Car Accident Shoulder Injuries – What You Must Know

Shoulder injuries in a car accident are common. They are caused mostly by the jerking movements that occur in an accident and may be further aggravated by seat belt shoulder straps. Shoulder injuries may also be related to neck injuries. Understanding more about shoulder injuries will allow you to recognize them quickly and seek treatment to prevent further discomfort and problems.

Causes of Shoulder Injuries

In a car accident shoulder injuries can be caused in three main ways. The first is as a result of a neck injury. A neck injury can radiate pain down the arm due to nerves being injured. The injury to the neck will then cause problems in the shoulder.

The next cause is direct damage to the shoulder from impact during the crash. This causes immediate pain and is easily recognized.

The last cause is from whiplash. Whiplash is usually associated with the neck, but it can cause pain in the shoulders as well. It may not cause pain right away after the crash, but may develop over time.


Shoulder injuries are usually found through an x-ray or and MRI. Most shoulder injuries are not severe and merely require rest and pain medication for proper healing. If the injuries are more severe then surgery or extensive therapy may be needed.

The earlier treatment is sought for a shoulder injury, the better. Early recognition of a shoulder injury and early treatment help to insure the problem is cared for correctly and prevents further damage from occurring. You should always make sure that any medical care you receive is documented and that you keep a copy for your records.

What to do After an Accident

Since some shoulder injuries may not develop symptoms right away it is always smart to have a complete medical check following the accident. If you fail to get checked out and have your medical attention documented then you may not be able to recover damages later on if symptoms do appear.

When you are in an accident it is smart to exchange information with the other driver. You should get their name, address, telephone, number, insurance information and license information. Make sure that you do not speak with them about the actual accident. You should only speak with the police to give your statement. You may also wish to gather information from witnesses.

You want to document everything about the accident so that any shoulder injury found in the future that can be linked to the accident can be claimed. If you are careful in how you handle an accident you should be able to make a claim against the other person for your shoulder injury.

Shoulder injuries from a car accident are usually not too severe, but they are severe enough to make you lose time at work and to rack up medical bills that can be costly. It is important that if you suffer from a shoulder injury resulting from a car accident that you report it to the insurance and make a claim so you can recover your costs.

Cerebral Palsy and Erb’s Palsy

The birth of a child is one of life’s most treasured and joyous events. That joy can be tainted or destroyed when the child suffers a debilitating or fatal birth injury due to a medical error.

Most birth injuries are preventable by proper monitoring of both the mother and the fetus during pregnancy and delivery. Children who suffer birth injuries can be disabled for life, require extensive medical care immediately after delivery, and may require life-long care.

The physical, emotional, and financial hardships that families experience can be overwhelming and life-altering. In some cases one or both parents will have to quit their jobs to care for the child, sometimes for the rest of that child’s life.

Cerebral palsy

Cerebral palsy is caused by brain injury to a baby during pregnancy, delivery, or shortly after delivery. It affects muscle control and it can cause learning disabilities. Proper medical care and therapy are your child’s best hope of leading a normal life, but most children with cerebral palsy require life-long care.

Cerebral palsy will affect each child differently but some of the problems it can cause include speech impairment, visual impairment, hearing impairment, difficulty walking, difficulty eating, limited motor skills, paralysis, drooling, seizures, and incontinence.

Cerebral palsy causes include:

  • Lack of oxygen
  • Umbilical cord strangulation
  • Unreasonable delay in performing a c-section
  • Rh incompatibility
  • Bleeding in the brain
  • Infection in mother or baby during pregnancy
  • Inappropriate medications during pregnancy
  • Kidney and urinary tract infections in the mother
  • Severe jaundice
  • Stroke
  • Failure to respond to fetal distress
  • Inappropriate use of forceps
  • Failure to treat infant seizures

Erb’s palsy

Another common birth injury is Erb’s palsy. Erb’s palsy does not affect the brain. It affects the shoulder, arm, and hand. In most cases, Erb’s palsy can be treated with therapy and exercise. In about 20% of cases, surgery is required. Most children can make a full recovery, but some are permanently disabled.

Erb’s palsy is caused by an injury to the brachial plexus during delivery. It is entirely preventable. The brachial plexus is a nerve bundle between the neck and shoulder. This nerve bundle can be damaged by too much force during delivery when the baby’s should is wedged behind the mother’s pubic bone. This is called shoulder dystocia.

Caesarian section is the best way to prevent Erb’s palsy, but when shoulder dystocia is not detected early enough to perform a C-section, there are several delivery methods that doctors can used to help prevent the trauma.

There are many warning signs doctors should look for that indicate a high risk of shoulder dystocia including:

  • Obesity in the mother
  • Advanced age of mother
  • Short or small mother
  • Diabetes in the mother
  • Flat, contracted or exceptionally small pelvis in the mother
  • Above-normal weight gain during pregnancy
  • High pre-birth weight of the baby
  • Abnormally long gestation period
  • Prolonged labor
  • Breech position

Hiatal Hernia Massage – Useful Do It Yourself Tips

I did not know much about hiatal hernias’ until I thought I had one. A trip to the hospital is all it took to give me a wakeup call. I did not have one but the first thought the doctors had was that my symptoms matched. As it turned out, I had gall stones. After a 12-hour surgery and a 4-day hospital stay, I decided to do some research. If the situation arises, I now know what to do for it. The hiatal hernia massage is a tried and true method that you can do for yourself. The hiatus is the opening juncture where the esophagus passes through the diaphragm connecting the stomach to the mouth. I was never big on anatomy, so I for one found this very interesting. The diaphragm separates our chest cavity from our stomachs.

It seems that every school today is pitching ads for massage therapist training. I knew massage was a big thing for athletes and sore muscles but heartburn caused by this hernia, I was intrigued. To my way of thinking one of the hardest things to do is to adequately massage your own body. For this one problem I could not have been more wrong. As I soon learned, this technique is not a new one, just a little dusty from disuse. The hiatal hernia massage takes only minutes a day. One of the symptoms of having this condition is constipation. This blockage is more than likely the culprit in the first place. I’ll tell you why, not being able to eliminate the body’s waste products prevents normal flagellation. This then trapped gas expands, this causes that bloated feeling as the stomach diligently tries to process the meals you continue to eat it creates more gas. This expands the stomach even more eventually causing the muscles and surrounding tissues near the hiatus to weaken. When this happens, the gas pushes part of the stomach through this now fragile sheet. If left unchecked this bulge gets bigger and puts pressure on vital arteries and veins, that is why so many with this condition have poor circulation in their lower bodies. Before I take you through the steps of this massage, might I suggest that you take one week to relieve your constipation issues and get the blood circulating freely,  by releasing the pent up gases you remove the pressure on those arteries and veins.  This is not an overnight cure, it will take practice and diligence, but you can pull the stomach back through using the hiatal hernia massage technique. First sit in an upright position. Next find the bottom of your breast bone, then using the tips of your finger, both hands, go down about an inch or so. Now you are ready to begin. You’re going to apply steady pressure while pushing in, up and down. If it feels like a circular motion then you are doing it the correct way. As with exercising any muscle you may experience a little tenderness at first, don’t stop! Just reduce the number of repetition and times per day.  In a month or two you will see that the stomach is returning to its place. Say Good-bye hernia!  The hiatal hernia massage will make you think it’s a miracle, but it’s just plain common sense.

