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The hepatitis E virus, responsible for major epidemics of viral hepatitis in subtropical and tropical countries, was cloned only 7 years ago.1 Hepatitis E was found to belong to the family of Caliciviridae, which includes the Norwalk virus—a common cause of gastroenteritis in humans—and consists of a single, plus-strand RNA genome of approximately 7.2 kb without an envelope (Fig. 1). The virus contains at least three open reading frames encoding viral proteins against which antibodies are made on exposure. These antibodies, especially those against the capsid protein derived from the second open reading frame2 and a protein of unknown function derived from the third open reading frame, are detected by currently available serologic assays. Retrospective studies on stored sera of past epidemics of viral hepatitis in Mexico, Africa, Afghanistan, Pakistan, India, Bangladesh, Burma, Nepal, and Borneo have revealed that all were caused by strains of hepatitis E. In addition, hepatitis E was found to be responsible for the hepatitis epidemic in the southern part of Xinjiang, China, in which 120,000 persons became infected between September 1986 and April 1988.3 Hepatitis E predominantly affects young adults (15 to 40 years old). The symptoms of hepatitis E are similar to those of hepatitis A. Frequently, a prodrome consisting of anorexia, nausea, low-grade fever, and right upper abdominal pain is present 3 to 7 days before jaundice develops. Aminotransferase levels peak (usually between 1,000 and 2,000 U/L) near the onset of symptoms; bilirubin levels (10 to 20 mg/dL) peak later. Jaundice usually resolves after 1 to 2 weeks. In about 10% of cases, the disease is fulminant—especially in pregnant women, among whom mortality rates as high as 20% due to hemorrhagic and thrombotic complications have been reported. No evidence has suggested that hepatitis E can cause chronic infection. Transmission is by the fecal-oral route, predominantly through fecally contaminated drinking water supplies. In addition, however, preliminary reports have suggested transmission of the hepatitis E virus through blood transfusions. Volunteer studies confirmed the presence of the virus in serum and feces before and during clinical disease.4 The virus is shed into feces approximately 1 week before symptoms develop. The incubation period varies from 2 to 9 weeks (mean duration, approximately 45 days). Until now, a few reports had described symptomatic hepatitis E acquired in Europe;5, 6 all patients with symptomatic hepatitis E in the United States were travelers returning from Mexico, Africa, or the Far East, in whom hepatitis E developed after their return home.7 In this issue of the Mayo Clinic Proceedings (pages 1133 to 1136), Kwo and associates describe a case of hepatitis E in a man who had not left the United States during the previous 10 years. Specific serologic tests for hepatitis E virus IgG (enzyme immunoassays and a fluorescent antibody blocking assay) and IgM8 (US strain-specific enzyme-linked immunosorbent assay with use of synthetic polypeptides deduced from the viral genome, as shown in Figure 1), developed at Abbott Laboratories (IgG and IgM) as well as at the Centers for Disease Control and Prevention (IgG), were used to prove that the patient indeed had acute hepatitis E. Researchers at Abbott Laboratories have prepared a report that describes most of the viral genome in this patient (Fig. I).8 Their results are interesting because this strain from the United States differs considerably from hepatitis E strains isolated in Mexico, Burma, Pakistan, or China. Furthermore, the sequence of the US strain is highly homologous (98% and 94% homology at the amino acid level to the second and third open reading frames, respectively) to a recently isolated hepatitis E strain from American swine.9 This finding suggests that, in the United States, hepatitis E is a zoonosis with the swine population as one of its hosts. This relationship would confirm earlier studies in Asia, where swine were also found to carry variants of the hepatitis E virus.10 Why are these two recent discoveries important for medicine in the United States? First, other sporadic, locally acquired cases of acute hepatitis may be caused by hepatitis E. Second, these back-to-back discoveries strongly suggest that a common natural host for hepatitis E is present in countries with more moderate climates. Because swine do not seem to experience any symptoms associated with infection and because symptoms in humans can be minor or absent, we now may also have an explanation for the 1 to 2% of positive hepatitis E serologic results in blood donors in the United States,11 Netherlands,12 and Italy,6 countries with large swine staples. Clearly, more research needs to be done to confirm this hypothesis. Third, in countries with more moderate climates, hepatitis E may often result in a subclinical infection. Is this variation in manifestation due to less virulent strains, and do sequence variations determine virulence? Fourth, swine may be used as an animal model for study of the disease as well as vaccine development.
