Kawasaki disease, also known as the cutaneo adenopathy syndrome, or Kawasaki syndrome, is a multi-systemic disease, febrile, acute in children, characterized by inflammation of blood vessels. The condition was named after a Japanese pediatrician, Tomisaku Kawasaki, who first described it in 1967. Although it is most common among Asian children, the disease can affect children of all races.



The Kawasaki disease is characterized by inflammation of blood vessels in the whole body, but there is no specific test for the diagnosis; the diagnosis is relying on a series of signs and symptoms. The Kawasaki disease symptoms are: -fever that can last for over 5 days -erythema, severe growth areas; -conjunctival congestion -red, swollen, dry lips;  -strawberry-language with bright red dots on the top -pulp; skin-peeling fingers; -redness and swelling of the fingers, lips, palms, soles; -lymphadenopathy.

Most children having the Kawasaki disease symptoms are aged between 1 and 8 years old, but this disease can affect teens too, and it is twice more common in boys than in girls. 50% of children develop heart problems such as arrhythmia after 4 weeks of evolution of this disease, arterial aneurysms, formation of blood clots. Other meningitis symptoms include inflammation of the brain, the joints and bladder complications. These problems can be solved in time without permanent damage of the affected organs.

Patients recover if all coronary arteries are not affected in the first 8 weeks. For those with impaired survival depends on the severity of this disease. Following treatment, less than 1% of children die. Those who do not survive- death occurs within the first month, but even the several aneurysms resolve in matter of years. Almost every year, those who do not resolve their problems in this period progress to dissection.

The treatment uses high doses of aspirin to reduce inflammation and prevent the formation of clogs. There can also be used an intravenous treatment based on gamma globulin. This treatment proved effective in reducing the formation of aneurysms in coronary arteries.

Pathogenic aspects - Coronary artery is observed in almost all fatal cases. It is a typical proliferation and an infiltration of the vascular wall with mono nuclear cells. Aneurysms and thrombosis can be seen in patients suffering from the Kawasaki disease. Other events include myocardial infarction, pericarditis, cardiomegaly, myocardial infarction and myocardial ischemia.

Causes of the Kawasaki disease - The Kawasaki disease causes are unknown, but researchers believe the disease is not contagious. There are a developed number of theories according to which some bacterial or viral infections or environmental factors could trigger the Kawasaki disease. There is a common belief that there is a close connection between an unusual form of Staphylococcus aureus to eliminate toxins from a septic shock syndrome and Kawasaki syndrome. Some risk factors for KS includes: -age between 2 and 5 years; -male gender; -part of an ethnic-Asians group

In the category of sexually transmitted diseases (STDs), the sexually transmitted disease symptoms are caused by various microorganisms that are associated with sexual activity. Not all diseases included in this category are transmitted sexually and their effects are not restricted to reproductive organs. There are approximately 24 STDs but we will stop here on the most popular.



Syphilis is an infectious disease caused by Treponema Pallidum, most often transmitted sexually (90% of cases) but also by kissing, accidental inoculation through bites or stings, transfusion of fresh blood, open sores of skin diseases (herpes , acne) and quite exceptional by contaminated objects. Syphilis can be transmitted from a sick mother to the child starting with 3.4 months of pregnancy. The average incubation period is 21 days.

The sexually transmitted disease symptoms for syphilis begin with the appearance of syphilitic chancre (erosion with smooth edge, clean bottom and the last, covered by a serosity without inflammation and painless). Secondary syphilis occurs as 6-8 weeks after the appearance of chancre and is characterized by a number of skin manifestations, usually accompanied by visceral poly-adenopathy.

Some of the symptoms may be erythematous, erosive mucosa (the lining of the mouth, genital, anal, etc.), or pigmentation and ulcer. The hair can be affected(syphilitic alopecia), as well as the nails. General symptoms are represented by fever, moderate weight loss, decreased appetite, headache, bone or muscle.

Latent syphilis is a seemingly quiet period after secondary infection symptoms were off and can take years. Tertiary syphilis occurs after a variable period of onset of the disease (between 3 and 20 years) and is not necessarily an evolutionary stage skin. Diagnosis is serological: RBW test (now abandoned) or VDRL. Gonorrhea (gonorrhea) is a bacterial infection almost always sexually contacted. The incubation period is 3-5zile.