Some Common Problems Associated With Spinal Cord

<!– @page { margin: 2cm } P { margin-bottom: 0.21cm } –>

The spine is what determines how comfortably we walk, stand, sit or even rest. There are some problems associated with the spinal cord that cause a great deal of discomfort to the patient. Some of them are discussed below.

Cervical spondylosis

A common symptom is pain in the neck. It may be a natural consequence of aging for those above 50 years of age. Like the other parts of our body, bones in the neck also tend to progressively degenerate as we age. Cervical spondylosis may be a result of bony spurs besides problems with ligaments and discs. The spinal canal may tend to narrow leading to compression of the spinal cord which may pinch the nerves leading to the arms. Spinal cord compression can be a result of injuries as well. This may lead to pain ranging from mild discomfort to severe dysfunction.

Spinal cord damage

There are many ways in which the spinal cord can get damaged. It can get cut in an accident, compressed or get destroyed due to an infection. The spinal cord may also get damaged when its blood supply gets cut off, or it is affected by diseases like cervical spondylosis, spinal cord cysts or multiple sclerosis which tend to alter its nerve function.

Bony Dysfunction

Following spinal cord infection, joint as well as muscle contractures can occur rapidly which tends to complicate rehabilitation later on. Early stabilization of the spine fracture means early mobilization leading to fewer complications. Each complication increases the hospital stay as well as increasing the rehab stay.

Cardiovascular Disease

A major long-term risk of spinal cord injury is cardiovascular disease. People who are suffering from spinal cord injury tend to lead rather sedentary lives and are at a higher risk of cardiovascular disease. Thus, careful assessment of cardiovascular function as well as the encouragement of exercise programs is a necessary long-term aspect of spinal cord injury management and care.

Deep Vein Thrombosis (DVT)

Deep vein thrombosis (DVT) is a potentially severe complication of spinal cord injury. In fact, DVT in the lower leg is nearly universal during the early phase of rehabilitation. Thromboses in the thigh is of a great concern as there is a high risk of it becoming dislodged and passing through the vascular tree to the lungs, where a major obstruction of the arteries which lead to the lung can even be fatal.

Heterotopic Ossification (HO) and Cysts

Heterotopic ossification (HO) refers to the development of abnormal bone in non-skeletal tissue, mainly in the region of the hip and knee joints. It can occur in many spinal cord injured individuals and tends to develop within days following the injury or it may even take place after several months. Though there is usually no significant additional physical limitation, but in some patients, HO may lead to a major limitation of joint motion.

Symptoms include difficulty in the ability to perform activities of daily living, especially those activities which require bending at the hips. The other symptoms include increased spasticity, swelling of the entire leg, as well as elevated temperature.

These are but a few problems related to the dysfunction of the spinal cord itself and complications arising out of the dysfunction.

Shingles Distribution on the Skin

Shingles is a condition characterized by painful blisters that typically appear in a linear distribution on the skin following nerve pathways. Shingles is caused by reactivation of a previous infection with the varicella-zoster virus. Shingles is a herpes virus infection (herpes zoster) that usually affects a nerve, causing pain in one area of the body. Infection of the ganglia of the posterior roots of the spinal nerves or the fifth cranial nerve by the varcella-zoster virus (shingles), which also causes chicken pox; it is marked by a painful eruption of vesicles usually on one side of the body along the course of one or more cutaneous nerves.

Shingles is derived from the Latin and French words for belt or girdle, reflecting distribution of the rash in a broad band. This band is usually only on one side of the body and represents a dermatome—the area that a single sensory nerve supplies in the skin.

Today’s treatments provide a variety of ways to shorten the duration of a shingles outbreak and to control the associated pain. Sometimes, however, shingles leads to a chronic painful condition called post-herpetic neuralgia (PHN) that can be difficult to treat. Putting a medicated lotion (two brand names: Benadryl, Caladryl) on the blisters might reduce the pain and itching. Putting cool compresses soaked in an astringent liquid (two brand names: Bluboro, Domeboro) on the blisters and sores might make them hurt or itch less.

The first sign of shingles is often burning or tingling pain, or sometimes numbness or itch, in one particular location on only one side of the body. After several days or a week, a rash of fluid-filled blisters, similar to chickenpox, appears in one area on one side of the body. Shingles pain can be mild or intense. Some people have mostly itching; some feel pain from the gentlest touch or breeze. The most common location for shingles is a band, called a dermatome, spanning one side of the trunk around the waistline.

Yes, shingles is contagious. Shingles can be spread from an affected person to children or adults who have not had chickenpox. Instead of developing shingles, these people develop chickenpox. Once they have had chickenpox, people cannot catch shingles (or contract the virus) from someone else. Once infected, however, people have the potential to develop shingles later in life.

Doctors can distinguish shingles from chickenpox (or dermatitis or poison ivy) by the way the spots are distributed. Since shingles occurs in an area of the skin that is supplied by sensory fibers of a single nerve–called a dermatome–the rash usually appears in a well-defined band on one side of the body, typically the torso; or on one side of the face, around the nose and eyes. (Shingles’ peculiar name derives from the Latin cingulum, which means girdle or belt.) If a diagnosis is in doubt, lab tests can confirm the presence of the virus.

To help with the pain of shingles, your doctor might have you take an over-the-counter pain medicine like acetaminophen (one brand name: Tylenol) or ibuprofen (one brand name: Motrin). Aspirin is not recommended because using it might cause a liver problem called Reye’s syndrome.

Vaccines can help reduce the risk of shingles, while early treatment can help shorten a shingles infection and minimize the chance of complications. If shingles causes severe pain, your doctor might have you take a prescription pain medicine.

Good home care can help you feel better faster. Take care of any skin sores, and keep them clean. Take your medicines as directed. And use over-the-counter pain medicines to relieve pain.

Avoid contact with people until the rash heals. While you have shingles, you can spread chickenpox to people who have never had chickenpox. Be extra careful to avoid people with weak immune systems and pregnant women and babies who have never had chickenpox.

Causes of Butt Pain

There are many causes of buttocks or butt pain, depending on how you describe it.

Pain in the Buttock/Butt muscle – Do you have pain in the big muscle of your butt while sitting, standing, walking, or during sex or other physical exercise? If you push on the center of your butt muscle does it hurt worse? How about during massage when they rub you hard in that area – do you just about jump off the table in pain? Does the pain radiate down either or both legs? Is it sharp, dull, burning, or aching, there all the time? Does it keep you from sleeping? Is it crampy? All of these could be describing butt pain caused by your sciatic nerve.

What is the sciatic nerve? – The sciatic nerve is a big nerve that comes out of your spine at the lower back, runs through your butt muscle and down your legs. It can easily be irritated by stress. When stressed, your muscles become strained and squeeze down on that nerve, causing all sorts of symptoms and generally making your life pretty miserable.

Pain in low back/butt – The lower back and buttocks are closely connected, so often if you have pain in one area you will also have pain in the other. The sciatic nerve runs through both your lower back and your buttock. Some people have pain only in the lower back, some only the butt or just one butt cheek, some people have pain in the low back radiating down one butt muscle all the way down the leg. All of these describe a typical sciatic nerve issue.

