Tuesday, December 23, 2014

Bodybuilding reduces lipodystrophy in patients with HIV

A common disease among HIV patients is lipodystrophy, which is characterized by irregular distribution of body fat, which causes the accumulation or loss of same in some areas. At the end of sessions, both lipodystrophy and high cholesterol and triglycerides showed improvement.

The author of the study, the physical educator Pedro Pinheiro Neto Paes says that nowadays, with the use of antiretroviral drugs, patients live longer and better with the AIDS virus, but prolonged use of medication has side effects such as lipodystrophy. Furthermore, it is common to high cholesterol and triglycerides. Because of lipodystrophy in the case of a maldistribution of body fat, the teacher thought the exercise as a way to combat the disease in order to verify the relationship between physical activity and negative variables altered by antiretroviral therapy.

Research volunteers for health education and physical activity in promoting quality of life of people living with HIV / AIDS conducted 36 training sessions spread over 12 weeks. Each session was made by heating, strength training and relaxation. At the end of the process, all variables showed a decrease negative. And besides, they also adopted a practice of regular physical activity that positively influenced the quality of life of this group of people. It was observed that lipodystrophy and triglycerides were the problems with most significant improvement.

What the author of the study highlights, however, is the improvement of self-esteem reported by them. The practice outside of our training sessions promoted the reintegration into society through physical activity, which was a great gain qualitative research. Although the quantitative effects have been very positive, the biggest complaint of them is still prejudice, which is decreased with this social integration. For the educator, it is important to encourage physical activity in this group because it shows an alternative therapy. That is, gives results and does not involve drugs.

When you think about losing fat, is usually the first association with aerobic exercises, including literature, but we went the other way: the strength training, says study author. He said this was one of the differentials of their study, who worked with high loads of strength: the patients came to lift more than 80% of its maximum capacity for each individual year, during the specific training.

Neto explains that aerobic exercises require much practice time for fat loss and ergogenic factor (calories burned) occurs mainly during the activity. Meanwhile, the activity of force causes the metabolic rate increases, and fat loss occurs throughout the day. And in addition to fat loss, there is still gain muscle mass.

Many note that water retention occurs due to the use of Deca Durabolin. This isn’t something you can do about, but the good news is that the total aromatase rate is just 20 percent of testosterone. You can limit the amount of water retention that occurs by using an anti-estrogen supplement. You may need to increase your anti-estrogen dose to limit the retention, but it could also mean that you are eating too many calories. Over-eating carbohydrates is common, and this leads to water holding. This happens with or without this anabolic steroid, so diet control remains extremely important. A remarkable property of Deca is its capability to develop collagen synthesis in addition to bone mineral content, which is an enormous benefit to athletes with joint maladies such as inflammation and connective tissue problems. Since it is a progestin, it aids the immune mediated anti-inflammatory process, and in so doing alleviates joint pain.

Deca results effectively stimulates weight gain in AIDS patients suffering from its wasting effect, athletes, and bodybuilders. Deca is the preferred anabolic steroid to use for cutting and bulking cycles. While the shorter estered version of Deca Durabolin or the chemical name of Nandrolone Phenylpropionate, is the preference to use for cutting cycles.

The fact that Deca Durabolin has a very long active life requires the administration of injections at intervals of one week, irrespective of total dose. Due to this fact, Deca Durabolin is routinely used for a period of no less than ten weeks, and customarily for twelve weeks.

Many users have noted they are dissatisfied when they first start taking Deca Durabolin. Despite being an anabolic steroid, you will not see large results straight away. The steroid just does not work that way. This is a slow process and you will need some patience. There are steroids out there that will do it quicker, but then there will also be more water retention rather than muscle mass. Dianabol and Anadrol over lead to weight gains of 20-30 pounds in a few weeks, but that is not going to be 20 to 30 pounds of muscle! Deca is stable and will lead to muscle mass increase instead of other weight, as long as you use it properly.

