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Nerium oleander (Korobi)

Botanical Name : Nerium oleander
Family: Apocynaceae
Subfamily: Apocynoideae
Tribe: Wrightieae
Genus: Nerium L.
Species: N. oleander
Kingdom: Plantae
Order: Gentianales

Common Names: oleande, rokttokarobi  or korobifull (bengali name)

Habitat :Nerium oleander is either native or naturalized to a broad area from Mauritania, Morocco, and Portugal eastward through the Mediterranean region and the Sahara (where it is only found sporadically), to the Arabian peninsula, southern Asia, and as far East as Yunnan in southern parts of China. It typically occurs around dry stream beds. Nerium oleander is planted in many subtropical and tropical areas of the world. On the East Coast of the US, it can be planted as far north as Virginia Beach, Virginia, while in California and Texas it is naturalized as a median strip planting.It is so widely cultivated that no precise region of origin has been identified, though southwest Asia has been suggested. The ancient city of Volubilis in Morocco may have taken its name from the Berber name oualilt for the flower

Description:
Nerium oleanderis an evergreen shrub or small tree. It grows to 2–6 m (6.6–20 ft) tall, with erect stems that splay outward as they mature; first-year stems have a glaucous bloom, while mature stems have a grayish bark. The leaves are in pairs or whorls of three, thick and leathery, dark-green, narrow lanceolate, 5–21 cm (2.0–8.3 in) long and 1–3.5 cm (0.39–1.4 in) broad, and with an entire margin. The flowers grow in clusters at the end of each branch; they are white, pink to red, 2.5–5 cm (0.98–2.0 in) diameter, with a deeply 5-lobed fringed corolla round the central corolla tube. They are often, but not always, sweet-scented. The fruit is a long narrow capsule 5–23 cm (2.0–9.1 in) long, which splits open at maturity to release numerous downy seeds.

 

Click to see the pictures….>….(01)……..(1)...(2)...(3)....(4).(5)..(6)..…(7)...(8)..

Medicinal Uses:
Medicinal uses of nerium oleander include treating ulcers, hemorrhoids, and leprosy. In addition, oleander has been used to treat ringworm, herpes, and abscesses. Although people have used this supplement for centuries to treat a variety of ailments, nerium oleander is very toxic and has been determined to be unsafe for human use.

Oleander poisoning can occur with uses of even small doses and can cause nausea, vomiting, bloody diarrhea, and dizziness. In addition, nerium oleander toxicity can cause loss of appetite and dilated pupils. The symptoms of toxicity typically occur within three hours of consumption and without emergency medical intervention, serious health consequences can occur. If these and other symptoms such as shortness of breath and difficulty breathing occur, 911 should be notified.

Serious effects of oleander toxicity can include seizures, heart irregularities, and hypotension. In addition, fatal cardiac complications and loss of consciousness can occur as well. Treatment for this medical emergency includes the administration of activated charcoal and intravenous fluids. In addition, gastric lavage, or stomach pumping, may be done to remove as much of the substance as possible from the stomach.

Drugs derived from Nerium oleander have been investigated as a treatment for cancer. According to the American Cancer Society the trials have produced no evidence of benefit, but they did however cause adverse side-effects.

Other Uses:
Oleanderis a Ornamental gardening plant. It grows well in warm subtropical regions, where it is extensively used as an ornamental plant in landscapes, in parks, and along roadsides. It is drought-tolerant and will tolerate occasional light frost down to ?10 °C (14 °F).It is commonly used in landscaping freeway medians in California, Texas and other mild-winter states in the Continental United States because it is upright in habit and easily maintained. Its toxicity renders it deer-resistant. It is tolerant of poor soils and drought. Oleander can also be grown in cooler climates in greenhouses and conservatories, or as indoor plants that can be kept outside in the summer. Oleander flowers are showy and fragrant and are grown for these reasons. Over 400 cultivars have been named, with several additional flower colours not found in wild plants having been selected, including red, purple, pink, and orange; white and a variety of pinks are the most common. Many cultivars also have double flowers. Young plants grow best in spaces where they do not have to compete with other plants for nutrients.

Known Hazards:Oleander is one of the most poisonous of commonly grown garden plants.It has historically been considered a poisonous plant because some of its compounds may exhibit toxicity, especially to animals, when consumed in high amounts. Among these compounds are oleandrin and oleandrigenin, known as cardiac glycosides, which are known to have a narrow therapeutic index and can be toxic when ingested.

Toxicity studies of animals administered oleander extract concluded that rodents and birds were observed to be relatively insensitive to oleander cardiac glycosides. Other mammals, however, such as dogs and humans, are relatively sensitive to the effects of cardiac glycosides and the clinical manifestations of “glycoside intoxication”.

