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Prostate cancer

Other Name : Carcinoma of the man’s prostate,adenocarcinoma, or glandular cancer

Definition:
Prostate cancer is cancer that occurs in a man’s prostate— a small walnut-shaped gland that produces the seminal fluid that nourishes and transports sperm for  male reproductive system.

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Prostate cancer is one of the most common types of cancer in men. Most prostate cancers are slow growing; however, some grow relatively fast.Initially remains confined to the prostate gland,  where it may not cause serious harm. While some types of prostate cancer grow slowly and may need minimal or no treatment, other types are aggressive and can spread quickly.

Prostate cancer that is detected early — when it’s still confined to the prostate gland — has a better chance of successful treatment.

Factors that increase the risk of prostate cancer include: older age, a family history of the disease, and race. About 99% of cases occur in those over the age of 50. Having a first degree relative with  the disease increases the risk 2 to 3 fold. In the United States it is more common in the African American population than the Caucasian population. Other factors that may be involved include a diet  high in processed, red meat, or milk products or low in certain vegetables. Prostate cancer is diagnosed by biopsy. Medical imaging may then be done to determine if the cancer has spread to other  parts of the body.

Symptoms:
Early prostate cancer usually causes no symptoms. Sometimes, however, prostate cancer does cause symptoms, often similar to those of diseases such as benign prostatic hyperplasia. These include frequent urination, nocturia (increased urination at night), difficulty starting and maintaining a steady stream of urine, hematuria (blood in the urine), and dysuria (painful urination). A study  based on the 1998 Patient Care Evaluation in the US found that about a third of patients diagnosed with prostate cancer had one or more such symptoms, while two thirds had no symptoms.

Prostate cancer is associated with urinary dysfunction as the prostate gland surrounds the prostatic urethra. Changes within the gland, therefore, directly affect urinary function. Because the vas  deferens deposits seminal fluid into the prostatic urethra, and secretions from the prostate gland itself are included in semen content, prostate cancer may also cause problems with sexual function  and performance, such as difficulty achieving erection or painful ejaculation.

Advanced prostate cancer can spread to other parts of the body, possibly causing additional symptoms. The most common symptom is bone pain, often in the vertebrae (bones of the spine), pelvis,  or ribs. Spread of cancer into other bones such as the femur is usually to the proximal part of the bone. Prostate cancer in the spine can also compress the spinal cord, causing leg weakness and  urinary and fecal incontinence.

Causes:
The  causes of prostate cancer  is still not very clear.
Doctors know that prostate cancer begins when some cells in your prostate become abnormal. Mutations in the abnormal cells’ DNA cause the cells to grow and divide more rapidly than normal cells  do. The abnormal cells continue living, when other cells would die. The accumulating abnormal cells form a tumor that can grow to invade nearby tissue. Some abnormal cells can break off and  spread (metastasize) to other parts of the body.

Risk Factors:
The primary risk factors are obesity, age and family history. Prostate cancer is very uncommon in men younger than 45, but becomes more common with advancing age. The average age at the time  of diagnosis is 70. However, many men never know they have prostate cancer. Autopsy studies of Chinese, German, Israeli, Jamaican, Swedish, and Ugandan men who died of other causes have  found prostate cancer in 30% of men in their 50s, and in 80% of men in their 70s. Men who have first-degree family members with prostate cancer appear to have double the risk of getting the  disease compared to men without prostate cancer in the family. This risk appears to be greater for men with an affected brother than for men with an affected father.   Men with high blood pressure are more likely to develop prostate cancer.  There is a small increased risk of prostate cancer associated with lack of exercise. A 2010 study found that prostate basal cells were the most common  site of origin for prostate cancers.

Genetic factors :
Genetic background may contribute to prostate cancer risk, as suggested by associations with race, family, and specific gene variants. Men who have a first-degree relative (father or brother) with prostate cancer have twice the risk of developing prostate cancer, and those with two first-degree relatives affected have a fivefold greater risk compared with men with no family history. In the

United States, prostate cancer more commonly affects black men than white or Hispanic men, and is also more deadly in black men. In contrast, the incidence and mortality rates for Hispanic men  are one third lower than for non-Hispanic whites. Studies of twins in Scandinavia suggest that 40% of prostate cancer risk can be explained by inherited factors.

No single gene is responsible for prostate cancer; many different genes have been implicated. Mutations in BRCA1 and BRCA2, important risk factors for ovarian cancer and breast cancer in women, have also been implicated in prostate cancer. Other linked genes include the Hereditary Prostate cancer gene 1 (HPC1), the androgen receptor, and the vitamin D receptor.  TMPRSS2-ETS gene  family fusion, specifically TMPRSS2-ERG or TMPRSS2-ETV1/4 promotes cancer cell growth.