Acute infection is rarely met in women but when it is characterized by burn sensations and pain when urinating, vaginal and urethral yellowish secretion. Chronic infection, almost asymptomatic, is mostly met in women. The man has an acute infection that starts with previous urethritis itching, redness and swelling of the area. Then the yellow-green secretion is being associated with urethral burning and pain on urination.

Trichomoniaza is an infection caused by a parasite (Trichomonas vaginalis) transmitted sexually. After some statistics is the most common sexually transmitted disease. The transmission can also occur by water in swimming pools, toilet cover sites, toilet articles, but these are extremely rare cases. The main transmitter of the disease is the man who most often presents as an asymptomatic.

In women the disease is evolving as a sub-acute vulvo-vaginitis characterized by itching, burning, vaginal discomfort associated with whitish secretion, creamy yellow or greenish ugly smelly secretion. Untreated, this disease will become chronic with relapsed pre-and post-menstrual and pregnancy. Non-specific infections are often caused by Chlamydia trachomatis.

In women, most often, these infections are asymptomatic but may manifest through the vagina, cervical or urethral syndrome. In men, urethritis is often sub acute, with frequent urination, mild dysuria, clear urethral secretion, or white lining. Evocative symptoms are severe itching in the pubic symphysis, especially in the evening and night, caused by parasites stings.

BSE - mad cow disease; It had been several years already since the first case in England had been diagnosed. A previously unknown neurological disease in cattle: “cow 133” died in 1985 after the presence of head tremor, weight loss and coordination disorders.



Specialists had blamed the early symptoms of mad cow disease on a "progressive spongiform encephalopathy of cattle", a new disease, which was then called "mad cow disease" because of how weird the sick animals were acting. Later it became clear that there was an epidemic outbreak of this new disease. The epidemic peak was reached in 1992-1993, with over 100,000 confirmed cases of disease in cattle.

Despite protection measures, which most European countries have taken, prohibiting the imports of cattle and beef products from Britain, the disease has gone beyond Britain's borders. There were over 180,000 reported cases of bovine spongiform encephalopathy (BSE) in Great Britain and more than 1,500 cases in several countries in Western Europe.

The disease appeared in cows due to the unfortunate practice of using food supplement with scraps of meat from sheep suffering from scrapie ( "Pimiento"), in order to increase production of milk and meat. This mode of feeding began to be used in 1930 and has become a rule in animal breeding farms around the world.

vCJD - the human variant of the disease - Although initially officials denied reports that BSE can be transmitted to humans, in 1996 the British government officially recognized that there were already victims of the new human brain disease, related to mad cow disease. This disease - the specialists called it variant Creutzfeldt-Jakob disease (vCJD) - was assigned in the class of transmissible spongiform encephalopathies (TSE), along with the Creutzfeldt-Jakob disease and the Kuru disease.

They form a family of degenerative brain diseases affecting man and some domestic and wild animals. The incubation period is very long, for months or years. There is no treatment to cure these diseases, their evolution always leading to death.

As for the early symptoms of mad cow disease in humans, vCJD differs from traditional forms of Creutzfeldt-Jakob disease by impairing the younger patients (average age is 29 years, as opposed to 65 years), vCJD has a longer incubation (years or decades) and a longer duration (on average 14 months). The nature of the agent has not been fully elucidated, but the most credible theory is that there is a new pathogen, called prion, a protein with the same composition as one of the proteins in the brain, but with an abnormal three-dimensional structure.

Prions can be transmitted from animals to humans by eating diseased meat or their penetration into the human body is possible through neuro-surgical instruments, procedures or medical products (transplanted corneas and dura mater, pituitary hormone extract, human growth hormone etc..). Also, there is the possibility of transmission by the bite of pets or wild animals that carry the prions. Unlike other microbial agents, prions seem to lack genetic material and are very resistant to high temperatures, regular or antibacterial agent inactivation or sterilization procedures.