However, despite the common “poisonous” designation of this plant, very few toxic events in humans have been reported. According to the Toxic Exposure Surveillance System (TESS) in 2002 there were 847 human exposures to oleander reported to poison centers in the United States. Despite this exposure level, from 1985 through 2005, only three deaths were reported. One cited death was apparently due to the ingestion of oleander leaves by a diabetic man. His blood indicated a total blood concentration of cardiac glycosides of approximately 20 ?g/L which is well above the reported fatal level. Another study reported on the death of a woman who self-administered “an undefined oleander extract” both orally and rectally and her oleandrin tissue levels were 10 to 39 ?g/g which were in the high range of reported levels at autopsy. And, finally, one study reported the death of a woman who ingested oleander ‘tea’. Few other details were provided.

In contrast to consumption of these undefined oleander derived materials, there is no toxicity or deaths reported from topical administration or contact with Nerium oleander or specific products derived from them. In reviewing oleander toxicity Lanford and Boor concluded that, except for children who might be at greater risk, “the human mortality associated with oleander ingestion is generally very low, even in cases of moderate intentional consumption (suicide attempts)”.

Toxicity studies that have been conducted in dogs and rodents administered oleander extracts by intramuscular (IM) injection indicated that on an equivalent weight basis, doses of an oleander extract with glycosides ten times in excess of those likely to be administered therapeutically to humans are still safe and without any “severe toxicity observed.

Disclaimer:
The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.

Resources:
https://en.wikipedia.org/wiki/Nerium
http://www.wisegeek.com/what-are-the-medical-uses-of-nerium-oleander.htm

ROKTTOKOROBI~রক্তকরবী================"রক্তকরবী ফুল""ROKTTOKOROBI"The Bengali Flower…Color-> RedScientific Name- "…

Posted by ~TREE PLANTATION~ on Sunday, June 5, 2011

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Silicosis

Alternative Names:Potter’s rot,  Acute silicosis; Chronic silicosis; Accelerated silicosis; Progressive massive fibrosis; Conglomerate silicosis; Silicoproteinosis

Definition:
Silicosis is a respiratory disease caused by breathing in (inhaling) silica dust. It is an occupational lung disease that develops over time when dust that contains silica is inhaled into the lungs. Other examples of occupational lung disease include coalworker’s pneumoconiosis and asbestosis.

click to see the pictures

The name silicosis (from the Latin silex, or flint) was originally used in 1870 by Achille Visconti (1836-1911), prosector in the Ospedale Maggiore of Milan. The recognition of respiratory problems from breathing in dust dates to ancient Greeks and Romans. Agricola, in the mid-16th century, wrote about lung problems from dust inhalation in miners. In 1713, Bernardino Ramazzini noted asthmatic symptoms and sand-like substances in the lungs of stone cutters. With industrialization, as opposed to hand tools, came increased production of dust. The pneumatic hammer drill was introduced in 1897 and sandblasting was introduced in about 1904, both significantly contributing to the increased prevalence of silicosis.

Classification:
Classification of silicosis is made according to the disease’s severity (including radiographic pattern), onset, and rapidity of progression. These include:

Chronic simple silicosis
Usually resulting from long-term exposure (10 years or more) to relatively low concentrations of silica dust and usually appearing 10–30 years after first exposure. This is the most common type of silicosis. Patients with this type of silicosis, especially early on, may not have obvious signs or symptoms of disease, but abnormalities may be detected by x-ray. Chronic cough and exertional dyspnea are common findings. Radiographically, chronic simple silicosis reveals a profusion of small (<10 mm in diameter) opacities, typically rounded, and predominating in the upper lung zones.

..Click to see the pictures………..(2)….(1)
Accelerated silicosis
Silicosis that develops 5–10 years after first exposure to higher concentrations of silica dust. Symptoms and x-ray findings are similar to chronic simple silicosis, but occur earlier and tend to progress more rapidly. Patients with accelerated silicosis are at greater risk for complicated disease, including progressive massive fibrosis (PMF).

Complicated silicosis
Silicosis can become “complicated” by the development of severe scarring (progressive massive fibrosis, or also known as conglomerate silicosis), where the small nodules gradually become confluent, reaching a size of 1 cm or greater. PMF is associated with more severe symptoms and respiratory impairment than simple disease. Silicosis can also be complicated by other lung disease, such as tuberculosis, non-tuberculous mycobacterial infection, and fungal infection, certain autoimmune diseases, and lung cancer. Complicated silicosis is more common with accelerated silicosis than with the chronic variety.
Click to see the picture

Acute silicosis
Silicosis that develops a few weeks to 5 years after exposure to high concentrations of respirable silica dust. This is also known as silicoproteinosis. Symptoms of acute silicosis include more rapid onset of severe disabling shortness of breath, cough, weakness, and weight loss, often leading to death. The x-ray usually reveals a diffuse alveolar filling with air bronchograms, described as a ground-glass appearance, and similar to pneumonia, pulmonary edema, alveolar hemorrhage, and alveolar cell lung cancer.