Pain in your rectum (or butthole) – This is more than likely hemorrhoids. Hemorrhoids are veins in your rectum, or right outside of it, that become swollen, hard, and very sensitive. Sometimes you can even see the hemorrhoids if you aim your butt toward a mirror, bend over, and spread your butt cheeks. They may look like little, round purple balls (that is the vein,) or they might be red and swollen. (Google ‘hemorrhoids’ and select images.) Hemorrhoids are caused by sitting (truck drivers often suffer from them), bowel obstruction (straining while trying to defecate will create hemorrhoids over time), pregnancy (due to constipation and pressure from the growing baby), and dehydration. Lack of hydration is one of the main causes of constipation, and therefore, hemorrhoids. Drink 2 quarts of water, minimum, each day. Coffee, tea, and soft drinks don’t count. Buy Preparation H at your local drug store which will provide temporary relief of the itching, burning, and swelling. But to really get rid of them for good you have to intake more water to your diet, and more fiber. I like to drink 2-3 quarts of water per day PLUS eat lots of fresh fruits and vegetables. I don’t get hemorrhoids any longer because of these changes. If you think it is hemorrhoids, but it doesn’t go away after a couple weeks of drinking more water and curing your constipation, please see your physician. P.S. the toilet is NOT a library. Don’t sit there for hours and read – that is one of the main causes of hemorrhoids.

Pain or burning in the top of the gluteal cleft – If you have soreness, redness, itching, burning, and/or mild bleeding at the top of your butt crack, you could have a pilonidal cyst.

From Wikipedia: “Pilonidal cysts are quite painful, afflict men more frequently than women, and typically occur between the ages of 15 and 24. Although usually found near the coccyx, the condition can also affect the navel, armpit or penis.”

These cysts often get bacterial or fungal infections. To try treating it yourself, get an over-the-counter anti-bacterial cream and treat yourself twice a day after showering. If you still have the issue after a couple weeks, you might want to see your physician. I know, embarrassing. I had to go to the doctor once for an extremely painful hemorrhoid. Please check out Wikipedia for more on this issue.

Anne West is an author and publisher of self-help eBooks on natural healing methods, including buttock pain. Her passions are nutrition, self-healing, and finding natural solutions to optimum health that will provide vitality and longevity. Her bestselling eBook has sold thousands of copies worldwide.

Strep throat – How Long Does It Last?

Strep throat is considered to be the most common reaction of a sore throat and sometimes it improves by its own with any sort of treatment and antibiotics. Are you suffering from the strep throat, then you should visit the doctor to get a proper treatment for this? If doctor diagnosis the strep throat then he will definitely suggest you something to control your fever, pain, infection and to kill the bacteria. Read this article to know more about the strep throat and how long does strep throat last?


You will normally observe the symptoms of strep throat after several days after the exposure of the bacteria. A sore throat is the most common symptom of it. Apart from it, fever, stomach ache, headache, vomiting, and fatigue are other common symptoms of a sore throat.

Do antibiotics provide you relief from the strep throat?

Antibiotics are the best thing to reduce the duration and pain of the strep throat. The longer the time of strep throat will be the more infection will spread in your body. The reliving period after taking the antibiotics is 24 hours to 36. Apart from the antibiotics, doctors also recommend the throat lozenges, acetaminophen, and gargling with warm salt water to overcome the pain instantly.

How long does strep throat last?

If you like to take the antibiotics for the relief then it is good you will notice improvement quickly. One thing I want to know you that completes the full course of strep throat treatment don’t stop taking the medications after two or three times. This can be dangerous for your health and the chances are there that you will again face it after some days. So even though you feel good but, it’s important to complete the whole prescription cycle.

The symptoms of strep throat go away within 24 hours after starting the treatment but on the other hand, it may happen that this disease lasts longer for more than five days. If you are not taking any treatment for strep throat or not taking the medicine that has been prescribed by the doctor then the chances are there that you have to face the rheumatic fever.

In some cases, strep throat symptoms improve in 3-5 days regardless of the treatment that you prefer for it. The best thing about treating the strep throat with antibiotics is it reduces the complications risk. ; As compare to the adults the complications risk more in the children’s. According to one research, Strep throat normally goes within 3 to 7 days with or without treatment but doctors normally recommend you to treat it with the antibiotics even though you are not willing to take it.

To conclude, after starting the treatment, an individual is normally feeling better within 24 but one should complete the medication duration that is normally prescribed by the doctor to prevent the strep throat. You should rest at home in these days. Don’t go to work and school, drink water as much as you can, avoid ice and the things that can irritate your throat. Also, the best thing to do is gargling with warm salt water.

How to get rid of tonsil stones now

When bacteria and viruses are ingested by white blood cells, can develop a minor infection of the tonsils. This infection then stimulates the immune system to produce antibodies against future infections.

Sometimes the tonsils are not against bacterial or viral infection and swollen, becomes inflamed. The result is tonsillitis. Viral tonsillitis usually lasts 4 to 10 days it takes something more bacterial tonsillitis. If symptoms include sore throat, fever over 38.3 ° C and swollen lymph nodes, may be caused by streptococcus infection.

 Get rid of tonsil stones-

A number of viruses can cause tonsillitis, including Epstein-Barr virus. This is the same virus that causes infectious mononucleosis. Certain strains of bacteria can also cause tonsillitis. The most common culprit is the same bacteria that causes strep throat pain. It is Streptococcus pyogenes, or strep group A beta-hemolytic. Intimate contact with an infected person is at greater risk factor for tonsillitis. Viruses and bacteria tend to flourish where people – especially children – are in close contact for several hours each day, for example at school or kindergarten.
The most common problems that occur with tonsils and adenoids are recurrent or chronic infections and their significant increase (hypertrophy). Tonsillitis is an infection or inflammation of the tonsils. The tonsils are round and consist of lymphoid tissue. They are located on both sides of the neck, above and behind the tongue and part of the immune system. Treated with appropriate antibiotics, symptoms of bacterial tonsillitis should disappear in a few days. Surgery is necessary only if tonsillitis affects the child’s breathing or swallowing, or if it recurs frequently.

Acute tonsillitis is an infection of the tonsils caused by one or more types of bacteria or viruses. Acute tonsillitis is characterized by a gradual or rapid onset of pain in the neck, usually associated with fever. The patient may stop swallowing saliva, salivating, to complain of ear pain in swallowing or have bad breath. Tonsils become red-lit area, with or without a white-gray deposit (exudate). Swollen neck lymph nodes and fever may occur.

Chronic tonsillitis is a persistent infection of the tonsils. Repeated infections can cause the formation of small pockets (crypts) in the amygdala, which are home to bacteria. Frequently, these tombs was found smelling stones. These stones (tonsillitis) may contain large amounts of sulfur. When crushed, appears characteristic rotten egg smell that’s causing bad breath. They give the patient a feeling it has something that keeps the bottom of the neck.