Two large genome-wide association studies linking single nucleotide polymorphisms (SNPs) to prostate cancer were published in 2008. These studies identified several SNPs which substantially  affect the risk of prostate cancer. For example, individuals with TT allele pair at SNP rs10993994 were reported to be at 1.6 times higher risk of prostate cancer than those with the CC allele pair. This

SNP explains part of the increased prostate cancer risk of African American men as compared to American men of European descent, since the C allele is much more prevalent in the latter; this SNP is located in the promoter region of the MSMB gene, thus affects the amount of MSMB protein synthesized and secreted by epithelial cells of the prostate.

Dietary factors:
While some dietary factors have been associated with prostate cancer the evidence is still tentative.  Evidence supports little role for dietary fruits and vegetables in prostate cancer occurrence. Red  meat and processed meat also appear to have little effect in human studies.  Higher meat consumption has been associated with a higher risk in some studies.

Lower blood levels of vitamin D may increase the risk of developing prostate cancer.

Folic acid supplements have no effect on the risk of developing prostate cancer.

Viral factors:
In 2006, a previously unknown retrovirus, Xenotropic MuLV-related virus or XMRV, was associated with human prostate tumors,  but subsequent reports on the virus were contradictory,  and the original 2006 finding was instead due to a previously undetected contamination.

Sexual factors:
Several case-control studies have shown that having many lifetime sexual partners or starting sexual activity early in life substantially increases the risk of prostate cancer. This correlation suggests  a sexually transmissible infection (STI) may cause some prostate cancer cases; however, many studies have unsuccessfully attempted to find such a link, especially when testing for STIs shortly  before or after prostate cancer diagnosis.  Studies testing for STIs a decade or more prior to prostate cancer diagnosis find a significant link between prostate cancer and various STIs (HPV-16, HPV-18 and HSV-2). This evidence could be explained by a yet-to-be-identified sexually transmissible infection and a long latency period between onset of infection and prostate cancer.

On the other hand, while the available evidence is weak,  tentative results suggest that frequent ejaculation may decrease the risk of prostate cancer.  A study, over eight years, showed that those  that ejaculated most frequently (over 21 times per month on average) were less likely to get prostate cancer.  The results were broadly similar to the findings of a smaller Australian study

Medication exposure:
There are also some links between prostate cancer and medications, medical procedures, and medical conditions. Use of the cholesterol-lowering drugs known as the statins may also decrease  prostate cancer risk.

Infection or inflammation of the prostate (prostatitis) may increase the chance for prostate cancer while another study shows infection may help prevent prostate cancer by increasing blood to the  area. In particular, infection with the sexually transmitted infections chlamydia, gonorrhea, or syphilis seems to increase risk. Finally, obesity  and elevated blood levels of testosterone   may increase the risk for prostate cancer. There is an association between vasectomy and prostate cancer however more research is needed to determine if this is a causative relationship.

Pathophysiology:
The prostate is a part of the male reproductive system that helps make and store seminal fluid. In adult men, a typical prostate is about 3 centimeters long and weighs about 20 grams. It is located in the pelvis, under the urinary bladder and in front of the rectum. The prostate surrounds part of the urethra, the tube that carries urine from the bladder during urination and semen during ejaculation.  Because of its location, prostate diseases often affect urination, ejaculation, and rarely defecation. The prostate contains many small glands which make about 20 percent of the fluid  constituting semen.  In prostate cancer, the cells of these prostate glands mutate into cancer cells. The prostate glands require male hormones, known as androgens, to work properly. Androgens  include testosterone, which is made in the testes; dehydroepiandrosterone, made in the adrenal glands; and dihydrotestosterone, which is converted from testosterone within the prostate itself.

Androgens are also responsible for secondary sex characteristics such as facial hair and increased muscle mass.

Prostate cancer is classified as an adenocarcinoma, or glandular cancer, that begins when normal semen-secreting prostate gland cells mutate into cancer cells. The region of prostate gland where  the adenocarcinoma is most common is the peripheral zone. Initially, small clumps of cancer cells remain confined to otherwise normal prostate glands, a condition known as carcinoma in situ or  prostatic intraepithelial neoplasia (PIN). Although there is no proof that PIN is a cancer precursor, it is closely associated with cancer. Over time, these cancer cells begin to multiply and spread to the  surrounding prostate tissue (the stroma) forming a tumor. Eventually, the tumor may grow large enough to invade nearby organs such as the seminal vesicles or the rectum, or the tumor cells may develop the ability to travel in the bloodstream and lymphatic system. Prostate cancer is considered a malignant tumor because it is a mass of cells that can invade other parts of the body. This invasion of other organs is called metastasis. Prostate cancer most commonly metastasizes to the bones, lymph nodes, and may invade rectum, bladder and lower ureters after local progression.

The route of metastasis to bone is thought to be venous as the prostatic venous plexus draining the prostate connects with the vertebral veins.

