gradually this should be increased to an hour by the age of 18 years.

Smoking (even second-hand smoke), using snuff or chewing tobacco releases chemicals into the body which damage the blood vessels, making them narrow and thus increasing the BP.

Salt makes the body retain fluid, which in turn increases the BP. Limit your intake to 5gm a day. Sodium can be balanced by potassium found in fresh fruits and vegetables. Eat four to six helpings of this a day.

Vitamin D obtained through the diet and by exposure to sunlight affects the levels of a BP-regulating enzyme in the kidneys. Inadequate levels can indirectly elevate the BP.

Heavy drinking can cause permanent heart damage. Even two or three drinks in a single sitting can cause the release of chemicals that temporarily elevate the BP.

Stress can elevate the BP. It needs to tackled with meditation and yoga. Chronic diseases like diabetes, high cholesterol, kidney disease and sleep apnoea need to be controlled as they contribute to the risk of high BP.

Children too are at risk from as early as six or eight years if they are obese, inactive and eat high sodium snacks. These lifestyle changes, therefore, need to be initiated from a young age.

You may click to see :10 Ways to Lower Your Blood Pressure Without Medication

Source: The Telegraph (Kolkata, India)

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Nattokinase May Soon be Sold as Aspirin Replacement to Treat Thromboses

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What Is Nattokinase?
Nattokinase is a potent fibrinolytic (anti-clotting) enzyme complex extracted and highly purified from a traditional Japanese food called Natto. Natto is a fermented cheese-like food that has been used in Japanese culture for more than 1,000 years for its popular taste, and as a folk remedy for heart and vascular diseases. Research has shown that Nattokinase supports the body in breaking up and dissolving the unhealthy coagulation of blood. In fact, it has been shown to have four times greater fibrinolytic activity than plasmin.4

click & see the pictures….…...Natto……...Nattokinase

How is it made?
Natto is produced by a fermentation process by adding the bacteria Bacillus subtilis to boiled soybeans. The resulting Nattokinase enzyme is produced when Bacillus subtilis acts on the soybeans. While other soy foods contain enzymes, it is only the natto preparation that contains the specific Nattokinase enzyme.

How was Nattokinase discovered?… Japanese researcher Dr. Hiroyuki Sumi had spent many years searching for a natural thrombolytic agent that could successfully dissolve blood clots associated with heart attacks and stroke. Finally in 1980, after testing more than 173 natural foods, Sumi found what he was looking for.

Natto, a traditional Japanese soy cheese(commonly eaten for breakfast in Japan), was dropped onto an artificial thrombus (fibrin) in a petri dish and allowed to stand at 37ºC (approximately body temperature). Over the next 18 hours, the thrombus around the natto completely dissolved! Sumi named the newly discovered enzyme Nattokinase, which means “enzyme in natto.” Dr. Sumi remarked that Nattokinase showed “a potency matched by no other enzyme.”

 

You may click to see :Natto and Nattokinase

The American Academy of Orthopedic Surgeons has said that taking aspirin may not prevent deep vein thrombosis (DVT), which is the formation of a clot in the blood vessels, usually in a vein deep within the legs or hips.

How does  Nattokinase work
Nattokinase enhances the body’s natural ability to fight blood clots, and has an advantage over blood thinners because it has a prolonged effect without side effects.

*Supports normal blood pressure
*Prevents blood clots from forming
*Dissolves existing blood clots
*Dissolves fibrin
*Enhances the body’s production of plasmin and other clot-dissolving agents, including urokinase

Research studies
Nattokinase has been the subject of 17 studies, including two small human trials. In 1990, Dr. Sumi’s research team published a series of studies demonstrating the fibrinolytic effects of Nattokinase.9 Here are some of them:

Dissolves blood clots
Researchers from JCR Pharmaceuticals, Oklahoma State University, and Miyazaki Medical College, tested Nattokinase on 12 healthy Japanese volunteers (6 men and 6 women, between the ages of 21 and 55). The researchers gave the volunteers 7 ounces of natto (the food) before breakfast, and then tracked fibrinolytic activity through a series of blood plasma tests....click & see

In one test, a blood sample was taken and a thrombus (clot) was artificially induced. The amount of time needed to dissolve the clot was cut in half within 2 hours of treatment, compared to the control group. Additionally, the volunteers retained an enhanced ability to dissolve blood clots for up to 8 hours.9

Dr. Sumi’s team also induced blood clots in a major leg vein in male dogs that had been given either four capsules of Nattokinase (250 mg per capsule) or four placebo capsules. Angiograms (x-rays of blood vessels) showed that the blood clots in the dogs that received Nattokinase had completely dissolved within 5 hours of treatment, and that normal blood circulation had been restored. Blood clots in the dogs who received the placebo showed no sign of dissolving 18 hours after the treatment.9

Researchers from Biotechnology Research Laboratories and JCR Pharmaceuticals Co. of Kobe, Japan, tested Nattokinase’s ability to dissolve a blood clot in the carotid arteries of rats. Animals treated with Nattokinase regained 62 percent of blood flow, whereas those treated with plasmin regained just 15.8 percent of blood flow.19

In another laboratory study, endothelial damage was induced in the femoral arteries of rats that had been given Nattokinase. In normal circumstances, a thickening of the artery walls and blood clotting would occur, but they were both suppressed because of Nattokinase’s fibrinolytic activity.

A recent study found that airline passengers given three daily doses of nattokinase were less likely to develop a DVT during a flight.


Helps reduce high blood pressure
Human volunteers with high blood pressure were given 30 grams of natto extract (equivalent to 7 ounces of natto food), orally for 4 consecutive days. In 4 out of 5 volunteers, the systolic blood pressure decreased on average from 173.8 to 154.8. Diastolic blood pressure decreased on average from 101.0 to 91.2. This data represents about a 10.9 percent drop in systolic blood pressure and a 9.7 percent drop in diastolic blood pressure.5911

Wistar rats that were given natto extract showed a significant drop in systolic blood pressure also, from an average of 166 to 145 in just two hours, which further decreased to an average of 144 in 3 hours. This data represents an approximate 12.7 percent drop in systolic blood pressure also, from an average of 166 to 145 in just two hours, which further decreased to an average of 144 in three hours. This data represents an approximate 12.7 percent drop in systolic blood pressure within two hours.5,9,11

These tests all indicate that Nattokinase generates a heightened ability in the body to dissolve blood clots.

Restores blood circulation
This is one of the most dramatic, documented stories about the effects of Nattokinase. A 58-year-old man had a blood clot in the retina of his right eye that caused fluid build up and bleeding. He started losing his vision in that eye and was admitted to a university hospital, where researchers prescribed a 3-ounce dose of natto to be taken before bed every night, in order to get the benefit of Nattokinase.

The man’s bleeding completely stopped by the tenth day, and by the 20th day, his vision returned and he was released from the hospital. He continued to eat natto twice a week. When he had a retinal angiogram two months later, it showed that the blood clot was completely gone.12

The traditional Japanese food Natto has been used safely for more than 1,000 years. The safety record of its potent fibrinolytic enzyme, Nattokinase, is based upon the long-term traditional use of the food and recent scientific studies.

Nattokinase has many benefits including its prolonged effects, cost effectiveness, and its ability to be used preventatively. It is a naturally occurring, food-based dietary supplement that has demonstrated stability in the gastrointestinal tract, as well as to changes in pH and temperature. It is definitely a nutritional supplement to consider adding to a cardiovascular health maintenance plan.

While currently it is rarely used clinically, the article in the JAAPA suggests that further clinical trials of nattokinase may cement its potential health benefits.

Resources:
*Better Health Research :
*Smart Publications :
*http://www.naturalypure.com/NattokinasePlus.htm

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