Side Effects:

Erectile dysfunction is considered one of the side effects that can result from Deca Durabolin. This can occur even when using testosterone supplements. Some individuals just believe that their bodies struggle to respond to this hormone, no matter how much they use. However, there are high chances that you are doing something wrong if you notice this issue with each use of the steroid. You could try to increase the amount of testosterone, but this can make the problem worse. You will now have more estrogenic activity in the body, which affects the dysfunction. Anti-estrogens can affect the sexual performance, especially those that are aromatase inhibitors.

It is extremely important to keep your estrogen to testosterone ratio at a healthy and correct level. Sexual dysfunction can occur if you have large testosterone doses without the aromatase inhibitors. The same effect can be gained from the exact opposite, while large amounts of aromatase inhibitors and large levels of testosterone can also cause the effect. You need to find the right balance for yourself.

Wednesday, December 17, 2014

Anabolic steroid and HIV therapy

Sometimes, athletes who use anabolic steroids may share the needles, syringes or other equipment they use to inject these drugs. By sharing needles, syringes or other equipment, a person becomes a high risk for HIV transmission. HIV is the virus that causes AIDS. If a person shares needles, syringes and other equipment to inject steroids into the vein (IV), in the muscles or under the skin, small amounts of blood from the person infected with HIV may be injected into the bloodstream of the next person to use the equipment.

HIV attacks the body's defense system, making the body less able to fight off infections and cancers. There's no vaccine or cure for HIV or AIDS. People who may have been exposed to HIV should be tested. If they find out they have the virus, they can start treatment early. You can't tell just be looking at someone if he or she has HIV. And, since someone can be infected with HIV for many years without having any symptoms, some people may not know they have HIV. Anyone who has ever shared a needle to shoot any drugs even once could become infected with HIV and should be tested.

These have shown some benefit in a variety of human disorders, including HIV-related muscle wasting and other catabolic conditions such as chronic obstructive pulmonary disease, severe burn injuries, and alcoholic hepatitis. Because of their diverse biological actions, anabolic steroids have been used to treat a variety of other conditions, including bone marrow failure syndromes, constitutional growth retardation in children, and hereditary angioedema.

Anabolic steroid side effect, safety, risks and danger:

Anabolic steroid therapy is associated with various side effects that are generally dose related, therefore, illicit use of mega doses for the purpose of bodybuilding and enhancement of athletic performance can lead to serious and irreversible organ damage. The most common side effects of anabolic steroids are some degree of masculinization in women and children, behavioral changes (eg, aggression), liver damage, and alteration of blood lipid levels and coagulation factors. Anabolic steroids could also raise levels of homo cysteine. Bodybuilders who used the muscle-building anabolic steroids have increased levels of homo cysteine, an amino acid tied to increased mortality, heart disease risk and blood vessel damage.

HIV (human immunodeficiency virus) is the virus that causes AIDS (acquired immune deficiency syndrome). The HIV retrovirus may be passed from one person to another when infected blood, semen, vaginal secretions or other bodily fluids come in contact with an uninfected person's broken skin or mucous membranes. People with HIV have what is called HIV infection and are fit and well. Some of these people will develop AIDS as a result of their HIV infection. Growth hormone is a popular bodybuilding and performance enhancing aid, and the use of recombinant human growth hormone (rHGH, or simply GH) to treat various conditions in HIV infection has been debated with excitement for years. Indeed it is licensed for the treatment of wasting syndrome in advanced stages of AIDS. GH is also a commonly used bodybuilding and performance enhancing drug, which can be purchased on the black market; used to help both muscle anabolism / strength and reduction in body fat levels. Both of these applications have possible significance in the treatment of HIV.

Other than in the treatment of wasting disease, results from the studies using rHGH to treat body changes associated with HIV and/or drugs used to treat HIV have been very favourable. One which has been studied extensively is the use of rHGH in reducing HIV-associated adipose redistribution syndrome (HARS). However, the positive effects of HGH treatment in HIV may be more direct. Several studies have proposed that rHGH may bolster the immune system in ways that might improve clinical outcomes in HIV. HIV-associated adipose redistribution syndrome (HARS)
HARS is a type of lipodystrophy (abnormal distribution of body fat), where there is accumulation of excess truncal fat and visceral adipose tissue, as opposed to regular gynoid (glutes and hips) or android (abdomen) deposition. This is observed in HIV infected people, moreso as virus load increases. Although not a debilitating condition in itself (indeed extra body fat can prolong life if followed by wasting), HARS is unpleasant for the individual, giving reduced confidence in body image; another negative aspect of the disease.

rHGH therapy has been shown to significantly reduce HARS, leading to an improved body image, and significant improvement in psychological well-being. Numerous studies have demonstrated the benefits of this, leading to rHGH being licesenced for the treatment of HARS in some countries. It should also be noted that improvement in psychological well-being could also contribute to a positive clinical outcome, in that it reduces the effects of wasting.