Symptoms:
Because chronic silicosis is slow to develop, signs and symptoms may not appear until years after exposure. Signs and symptoms include:

*Dyspnea (shortness of breath) exacerbated by exertion

*Cough, often persistent and sometimes severe

*Fatigue

*Tachypnea (rapid breathing) which is often labored

*Loss of appetite and weight loss

*Chest pain

*Fever

*Gradual dark shallow rifts in nails eventually leading to cracks as protein fibers within nail beds are destroyed.

In advanced cases, the following may also occur:

*Cyanosis (blue skin)

*Cor pulmonale (right ventricle heart disease)

*Respiratory insufficiency

Patients with silicosis are particularly susceptible to tuberculosis (TB) infection—known as silicotuberculosis. The reason for the increased risk—3 fold increased incidence—is not well understood. It is thought that silica damages pulmonary macrophages, inhibiting their ability to kill mycobacteria. Even workers with prolonged silica exposure, but without silicosis, are at a similarly increased risk for TB.

Pulmonary complications of silicosis also include Chronic Bronchitis and airflow limitation (indistinguishable from that caused by smoking), non-tuberculous Mycobacterium infection, fungal lung infection, compensatory emphysema, and pneumothorax. There are some data revealing an association between silicosis and certain autoimmune diseases, including nephritis, Scleroderma, and Systemic Lupus Erythematosus, especially in acute or accelerated silicosis.

In 1996, the International Agency for Research on Cancer (IARC) reviewed the medical data and classified crystalline silica as “carcinogenic to humans.” The risk was best seen in cases with underlying silicosis, with relative risks for lung cancer of 2-4. Numerous subsequent studies have been published confirming this risk. In 2006, Pelucchi et al. concluded, “The silicosis-cancer association is now established, in agreement with other studies and meta-analysis

Causes:
Silica in crystalline form is toxic to the lining of the lungs. When the two come into contact, a strong inflammatory reaction occurs. Over time this inflammation causes the lung tissue to become irreversibly thickened and scarred – a condition known as fibrosis.

Common sources of crystalline silica dust include:

•Sandstone
•Granite
•Slate
•Coal
•Pure silica sand

People who work with these materials, as well as foundry workers, potters and sandblasters, are most at risk. Other forms of silica, such as glass, are less of a health risk as they aren’t as toxic to the lungs.

Men tend to be affected more often than women, as they are more likely to have been exposed to silica.

Risk Factors:
Silicosis is most commonly diagnosed in people over 40, as it usually takes years of exposure before the gradually progressive lung damage becomes apparent.

There are now fewer than 100 new cases of silicosis diagnosed each year in the UK. This is mostly the result of better working practices, such as wet drilling, appropriate ventilation, dust-control facilities, showers and the use of face masks. Many foundries are also replacing silica sand with synthetic materials.

With these measures and an increased awareness of the risks of silica exposure, the number of cases should fall even further in the future.

When silicosis is suspected, a chest x-ray will look for any damaged areas of the lungs to confirm the diagnosis. Lung function tests are often performed to assess the amount of damage the lungs have suffered and to guide treatment.

Possible Complications:
•Connective tissue disease, including rheumatoid arthritis, scleroderma (also called progressive systemic sclerosis), and systemic lupus erythematosus
•Lung cancer
•Progressive massive fibrosis
•Respiratory failure
•Tuberculosis

You may click to see the pictures:    ->(1) Simple  silicosis    :   (2)  Complicated silicosis    :(3) Silicosis.ILO Classification 2-2 R-R  :

Diagnosis:
There are three key elements to the diagnosis of silicosis. First, the patient history should reveal exposure to sufficient silica dust to cause this illness. Second, chest imaging (usually chest x-ray) that reveals findings consistent with silicosis. Third, there are no underlying illnesses that are more likely to be causing the abnormalities. Physical examination is usually unremarkable unless there is complicated disease. Also, the examination findings are not specific for silicosis. Pulmonary function testing may reveal airflow limitation, restrictive defects, reduced diffusion capacity, mixed defects, or may be normal (especially without complicated disease). Most cases of silicosis do not require tissue biopsy for diagnosis, but this may be necessary in some cases, primarily to exclude other conditions.

For uncomplicated silicosis, chest x-ray will confirm the presence of small (< 10 mm) nodules in the lungs, especially in the upper lung zones. Using the ILO classification system, these are of profusion 1/0 or greater and shape/size “p”, “q”, or “r”. Lung zone involvement and profusion increases with disease progression. In advanced cases of silicosis, large opacity (> 1 cm) occurs from coalescence of small opacities, particularly in the upper lung zones. With retraction of the lung tissue, there is compensatory emphysema. Enlargement of the hilum is common with chronic and accelerated silicosis. In about 5-10% of cases, the nodes will calcify circumferentially, producing so-called “eggshell” calcification. This finding is not pathognomonic (diagnostic) of silicosis. In some cases, the pulmonary nodules may also become calcified.

A computed tomography or CT scan can also provide a mode detailed analysis of the lungs, and can reveal cavitation due to concomitant mycobacterial infection.

Treatment:
Silicosis is an irreversible condition with no cure.  Treatment options currently focus on alleviating the symptoms and preventing complications. These include:

*Stopping further exposure to silica and other lung irritants, including tobacco smoking.