The prostate is a zinc-accumulating, citrate-producing organ. The protein ZIP1 is responsible for the active transport of zinc into prostate cells. One of zinc’s important roles is to change the metabolism of the cell in order to produce citrate, an important component of semen. The process of zinc accumulation, alteration of metabolism, and citrate production is energy inefficient, and  prostate cells sacrifice enormous amounts of energy (ATP) in order to accomplish this task. Prostate cancer cells are generally devoid of zinc. This allows prostate cancer cells to save energy not  making citrate, and utilize the new abundance of energy to grow and spread. The absence of zinc is thought to occur via a silencing of the gene that produces the transporter protein ZIP1. ZIP1 is now called a tumor suppressor gene product for the gene SLC39A1. The cause of the epigenetic silencing is unknown. Strategies which transport zinc into transformed prostate cells effectively  eliminate these cells in animals. Zinc inhibits NF-?B pathways, is anti-proliferative, and induces apoptosis in abnormal cells. Unfortunately, oral ingestion of zinc is ineffective since high  concentrations of zinc into prostate cells is not possible without the active transporter, ZIP1.

Loss of cancer suppressor genes, early in the prostatic carcinogenesis, have been localized to chromosomes 8p, 10q, 13q, and 16q. P53 mutations in the primary prostate cancer are relatively low  and are more frequently seen in metastatic settings, hence, p53 mutations are late event in pathology of prostate cancer. Other tumor suppressor genes that are thought to play a role in prostate  cancer include PTEN (gene) and KAI1. “Up to 70 percent of men with prostate cancer have lost one copy of the PTEN gene at the time of diagnosis”   Relative frequency of loss of E-cadherin and  CD44 has also been observed.

RUNX2 is a transcription factor that prevents cancer cells from undergoing apoptosis thereby contributing to the development of prostate cancer.

The PI3k/Akt signaling cascade works with the transforming growth factor beta/SMAD signaling cascade to ensure prostate cancer cell survival and protection against apoptosis. X-linked
inhibitor of apoptosis (XIAP) is hypothesized to promote prostate cancer cell survival and growth and is a target of research because if this inhibitor can be shut down then the apoptosis cascade  can carry on its function in preventing cancer cell proliferation.  Macrophage inhibitory cytokine-1 (MIC-1) stimulates the focal adhesion kinase (FAK) signaling pathway which leads to prostate  cancer cell growth and survival.

The androgen receptor helps prostate cancer cells to survive and is a target for many anti cancer research studies; so far, inhibiting the androgen receptor has only proven to be effective in mouse  studies.   Prostate specific membrane antigen (PSMA) stimulates the development of prostate cancer by increasing folate levels for the cancer cells to use to survive and grow; PSMA increases  available folates for use by hydrolyzing glutamated folates.

Diagnosis :
The American Cancer Society’s position regarding early detection is “Research has not yet proven that the potential benefits of testing outweigh the harms of testing and treatment. The American  Cancer Society believes that men should not be tested without learning about what we know and don’t know about the risks and possible benefits of testing and treatment. Starting at age 50, (45 if African American or brother or father suffered from condition before age 65) the man should  talk to the doctor about the pros and cons of testing so  the person can decide if testing is the right choice for  him.”

The only test that can fully confirm the diagnosis of prostate cancer is a biopsy, the removal of small pieces of the prostate for microscopic examination. However, prior to a biopsy, less invasive  testing can be conducted.

There are also several other tests that can be used to gather more information about the prostate and the urinary tract. Digital rectal examination (DRE) may allow a doctor to detect prostate  abnormalities. Cystoscopy shows the urinary tract from inside the bladder, using a thin, flexible camera tube inserted down the urethra. Transrectal ultrasonography creates a picture of the prostate  using sound waves from a probe in the rectum.

Prostate screening tests :

*Digital rectal exam (DRE). During a DRE, your doctor inserts a gloved, lubricated finger into your rectum to examine your prostate, which is adjacent to the rectum. If your doctor finds any
abnormalities in the texture, shape or size of your gland, you may need more tests.

*Prostate-specific antigen (PSA) test. A blood sample is drawn from a vein in your arm and analyzed for PSA, a substance that’s naturally produced by your prostate gland. It’s normal for a small  amount of PSA to be in your bloodstream. However, if a higher than normal level is found, it may be an indication of prostate infection, inflammation, enlargement or cancer.
PSA testing combined with DRE helps identify prostate cancers at their earliest stages, but studies have disagreed whether these tests reduce the risk of dying of prostate cancer. For that reason,  there is debate surrounding prostate cancer screening.

If an abnormality is detected on a DRE or PSA test, your doctor may recommend tests to determine whether you have prostate cancer, such as:

*Ultrasound. If other tests raise concerns,  the doctor may use transrectal ultrasound to further evaluate your prostate. A small probe, about the size and shape of a cigar, is inserted into  the rectum. The probe uses sound waves to make a picture of the  prostate gland.

*Collecting a sample of prostate tissue. If initial test results suggest prostate cancer, your doctor may recommend a procedure to collect a sample of cells from your prostate (prostate biopsy).