Heart failure, sometimes known as congestive heart failure, occurs when your heart muscle doesn't pump blood as well as it should. Certain conditions, such as narrowed arteries in your heart (coronary artery disease) or high blood pressure, gradually leave your heart too weak or stiff to fill and pump efficiently. Not all conditions that lead to heart failure can be reversed, but treatments can improve the signs and symptoms of heart failure and help you live longer. Lifestyle changes — such as exercising, reducing salt in your diet, managing stress and losing weight — can improve your quality of life. One way to prevent heart failure is to control conditions that cause heart failure, such as coronary artery disease, high blood pressure, diabetes or obesity.
What is polycystic kidney disease? Polycystic kidney disease (also called PKD) causes numerous cysts to grow in the kidneys. These cysts are filled with fluid. If too many cysts grow or if they get too big, the kidneys can become damaged. PKD cysts can slowly replace much of the kidneys, reducing kidney function and leading to kidney failure. How common is PKD? In the United States about 600,000 people have PKD. It is the fourth leading cause of kidney failure. It is found in all races and occurs equally in men and women. It causes about 5% of all kidney failure. What other organs besides the kidney are affected by PKD? PKD can affect other organs besides the kidney. People with PKD may have cysts in their liver, pancreas, spleen, ovaries, and large bowel. Cysts in these organs usually do not cause serious problems, but can in some people. PKD can also affect the brain or heart. If PKD affects the brain, it can cause an aneurysm. An aneurysm is a bulging blood vessel that can burst, resulting in a stroke or even death. If PKD affects the heart, the valves can become floppy, resulting in a heart murmur in some patients. What are the clues that someone has PKD? Most people do not develop symptoms until they are 30 to 40 years old. The first noticeable signs and symptoms may include: Back or side pain An increase in the size of the abdomen Blood in the urine Frequent bladder or kidney infections High blood pressure High blood pressure is the most common sign of PKD. Occasionally, patients may develop headaches related to high blood pressure or their doctors may detect high blood pressure during a routine physical exam. Because high blood pressure can cause kidney damage, it is very important to treat it. In fact, treatment of high blood pressure can help slow or even prevent kidney failure. Fluttering or pounding in the chest About 25% of PKD patients have a so-called floppy valve in the heart, and may experience a fluttering or pounding in the chest as well as chest pain. These symptoms almost always disappear on their own but may be the first hint that someone has PKD. How is PKD diagnosed? Ultrasound is the most reliable, inexpensive and non-invasive way to diagnose PKD. If someone at risk for PKD is older than 40 years and has a normal ultrasound of the kidneys, he or she probably does not have PKD. Occasionally, a CT scan (computed tomography scan) and MRI (magnetic resonance imaging) may detect smaller cysts that cannot be found by an ultrasound. MRI is used to measure and monitor volume and growth of kidneys and cysts. In some situations, genetic testing might also be done. This involves a blood test that checks for abnormal genes that cause the disease. Genetic testing is not recommended for everyone. The test is costly, and it also fails to detect PKD in about 15% of people who have it. However, genetic testing can be useful when a person: has an uncertain diagnosis based on imaging tests has a family history of PKD and wants to donate a kidney is younger than 30-years old with a family history of PKD and a negative ultrasound, and is planning to start a family
Most of the time, treatment for hemorrhoids involves steps that you can take on your own, such as lifestyle modifications. But sometimes medications or surgical procedures are necessary. Medications If your hemorrhoids produce only mild discomfort, your doctor may suggest over-the-counter creams, ointments, suppositories or pads. These products contain ingredients, such as witch hazel or hydrocortisone, that can relieve pain and itching, at least temporarily. Don't use an over-the-counter cream or other product for more than a week unless directed by your doctor. These products can cause side effects, such as skin rash, inflammation and skin thinning. Minimally invasive procedures If a blood clot has formed within an external hemorrhoid, your doctor can remove the clot with a simple incision, which may provide prompt relief. For persistent bleeding or painful hemorrhoids, your doctor may recommend another minimally invasive procedure. These treatments can be done in your doctor's office or other outpatient setting. Rubber band ligation. Your doctor places one or two tiny rubber bands around the base of an internal hemorrhoid to cut off its circulation. The hemorrhoid withers and falls off within a week. This procedure — called rubber band ligation — is effective for many people. Hemorrhoid banding can be uncomfortable and may cause bleeding, which might begin