*Cough suppressants.

*Antibiotics for bacterial lung infection.

*TB prophylaxis for those with positive tuberculin skin test or IGRA blood test.

*Prolonged anti-tuberculosis (multi-drug regimen) for those with active TB.

*Chest physiotherapy to help the bronchial drainage of mucus.

*Oxygen administration to treat hypoxemia, if present.

*Bronchodilators to facilitate breathing.

*Lung transplantation to replace the damaged lung tissue is the most effective treatment, but is associated with severe risks of its own.

*For acute silicosis, Whole-lung lavage (see Bronchoalveolar lavage) may alleviate symptoms, but does not decrease overall mortality.

Experimental treatments include:

*Inhalation of powdered aluminium, d-penicillamine and polyvinyl pyridine-N-oxide.

*Corticosteroid therapy.

*The herbal extract tetrandine may slow progression of silicosis.

Support Groups:
Joining a support group where you can meet other people with silicosis or related diseases can help you understand your disease and adapt to its treatments.

Prognosis:
The outcome varies depending on the amount of damage to the lungs.

Prevention:
The best way to prevent silicosis is to identify work-place activities that produce respirable crystalline silica dust and then to eliminate or control the dust (“primary prevention”). Water spray is often used where dust emanates. Dust can also be controlled through dry air filtering.

Following observations on industry workers in Lucknow (India), experiments on rats found that jaggery (a traditional sugar) had a preventive action against silicosis.

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/Silicosis
http://www.nlm.nih.gov/medlineplus/ency/article/000134.htm
http://www.smianalytical.com/dust-sampling/what-is-silicosis.html
http://www.bbc.co.uk/health/physical_health/conditions/silicosis1.shtml

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Sarcoidosis

Alternative Names : Sarcoid, Besnier-Boeck disease or Besnier-Boeck-Schaumann disease

Definition:
Sarcoidosis (from sarc meaning flesh, -oid, like, and -osis, process)  is a disease in which abnormal collections of chronic inflammatory cells (granulomas) form as nodules in multiple organs. The cause of sarcoidosis is unknown. Granulomas most often appear in the lungs or the lymph nodes, but virtually any organ can be affected. Normally the onset is gradual. Sarcoidosis may be asymptomatic or chronic. It commonly improves or clears up spontaneously. More than 2/3 of people with lung sarcoidosis have no symptoms after 9 years. About 50% have relapses. About 10% develop serious disability. Lung scarring or infection may lead to respiratory failure and death.

CLICK & SEE THE PICTURES

Sarcoidosis most commonly affects young adults of both sexes, although studies have reported more cases in females. Incidence is highest for individuals younger than 40 and peaks in the age-group from 20 to 29 years; a second peak is observed for women over 50.

Sarcoidosis occurs throughout the world in all races with an average incidence of 16.5/100,000 in men and 19/100,000 in women. The disease is most prevalent in Northern European countries, and the highest annual incidence of 60/100,000 is found in Sweden and Iceland. In the United States, sarcoidosis is more common in people of African descent than Caucasians, with annual incidence reported as 35.5 and 10.9/100,000, respectively. Sarcoidosis is less commonly reported in South America, Spain, India, Canada, and the Philippines.

The differing incidence across the world may be at least partially attributable to the lack of screening programs in certain regions of the world and the overshadowing presence of other granulomatous diseases, such as tuberculosis, that may interfere with the diagnosis of sarcoidosis where they are prevalent. There may also be differences in the severity of the disease between people of different ethnicities. Several studies suggest that the presentation in people of African origin may be more severe and disseminated than for Caucasians, who are more likely to have asymptomatic disease.

Manifestation appears to be slightly different according to race and sex. Erythema nodosum is far more common in men than in women and in Caucasians than in other races. In Japanese patients, ophthalmologic and cardiac involvement are more common than in other races.

Sarcoidosis is one of the few pulmonary diseases with a higher prevalence in non-smokers

Classification:
Sarcoidosis may be divided into the following types:

*Annular sarcoidosis
*Erythrodermic sarcoidosis
*Ichthyosiform sarcoidosis
*Hypopigmented sarcoidosis
*Löfgren syndrome
*Lupus pernio
*Morpheaform sarcoidosis
*Mucosal sarcoidosis
*Neurosarcoidosis
*Papular sarcoid
*Scar sarcoid
*Subcutaneous sarcoidosis
*Systemic sarcoidosis
*Ulcerative sarcoidosis

Symptoms:
Sarcoidosis is a systemic disease that can affect any organ. Common symptoms are vague, such as fatigue unchanged by sleep, lack of energy, weight loss, aches and pains, arthritis, dry eyes, swelling of the knees, blurry vision, shortness of breath, a dry hacking cough or skin lesions. Sarcoidosis and cancer may mimic one another, making the distinction difficult.  The cutaneous symptoms vary, and range from rashes and noduli (small bumps) to erythema nodosum or lupus pernio. It is often asymptomatic.