Immune system:

Of most interest in HIV therapy are the possible benefits of rHGH use on the immune system, since HIV's primary adverse effect is reduction in the immune system. It has been clearly demonstrated that rHGH does benefit the immune system, but the method by which it helps is still under debate. One theory is that rHGH may stimulate renewal of the thymus gland, an important organ in the immune system. This may, in turn, lead to improved immune health in people with HIV. Studies are now examining whether or not renewing thymus tissue leads to better health and longer survival.

The thymus is necessary for developing new T-lymphocytes, which are key immune cells in the defense against disease, and numbers of which steadily reduce in HIV as infection progresses. In particular the thymus gland is involved in the development of CD4+ and CD8+ cells, and it is the CD4+ level which is a very critical marker in HIV outcome. Without some thymus activity, immune reconstitution that produces a wide range of functional CD4+ cells is not believed to be possible. Thus, the state of the thymus in HIV disease and how therapies affect it are of great interest to those researching ways to restore the immune system.

Napolitano et al (2002) researched rHGH and its impact on the thymus in HIV. Doses ranged from 1.5 (4.5IU) to 3.0mg (9IU) per day for 6–12 months in healthy HIV volunteers. After six months, marked increases in thymus mass were noted, beyond what has been seen using anti-HIV therapy alone. This increase was sustained during the course of rHGH therapy and correlated with a higher CD4+ count, suggesting that the thymus is functioning properly and helping make new T-cells, further suggesting a stronger immune system. When rHGH was stopped, there was a loss of thymus mass; however, CD4+ cell count increases seen over the course of therapy were sustained despite this loss of mass.

Napolitano later (2003) did a twenty-person study using 3mg (9IU) rHGH a day injected under the skin (subcutaneous injection). This was followed by 1.5mg (4.5IU) rHGH a day for another six months, for a total of one year of daily therapy. Of the 20 volunteers (all of whom stayed on anti-HIV therapy during the study), ten took one year of rHGH according to the schedule described above while the other ten were merely observed. After one year, the group on rHGH stopped therapy and were observed for a second year, while the group who hadn't taken rHGH therapy then started one year of it. The size of the thymus increased in those on rHGH during the first year, but not among the second group. Those on rHGH had a significant increase in thymus mass while those only on anti-HIV therapy actually had a slight decrease. Interestingly the most pronounced increase in both naïve and total CD4+ cell counts were seen among those on rHGH with a rise in the hormone IGF-1 (insulin-like growth factor-1) which is also associated with immune function. In subjects with pronounced increase in IGF-1 levels due to rHGH use, naïve cells increased by 95% and CD4+ increased by 25%.

Tuesday, December 9, 2014

The anabolic steroids and Hepatitis C

The anabolic steroids have been studied as a treatment for wasting caused by HIV and have been shown to be safe and effective, helping the formation of lean muscle mass. To be most effective, anabolic steroid treatment should be combined with an exercise program of resistance (weight) training. Studies have mostly been restricted to men because of concerns about the side-effects of steroid treatment for women. It is estimated that as many as 40% of HIV-positive men who are ill because of HIV have low levels of testosterone (hypogonadism). Low testosterone can result in decreased appetite, depression, poor metabolism of food, and sexual problems, including the inability to obtain and maintain an erection.