Lipid Metabolism,Pathways and its disorders

Lipid Metabolism is nothing but a series of chemical reaction process responsible for the synthesis and breakdown of glycerides, sterols and phospholipids. Lipids are mostly comprised of oxygen, hydrogen and carbon. Glycerides are available in the form of fat which is stored as a fuel purpose, and the remaining two forms sterols and phospholipids where found as cholesterol. Glycerides exist in two forms, chylomicrons and lipoproteins for the purpose of yielding energy when consumed by the cell. Before consuming the glycerides, it must be hydrolyzed as it cannot be taken directly by the tissues.

By the use of carbohydrates, fat cells (adiposities), amino acids and diet, we can obtain fatty acids. These fatty acids are supplied through the body by the blood stream in the form of chylomicrons which are the easiest form to transform energy to the required cells.

Lipolysis, ketosis, lipogenesis and betaoxidation are the metabolic pathways of lipid metabolism.

Beta oxidation and Lipolysis were carried in the cell mitochondria for the removal of two carbons in the form of acetyl CoA from fatty acid cycle, and later enters into the citric acid cycle to produce energy packets (Adenosine triphosphate), water and co2. These are the output products of Lipolysis and beta oxidation metabolic pathways.
If the rate of change of ketones formation by the liver is in high rate due to prolonged starvation, then this ketosis metabolic pathway occurs. This process also occurs when large amount of fat foods are consumed with less carbohydrates content.
The metabolic pathway of lipogenesis occurs in the cytosol of cell membrane. Lipogenesis causes Triglyceride (basic form of glycerides) to synthesize in liver, intestinal mucosa and muscle tissues as these are the main sites for the occurrence of this process. The production of fatty acids is done from hydrolysis of some fats, oxidation of amino acids, glucose and also from the synthesis of acetyl CoA.
Lipid is the only nutrient that contains hydrogen which plays the key role for the formation of glycerides, sterols and phospholipids. Lipids are the organic compounds of fatty acids, glycerolipids, glycerophospholipids, sterol lipids, prenol lipids, saccharolipids and polyketides which are the essential nutrients in building the muscle tissue and organs. Glycerolipids are very essential for building the cell structures. If the presences of glycerolipids are in excess state then it was converted into fat and later used for energy metabolism.

The body exposes to prolonged starvation or illness due to the breakdown of lipids by the inadequate supply of energy .Brain tissues uses the preference of liver for utilizing the organic compounds of lipids in it. Liver cells and kidney cells are the only two organs to contain the lipogenesis pathway which are used for the conversion of this organic compound into fats.

The Lipid metabolism is carried in two path ways:
Lipid catabolism: Lipid catabolism is the process of breaking down the lipid groups (glycerides, sterols and phospholipids) into smaller units for the easy transfer of energy through blood to the cells. Lipid catabolism is also referred to as digestion process of nutrients. Carbon dioxide, water and ATP are the final products of lipid catabolism.

Lipid anabolism: lipid Anabolism is the process of grouping the smaller lipid groups into larger molecules for building up the organs and muscle tissues.
Lipid metabolism disorder causes severe damage to the major organs due to accumulation of excess fatty acids in cells and tissues of brain, liver, nervous system, spleen and bone marrow.
Neurological complications, pains in arms and legs, eye paralysis and muscle tone disease are caused due to the disorder of lipid metabolism.

Diabetic Skin Care

Diabetes mellitus is characterized by high blood glucose (hyperglycemia) which can be due to: a) decreased production of insulin (called Type I diabetes mellitus) due to destruction of the pancreas on an autoimmune basis or b) decreased peripheral sensitivity to insulin (called type II which also has some decreased production of insulin by the pancreas) associated with obesity and lack of physical activity. Only about 5-10% of the total have type I disease, the rest have type II.

The most recent statistics available (2005) reveal 20.8 million people (7% of the population) with diabetes of which 14.6 million were actually diagnosed leaving 6.2 million unaware of the presence of this serious disease. Moreover, its prevalence has increased 40% in the last decade and is expected to increase by 165% between 2000 and 2005 (figure 1). It has been estimated that fully 1/3 of the population born in 2000 will develop diabetes. In addition to patient suffering and disability, the economic impact in direct and indirect costs is enormous, amounting to $132 billion in 2002 representing 1/10th of all health care costs.

There were 224,092 deaths attributable to diabetes in the USA in 2002 (probably an underestimation). The risk for death in patients with diabetes is twice that for people of the same age without diabetes, and this decreased longevity is due to cardiovascular disease. Diabetes increases the risk of heart disease and stroke 2-4 fold over that for people without diabetes. Its microvascular complications of retinopathy, nephropathy, and neuropathy make diabetes mellitus the leading cause of blindness, end-stage renal disease, and non-traumatic lower extremity amputations in the U.S.A.2 The frequency of the last complication is increasing (figure 2).


The macrovascular and microvascular complications of diabetes are closely related to hyperglycemia and oxidative stress, which is when cells fail to detoxify the reactive oxygen species (ROS) produced during metabolism. Four hypotheses have been proposed to explain how hyperglycemia causes complications: 1) increased polyol pathway flux, 2) increased intracellular formation of advanced glycation end-products (AGE), 3) activation of protein kinase C (PKC) isoforms, and 4) increased flux through the hexosamine pathway.

A unifying concept is that hyperglycemia-induced mitochondrial superoxide overproduction activates these 4 pathways. Excess superoxide partially inhibits the glycolytic enzyme glyceraldehyde 3-phosphate dehydrogenase (GAPDH) thereby diverting upstream metabolites from glycolysis to pathways of glucose over-utilization. Superoxide anion achieves this by causing DNA strand breaks that result in activation of poly ADP ribose polymerase (PARP) which in turn ribosylates and deactivates GAPDH. By preventing their metabolism, this process increases energy substrates resulting in increased flux of dihydroxyacetone phosphate (DHAP) to diacylglycerol (DAG), an activator of PKC, and of triose phosphates to methylglyoxol, which is the main intracellular AGE precursor. Increased flux of fructose-6-phosphate to UDP-N-acetylglucosamine in the hexosamine pathway increases modification of proteins by O-linked N-acetylglucosamine and increased glucose flux through the polyol pathway consumes the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) and depletes GSH (reduced glutathione, a natural potent anti-oxidant).

Several mechanisms have been postulated to explain why increasing the polyol pathway flux is detrimental. These are sorbitol-induced osmotic stress, decreased (Na++K+) ATPase activity, increased cytosolic NADH/NAD+ and decreased cytosolic NADPH.