CLICK & SEE THE PICTURES

 

The combination of erythema nodosum, bilateral hilar lymphadenopathy and arthralgia is called Löfgren syndrome. This syndrome has a relatively good prognosis.

Renal, liver (including portal hypertension), heart or brain involvement may cause further symptoms and altered functioning. Sarcoidosis affecting the brain or nerves is known as neurosarcoidosis.

Cardiac sarcoidosis:
Although cardiac involvement is present in 20% to 30% of patients with sarcoidosis, only about 5% of patients with systemic sarcoidosis are symptomatic.

The presentation of cardiac sarcoidosis can range from asymptomatic conduction abnormalities to fatal ventricular arrhythmia. Myocardial sarcoidosis can be a rare cause of sudden cardiac death.

Eye:
Manifestations in the eye include uveitis, uveoparotitis, and retinal inflammation, which may result in loss of visual acuity or blindness. The combination of anterior uveitis, parotitis, VII cranial nerve paralysis and fever is called uveoparotid fever, and is associated with Heerfordt-Waldenstrom syndrome. (D86.8)

Nervous system:
The central nervous system is involved in fewer than 1% of patients with sarcoidosis. There is usually granulomatous involvement of the basal meninges that subsequently affects the cranial nerves. Myelopathy may be the initial clinical presentation of intramedullary neurosarcoidosis.

Scalp:
Sarcoidosis of the scalp presents with diffuse or patchy hair loss.

Causes and pathophysiology:
The exact cause of sarcoidosis is not known. The current working hypothesis is that in genetically susceptible individuals sarcoidosis is caused through alteration in immune response after exposure to an environmental, occupational, or infectious agent.

Dysregulation of the immune system:
Granulomatous inflammation is characterized primarily by accumulation of monocytes, macrophages and activated T-lymphocytes, with increased production of key inflammatory mediators, TNF-alpha, IFN-gamma, IL-2 and IL-12, characteristic of a Th1-polarized response (T-helper lymphocyte-1 response). Sarcoidosis has paradoxical effects on inflammatory processes; it is characterized by increased macrophage and CD4 helper T-cell activation resulting in accelerated inflammation, however, immune response to antigen challenges such as tuberculin is suppressed. This paradoxic state of simultaneous hyper- and hypo- activity is suggestive of a state of anergy. The anergy may also be responsible for the increased risk of infections and cancer. It appears that regulatory T-lymphocytes in the periphery of sarcoid granulomas suppress IL-2 secretion which is hypothesized to cause the state of anergy by preventing antigen-specific memory responses.

While it is widely believed that TNF-alpha plays an important role in the formation of granulomas, it was observed that sarcoidosis can be triggered by treatment with the TNF-alpha antagonist etanercept.

Genetic associations:
Investigations of genetic susceptibility yielded many candidate genes but only few were confirmed by further investigations and no reliable genetic markers are known. Currently, the most interesting candidate gene is BTNL2; several HLA-DR risk alleles are also being investigated.  In persistent sarcoidosis the HLA haplotype HLA-B7-DR15 are either cooperating in disease or another gene between these two loci is associated. In non-persistent disease there is a strong genetic association with HLA DR3-DQ2.[19] Siblings have only a modestly increased risk (hazard ratio 5-6) of developing the disease, indicating that genetic susceptibility plays only a small role. The alternate hypothesis that family members share similar exposures to environmental pathogens is quite plausible to explain the apparent hereditary factor.

Infectious agents:
Several infectious agents appear to be significantly associated with sarcoidosis but none of the known associations is specific enough to suggest a direct causative role. Propionibacterium acnes can be found in bronchoalveolar lavage of approximately 70% patients and is associated with disease activity, however it can be also found in 23% of controls. A recent meta-analysis investigating the role of mycobacteria in sarcoidosis found it was present in 26.4% of cases, however the meta-analysis also detected a possible publication bias, so the results need further confirmation.

There have also been reports of transmission of sarcoidosis via organ transplants.

Vitamin D dysregulation:
Sarcoidosis frequently causes an increase in vitamin D production outside the kidney. Macrophages inside the granulomas convert vitamin D to its active form, resulting in elevated levels of the hormone 1,25-dihydroxyvitamin D and symptoms of hypervitaminosis D that may include fatigue, lack of strength or energy, irritability, metallic taste, temporary memory loss or cognitive problems. Physiological compensatory responses (e.g., suppression of the parathyroid hormone levels) may mean the patient does not develop frank hypercalcemia. This condition may be aggravated by high levels of estradiol and prolactin such as in pregnancy, leading to hypercalciuria and/or compensatory hypoparathyroidism.High levels of Vitamin D are also implicated in immune-system dysfunctions which tie into the sarcoid condition.