In the early symptoms of mad cow disease in humans, patients see discrete psychiatric symptoms most often in the form of depression. Less often it mimics a psychosis similar to schizophrenia. Then there are a number of unusual symptoms, such as skin feeling sticky, and neurological signs, the most common being motor instability, difficulty walking and performing voluntary movements, lack of coordination. The patient's condition progressively gets worse, so eventually the patient becomes completely still and mute, then dies.

Hyperthyroidism is the hyper function of the thyroid gland. Graves disease is also known as Basedow's disease or Parry disease and is a disease that is characterized by 3 major manifestations: hyperthyroidism with diffuse goiter, dermopathy and ophthalmopathy. These major events do not always occur together.



Basedow disease is a relatively common disease that may occur at any age but is most common in 3rd and 4th decades of life, its frequency being increased in women. In geographical areas where goiter is endemic men to women ratio is 7:1 compared to geographical regions with endemic goiter where the ratio is much lower.

Graves disease symptoms are classified to reflect events associated to thyrotoxicosis and Basedow disease specific. The most common Graves disease symptoms are: emotional lability, nervousness, tremors, insomnia, excessive sweating and intolerance to heat and increased peristalsis. Also weight loss is common despite maintenance or increased appetite. The presence of proximal muscle weakness with reduction in force is often manifested by difficulty in ascending the stairs.

Periomenopause in women tends to trace the appearance of amenorrhea. Young people are generally dominated by nervous symptoms while the predominant symptoms in the elderly are cardiovascular and eye tests. Specific manifestations of Graves disease are: - Hyper functional diffuse goiter; - Dermopathy; - ophthalmopathy.

These symptoms occur in different combinations and with a highly variable frequency, the most common being goiter. Diffuse goiter and lobular hyper functions may be asymmetrical. Detection of the thyroid gland usually indicates this thyrotoxicosis, but this sign is sometimes present in other forms of thyroid hyperplasia. Differential diagnosis is made with the murmur of breath, venous and carotid. On palpation of thyroid can be detected an increased pyramidal lobe.

Dermopathy usually manifests itself in the rear part of the legs and is called pretibial mixed. This is a late phenomenon that occurs in approximately half of patients in active stage of thyrotoxicosis and virtually in all patients with ophthalmopathy.

Dermopathy (manifestations of skin) is characterized by: - Skin is soft, warm, moist, fine, erythematous (redness especially the emotions in the region prior to the neck and chest); - Itching skin; - Hyper pigmentation in the certain areas (Jellinek sign), and at the elbows, hands or diffuse hyper pigmentation; - Vitiligo; - Alopecia (in the scalp is low, soft, very friable); - The hair on the body is fine and reduced - Nails are thinner; they become soft, loose and shiny.

Ophthalmopathy is characterized by:
- Upper eyelid retraction determine the discovery of a large portion of the sclera giving the patient a fixed, fearful that creates the impression of apparent exophthalmia. This causes delay in achieving the upper eyelid descent causing strange movements of the eye. The reasons for this mechanism are represented by high muscle spasm due to higher eyelid increased sympathetic nervous system activity (activity blockers)

- Corneal surface moist and glossy
- Exophthalmia - it consists in prominent eyeballs. Exophthalmia is commonly bilateral and rarely meets unilaterally. The look here is fixed and due to excessive opening of the fissure and tears to the eyes is double. Sometimes exophthalmia can progress to malignant form, setting up blindness.

- Congestion of the conjunctiva which is more intense at the edge of circumscribing the eyelids accompanied by hyper secretion; - limiting upward movement of the eyeball to a certain threshold; - inability to perform eye movements

Autoimmune diseases are conditions characterized by the fact that the body is attacked by its own immune system.
- Organ specific diseases are different: Hashimoto's thyroiditis, myasthenia, juvenile insulin dependent diabetes.
- Non-specific organ diseases include disseminated lupus erythematosus, rheumatoid arthritis and dermatopolimyositis.



Treatment of most autoimmune diseases may act only on the symptoms and usually calls mainly on corticosteroids and immunosuppressants, and, sometimes, to plasmaphereses (consisting of plasma exchange in the extraction of unwanted substances in the blood). The autoimmune disease list of symptoms is long and the symptoms are highly complex, but instead of an autoimmune disease list of symptoms I will try to describe the diseases in general terms and name some of the symptoms.