Prostate biopsy is often done using a thin needle that’s inserted into the prostate to collect tissue. The tissue sample is analyzed in a lab to determine whether cancer cells are present.

Now to Determining whether prostate cancer is aggressive:

When a biopsy confirms the presence of cancer, the next step is to determine the level of aggressiveness (grade) of the cancer cells. In a laboratory, a pathologist examines a sample of the cancer cell to determine how much cancer cells differ from the healthy cells. A higher grade indicates a more aggressive cancer that is more likely to spread quickly.

The most common scale used to evaluate the grade of prostate cancer cells is called a Gleason score. Scoring combines two numbers and can range from 2 (nonaggressive cancer) to 10 (very aggressive cancer).

For  determining how far the cancer has spread:

Once a prostate cancer diagnosis has been made, your doctor works to determine the extent (stage) of the cancer. If your doctor suspects your cancer may have spread beyond your prostate, imaging tests such as these may be recommended:

*Bone scan
*Ultrasound
*Computerized tomography (CT) scan
*Magnetic resonance imaging (MRI)
*Positron emission tomography (PET) scan

It is not every person should have every test. The doctor will determine which tests are best for  every  individual case.

Once testing is complete,  the doctor assigns the stage and this helps determination of  treatment options. The prostate cancer stages are:

Stage I. This stage signifies very early cancer that’s confined to a small area of the prostate. When viewed under a microscope, the cancer cells aren’t considered aggressive.

Stage II. Cancer at this stage may still be small but may be considered aggressive when cancer cells are viewed under the microscope. Or cancer that is stage II may be larger and may have grown to  involve both sides of the prostate gland.

Stage III. The cancer has spread beyond the prostate to the seminal vesicles or other nearby tissues.

Stage IV. The cancer has grown to invade nearby organs, such as the bladder, or spread to lymph nodes, bones, lungs or other organs.

Treatment:
Prostate cancer treatment options depend on several factors, such as how fast your cancer is growing, how much it has spread and the overall health  and age of the patient , as well as the benefits  and the potential side effects of the treatment.Immediate treatment may not be necessary for men diagnosed with very early-stage of  prostate cancer. Some men may never need treatment. Instead, doctors sometimes recommend active  surveillance.

In active surveillance, regular follow-up blood tests, rectal exams and possibly biopsies may be performed to monitor progression of your cancer. If tests show your cancer is progressing, you may opt for a prostate cancer treatment such as surgery or radiation.

Active surveillance may be an option for cancer that isn’t causing symptoms, is expected to grow very slowly and is confined to a small area of the prostate. Active surveillance may also be

considered for a man who has another serious health condition or an advanced age that makes cancer treatment more difficult.

Active surveillance carries a risk that the cancer may grow and spread between checkups, making it less likely to be cured.

For other cases the the following treatment is recomended:

*Radiation therapy : Radiation therapy uses high-powered energy to kill cancer cells. Prostate cancer radiation therapy can be delivered in two ways:

Radiation that comes from outside of  the body (external beam radiation). During external beam radiation therapy, the patient   lie on a table while a machine moves around the body, directing high-

powered energy beams, such as X-rays or protons, to   prostate cancer.The patient  typically undergo external beam radiation treatments five days a week for several weeks.

Radiation placed inside  the body (brachytherapy). Brachytherapy involves placing many rice-sized radioactive seeds in your prostate tissue. The radioactive seeds deliver a low dose of radiation

over a long period of time. The doctor implants the radioactive seeds in patient’s prostate using a needle guided by ultrasound images. The implanted seeds eventually stop giving off radiation and  don’t need to be removed.

Side effects of radiation therapy can include painful urination, frequent urination and urgent urination, as well as rectal symptoms, such as loose stools or pain when passing stools. Erectile dysfunction can also occur.

Hormone therapy:
Hormone therapy is treatment to stop  the patient’s body from producing the male hormone testosterone. Prostate cancer cells rely on testosterone to help them grow. Cutting off the supply of hormones may cause cancer cells to die or to grow more slowly.

Options of hormone therapy:
*Medications that stop the body from producing testosterone. Medications known as luteinizing hormone-releasing hormone (LH-RH) agonists prevent the testicles from receiving messages to make testosterone. Drugs typically used in this type of hormone therapy include leuprolide (Lupron, Eligard), goserelin (Zoladex), triptorelin (Trelstar) and histrelin (Vantas). Other drugs sometimes used include ketoconazole and abiraterone (Zytiga).

*Medications that block testosterone from reaching cancer cells. Medications known as anti-androgens prevent testosterone from reaching your cancer cells. Examples include bicalutamide (Casodex), flutamide, and nilutamide (Nilandron). The drug enzalutamide (Xtandi) may be an option when other hormone therapies are no longer effective.