Hyperprolactinemia:
Prolactin is frequently increased in sarcoidosis, between 3–32% cases have hyperprolactinemia,  this frequently leads to amenorrhea, galactorrhea or nonpuerperal mastitis in women. Prolactin also has a broad spectrum of effects on the immune system and increased prolactin levels are associated with disease activity or may exacerbate symptoms in many autoimmune diseases and treatment with prolactin lowering medication has been shown effective in some cases. However it is unknown if this relation holds in sarcoidosis and the gender predilection in sarcoidosis is less pronounced than in some other autoimmune diseases where such relation has been established. In pregnancy, the effects of prolactin and estrogen counteract each other to some degree, with a slight trend to improve pulmonary manifestations of sarcoidosis while lupus, uveitis and arthralgia might slightly worsen.   Lupus, uveitis and arthralgia are known to be in some cases associated with increased prolactin levels and respond to bromocriptin treatment but so far this has not been investigated specifically for sarcoidosis. The reasons for increased prolactin levels in sarcoidosis are uncertain. It has been observed that prolactin is produced by T-lymphocytes in some autoimmune disorders in amounts high enough to affect the feedback by the hypothalamic dopaminergic system.

The extrapituitary prolactin is believed to play a role as a cytokine like proinflammatory factor. Prolactin antibodies are believed to play a role in hyperprolactinemia in other autoimmune disorders and high prevalence endocrine autoimmunity has been observed in patients with sarcoidosis.[30] It may also be a consequence of renal disease or treatment with steroids. Neurosarcoidosis may occasionally cause hypopituiarism but has not been reported to cause hyperprolactinemia.

Thyroid disease:
In women, a substantial association of thyroid disease and sarcoidosis has been reported. The association is less marked but still significant for male patients. Female patients have a significantly elevated risk for hypothyroidism, hyperthyroidism and thyroid autoimmunity and it appears that autoimmunity is very important in the pathogenesis of thyroid disease in this population. Thyroid granulomatosis on the other hand is uncommon.

Hypersensitivity/autoimmune:
Association of autoimmune disorders has been frequently observed. The exact mechanism of this relation is not known but some evidence supports the hypothesis that this is a consequence of Th1 lymphokine prevalence.

Sarcoidosis has been associated with celiac disease. Celiac disease is a condition in which there is a chronic reaction to certain protein chains, commonly referred to as glutens, found in some cereal grains. This reaction causes destruction of the villi in the small intestine, with resulting malabsorption of nutrients.

An association with type IV hypersensitivity has been described. Tests of delayed cutaneous hypersensitivity have been used to measure progression.

Other:
While disputed, some cases have been associated with inhalation of the dust from the collapse of the World Trade Center after the September 11, 2001 attacks . Chicago comedian, Bernie Mac, suffered from sarcoidosis and died of pneumonia as a result of his compromised immune system. Reggie White, a former standout National Football League player, also suffered from sarcoidosis, and the disease played a major role in his death.

Risk Factors:
While anyone can develop sarcoidosis, factors that may increase your risk include:

*Age and sex. Sarcoidosis usually occurs between the ages of 20 and 40. Women are slightly more likely to develop the disease than are men.

*Race. Black Americans have a higher incidence of sarcoidosis than do white Americans. Also, sarcoidosis may be more severe in blacks and more likely to cause skin problems.

*Ethnicity. Worldwide, sarcoidosis is most commonly reported in people whose families originally came from Northern Europe — particularly Scandinavia and Britain. People with Japanese ancestry are more likely to develop eye or cardiac complications from sarcoidosis.

*Family history. If someone in your family has had sarcoidosis, you are more likely to develop the disease yourself.

Complications:
In about two-thirds of people with sarcoidosis, the condition resolves with no lasting consequences. But in some people, sarcoidosis can become chronic and lead to complications that may affect different parts of our body, such as : Lungs,Eyes,Kidneys,Heart, Nervous system  and Reproductive system.

Diagnosis:
Sarcoidosis can be difficult to diagnose, partly because the disease produces few signs and symptoms in its early stages. And when symptoms do occur, they vary by organ system affected and can mimic those of other disorders. A variety of diagnostic tests can narrow the possibilities and rule out other conditions.

Imaging tests
*X-ray. A simple chest X-ray can reveal evidence of lung damage or enlarged lymph nodes in your chest. In fact, some people have been diagnosed with sarcoidosis before they have any symptoms — from the evidence provided by chest X-rays taken for other reasons.

*CT scan. Computerized tomography (CT) uses a computer to combine a large number of X-rays views taken from many different directions into detailed, cross-sectional images of your internal structures.

Lab tests
Samples of your blood may be tested to check your general health and to see how well your kidneys and liver are functioning.

Lung function tests
These tests typically measure:

…#The volume of your lungs
…#How much air you can breathe in and out
…#How fast you can breathe air out
…#How well your lungs deliver oxygen to your blood

Biopsies
A biopsy is a small sample of tissue taken from a part of your body believed to be affected by sarcoidosis. The sample can be tested for the types of granulomas that are commonly seen in sarcoidosis. Biopsies can most easily be taken from your skin, from lymph nodes right under the skin, or from the outer membrane of your eye.