A blood test can show if you have low levels of testosterone and your doctor may prescribe either a short course of oral testosterone replacement therapy, testosterone patches or testosterone gel. Although testosterone is usually considered to be the male sexual hormone, it also occurs naturally in women. Testosterone patches have been examined as a treatment for wasting caused by HIV in women. It was found that weight and quality of life improved for some of the women, and the development of male characteristics was not reported. Side-effects from testosterone replacement therapy are rare, but can include the shutting down of natural testosterone production, shrinking of the testicles, hair loss, increased sexual desire, and aggression. In women, male characteristics, such as the deepening of the voice, and facial hair may develop. Hepatitis C is usually transmitted through blood-to-blood contact. Needles, syringes and other equipment used to inject drugs, and equipment used to sniff drugs such as straws or banknotes, should never be shared.

The sexual transmission of hepatitis C is now an issue of concern. It used to be thought that this was very rare. However, there have been recent reports of increasing numbers of gay men testing positive for hepatitis C. Many of these men are HIV positive and their only risk activity appears to be unprotected anal sex. Sexual activity that carries a risk of contact with blood, such as rougher anal sex, use of sex toys and fisting, seems to have a particular risk of hepatitis C transmission. Group sex, especially in the context of drug use, is also an important risk factor. Using condoms correctly, every time you have sex, not sharing sex toys or washing them between use, and not sharing pots of lubricant can reduce the risk. Mother-to-baby transmission of hepatitis C is thought to be uncommon, but the risk is increased if the mother is also HIV positive. A high hepatitis C viral load increases the risk that a mother will pass on hepatitis C to her baby and, as with HIV, a caesarean delivery reduces the risk. It’s best not to share razors, hair and nail clippers, nail scissors or toothbrushes if you have hepatitis C.

Very few people experience symptoms when they are first infected with hepatitis C. When they do occur, symptoms include jaundice, diarrhoea and feeling sick. In the longer term, about 50% of people with hepatitis C will experience some symptoms. The most common ones are feeling generally unwell, extreme tiredness, weight loss, depression and intolerance of fatty food and alcohol. Although a small proportion of people infected with hepatitis C clear the infection naturally, about 85% will go on to develop chronic hepatitis C. About a third of people will develop severe liver disease within 15 to 25 years. The severity of disease can be affected by the strain of hepatitis C you are infected with. Men, people who drink alcohol, people who are infected with hepatitis C when they are already into middle age, and people with HIV seem to experience faster hepatitis C disease progression. Hepatitis C can cause liver fibrosis (hardening) and cirrhosis (scarring). This damages the liver to such an extent that it cannot work properly, causing jaundice, internal bleeding and swelling of the abdomen. Chronic infection with hepatitis C can cause liver cancer (hepatocellular carcinoma, or HCC). HCC is especially likely to happen in people with cirrhosis, particularly if they drink heavily. There’s also some evidence that smoking can speed up the rate of cirrhosis and increase the risk of liver cancer. Surgery is the most effective form of treatment for liver cancer, but  other options include chemotherapy and treatment with drugs.

You should be tested soon after your diagnosis with HIV to see if you are also infected with hepatitis C. Unlike hepatitis B, there is no vaccine against hepatitis C. If you are in a group at high risk of infection with hepatitis C, it’s recommended that you have regular tests to see if you have been infected. A test is available to measure hepatitis C viral load. Unlike the HIV viral load test, this is not an indicator of when to start treatment. However, it is used to show how effective treatment any hepatitis C is being and how long it should continue. Liver function tests can give an indication of the extent to which hepatitis C has damaged your liver. Liver ultrasounds and biopsies may also be used. People co-infected with HIV and hepatitis C are more likely to develop liver damage than people who are only infected with hepatitis C. However, hepatitis C does not increase your risk of becoming ill due to HIV or responding less well to HIV treatment.

HIV treatment can be used safely and effectively if you are co-infected with HIV and hepatitis C. HIV treatment that suppresses viral load and increases your CD4 cell count can slow the rate of HCV-related liver damage. However, you may be at greater risk of experiencing the liver side-effects which some anti-HIV drugs can cause, and you and your doctor should have this in mind when selecting which anti-HIV drugs to take. It also seems to be the case that people co-infected with HIV and hepatitis C are at greater risk of developing some of the metabolic disorders which anti-HIV drugs can cause (particularly insulin resistance and diabetes).