two to four days after the procedure but is rarely severe. Injection (sclerotherapy). In this procedure, your doctor injects a chemical solution into the hemorrhoid tissue to shrink it. While the injection causes little or no pain, it may be less effective than rubber band ligation. Coagulation (infrared, laser or bipolar). Coagulation techniques use laser or infrared light or heat. They cause small, bleeding, internal hemorrhoids to harden and shrivel. While coagulation has few side effects, it's associated with a higher rate of hemorrhoids coming back (recurrence) than is the rubber band treatment. Surgical procedures If other procedures haven't been successful or you have large hemorrhoids, your doctor may recommend a surgical procedure. Surgery can be performed on an outpatient basis or you may need to stay in the hospital overnight. Hemorrhoid removal. During a hemorrhoidectomy, your surgeon removes excessive tissue that causes bleeding. Various techniques may be used. The surgery may be done with a local anesthetic combined with sedation, a spinal anesthetic or a general anesthetic. Hemorrhoidectomy is the most effective and complete way to treat severe or recurring hemorrhoids. Complications may include temporary difficulty emptying your bladder and urinary tract infections associated with this problem. Most people experience some pain after the procedure. Medications can relieve your pain. Soaking in a warm bath also may help. Hemorrhoid stapling. This procedure, called stapled hemorrhoidectomy or stapled hemorrhoidopexy, blocks blood flow to hemorrhoidal tissue. Stapling generally involves less pain than hemorrhoidectomy and allows an earlier return to regular activities. Compared with hemorrhoidectomy, however, stapling has been associated with a greater risk of recurrence and rectal prolapse, in which part of the rectum protrudes from the anus. Talk with your doctor about what might be the best option for you.
Severe combined immunodeficiency (SCID) is a life-threatening syndrome of recurrent infections, diarrhea, dermatitis, and failure to thrive. It is the prototype of the primary immunodeficiency diseases and is caused by numerous molecular defects that lead to severe compromise in the number and function of T cells, B cells, and occasionally natural killer (NK) cells. Clinically, most patients present before age 3 months. Without intervention, SCID usually results in severe infection and death in children by age 2 years. A committee of experts, initially sponsored by the World Health Organization (WHO), meets every 2 years with the goal to classify the group of primary immunodeficiency diseases according to current understanding of the pathways that become defective in the immune system.[1] Eight classification groups have been determined, with SCID being one of the best studied. Over the past few decades, the diverse molecular genetic causes of SCID have been identified with progress from studies of the immune system.[2] SCID is considered a pediatric emergency because survival depends on expeditious stem cell reconstitution, usually by bone marrow transplantation (BMT). Appropriate diagnosis is essential because instituting proper treatment is lifesaving. Despite the heterogeneity in the pathogenesis of immune defects, common cutaneous manifestations and typical infections can provide clinical clues in diagnosing this pediatric emergency.[3] Skin manifestations were prevalent in primary immunodeficiency disorders studied in 128 pediatric patients in Kuwait; skin infections were the most prevalent findings, seen in 39 patients (30%), followed by dermatitis in 24 (19%).[4] Skin infections were significantly more prevalent in those with congenital defects in phagocyte number, function, or both, as well as in those with well-defined immunodeficiencies. Dermatitis was evident in all patients with hyper–immunoglobulin (Ig) E syndrome and Wiskott-Aldrich syndrome.[4] Erythroderma of infancy with diffuse alopecia was seen exclusively in patients with SCID disorders, and telangiectasia in patients with ataxia telangiectasia; and partial albinism with silvery gray hair was associated with Chediak-Higashi syndrome. With the advances in BMT and gene therapy, patients now have a better likelihood of developing a functional immune system in a previously lethal genetic disease. However, once an infant develops serious infections, intervention is rarely successful.
Guillain-Barre syndrome is a rare disorder in which your body's immune system attacks your nerves. Weakness and tingling in your extremities are usually the first symptoms. These sensations can quickly spread, eventually paralyzing your whole body. In its most severe form Guillain-Barre syndrome is a medical emergency. Most people with the condition must be hospitalized to receive treatment. The exact cause of Guillain-Barre syndrome is unknown. But it is often preceded by an infectious illness such as a respiratory infection or the stomach flu. There's no known cure for Guillain-Barre syndrome, but several treatments can ease symptoms and reduce the duration of the illness. Most people recover from Guillain-Barre syndrome, though some may experience lingering effects from it, such as weakness, numbness or fatigue.