Surgery to remove the testicles (orchiectomy).
Removing  the testicles reduces testosterone levels in the body.
Hormone therapy is used in men with advanced prostate cancer to shrink the cancer and slow the growth of tumors. In men with early-stage prostate cancer, hormone therapy may be used to shrink tumors before radiation therapy. This can make it more likely that radiation therapy will be successful.

Side effects of hormone therapy may include erectile dysfunction, hot flashes, loss of bone mass, reduced sex drive and weight gain.

Surgery to remove the prostate:
Surgery for prostate cancer involves removing the prostate gland (radical prostatectomy), some surrounding tissue and a few lymph nodes. Ways the radical prostatectomy procedure can be performed include:

*Using a robot to assist with surgery. During robot-assisted surgery, the instruments are attached to a mechanical device (robot) and inserted into  the abdomen through several small incisions. The surgeon sits at a console and uses hand controls to guide the robot to move the instruments. Robotic prostatectomy may allow the surgeon to make more-precise movements with surgical tools than is possible with traditional minimally invasive surgery.

*Making an incision in  the abdomen. During retropubic surgery, the prostate gland is taken out through an incision in  the lower abdomen. Compared with other types of prostate surgery, retropubic prostate surgery may carry a lower risk of nerve damage, which can lead to problems with bladder control and erections.

*Making an incision between  the anus and scrotum. Perineal surgery involves making an incision between  the anus and scrotum in order to access  the prostate. The perineal approach to surgery may allow for quicker recovery times, but this technique makes removing the nearby lymph nodes and avoiding nerve damage more difficult.

*Laparoscopic prostatectomy. During a laparoscopic radical prostatectomy, the doctor performs surgery through small incisions in the abdomen with the assistance of a tiny camera (laparoscope). This procedure requires great skill on the part of the surgeon, and it carries an increased risk that nearby structures may be accidentally cut. For this reason, this type of surgery is not commonly performed for prostate cancer in the U.S. anymore.

The Doctor should decide which type of surgery is best for  the specific situation.

Radical prostatectomy carries a risk of urinary incontinence and erectile dysfunction. The riskfactors that the patient   may face based on the situation, the type of procedure the patient may select, according to his age, body type and  overall health.

Freezing of prostate tissue:
Cryosurgery or cryoablation involves freezing tissue to kill cancer cells.

During cryosurgery for prostate cancer, small needles are inserted in the prostate using ultrasound images as guidance. A very cold gas is placed in the needles, which causes the surrounding tissue to freeze. A second gas is then placed in the needles to reheat the tissue. The cycles of freezing and thawing kill the cancer cells and some surrounding healthy tissue.

Initial attempts to use cryosurgery for prostate cancer resulted in high complication rates and unacceptable side effects. However, newer technologies have lowered complication rates, improved cancer control and made the procedure easier to tolerate. Cryosurgery may be an option for men who haven’t been helped by radiation therapy.

Chemotherapy:
Chemotherapy uses drugs to kill rapidly growing cells, including cancer cells. Chemotherapy can be administered through a vein in your arm, in pill form or both.

Chemotherapy may be a treatment option for men with prostate cancer that has spread to distant areas of their bodies. Chemotherapy may also be an option for cancers that don’t respond to hormone therapy.

Biological therapy:
Biological therapy (immunotherapy) uses your body’s immune system to fight cancer cells. One type of biological therapy called sipuleucel-T (Provenge) has been developed to treat advanced, recurrent prostate cancer.

This treatment takes some of the patient’s own immune cells, genetically engineers them in a laboratory to fight prostate cancer, then injects the cells back into your body through a vein. Some men do respond to this therapy with some improvement in their cancer, but the treatment is very expensive and requires multiple treatments.

Alternative therapy:
It is believed that regular Yoga exercise with Pranayama  and Meditation under the guideline of some expart  may help a lot to cope with the distress of the patient.

Prevention:
Diet and lifestyle

The data on the relationship between diet and prostate cancer is poor.   In light of this the rate of prostate cancer is linked to the consumption of the Western diet.  There is little if any evidence to support an association between trans fat, saturated fat and carbohydrate intake and risk of prostate cancer.  Evidence regarding the role of omega-3 fatty acids in preventing prostate cancer does not suggest that they reduce the risk of prostate cancer, although additional research is needed. Vitamin supplements appear to have no effect and some may increase the risk.  High calcium intake has been linked to advanced prostate cancer. Consuming fish may lower prostate cancer deaths but does not appear to affect its occurrence.  Some evidence supports lower rates of prostate cancer with a vegetarian diet.  There is some tentative evidence for foods containing lycopene and selenium.  Diets rich in cruciferous vegetables, soy, beans and other legumes may be associated with a lower risk of prostate cancer, especially more advanced cancers.

Men who get regular exercise may have a slightly lower risk, especially vigorous activity and the risk of advanced prostate cancer.