Activation of the hexosamine pathway results in intracellular glycosylation and donation of N-acetyl glucosamine to serine and threonine residues of transcription factors such as Sp1 resulting in increased production of factors such as plasminogen activator inhibitor-1 (PAI-1) and transforming growth factor beta 1 (TGF-beta 1).5

Production of intracellular AGEs damages target cells by three mechanisms. Intracellular proteins modified by AGEs have altered function (like neurotropism, axonal transport, and gene expression). Secondly, extra-cellular matrix components modified by AGE precursors interact abnormally with other matrix components and with the receptors for matrix proteins (integrins) on cells. Thirdly, plasma proteins modified by AGE precursors bind to AGE receptors (RAGE) on endothelial cells, mesangial cells, and macrophages inducing receptor-mediated production of ROS as a second messenger to activate the nuclear factor kappa B (NF-kappa B), a transcription factor causing pathological changes in gene expression.5

Hyperglycemia-induced activation of PKC has a number of pathogenic consequences by affecting expression of endothelial nitric oxide synthetase (eNOS), endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), TGF-beta 1, and PAI-1, and by activating NF-kappa B and NAD(P)H oxidases. Increased eNOS and decreased ET-1 decrease blood flow causing hypoxia. Increased VEGF causes increased vascular permeability and angiogenesis. Increased TGF-beta leads to increased collagen, fibronectin, extra-cellular matrix, and basement membrane resulting in capillary occlusion. Increased PAI-1 decreases fibrinolysis leading to vascular occlusion. Increased NF-kappa B causes an increase in pro-inflammatory gene expression. Increased NAD(P)H oxidase causes increased ROS (resulting in DNA damage, oxidation of polydesaturated fatty acids in lipids, and oxidation of amino acids in proteins). These pathogenic mechanisms can all be characterized as a result of ROS effects on genes and proteins.5

Diabetic Skin

The skin of the diabetic is prematurely aged and is subjected to the problems of neuropathy, macrovascular disease, and microvascular disease. In addition, diabetes is associated with poor wound healing, susceptibility to infection, and decreased cell-mediated immunity. This battle may go on unrecognized to the naked eye and dictates a keen vigilance by both doctor and patient to prevent the dreaded complications of this disease. The struggle is against oxidative stress and inflammation, ischemia and necrosis.

Clinical manifestations

1. Diabetic dermopathy is the most common dermatological manifestation of diabetes and is due to microvascular changes. Because it is associated with but not specific for diabetes mellitus, it serves as a marker for the disease. This dermopathy is most often seen in diabetic men over the age of 50 but may also be seen in euglycemic diabetics and healthy individuals. The lesion is so named because of typical changes in the microvasculature. Irregularly shaped patches of skin with a depressed surface are found primarily over the anterior aspect of the lower legs but may occur on the upper arms and thighs and over bony prominences. The lesions are light brown in color due to extravasated red blood cells and deposition of hemosiderin in histiocytes. They appear in crops and resolve over 12-18 months. Since the lesions are asymptomatic, no specific treatment is required except to protect the area from trauma and secondary infection.

2. The skin of the diabetic foot is usually dry due to decreased sweating as a result of the autonomic neuropathy of diabetes. Sweating normally helps hydrate the stratum corneum, and dry skin is prone to callus formation with cracking and fissuring.

3. The “diabetic foot” is due to neurovascular and ischemic changes. It is a very serious complication of this disease. Loss of sensation means that the diabetic patient is no longer able to sense and avoid injuring agents in the environment. Thermal trauma can have horrific results. Even minor mechanical trauma to the skin of the diabetic foot can result in blisters, sores, and ulcers. This is compounded by motor loss to the intrinsic muscles of the foot leading to deformities including a high plantar arch and “hammer toes.” Bony prominences are created at the heel, toes, and metatarsal heads that become pressure points over which the skin can break down. This can lead to ulceration; infection of skin, soft tissues, and bone (osteomyelitis); gangrene (which can be either “wet” due to necrosis with infection or “dry” due to necrosis without infection); and ultimately amputation. The skin over pressure points can become thickened as a callus or corn or develop blisters that can get infected. The skin between the toes can become macerated which fosters secondary infection by bacteria and fungi. The bones of the feet can degenerate producing fractures (Charcot foot). One dreaded complication from this is a “rocker-bottom foot” that often results in skin breakdown and infection. A “diabetic foot” is usually asymptomatic until late in the game. Special attention is required: the patient should inspect his or her feet daily to avoid the complication, and a physician with expertise in this field is required for optimal results.


Control of hyperglycemia: The first step in controlling hyperglycemia in type II diabetics is diet and exercise. Then oral hypoglycemic agents are added of which there are many. Ultimately, insulin may be required by injection. Insulin is the first therapeutic step in type I diabetics. Unfortunately, control of blood glucose is difficult particularly in type II patients probably related to poor compliance. It is at this level that the patient can be most helpful. Make sure the patient takes control of their blood glucose, exercises, has proper diet, attends to their skin, and uses appropriate medications. Patients should check their blood sugar often and their feet daily. The best results come from treatment based on pathogenesis, and prevention is the name of the game.


Corneotherapy is made possible by what is known as the 500 Dalton Rule. The 500 Dalton Rule is used in the development of topical drugs and trans-dermal delivery systems. The skin’s barrier is effective in blocking molecules with an atomic weight more than 500 Daltons, but molecules of less weight pass through the skin’s barrier. Topical drugs like cyclosporine, tacrolimus, and ascomycins can be effectively delivered through the skin because the molecules of these drugs are all smaller than 500 Daltons.

While the stratum corneum’s physicochemical barrier resists the penetrations of large molecules, smaller molecules with a molecular weight of less than 500 Daltons pass transcutaneously. Molecular size is an important factor governing passage of substances through the skin, giving substances with higher molecular weights self-limiting properties. Passive delivery of substances, due to their low molecular weight, provides novel delivery opportunities. Included in these low molecular weight substances are vitamins, amino acids, ?-3 and ?-6 essential fatty acids, and antioxidants like hydroxytyrosol.

Instructions for Patients to Prevent Diabetic Foot Problems
You should start taking good care of your feet. Set a time every day to check them. Now is the time for you to play an active role in your health care with these 10 steps:

1.Test your blood glucose often. Work with your health care team to keep your blood glucose in your target range with proper diet and exercise.
2.Avoid foot problems by early detection of changes before they get worse. Look at your bare feet daily for red spots, cuts, swellings, and blisters. If you cannot see the bottoms of your feet, use a mirror or ask someone for help.
3.Get active. Plan your physical activity program with your health care team.
4.Get informed. Ask your doctor about Medicare coverage for special shoes (orthotics).
5.Wash (not soak) your feet every day in lukewarm water and dry them carefully, especially between the toes.
6.Keep your skin soft and smooth. Rub a thin coat of skin cream over the tops and bottoms of your feet, but not between your toes.
7.If you can see and reach your toenails, trim them when needed. Trim your toenails straight across and file the edges with an emery board or nail file.
8.Wear shoes and socks at all times. Never go barefoot. Wear comfortable shoes that fit well and protect your feet. Check inside your shoes before wearing them. Make sure the lining is smooth and there are no objects inside.
9.Protect your feet from hot and cold. Wear shoes at the beach or on hot pavement. Don’t put your feet into hot water. Test water before putting your feet in it just as you would before bathing a baby. Never use hot water bottles, heating pads, or electric blankets. You can burn your feet seriously without realizing it.
10.Keep the blood flowing to your feet. Put your feet up when sitting. Wiggle your toes and move your ankles up and down for 5 minutes, two (2) or three (3) times a day. Don’t cross your legs for long periods of time. Don’t smoke!

Remedy® Description:

Clinical Pharmacology: The active ingredient in these preparations is dimethicone 1.5% that protects the skin. Olivamine® is a patent pending blend of antioxidants and anti-inflammatory agents that helps repair cell membranes and restore cells to a healthy state. Olivamine® contains the following:


3,4-dihdroxyphenylethanol (hydroxytyrosol: DOPET) is the major component in the phenolic fraction of olive oil. It is a hydro-soluble and lipid soluble molecule that is an efficient scavenger of peroxyl radicals. Experiments demonstrate that DOPET effectively counteracts the cytotoxic effects of reactive oxygen species (ROS) in various human cellular systems. In studies using DOPET pre-incubated cells, it was found that damage due to oxidative stress, such as lipid peroxidation and alterations of cell permeability, could be prevented and that DOPET exerted a protective effect against H2O2 induced oxidative hemolysis.