Clopidogrel keeps the platelets in your blood from coagulating (clotting) to prevent unwanted blood clots that can occur with certain heart or blood vessel conditions. Clopidogrel is used to prevent blood clots after a recent heart attack or stroke, and in people with certain disorders of the heart or blood vessels. Clopidogrel may also be used for other purposes not listed in this medication guide
Hyperkalemia is defined as a serum potassium concentration higher than the upper limit of the normal range; the range in infants and children is age-dependent, whereas the range for adults is approximately 3.5-5.5 mEq/L. The upper limit may be considerably higher in young or premature infants, as high as 6.5 mEq/L.[5] Degrees of hyperkalemia are defined as follows[6] : 5.5-6.0 mEq/L – Mild 6.1-7.0 mEq/L – Moderate ≥7.0 mEq/L – Severe levels higher than 7 mEq/L can lead to significant hemodynamic and neurologic consequences. levels exceeding 8.5 mEq/L can cause respiratory paralysis or cardiac arrest and can quickly be fatal. Because of a paucity of distinctive signs and symptoms, hyperkalemia can be difficult to diagnose. Indeed, it is frequently discovered as an incidental laboratory finding. The physician must be quick to consider hyperkalemia in patients who are at risk for this disease process. (See Etiology.) However, any single laboratory study demonstrating hyperkalemia must be repeated to confirm the diagnosis, especially if the patient has no changes on electrocardiography (ECG). Because hyperkalemia can lead to sudden death from cardiac arrhythmias, any suggestion of hyperkalemia requires an immediate ECG to ascertain whether ECG signs of electrolyte imbalance are present (see Workup). Continuous ECG monitoring is essential if hyperkalemia is confirmed. Other testing is directed toward uncovering the condition or conditions that led to the hyperkalemia (see Workup). The aggressiveness of therapy for hyperkalemia is directly related to the rapidity with which the condition has developed, the absolute level of serum potassium, and the evidence of toxicity. The faster the rise of the potassium level, the higher it has reached, and the greater the evidence of cardiotoxicity, the more aggressive therapy should be. In severe cases, treatment focuses on immediate stabilization of the myocardial cell membrane, rapid shifting of potassium to the intracellular space, and total body potassium elimination. In addition, all sources of exogenous potassium should be immediately discontinued. (See Treatment.)
Atopic dermatitis (eczema) is a condition that makes your skin red and itchy. It's common in children but can occur at any age. Atopic dermatitis is long lasting (chronic) and tends to flare periodically and then subside. It may be accompanied by asthma or hay fever.
Constipation is a common problem. It means either going to the toilet less often than usual to empty the bowels, or passing hard or painful stools (faeces). Constipation may be caused by not eating enough fibre, or not drinking enough fluids. It can also be a side-effect of certain medicines, or related to an underlying medical condition. In many cases, the cause is not clear. Laxatives are a group of medicines that can treat constipation. Ideally, laxatives should only be used for short periods of time until symptoms ease. Note: there is a separate leaflet on constipation in children. What is constipation? Constipation is common. If you are constipated it causes one or more of the following: Stools (faeces) become hard and difficult or painful to pass. The time between toilet trips increases compared with your usual pattern. (Note: there is a large range of normal bowel habit. Some people normally go to the toilet to pass stools 2-3 times per day. For others, 2-3 times per week is normal. It is a change from your usual pattern that may mean that you are constipated.) Sometimes, crampy pains occur in the lower part of your tummy (abdomen) You may also feel bloated and feel sick if you have severe constipation. What are the causes of constipation? Known causes include the following: Not eating enough fibre (roughage) is a common cause. The average person in the UK eats about 12 g of fibre each day. But, 18 g per day is recommended by the British Nutrition Foundation. Fibre is the part of plant food that is not digested. It remains in your gut. It adds bulk to the stools (faeces) and helps your bowels to work well. Foods high in fibre include fruit, vegetables, cereals and wholemeal bread. Not drinking much may make constipation worse. Stools are usually soft and easily passed if you eat enough fibre and drink enough fluid. However, some people need more fibre and/or fluid than others in order to avoid constipation. Some special slimming diets are low in fibre and may cause constipation. Some medicines can cause constipation as a side-effect. Examples are painkillers (particularly those with codeine, such as co-codamol, or very strong painkillers, such as morphine), some antacids, some antidepressants (including amitriptyline) and iron tablets; however, there are many others. See the list of possible side-effects on the leaflet that comes with any medicine that you may be taking. Tell a doctor if you suspect a medicine is making you constipated. A change of medication may be possible. Various medical conditions can cause constipation. For example, an underactive thyroid gland, irritable bowel syndrome, some gut disorders and conditions that cause poor mobility, particularly in the elderly. Pregnancy. About 1 in 5 pregnant women will become constipated. It is due to the hormonal changes of pregnancy that slow down the gut movements. In later pregnancy, it can simply be due to the baby taking up a lot of room in the tummy and the bowels being pushed to one side.