Drugs are available for the treatment of hepatitis C and you should receive your treatment and care from doctors who are expert in the treatment of both HIV and hepatitis C. This may mean that, as well as seeing an HIV doctor, you also need to see a specialist liver doctor. If you have both HIV and hepatitis C, you should be assessed to see if you would benefit from starting hepatitis C treatment. If you and your doctor decide that you will start hepatitis C treatment now, and your CD4 cell count is between 350 and 500, you should start hepatitis C treatment first, then start HIV treatment. If your CD4 cell count is between 350 and 500 and you don’t yet need treatment for hepatitis C, you should start HIV treatment. If your CD4 cell count is under 350, you should start HIV treatment before starting hepatitis C treatment. A number of anti-HIV drugs have interactions with drugs used to treat hepatitis C. The choice of anti-HIV drugs you take will need to be made with these possible interactions in mind.

Before you start treatment for hepatitis C, it is important to know which strain, or genotype, of hepatitis C you have been infected with, as this can predict your response to treatment and the amount of time you will need to take treatment for. There are several hepatitis C genotypes. Type 1 is most common in the UK, and unfortunately responds least well to the currently available treatments for hepatitis C. Genotype 4 is also harder to treat. People with genotypes 2 or 3 respond better to treatment. However, there are new HCV drugs available, and more in development, which should improve the chances of a cure for people with harder-to-treat genotypes.

Factors such as your age, gender, how long you have had hepatitis C, the degree of liver damage and whether cirrhosis has developed are also important in predicting if treatment is likely to be effective. Unlike HIV treatment, treatment for hepatitis C is not lifelong. It consists of 24 or 48 weeks of treatment, and the length of treatment you receive will depend on the hepatitis C genotype you are infected with. A test after twelve weeks of treatment can predict if you are going to respond to treatment. Drugs are available for the treatment of hepatitis C. The backbone of treatment consists is pegylated interferon and ribavirin. These are taken in combination with an anti-HCV protease inhibitor. This sort of triple combination has been found to be much more effective than dual therapy with pegylated interferon and ribavirin alone. The aim of hepatitis C treatment is to eradicate infection with hepatitis C completely. Other aims of treatment include normalising liver function, reducing liver inflammation and reducing further damage to the liver. If you are ill because of HIV, then the aim of hepatitis C treatment is likely to focus on improving your tolerance of anti-HIV drugs, reducing the risk of death from liver problems and improving your overall quality of life. Hepatitis C treatment can have unpleasant side-effects, including a high temperature, joint pain, weight loss, nausea and vomiting and depression. Other side-effects include disturbances in blood chemistry.

Tuesday, December 2, 2014

Arthritis and HIV-infected patients

Musculoskeletal syndromes that occur in HIV-infected patients include manifestations of drug toxicity, reactive arthritis, Reiter's syndrome, infectious arthritis, and myositis. Principles to keep in mind when evaluating an HIV-infected patient with a musculoskeletal syndrome include the following:

Any musculoskeletal syndrome in non-HIV infected patients can occur in HIV-infected patients, such syndromes may not be related to the HIV infection.
HIV infection can alter clinical presentation and course. Reactive arthritis, inflammatory arthritis, or musculoskeletal infections may be more severe in presentation and course in HIV-infected persons. In some cases, musculoskeletal infections may be more insidious and subtle in onset.
Ruling out or correctly diagnosing infections is especially important to prevent the spread of infection in an immunocompromised patient.
The probability of an opportunistic infection as a cause for a musculoskeletal complaint depends on the stage of the patient's HIV disease. At early stages (CD4 count above 300), opportunistic infections are unlikely, although resistance to common bacterial pathogens may be reduced.
Generally, diagnostic tests and treatment regimens for musculoskeletal syndromes are the same as when the syndromes occur in non-HIV infected patients, except that the patient's HIV-related medications may cause side effects and interactions that impact differential diagnosis and limit therapeutic options, and there should be a very high threshold to using immunosuppressive drugs.