Autoimmune diseases are a heterogeneous collection of diseases with a subtle relation, which is difficult to understand. It is a list constantly added with new diseases. The diseases in this category have multiple symptoms and locations and are very different. A classification has been possible only in recent years due to scientific advances. And many, many questions. These are autoimmune diseases.

Naturally, each of us is aware that in one way or another we undermine our own health by smoking, alcohol abuse, inadequate nutrition with an excess of sweets and fats, inactivity stress and insufficient rest. Well, surprisingly, in some cases the body itself goes beyond control and uses its defense mechanisms against its own cells, as it happens in autoimmune diseases. Normally, the body reacts in a complex immune response in the face of antigens: bacteria, viruses, toxins, cancer cells, proteins, tissues, foreign bodies.

In autoimmune diseases such a response is prompt and intensive extends to the tissues the system considers foreign, and against which produce abnormal antibodies. It is still unclear exactly what causes the body to react in this devastating way. The usual suspects are genetic factors, organic or functional alterations of cells, which make them seem abnormal external factors (infectious, physical, chemical or drugs) that act on tissues or a correct initial response against a foreign antigen that is diverted later against a own components.

Red blood cells may be contested, blood vessels, liver or kidney tissues, endocrine glands, muscles, skin, joints, etc.. Sometimes the system attacks a single organ, such as the thyroid, sometimes the system attacks a tissue found in different organs, such as basal membrane of the lungs or kidneys, in Goodpasture's syndrome. Sometimes there coexist several autoimmune diseases (eg, thyroid and diabetes), sometimes a single disease is systemic in nature, such as lupus.

There is no common symptomatology for all these various diseases. However, usually the patients have a high fever or persistent dizziness, malaise and a chronic feeling of fatigue. What brings them to the doctor are usually manifestations of the disease in question, the result of severe functional and organic alterations.

Hashimoto thyroiditis is a chronic inflammation of the thyroid, evidenced by an increase in thyroid volume and evidence of thyroid failure (weight gain, rough skin, feeling of fatigue, decreased heart rate, etc.). In rare cases, the disease may progress to a hypersecretion of thyroid hormones. Graves disease is manifested by the appearance of a goiter, with signs of glandular hypersecretion (weight loss, nervousness, trouble sleeping, shaking of limbs, fatigue, muscle weakness, increased heart rate) and sensitivity to light, while the eyes seem to pop out of their orbits.

Pituitary tumors are pathological processes occurring in the pituitary gland, a structure with endocrine activity, located in the brain. Although its dimensions are very small, the pituitary has a very important role in the secretion of hormones that affect various organs and systems and participate generally in the maturing of the body.



Pituitary tumors represent 10-25% of all intracranial tumors by location. Pituitary disease symptoms are usually found in close examination because they are not immediately apparent as clear-cut signs of disease. Pituitary tumors are classified into 3 groups: Benign adenomas - tumors that are not cancer - They have a very slow growth rate and are not able to metastasize (to expand through the blood stream, the lymphatic system, in other parts of the body, at a distance from where the initial neoplasia took place).

Invasive pituitary adenomas - are tumors that are capable of expansion and invasion, especially in the cranial bones or sinuses located below the pituitary. Pituitary carcinomas - are malignancies (cancers). These are processes that extend into the central nervous system (brain and spinal cord) or outside it. Very few of pituitary tumors, however, are the result of neoplasia. This classification took into account the biological behavior of adenomas and their evolution, and is currently widely accepted by specialists in the field.

But most tumors are adenomas and only a small fraction of them are show pituitary disease symptoms. Invasive adenomas (35% of pituitary neoplasia cases) can invade the skull bones and the sphenoid sinus. Of all pituitary tumors, carcinomas represent 0.1-0.2%.

Pituitary adenomas can be classified according to:
The anatomy of the tumor – tumors are grouped according to size, which is determined from imagery measurements into: microadenomas (10 mm in diameter) and macroadenomas (over 1 cm diameter). Macroadenomas, in turn, can be split into encapsulated macroadenomas or invasive macroadenomas (localized or diffuse). Most tumors are microadenomas. This classification of adenomas according to size, extension and by exploring the invasineveness of the tumor using imagery is extremely detailed and complex.