Altering cellular osmolality to a hyperosmotic state results in a decrease in adenosine triphosphate (ATP) allied with necrosis and resultant necrosis. Glycine is a cytoprotectant against injury by ATP-depletion. Glycine protects ATP-depleted cells by low affinity interactions with multimeric channel protein, stabilization of which may other wise lead to formation of pathological pores. Such porous defects in membranes of ATP-depleted cells have been characterized recently, showing definable exclusion limits for molecules of increasing sizes. Glycine provided during ATP-depletion blocked the development of membranous pores completely. The relationship between necrosis and an extracellular depletion of ATP makes its protection and restoration imperative during the prelethal stages of necrosis or early necrosis.


L-Taurine can act as a direct antioxidant that scavenges or quenches oxygen free radicals intracellularly to block ROS mediated cell death. The beneficial effects of the ROS-scavenging capacity of L-taurine include attenuation of lipid peroxidation, reduction of membrane permeability, and inhibition of intracellular oxidation in different cells. Taurine prevents high glucose induced apoptosis in endothelial cells thru ROS inhibition and stabilization of intracellular calcium. Apart from its effect on antioxidant defense, L-taurine also functions as a principle modulator of intracellular Ca2+ homeostasis.


In research conducted by the Department of Microbiology and Immunology, SUNY Buffalo School of Medicine, Buffalo, NY, and the Free Radical & Radiation Biology Program, Department of Radiation Oncology, the University of Iowa, Iowa City, Iowa, we investigated the hypothesis that NAC-induced free radical-signaling delays G0/G1 cells progression to S phase by regulating the cell cycle regulatory protein cyclin D1 and the free radical-scavenging enzyme manganese superoxide dismutase (MnSOD). Treatment with NAC resulted in increased cellular glutathione levels indicating a shift to a more reducing environment. This shift in cellular redox environment was associated with delayed progression from G0/G1 to S. NAC treatment resulted in a decrease in cyclin D1 and an increase in MnSOD protein levels. The absence of NAC-induced G1 arrest in fibroblasts over-expressing cyclin D1 (or a non-degradable mutant of cyclin D1-T286A) indicates cyclin D1 regulates this delay in G0/G1 to S progression. These results support the hypothesis that cellular redox environment regulates cellular proliferation via regulating cell cycle regulatory protein levels. Furthermore, our results also suggest that inclusion of NAC in skin care formulations might help in appropriate wound healing by controlling proliferation and preventing scarring.


DNA synthesis is a vital part of cell life. In studies done in vivo and in vitro, L-proline was found to be the only amino acid that was involved in the stimulation of DNA synthesis. Further, epidermal growth factor (EGF) elicited no response without the addition of L-proline. Proline-deficient media such as Leibovitz’s L-15, Eagle’s minimal essential, and Dulebecco’s modified minimal essential did not induce DNA synthesis. However, using media such as Williams E, McCoy’s 5A and Ham’s F-12, which are rich in L-proline, there was DNA synthesis and marked proliferation. L-Proline is essential for the induction of cellular proliferation in vivo and in vitro through its effect on synthesis of intracellular collagen.

Vitamin B6 (Pyridoxine)

The term vitamin B6 is used to describe all biologically inter-convertible forms of pyridoxine including pridoxine, pyridoxal, pyridoxal 5-phosphate, and pyridoxamine. Vitamin B6 is an essential co-factor in numerous enzymatic reactions involved primarily in amino acid metabolism. In addition, vitamin B6 functions as an antioxidant by interacting with singlet molecular oxygen during oxidative stress.

Vitamin B3 (Niacinamide)

Niacinamide is a precursor of the coenzyme nicotinamide adenine dinucleotide (NAD+) used to generate ATP in the mitochondrial electron-transport chain. Niacinamide is involved in DNA integrity and maintains phosphatidylserine membrane asymmetry to prevent cellular inflammation and phagocytosis. Current research demonstrates that niacinamide prevents the induction of caspase-8, caspase-1, and caspase-2 activities during cellular injury. The cytoprotectant effects of niacinamide are involved in the maintenance and preservation of cellular membranes.

Methylsulfonylmethane (MSM)

Methylsulfonylmethane (MSM) is a naturally occurring organic compound containing 34% elemental sulfur. Sulfur is critical in the formation of collagen. The flexibility of bonds between cells, including skin, is dependent upon sulfur. MSM provides a bioavailable from of sulfur and supports the body’s ability to produce N-acetyl-L-cysteine and L-taurine that are sulfur-containing amino acids. MSM is an important volatile component in the sulfur cycle. Topically applied MSM is keratolytic through the formation of hydrogen sulfide. MSM aids in wound healing via keratin. Compounds containing sulfur are found in all body cells and are indispensable for life. Low levels of MSM are implicated in slow wound healing.

Indications and Usage

Remedy® with Olivamine® temporarily protects and helps relieve chapped or cracked skin in patients with dry skin or diabetes mellitus. It is useful in prevention of skin complications from diabetes.


Do not use products on deep or puncture wounds, animal bites, or serious burns.


These products are recommended for external use only.


When using this product do not get into eyes. Stop use and ask a physician if the condition worsens, symptoms last longer than 7 days, or symptoms clear up and then return within a few days. Keep out of reach of children. If swallowed, get medical help or contact a Poison Control Center right away. Protect the products from freezing and excessive heat.

Adverse Reactions

An allergic skin rash is possible with any of the components. If redness, itching, or hives occur, stop the product and seek medical care.

Dosage and Administration

Apply cleansing lotion to wet or dry skin and rub gently. Rinse or wipe with a moistened cloth. The cleanser acts without lathering. Apply the cream liberally until the entire area is covered. Both the cleansing lotion and the repair cream can be used as needed.

Bodybuilding Tactics Applied to the Obese

I used to interview elite bodybuilders on their training and eating for a living and did this for years and years. One reoccurring theme that kept popping up when talk turned to diet/nutrition was how much food top bodybuilders packed away on a daily basis. These men taught their bodies how to handle continually greater amounts of calories without becoming fat. Contrast this with the typical obese person who eats one meal a day and adds body fat at the drop of a hat. I am working with a crew of obese folks and having great success using modified bodybuilder eating tactics to help the obese lose body fat.

The first order of business for the obese is to establish a multiple meal schedule. The obvious advantage to this strategy is it divides the daily calories in smaller chunks. I require the obese person to eat every three hours and this usually works out to five feedings a day. Secondly we insist they clean up the food selections. Some foods are easily converted into body fat (sugar foods, manmade foods and saturated fat) and some foods are near impossible for the body to convert into fat (lean protein, fibrous carbohydrates). The body’s metabolism kicks into high gear to digest protein and fiber – creates what is called the thermogenic effect of food. Body temperature actually increases when the digestive system is faced with the daunting task of breaking down hard to digest protein and fiber.