Lung biopsies can be obtained during a bronchoscopy (brong-KOS-kuh-pee). This procedure uses a thin, flexible tube that contains a fiber-optic camera and a grasping tool. After the tube is inserted down your throat, a doctor uses the grasping tool to remove a small sample of lung tissue — about the size of a grain of rice. The sample is sent to a microbiology laboratory to look for specific organisms.

Treatment :
Currently, there’s no cure for sarcoidosis. For one in ten people the disease slowly gets worse over time and for one in 50 it proves fatal. However, for the majority of those with the disorder – around eight out of every ten people, in fact – the condition resolves spontaneously after a few years and never comes back.

Relief from symptoms can be found with anti-inflammatory painkillers, and steroids can also prove extremely effective. When used to treat chronic sarcoidosis, steroids may need to be used at a low dose for many months, sometimes a year or more. During this time, regular blood and lung function tests and chest x-rays are performed to monitor how well the treatment is working. In more severe cases, immunosuppressive drugs such as methotrexate are used. Newer drugs such as infliximab may also be prescribed.

Prognosis:
The disease can remit spontaneously or become chronic, with exacerbations and remissions. In some patients, it can progress to pulmonary fibrosis and death. Approximately half of the cases resolve without treatment or can be cured within 12–36 months and most within 5 years. Some cases persist several decades.  Where the heart is involved, the prognosis is poor.   Patients with sarcoidosis appear to be at significantly increased risk for cancer, in particular lung cancer, malignant lymphomas,[40] and cancer in other organs known to be affected in sarcoidosis.   In sarcoidosis-lymphoma syndrome, sarcoidosis is followed by the development of a lymphoproliferative disorder such as non-Hodgkin lymphoma. This may be attributed to the underlying immunological abnormalities that occur during the sarcoidosis disease process.  Sarcoidosis can also follow cancer   or occur concurrently with cancer. There have been reports of hairy cell leukemia,  acute myeloid leukemia,  and acute myeloblastic leukemia   associated with sarcoidosis.
In pregnancy:
Sarcoidosis generally does not prevent successful pregnancy and delivery; the endogenous estrogen in pregnancy may even have a slightly beneficial immunomodulatory effect. In most cases the course of sarcoidosis is unaffected by pregnancy; there is improvement in a few cases and worsening of symptoms in very few cases.
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/Sarcoidosis
http://www.bbc.co.uk/health/physical_health/conditions/sarcoidosis1.shtml
http://www.mayoclinic.com/health/sarcoidosis/DS00251

http://www.metrohealth.org/body.cfm?id=1554

Carbon Monoxide Poisoning

Introduction:
Carbon monoxide is a gas. It is a product of incomplete combustion of natural or petroleum gas.  It has no odor or color. You can’t see it, smell it, or taste it; but carbon monoxide can kill you. Inhaling the gas reduces the blood’s ability to carry oxygen, leaving the body’s organs and cells starved of oxygen.

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...Click to see the picture.
Common sources of carbon monoxide is automobiles on road and in  in the home include faulty central heating systems, gas appliances and fires. Blocked flues and chimneys mean the gas can’t escape and is inhaled by the unsuspecting individual.CO from these fumes can build up in places that don’t have a good flow of fresh air.  One  can be poisoned by breathing them in.

It is often hard to tell if someone has CO poisoning, because the symptoms may be like those of other illnesses. People who are sleeping or intoxicated can die from CO poisoning before they have symptoms. A CO detector can warn you if you have high levels of CO in your home.

Symptoms:
The symptoms of mild carbon monoxide poisoning may be non-specific and similar to those of viral cold and flu infections or food poisoning: headache, nausea, abdominal pain, dizziness, sore throat and dry cough.

The most common symptoms of CO poisoning are:
•Headache
•Dizziness
•Nausea
•Flu-like symptoms, fatigue
•Shortness of breath on exertion
•Impaired judgment
•Chest pain
•Confusion
•Depression
•Hallucinations
•Agitation
•Vomiting
•Abdominal pain
•Drowsiness
•Visual changes
•Fainting
•Seizure
•Memory and walking problems

In children, the symptoms are similar to those of a stomach upset, with nausea and vomiting.

More severe poisoning can result in a fast and irregular heart rate, hyperventilation, confusion, drowsiness and difficulty breathing. Seizures and loss of consciousness may also occur.

Some symptoms can occur a few days or even months after exposure to carbon monoxide. These may include confusion, loss of memory and problems with coordination.

Causes:
Carbon monoxide is formed when organic compounds burn. The most common sources are motor vehicle exhaust, smoke from fires, engine fumes, and nonelectric heaters. Carbon monoxide poisoning is often associated with malfunctioning or obstructed exhaust systems and with suicide attempts.