Neurologic and radiologic scans include (among others):
- X ray of the skull (profile) to view the walls of the pituitary, to measure its diameters and then to classify adenomas.
- pneumoencephalography or PEG - is a more complicated method by which to view the amount of air that will deploy in the cerebrospinal fluid space above the sella turcica.
- carotid artery angiography - an investigation is carried out routinely in the laboratory analysis of pituitary tumors, but only if there are suspected vascular lesions.
- polytomography - special tomography is a method which makes detailed images (by consecutive sections) of the structures difficult to access, using a special device, able to perform complex movements.
- CT (computer tomography) - the modern method which can do sections at 3 mm distance. It has many advantages: viewing the structures surrounding the adenoma, capsule, integrity of bone walls and the invasive nature of the adenoma.

According to radio-anatomic classification, there are 4 stages of adenomas, as follows: Stage 1 - adenoma 1 cm in diameter, without extension to the sella; Stage 2 - macroadenoma (over 1 cm diameter) with possible extension to the sella; Stage 3 - macroadenoma with enlargement and invasion of the supersellar space; Stage 4 - macroadenoma that goes beyond the sella and walls.

Niemann-Pick disease is a genetic disease of the metabolism in which the deficiency of the lysosomal enzyme acid –can cause pathological accumulation of lipids in all body cells but mainly in the spleen, liver, lung, bone marrow and brain. The disease is rare, and occurs in all races and both sexes.



Niemann Pick disease is transmitted autosomal recessive, which means that both parents were heterozygous-had one gene mutation present (but clinically healthy carriers of the mutation) and one in four children (25%) - heterozygous-will "inherit" the mutation genes from both parents and will become a patient. The gene that encodes the synthesis is located at chromosome 11p. There have been identified 12 mutations that can cause Niemann-Pick disease type A and type B.

Niemann Pick disease symptoms - The Niemann Pick disease symptoms are varied and differ depending on the type of the disease. There are described four types of Niemann-Pick disease, of which only type A and B are determined by scarcity (types C and D are determined by abnormal transport of cholesterol to brain cells, with accumulation of cholesterol in lysosomes).

Type A Niemann-Pick disease is the most common (almost 80% of cases) and is characterized by a normal aspect of the child at birth, possibly prolonged jaundice. By the age of 6 months there is evidence of hepatic and spleen enlargement and psychomotor retardation; neuropsychological deterioration is rapidly progressive. Manifestations of this disease are:

Eye: "cherry-red spot" in 50% of patients; Respiratory: - recurrent respiratory infections; Lung: diffuse reticular and fine nodular infiltrate; Abdominal: the increase in volume of the abdomen; Liver: hepatomegaly, jaundice neonatal; Spleen: spleen enlargement; Gastrointestinal: vomiting, constipation, difficulty eating; Skeletal disorders: osteoporosis; Neurological: Central nervous system: hypotonia, hyporeflexia, psychomotor retardation; stiffness; Blood: - anemia; "Niemann-Pick cells" in bone marrow biopsy;

Type B Niemann-Pick disease can begin during the infant or child in a routine consultation, the spleen-hepatomegaly, which is progressive and leads to increase in volume of the abdomen, in time, the associated impairment of the lung may be severe; around the age of 15-20 years is normal. Patients with type C Niemann-Pick disease have often prolonged jaundice (up to age 1-2 years) and progressive neuropsychological slow deterioration.

The spleen-hepatomegaly is less important compared with types A and B disease and survival is possible up to adult age. Specific diagnosis of Niemann-Pick disease is determining by the level of activity in leukocytes fibroblast cultures, which is very low (below 5%). In some countries this investigation is not yet available. In the absence of specific examination, histopathological examination of various tissues obtained by liver puncture biopsy= may bring evidence in favor of the diagnosis by revealing Niemann-Pick cell.

Niemann-Pick disease can be present in other diseases such as: Wolman disease, storage disease cholesterol esters or lipoprotein-lipase deficiency. Hematological evaluation can detect a decrease in the number of platelets, white cells and red blood cells. Ophthalmologic examination may reveal, for half of the patients' red cherry spot. Analysis of mutations is possible in specialized laboratories (not yet available in some countries), specifying the mutation is useful for a patient to identify the carriers in their families at risk and prenatal diagnosis.