A torn meniscus is one of the most common knee injuries. Any activity that causes you to forcefully twist or rotate your knee, especially when putting the pressure of your full weight on it, can lead to a torn meniscus. Each of your knees has two menisci — C-shaped pieces of cartilage that act like a cushion between your shinbone and your thighbone. A torn meniscus causes pain, swelling and stiffness. You also might have trouble extending your knee fully. Conservative treatment — such as rest, ice and medication — is sometimes enough to relieve the pain of a torn meniscus and give the injury time to heal on its own. In other cases, however, a torn meniscus requires surgical repair.
A Hundred Orgasms A Day follow the story of 3 women who were tormented every hour of everyday with the need to have orgasm. This documentary explain how Persistent Sexual Arousal Syndrome or PSAS causes this unusual condition. PSAS is a little know neurological disorder where women have symptoms of continuous uncontrollable genital arousal. This condition is unrelated to any kind of sensations of sexual desire. PSAS was initially documented by Doctor Sandra Leiblum in mid 2001, just recently recognized as a unique syndrome in medical science which has a comparable equivalent progressively more claimed by men. A few physicians makes use of the name Persistent Sexual Arousal Syndrome to reference the disorder in women; some others look at the syndrome of priapism in adult males to be a similar disorder. Most importantly, it is really not connected with hyper-sexuality, also known as nymphomania. Both hyper-sexuality, and nymphomania are not known diagnosable health conditions. Not only is it very rare, the disorder is also seldom reported by affected individual who may think it is embarrassing.
Any independent vertical movement of the transducer or the patient will affect the hydrostatic column of this fluid-filled system and thus alter the pressure measurements. At some time before or after PAC insertion, the system must therefore be zeroed to ambient air pressure. The reference point for this is the midpoint of the left atrium (LA), estimated as the fourth intercostal space in the midaxillary line with the patient in the supine position. With the transducer at this height, the membrane is exposed to atmospheric pressure, and the monitor is then adjusted to zero. Calibration Once zeroed, the monitoring system must be calibrated for accuracy. Currently, most monitors perform an automated electronic calibration. Two methods are used to manually calibrate and check the system. If the catheter has not been inserted, the distal tip of the PAC is raised to a specified height above the LA. For example, raising the tip 20 cm above the LA should produce a reading of approximately 15 mm Hg if the system is working properly (1 mm Hg equals 1.36 cm H 2 O). Alternatively, pressure can be applied externally to the transducer and adjusted to a known level using a mercury or aneroid manometer. The monitor then is adjusted to read this pressure, and the system is calibrated. Dynamic tuning Central pressures are dynamic waveforms (ie, they vary from systole to diastole) and thus have a periodic frequency. To monitor these pressures accurately, the system requires an appropriate frequency response. A poorly responsive system produces inaccurate pressure readings, and differentiating waveforms (eg, PA from pulmonary capillary wedge pressure [PCWP]) can become difficult. When signal energy is lost, the pressure waveform is dampened. Common causes of this are air bubbles (which are compressible), long or compliant tubing, vessel wall impingement, intracatheter debris, transducer malfunction, and loose connections in the tubing. A qualitative test of the frequency response is performed by flicking the catheter and observing a brisk high-frequency response in the waveform. After insertion, the system can be checked by using the rapid flush test. When flushed, an appropriately responsive system shows an initial horizontal straight line with a high-pressure reading. Once the flushing is terminated, the pressure drops immediately, which is represented by a vertical line that plunges below the baseline. A brief and well-defined oscillation occurs, followed by return of the PA waveform. A dampened system will not overshoot or oscillate, and causes a delay in returning to the PA waveform.
Pink eye (conjunctivitis) is an inflammation or infection of the transparent membrane (conjunctiva) that lines your eyelid and covers the white part of your eyeball. When small blood vessels in the conjunctiva become inflamed, they're more visible. This is what causes the whites of your eyes to appear reddish or pink. Pink eye is commonly caused by a bacterial or viral infection or an allergic reaction. It may affect one or both eyes. Pink eye can be irritating, but it rarely affects your vision. Treatments can help ease the discomfort of pink eye. Because pink eye can be contagious, early diagnosis and treatment can help limit its spread.