Multiple meals allow the body to deal with fewer calories at any one sitting and the repeated practice of eating 5-6 meals a day teaches the body to become adept at digesting and distributing food. Better to eat 3,000 “clean” calories a day divided into six five hundred-calorie daily meals than one 1,500 calorie mega-dirty fast-food meal.

The results are astounding when the obese buy into the approach. I have one male who has lost 40-pounds of bodyweight in 40 days while simultaneously adding 12-pounds of muscle. He started at 240 and yesterday he weighed 200. This is far more impressive because didn’t lose muscle in the process, he added muscle in the process. This was no ex-jock loaded with muscle memory; this is a 48-year old man with zero weight training experience.

Obese folks who slash calories end up losing as much fat as muscle and end up as miniaturized versions of the old fat selves. This modified bodybuilder approach melts fat while simultaneously adding muscle: the obese person eats more and as a direct result feels energized and vibrant during the process. Contrast this with the calorie-slasher who feels deprived, denied and continually on the verge of a binge. A person who eats wholesome foods every three hours is far less likely to binge and blow their diet than some poor obese person subsisting on 1200 calories a day. The calorie starved obese individual has set their caloric ceiling set so low that eating a candy bar or a bowl of ice cream causes them to add five pounds in 24-hours.

Adding functional muscle and building strength allows the obese person to become mobile and adept at climbing steps, getting out of a low chair and powering their bulk around. Compare this to the calorie-slasher who actually weakens their already weak body. Those who depend on deprivation to trigger bodyweight loss weaken the immune system and continually contract colds and sickness.

Those who live on 1000 to 1500 calories a day live in a stressful psychological world of denial. A person who has elevated their metabolism and consumes 3,000 calories a day can absorb an occasional binge far, far better than a person starving; I allow my folks a cheat meal once a week: this allows them to feel psychologically free. The interesting thing about the cheat meal (not cheat day – cheat meal) is that by “being good” the other 6 7/8’s of the time the sweets, fat and junk they crave and might eat are rejected by the body and classically results in diarrhea.

I train five obese folks I currently work with — one man and four women — and all are experiencing similarly spectacular results: all are losing unhealthy fat while building functional muscle and eating more food than they did before they commenced the process. This counterintuitive approach – eat more to lose fat – was torn right out of the playbook of champion bodybuilders and can be used to great effect by anyone interested in losing fat while adding muscle.

Know More About Sweat Rash And Treating It

Sweat Rash is a common skin ailment prevalent in hot and humid conditions, such as in the tropics characterized by skin and itchy rashes. It is more predominantly in children and infants because of under developed sweat glands. There are lots of other terms associated with skin rash like Milaria, prickly heat. Sweat rash usually develops under the arms, between the legs and the groin area where there is excessive sweat. Due to high moisture, fungal infection develops and leads to fungal skin infections.If neglected secondary bacterial infection may set in.

Sweat rash is common skin infection caused by Candida yeast infection. Symptoms of sweat rash include small red rashes called papules which may itch or more often cause prickling like sensation. These rashes may occur simultaneously at various parts of the body like face, neck, chest, under the arm, groin area and the scrotum.

Skin rashes may be associated with itching, tangling, burning, swelling and slight discomfort. Skin rash may be contagious or not contagious. Some skin rashes may be localized and some generalized. Some skin rashes are short-lived, some recurrent and some chronic.

Sweat rash treatment are generally quite basic which includes cooling the skin, keeping the affected part dry. Normally cool showers and loose fitting clothing usually does the trick. Also avoiding overcrowded, staying in the sun can be beneficial. Air conditioned or proper ventilation is necessary to avoid sweat reash. Calamine lotion is good treatment option for normal heat rashes.

If the skin is inflamed, treatment must be done both to relieve the inflammation and also treat the infection. Anti fungal agents are good to treat sweat rashes as they contain secondary anti bacterial properties that help to eliminate bacteria and fungi also. Most of these anti fungal creams contain hydrocortisone which helps down to soothen down the redness, itchiness and inflammation. There are lots of commercial anti fungal agents available in the market.

Even simple or treatable rashes can cause lot of frustration, especially if you do not know what to do, imagine rashes appearing on one fine day causing itchiness, burning sensation and you not knowing what to do. Self diagnosis is good if you had similar type of rashness before and most probably it would be the same one. It is always good to talk to your doctor or visit your health care professional if you are not sure about the type of skin rash.

How to Heal Cold Sores: What Should You Consider?

If you are looking for the best cold sore treatment, then here’s the good news: you are in luck. This great news will pave the way for the multitudes of options you have. It’s no longer a problem formulate your own techniques to wash away the pain you’re dealing with.

What Is Cold Sore?

Before you start looking for the ideal cold sore treatment, you must be aware of what the illness is. This can be referred to as fever blisters and would normally occur on both your upper and lower lips as well as in other parts of your mouth. Cold sore physically manifests by those small fluid-containing sacs on the skin or hard crusts. A cold sore may appear and linger for days or perhaps a couple of months. It depends on how severe or mild your cold sore is and, of course, the cold sore cure you are currently utilizing.

The major bummer of illness is called herpes simplex. It gets directly into the body any skin opening near your mouth. Another scenario is for you to get herpes simplex virus from individuals who are already infected with it by getting into fluid contact.

How to Get Rid of Cold Sores

Commonly, fever blisters will just go away after a few days. Simply put, there is no point for the sufferer to find any cold sore relief. Yet those small fluid-containing sacs on the skin can be excruciating. Sometimes they are embarrassing.

A very ideal cold sore remedy may be over the counter drugs. Normally, this drug would have tetracaine, dibucaine, or lidocaine that removes the itchy feeling as well as removes the pain. The medication can also decrease the painful sensation of the blisters. You must have an idea, meanwhile, that the over-counter-medicines do not last for a specific period of time. They may remove burning sensation and give you pain removal for not even an hour. You can also use moisturizers as well as skin protactants. You can prevent the occurrence several blisters or scabs. If you want to go out, bear in mind to wear UV-protected lip balms to avoid drying up your skin.

There are also prescribed medications if cold sores are already in their advanced stages. Definitely, you have to seek appointment with your own doctor before you can buy them online or offline. Make it a point to see your health care professional if the sores you’re having do not disappear after 14 days or the cold sores are already affecting your vision.

Herpes labialis don’t possess any cure yet. However, you can perhaps remove the sores immediately by means of improving the immune system in your body. You should be reminded of the dietary supplements religiously, especially the ones that have been filled with lots of good components such as vitamins and minerals. You may also relieve yourself of the burning sensation by putting ice compress. Be alert on the initial stages of cold sore, such as tingling feeling near the eyes or mouth.

Stop the Spread

You may also enhance the effects of cold sore treatments by doing preventive measures. If you have issues from the medical condition, you must resist the temptation of being intimate with someone. You must possess utensils not used by anyone but you , along with your make-up or grooming kit. Once your cold sore has completely disappeared, you have to immediately throw them away.

Don’t make it a habit to constantly touch parts of your body such as the eyes and even your genitals. You’re only spreading the virus then build sores in areas you constantly touch. Stress or worry may worsen the condition of the antibodies ; then there’s a good chance that you’re more at risk to the illness.