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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/Prostate_cancer
http://www.mayoclinic.org/diseases-conditions/prostate-cancer/basics/definition/con-20029597

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Lupus Nephritis

 

Alternative Names: Nephritis – lupus; Lupus glomerular disease

Definition:
Lupus nephritis is an inflammation of the kidney caused by systemic lupus erythematosus (SLE), a disease of the immune system. Apart from the kidneys, SLE can also damage the skin, joints, nervous system and virtually any organ or system in the body.

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Symptoms:
General symptoms of lupus include malar rash, discoid rash, photosensitivity, oral ulcers, nonerosive arthritis, pleuropericarditis, renal disease, neurological manifestations, and haematological disorders.

Clinically, SLE usually presents with fever, weight loss (100%), arthralgias, synovitis, arthritis (95%), pleuritis, pericarditis (80%), malar facial rash, photodermatosis, alopecia (75%), anaemia, leukopaenia, thrombocytopaenia, and thromboses (50%).

About half of cases of SLE demonstrate signs of lupus nephritis at one time or another. Renal-specific signs include proteinuria (100%), nephrotic syndrome (55%), granular casts (30%), red cell casts (10%), microhematuria (80%), macrohematuria (2%), reduced renal function (60%), RPGN (30%), ARF (2%), hypertension (35%), hyperkalemia (15%) and tubular abnormalities (70%).

The World Health Organization (WHO) developed a system to classify the six different stages of lupus nephritis:

Stage 1: no evidence of lupus nephritis:
In histology, Stage I (minimal mesangial) disease has a normal appearance under light microscopy, but mesangial deposits are visible under electron microscopy. At this stage urinalysis is typically normal.
Stage 2: mildest form, easily treated with corticosteroids:
Stage 2 disease (mesangial proliferative) is noted by mesangial hypercellularity and matrix expansion. Microscopic haematuria with or without proteinuria may be seen. Hypertension, nephrotic syndrome, and acute renal insufficiency are rare at this stage.
Stage 3: earliest stage of advanced lupus. Treatment requires high amounts of corticosteroids. The outlook remains favorable.

Stage 3 disease (focal lupus nephritis) is indicated by sclerotic lesions involving less than 50% of the glomeruli, which can be segmental or global, and active or chronic, with endocapillary or extracapillary proliferative lesions. Under electron microscopy, subendothelial deposits are noted, and some mesangial changes may be present. Immunofluorescence reveals the so-called “Full House” stain, staining positively for IgG, IgA, IgM, C3, and C1q. Clinically, haematuria and proteinuria is present, with or without nephrotic syndrome, hypertension, and elevated serum creatinine.
Diffuse proliferative lupus nephritis; photo shows the classic “flea-bitten” appearance of the cortical surface in the diffuse proliferative glomerulonephritides

Stage 4: advanced stage of lupus.

Stage 4 lupus nephritis (diffuse proliferative) is both the most severe, and the most common subtype. More than 50% of glomeruli are involved. Lesions can be segmental or global, and active or chronic, with endocapillary or extracapillary proliferative lesions. Under electron microscopy, subendothelial deposits are noted, and some mesangial changes may be present. Immunofluorescence reveals the so-called “Full House” stain, staining positively for IgG, IgA, IgM, C3, and C1q. Clinically, haematuria and proteinuria are present, frequently with nephrotic syndrome, hypertension, hypocomplementemia, elevated anti-dsDNA titres and elevated serum creatinine. There is the risk of kidney failure. Patients require high amounts of corticosteroids and immune suppression medications.
A wire-loop lesion may be present in stage III and IV. This is a glomerular capillary loop with subendothelial immune complex deposition that is circumferential around the loop. Stage V is denoted by a uniformly thickened, eosinophilic basement membrane. Stage III and IV are differentiated only by the number of glomeruli involved (which is subject to inherent sample bias), but clinically the presentation and prognosis are both expected to be more severe in stage 4 versus stage 3.
Stage 5:
Stage 5 (membranous lupus nephritis) is characterized by diffuse thickening of the glomerular capillary wall (segmentally or globally), with diffuse membrane thickening, and subepithelial deposits seen under electron microscopy. Clinically, stage V presents with signs of nephrotic syndrome. Microscopic haematuria and hypertension may also been seen. Plasma creatinine is usually normal or slightly elevated, and stage V may not present with any other clinical/serological manifestations of SLE (complement levels may be normal; anti-DNA Ab may not be detectable). Stage 5 also predisposes the affected individual to thrombotic complications such as renal vein thromboses or pulmonary emboli.Excessive protein loss and swelling. Doctors will treat with high amounts of corticosteroids. Doctors may or may not give immune-suppressing drugs.
A final stage is usually included by most practitioners, stage VI, or advanced sclerosing lupus nephritis. It is represented by Global sclerosis involving more than 90% of glomeruli, and represents healing of prior inflammatory injury. Active glomerulonephritis is usually not present. This stage is characterised by slowly progressive renal dysfunction, with relatively bland urine sediment. Response to immunotherapy is usually poor.