Some risk factors for HIV infection are also risk factors for other conditions that may present as musculoskeletal syndromes. Examples include injection drug use and arthritis associated with hepatitis B virus infection or endocarditis, sexual promiscuity and the arthritis syndromes associated with sexually transmitted infections such as gonorrhea and chlamydia, and hemophilia and hemarthrosis. Clinicians need to examine HIV-infected patients who present with acute or subacute musculoskeletal pains for evidence of infection in the joints and muscles. Careful examination of the skin may reveal a fungal infection that has spread to the joints. Septic arthritis may be difficult to differentiate from reactive arthritis, but cultures of the synovial fluid and blood will be sterile in cases of reactive arthritis. Septic arthritis in HIV-infected injection drug users (IDUs) is most commonly due to Staphylococcus aureus and usually responds well to treatment. In patients with advanced HIV disease who are not IDUs, clinicians must always consider opportunistic infections in joints, bones, and muscles. HIV-infected patients with muscle pain and weakness must be evaluated for idiopathic polymyositis, myositis secondary to zidovudine (AZT) toxicity, and infectious pyomyositis. Although many clinicians believe that HIV infection predisposes patients to musculoskeletal infections and has a negative impact on the outcome of the therapy, this hypothesis is not yet proved.
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Both Reiter's syndrome and septic bursitis can cause a monarticular arthritis in an HIV-infected patient. Evaluation of synovial fluid is necessary to rule out infection and make a diagnosis. Clues to help the clinician differentiate between infectious and reactive arthritis in patients with HIV disease include a history of urethritis, cervicitis, diarrhea, or conjunctivitis, and findings of psoriasiform lesions, nail changes and enthesopathy (inflammation of tendinous insertions), as these may accompany a reactive arthritis.

The onset of reactive arthritis in HIV-positive patients usually occurs in the foot and ankle, and the common types of inflammation are enthesopathy (involving the Achilles tendon, plantar fascia, or anterior and posterior tibial tendons) and multidigit dactylitis. Synovitis is rare but may occur in joints of the lower extremities. In the upper extremities, dactylitis and enthesopathy occur in the tendinous insertions in the lower part of the arms. Cutaneous symptoms include psoriasiform rashes, keratoderma blennorrhagicum, and onychodystrophy.

In reactive arthritis, the synovial fluid is usually inflammatory, with a few thousand white blood cells and a synovial glucose level that is at least two thirds the serum glucose level. Gram stain or culture of synovial fluid is the only reliable way to make the diagnosis of a septic arthritis or bursitis. If the diagnosis is entertained, aspiration and culture should be performed immediately. If the synovial fluid is purulent, it may be prudent to initiate broad antibiotic coverage while waiting for the results of definitive synovial fluid cultures. Also, if the synovial fluid is initially unobtainable (as in axial joint infection), it is prudent to initiate antibiotic coverage. Blood cultures should be obtained during the work-up of the arthritis, as they may become positive before the synovial fluid cultures. HIV-infected patients who are at high risk for septic arthritis include IDUs and hemophiliacs. Clinicians must always consider and rule out acute infectious synovitis in these patients.

Gram-positive bacteria, such as S. aureus and Streptococcus pneumoniae, commonly found in non-HIV infected patients with septic arthritis and bursitis, are causative factors in most reported cases of septic arthritis and bursitis in HIV-infected persons. Infections with organisms not common to the skin have also been reported. One report described osteomyelitis in HIV-infected patients, but usually it results from direct extension from a septic joint. Clinicians must frequently re-examine HIV-infected patients treated for septic arthritis for evidence of worsening or unchanging symptoms and signs. If bone pain and fever continue despite antibiotic coverage, extension of the infection to the surrounding bone should be considered, surgical debridement may be necessary.

In most HIV-infected patients with acute joint or bursa infections, broad antibacterial coverage to cover common skin organisms (including staphylococcal and streptococcal infections) should be initiated. Patients with advanced HIV disease occasionally have opportunistic joint infections, such as sporotrichosis, cryptococcosis and Mycobacterium avium intracellulare. Often these patients have extraarticular features suggestive of such infections, including typical skin lesions. These opportunistic infections often present with a more indolent course than that of a bacterial septic arthritis. If extra articular features of fungal infection are present or hyphae or budding yeasts are seen on direct synovial fluid examination, the patient should receive standard doses of intravenous amphotericin B.