To avoid creating a good entry for the virus, use sunblock lotion when you are on the road. Don’t forget about this during summer and winter. A drying skin may only worsen the condition of blisters developing on your skin and wounds.

You can surely treat the illness. It is only a must for you to discover and realize what you can do with them.

Vitamin D for Psoriasis

Oral doses of vitamin D have been considered as a treatment for psoriasis. This was sparked by experiments with cholecalciferol or 1,25 dihydroxyvitamin D3 (1,25 (OH)2D3), the active form of vitamin D made in the kidney, which showed promise in treating widespread psoriasis.

Using a one microgram daily dose of cholecalciferol, Japanese researchers in 1986 managed to treat 13 out of 17 psoriatic patents within three months. But there are risks involved with this therapy.

High doses of vitamin D often leads to hypercalcemia (high blood calcium levels) which is characterized by nausea, vomiting, drowsiness, confusion, high blood press­ure, kidney failure, and coma. This was observed in the Japanese study and can occur in those taking 1,000 lUs (international units) or more of vitamin D.

The topical use of cholecalciferol by the same research­ers proved to be more beneficial and less toxic. Sixteen out of 19 patients were treated within three weeks with a dose of 0.5 microgram per gram compared to three months with oral doses. Still, the possibility of hypercalcemia remained since vitamin D is absorbed by the skin.

That was until researchers at Leo Pharmaceutical Products in Denmark tried to develop a new form of vitamin D which could clear up psoriatic plaques minus the risks encountered in both oral and topical applications of cholecalciferol. That led to the discovery of calcipotriol.

Calcipotriol is a vitamin D3 derivative which is just as effective as cholecalciferol in controlling rapid cell growth in psoriatic skin yet 100 – 200 times less likely to produce hypercalcemia. Unlike other creams and ointments, it is colorless and odorless and generally well-tolerated by patients.

This vitamin D3 analogue is recommended for the treatment of plaque-type psoriasis and can be used alone or in combination with UVB radiation (which was tackled earlier in this series). The exact mechanism of calcipotriol is unknown but numerous studies have established the efficacy of this drug.

Controlled clinical trials have shown that calcipotriol is just as effective as some steroids and more effective than anthranol (both of which were discussed in this series) in treating plaque-type psoriasis. Patients using the recommended dose of 50 micrograms per gram twice daily for six months have not developed hypercalcemia, making calcipotriol safer than other conven­tional psoriasis regimens.

The long-term effects of calcipotriol, however, are unknown and its safety in children and pregnant women has not been established. Using more of the drug can also be dangerous. If you go beyond the recommended dose and use more than 100 grams a week, you may suffer from high blood calcium levels.

So far, the only side effect reported is a mild skin irritation that occurs in 10 to 20 percent of patients who use calcipotriol. But this can be controlled by means of careful application. Calcipotriol should not be used on the face and patients are advised to wash away traces of the ointment that accidentally get in other unaffected areas of the skin. If you experience skin irritation, stop treatment and consult a doctor immediately.

To strengthen your body, take Immunitril – your first line of defense in maintaining a healthy immune system. For details, visit

Dog Blastomycosis Fungal Disease

Blastomycosis of Blasto is a systemic fungal disease that primarily affects dogs and humans, but has also been known to infect cats, sea lions and horses. It is caused by the fungal organism Blastomyces dermatitidis, which is found as a mold in the soil or at room temperatures and as yeast in tissues or at body temperatures. Infection occurs primarily through inhalation. In the lung, alveolar macrophages phagocytize spores and the organism transforms to the yeast phase. Pulmonary macrophages transport the organism to the pulmonary interstitium. Other routes of infection include skin lesions or penetrating injuries that introduce the organism into the body.

Blastomycosis grows in forms: fungal form and yeast form. In fungal form, the bacteria occurs in the environment and the organism creates microscopically tiny spores that, once airborne, are able to pass far into the depths of the lungs. These spores are released from the fungus when the soil is disturbed by the dog digging for gophers or simply by the dog probing the soils following the odor trails that they love so much. Once the spores have taken hold, they grow as single celled yeast forms rather than the fungal form. This is why the Blasto organism is called a biphasic organism… it can grow in the environment as a fungus and within a mammal as a yeast. Blastomycosis is not generally considered a zoonotic disease, meaning one that is potentially contagious to people. If you have a pet with this infection, it indicates that you may be at risk for contracting the disease through a common environmental source such as contaminated soil near a waterway. Since it is the mold form that releases infective spores through the air, you cannot get blastomycosis from the air around your dog who is infected with the yeast form of the fungus.

After inhalation of organisms the incubation period for Blasto can be from a few days to many weeks before any signs of disease show up. Fever of 104 to 105 degrees, poor appetite, low grade deep cough, loss of exercise tolerance, and listlessness are cardinal signs of Blastomycosis. Similar to the other systemic fungal infections, Blastomycosis can spread throughout the body from the lungs and invade lymph nodes, joints, eye structures and skin. Often the first evidence a veterinarian has of Blastomycosis is a small draining ulcer that looks like a small abscess. Sudden blindness, lameness, and blood in the urine may be the first signs of disease… sometimes showing up before any coughing is noticed.

In one retrospective study, clinical signs of Blastomycosis includes respiratory tract problems, depression, anorexia, ocular problems, weight loss, dermatologic abnormalities, lethargy, fever of unknown origin, lameness, exercise intolerance, gastrointestinal tract problems, polyuria or polydipsia, mammary gland mass and urogenital tract problems. Cats show similar clinical signs as dogs, with respiratory difficulty characterized by dyspnea or chronic cough being the most common sign. Depression, dehydration, ocular disease, and CNS signs are also seen. Physical findings reflect clinical history and vary greatly. These include lymphadenopathy, fever, harsh lung sounds, draining skin lesions, chorioretinitis, anterior uveitis, cough, emaciation, retinal detachment, soft–tissue mass and more. Blastomycosis may be diagnosed by identification of the organisms in cytologic samples. Blastomyces dermatitidis usually is seen in the form of round yeast ranging from approximately 5-20 µm in diameter.

There are a few treatments and most of them are going to be drug related depending on how far the disease has progressed. If you do not seek treatment the disease can be life threatening. When the dog has been treated for the disease you should see an improvement over a three to five day period. The first drug usually provided for the disease is amphotericin B. This is an intravenous injection that goes directly to the source of the infection. Since the drug can have adverse effects the vet usually keeps the dog for a couple of days to make sure there is no kidney failure. Ketoconazole is also given. This drug is provided orally. Most often this drug takes ten to fourteen days to see any effects. It has been known to cure the issue, but sometimes both drugs may have to be given. Itraconazole is the newest treatment on the market; however some vets have yet to take up this medication because of the expense to the owner. It can cost about $1000 for treatment since they need to have several doses over a period of days for the effects to work.

Blastomycosis is rare fungal disease with a prevalence of 205/100,000 cases presenting to tertiary facilities.3 While it is a rare disease, it should be considered as a differential diagnosis in any case exhibiting the clinical signs discussed above. If other more common conditions have been excluded, blastomycosis should be investigated. It is an insidious disease that often is recognized only through extensive search for the organism or through a combination of clinical signs, history and signalment.