A tubuloreticular inclusion is also characteristic of lupus nephritis, and can be seen under electron microscopy in all stages. It is not diagnostic however, as it exists in other conditions. It is thought to be due to chronic interferon exposure.
Causes:
Systemic lupus erythematosus (SLE, or lupus) is an autoimmune disease. This means there is a problem with the body’s immune system.

Normally, the immune system helps protect the body from infection or harmful substances. But in patients with an autoimmune disease, the immune system cannot tell the difference between harmful substances and healthy ones. As a result, the immune system attacks otherwise healthy cells and tissue.

SLE may damage different parts of the kidney, leading to interstitial nephritis, nephrotic syndrome, and membranous GN. It may rapidly worsen to kidney failure.

Lupus nephritis affects approximately 3 out of every 10,000 people. In children with SLE, about half will have some form or degree of kidney involvement.

More than half of patients have not had other symptoms of SLE when they are diagnosed with lupus nephritis.

SLE is most common in women ages 20 – 40.
Diagnosis:
The diagnosis of lupus nephritis depends on blood tests, urinalysis, X-rays, ultrasound scans of the kidneys, and a kidney biopsy. On urinalysis, a nephritic picture is found and RBC casts, RBCs and proteinuria is found.

The World Health Organization has divided lupus nephritis into five stages based on the biopsy. This classification was defined in 1982 and revised in 1995.

* Class I is minimal mesangial glomerulonephritis which is histologically normal on light microscopy but with mesangial deposits on electron microscopy. It constitutes about 5% of cases of lupus nephritis. Renal failure is very rare in this form.[2]

*Class II is based on a finding of mesangial proliferative lupus nephritis. This form typically responds completely to treatment with corticosteroids. It constitutes about 20% of cases.[2] Renal failure is rare in this form.[2]

* Class III is focal proliferative nephritis and often successfully responds to treatment with high doses of corticosteroids. It constitutes about 25% of cases. Renal failure is uncommon in this form.

*Class IV is diffuse proliferative nephritis. This form is mainly treated with corticosteroids and immunosuppressant drugs. It constitutes about 40% of cases. Renal failure is common in this form.

* Class V is membranous nephritis and is characterized by extreme edema and protein loss. It constitutes about 10% of cases.[2] Renal failure is uncommon in this form.

Medicines are prescribed that decrease swelling, lower blood pressure, and decrease inflammation by suppressing the immune system: Patients may need to monitor intake of protein, sodium, and potassium. Patients with severe disease should restrict their sodium intake to 2 grams per day and limit fluid as well. Depending on the histology, renal function and degree of proteinuria, patients may require steroid therapy or chemotherapy regimens such as cyclophosphamide, azathioprine, mycophenolate mofetil, or cyclosporine.
Possible Complications:

*Acute renal failure
*Chronic renal failure
*End-stage renal disease
*Nephrotic syndrome
Treatment:

There is no cure for lupus nephritis. The goal of treatment is to keep the problem from getting worse. Stopping kidney damage early can prevent the need for a kidney transplant.

Treatment can also provide relief from lupus symptoms.

Common treatments include:

*minimizing intake of protein and salt
*taking blood pressure medication
*using steroids to reduce swelling and inflammation
*taking immune-suppression medicines like prednisone to reduce immune system damage to the kidneys

Extensive kidney damage may require additional treatment.

Drug regimens prescribed for lupus nephritis include mycophenolate mofetil (MMF), intravenous cyclophosphamide with corticosteroids, and the immune suppressant azathioprine with corticosteroids. MMF and cyclophosphamide with corticosteroids are equally effective in achieving remission of the disease. MMF is safer than cyclophosphamide with corticosteroids, with less chance of causing ovarian failure, immune problems or hair loss. It also works better than azathioprine with corticosteroids for maintenance therapy.

Prognosis:  How well you do depends on the specific form of lupus nephritis. You may have flare-ups, and then times when you do not have any symptoms.

Some people with this condition develop chronic kidney failure.

Although lupus nephritis may return in a transplanted kidney, it rarely leads to end-stage kidney disease.
Prevention: There is no known prevention for lupus nephritis.

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/Lupus_nephritis
http://www.nlm.nih.gov/medlineplus/ency/article/000481.htm
http://www.healthline.com/health/lupus-nephritis#Diagnosis3

Epilobium parviflorum

Botanical Name:Epilobium parviflorum
Family: Onagraceae
Genus: Epilobium
Species: E. parviflorumi
Kingdom: Plantae
Division: Magnoliophyta
Order: Myrtales

Common Names :Smallflower Hairy Willowherb or Willowherb

Habitat :Epilobium parviflorum grows  in most of Europe, including Britain, from Sweden to Northern Africa and Western Asia up to India, in USA and Canada.

Description:
Epilobium parviflorum  is a herbaceous perennial plant.