Sources of carbon monoxide:

•Gas water heaters
•Kerosene space heaters
•Charcoal grills
•Propane heaters and stoves
•Gasoline and diesel powered generators
•Cigarette smoke
•Propane-fueled forklifts
•Gasoline powered concrete saws
•Indoor tractor pulls
•Any boat with an engine
•Spray paint, solvents, degreasers, and paint removers

Risk Factors:
Risks for exposure to carbon monoxide include:
•Children riding in the back of enclosed pickup trucks (particularly high risk)
•Industrial workers at pulp mills, steel foundries, and plants producing formaldehyde or coke (a hard grey fuel)
•Personnel at fire scenes
•Using heating sources or electric generators during power outages
•Those working indoors with combustion engines or combustible gases
•Swimming near or under the stern or swim-step of a boat with the boat engine running
•Back drafting when a boat is operated at a high bow angle
•Mooring next to a boat that is running a generator or engine
•Improper boat ventilation

Diagnosis:
Because signs and symptoms of carbon monoxide poisoning are not specific, a blood test to look for it is the best way to make the diagnosis.

Treatment;
•The treatment for carbon monoxide poisoning is high-dose oxygen, usually using a facemask attached to an oxygen reserve bag.
•Carbon monoxide levels in the blood may be periodically checked until they are low enough to safely send you home.
•In severe poisoning, if available, a hyperbaric pressure chamber may be used to give even higher doses of oxygen.
•It is important to find the source of the carbon monoxide. Your local fire department or public service company will help find the source of carbon monoxide and make sure the building is safe.

Self-Care at Home:
•Move all family members and pets to fresh air away from the source of carbon monoxide (CO).
•No home therapy is available for carbon monoxide poisoning.
•You must seek medical care in a hospital emergency department.

Prognosis:
The prognosis for a person with carbon monoxide poisoning is difficult to predict.
•Death can result from severe cases.
•Even with proper treatment, some people develop long-term brain damage, resulting in complications such as severe memory loss, difficulty thinking, or other neurologic or psychiatric problems.
•Others appear to have no long-term problems.
*People who suffer mild poisoning invariably make a full recovery. Between ten and 50 per cent of those with severe poisoning may suffer long-term problems.

Prevention:
Your best protection is to install a carbon monoxide alarm on each level of your home or boat as your first line of defense. According to the National Fire Protection Association some 93% of homes have smoke alarms, yet the Consumer Product Safety Commission estimates that only 15% have carbon monoxide alarms. A carbon monoxide monitor with an audible alarm works much like a home smoke alarm and beeps loudly when the sensors detect carbon monoxide.

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•If the alarm sounds, evacuate the building. People who have symptoms of carbon monoxide poisoning should seek emergency medical care. Call the fire department or public service company to investigate.

•Inspect your home for hazards.

*Your home heating system, chimney, and flue must be inspected and cleaned by a qualified technician every year. Keep chimneys clear of bird and squirrel nests, leaves, and residue to ensure proper ventilation.

*Be sure your furnace and other appliances, such as gas ovens, ranges, and cook tops, are inspected for adequate ventilation.

*Do not burn charcoal inside your house (even in the fireplace). Have gas fireplaces inspected each fall to ensure the pilot light burns safely.

*Do not operate gasoline-powered engines in confined areas such as garages or basements. Do not leave your car, mower, or other vehicle running in an attached garage, even with the door open.

*Do not block or seal shut exhaust flues or ducts for appliances such as water heaters, ranges, and clothes dryers.

*Become familiar with the hazards of carbon monoxide poisoning and boating (please see Web Links section).

 

For More Information:
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You may click & see:-
*Environmental Protection Agency, Protect Your Family and Yourself from Carbon Monoxide Poisoning

*Centers for Disease Control – Prevent Carbon Monoxide Poisoning on Your Boat

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

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/carbonmonoxide1.shtml
http://www.emedicinehealth.com/carbon_monoxide_poisoning/article_em.htm
http://www.salem-news.com/articles/december212006/tips_122106.php
http://healthforworld.blogspot.com/2008/11/carbon-monoxide-poisoning.html

http://www.cdc.gov/co/faqs.htm

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Mercury Cancels Brain Benefits of Fish Oil

A long-term dietary study untangles the effects on brain development of two well-known but contrary exposures – beneficial oil and toxic methyl mercury – that accompany a fish-rich diet.

 CLICK & SEE THE PICTURES

Prenatal mercury exposure from a mother’s fish-rich diet can reduce the beneficial effects fish oil has on brain development, report an international group of researchers. The babies exposed in the womb to higher methyl mercury levels scored lower on skills tests as infants and toddlers than those exposed to lower levels of the pollutant.

Of five nutrients tested, only the benefits of the fish oil DHA were affected by the mercury. The extent to which methyl mercury interferes with fish oil’s brain benefits is uncertain.

Environmental Health News reports:

“The beneficial effects of eating fish during pregnancy on a baby’s brain development are relatively well accepted. However, some fish can contain high levels of mercury ... Government agency advisories suggest women of childbearing years eat fish with low mercury levels as well as limit consumption of fish that contain high levels.”


Resources:

Environmental Health News January 3, 2011
Environmental Research October 18, 2010

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