The biological form of the plant  is hemicryptophyte scapose, as its overwintering buds are situated just below the soil surface and the floral axis is more or less erect with a few leaves….

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Epilobium parviflorum reaches on average 30–80 centimetres (12–31 in) in height. The stem is erect and densely covered with hairs, especially in the lower part. The leaves are opposite, unstalked but not amplexicaul, lanceolate and toothed, rounded at the base, 4–10 centimetres (1.6–3.9 in) long. The tiny flowers are pale pink or pale purple, 6–7 millimetres (0.24–0.28 in) in diameter, with four petals, eight stamens and a 4-lobed stigma. Flowering occurs from June to August.  The hermaphroditic flowers are either self-fertilized (autogamy) or pollinated by insects (entomogamy). Fruit is a three-to seven-centimeter long capsule containing very small black seeeds (about 1 mm long), with white fibres that allow the dispersal by wind. This species is quite similar to Epilobium hirsutum, but the flowers are very smaller

Medicinal Uses:
Extracts of this plant have been used by traditional medicine in disorders of the prostate gland, bladder and kidney, having an antioxidant and antiinflammatory effect . Extracts of Epilobium have been shown to inhibit proliferation of human prostate cells in-vitro by affecting progression of the cell cycle.

Small-flowered willow herb has been used as remedies in folk medicine, particularly in Central Europe, for the treatment of prostate disorders and abnormal growths. This pleasant herb and flower tea was highly recommended by Austrian herbalist, Maria Treben, for ailing men with prostate abnormalities.  Enlarged prostate, prostatitis, kidney or bladder disorders, gastro-intestinal disorders, mouth mucus membrane lesions, rectal bleeding, menstrual disorders, cystitis, Preliminary (in vitro) studies at the Prostate Center of Vancouver found that very low concentrations of an extract from small-flowered willow herb tea, in the micrograms per ml level, was among the most active ever seen against abnormal cells and growths of the prostate. Several extracts from Epilobium parviflorum, were evaluated in biochemical assays with 5-alpha-reductase and aromatase, two enzymes involved in the etiology of benign prostatic hyperplasia (BPH). Aqueous extracts displayed inhibition of these enzymes and the active compounds identified were macrocyclic ellagitannins, oenothein A1, B1 and B2, which can make up to 14% of crude plant extracts. Out of a total of 92 plant phenolic extracts tested, small-flowered willow herb was also found to have high antioxidant activity.  Small-flowered willow herb tea is also recommended for treating urinary tract infections in women. Take as a tea for oral, vaginal, and intestinal candidias.  An ingredient of Swedish bitters.

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:
http://en.wikipedia.org/wiki/Epilobium_parviflorum
http://www.herbnet.com/Herb%20Uses_UZ.htm
http://en.wikipedia.org/wiki/File:Epilobium_parviflorum_0.7_R.jpg

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Transrectal Ultrasound and Biopsy of the Prostate

What is the test?
Your doctor is likely to recommend this test if you’ve had a rectal exam or blood tests that suggest that you might have prostate cancer. For this test, a urologist takes tissue samples from several places in your prostate, to be examined for cancer. A transrectal ultrasound helps the urologist see the prostate during the procedure.

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How do you prepare for the test?
Some doctors recommend that you have an enema before the test. Tell your doctor if you have any allergies, especially to antibiotics.

What happens when the test is performed?
In most cases, you lie on your side with your knees bent up to your chest. An ultrasound machine’s sensor-a short rod about the width around of two fingers-is covered with a condom and clear jelly and gently inserted into your rectum. You may feel some pressure similar to the sensation before a bowel movement. Once the sensor is in place, an image of your prostate appears on a video screen.

The ultrasound sensor surveys the whole prostate gland and pinpoints specific areas for biopsy. Then the doctor removes this ultrasound sensor and replaces it with a slightly smaller one. In addition to generating an ultrasound image, the smaller sensor has a small tube on its side called a needle guide. Your doctor points the needle guide at specific parts of your prostate. The guide releases a spring-loaded needle to take biopsies from different parts of the prostate. The spring-loading allows this needle to move into and out of the prostate very quickly. You are likely to feel some discomfort from each biopsy, but because the needle moves so quickly, any pain lasts only for a second at a time. Doctors usually collect multiple samples.Your doctor will probably give you antibiotics at the end of this procedure to prevent infection.

What risks are there from the test?
Many people have some blood in their urine or stool for a day or two after the biopsy. The only significant risk is the possibility of an infection in the prostate, but antibiotics can help prevent this.

Must you do anything special after the test is over?
Call your doctor if you develop a fever.

How long is it before the result of the test is known?
A pathologist will examine the biopsies under a microscope for cancer. This process usually requires several days.

For more knowledge & information you may click :-http://emedicine.medscape.com/article/457757-overview

Source:https://www.health.harvard.edu/fhg/diagnostics/transrectal-ultrasound-and-biopsy-of-the-prostate.shtml

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