The Lyme disease is a bacterial infection that is transmitted by a tick bite. Most frequent symptoms of Lyme disease are fever, fatigue, headache and eritema. Because these symptoms are encountered in many other diseases, there must be done a differential examination diagnose.



Isodex scapularis, the deer tick or black tick is the vector infectious bacterium Borrelia burgdorferi. It is responsible for the occurrence of the Lyme disease. It normally lives in mice, squirrels and other small animals.

The tick has three developmental stages: larva, nymph and adult. When an infected tick feeds on blood of a sick animal, and ingest it, the bacteria will live in the intestine. These ticks will then infect other men or animals at their next meal. Most cases of infection occur at the end of spring or summer when the tiny tick nymphs are most active in the environment and human activities are frequent.

The rest live in the fur deer ticks, which do not contract the Lyme disease. The treatment for the Lyme disease consists of antibiotics.

Causes - The deer tick is the principal vector of the Lyme disease but has not been shown whether other ticks may or may not become vectors.

Other modes of transmission of disease: -people contacts; -transmission during pregnancy; -by blood transfusion; -from the animals.

Interpersonal transmission: it has not yet been proven that the disease can be transmitted by kissing, touching or sex with an infected person.

During pregnancy, the disease can lead to infection of the placenta and abortion have not yet been registered, neither negative effects on the fetus. If the mother is treated properly after the transmission of the disease with antibiotics, there should not be any risks.

Although there were not yet registered any cases of infection through blood transfusions, it has been discovered that the bacterium survives in infected blood donations. The patients or infected people can donate blood preserved for 12 months after the last dose of antibiotic treatment.

Pets can have the Lyme disease but there is no evidence that they may become vectors for human beings, instead they bring ticks into the house and garden. The disease is not transmitted through the squirrel or deer meat, but it should still be properly cooked to appropriate temperatures before eating.

Symptoms - The first sign of infection is usually called a circular migratory erythema. It occurs in 70-80% of infected people and the area of the tick bite begins to get red, after a period of three to thirty days. A distinguishing feature of skin is gradual expansion of several days, reaching up to 30 cm. The erythema may become normal colored center as they expand as compared with an ox-eye. It can be warm and painless. Some people develop other flushes in different areas over several days.

Later symptoms of Lyme disease: -fatigue; -chills; fever; -headache; -cramps; -lymphadenopathy. In some cases, redness may be absent. The later symptoms of Lyme disease, left untreated can help the infection to spread to other parts of the body in a few weeks, causing a variety of symptoms:-motor weakness of both sides of the face-Bell's palsy;-severe headache and neck pain due to meningitis;- pain that leads to insomnia;-throb and dizziness due to arrhythmias; -migratory pain to joints. Most symptoms resolve even without treatment.

Some of the pain we are feeling is sometimes the symptom of a disease, but on other occasions it can only be something temporary that is caused by something unimportant and which goes away very soon. If you want to know if your pains are symptoms of severe liver disease, then you should know what that pain is. Generally, symptoms of severe liver disease involve less pain and more coloring, namely yellow.



A "tired" liver is wrapped in fat - After a high fat meal and "sprayed" with alcohol, pain may be caused by bile or pancreas. Many of us sometimes say "My liver hurts, it si from fatigue”. How true is this "saying"? People all over the world have adapted quickly to the fast pace of a market economy, with its continuous efforts. Fatigue and overwork are inherent and occurring in our lives everyday. We need to recognize this and know how to act. The liver, the "laboratory organ”, has at least 9 core functions and summarizes more than 2,500 known substances (and probably 25,000 unknown ones). Therefore, we must understand that the liver, necessarily grows "tired".

The liver has one of the best ways of regenerating the entire body. In particular, fatigue in the body does not create symptoms directly related to "place" where the liver is in the body. I mean, if you have pain in the right part of the abdomen, this does not automatically mean that you are feeling the pain caused by a tired liver. We must not forget, for example, that running in physical education class in school also caused the right side of the abdomen to hurt.

That pain, which disappear once we stopped running, had little connection with the liver, but with the large intestine which forms an elbow near the liver and gas starts going up, pressuring the. The pain is normal there, and not from an accumulation of blood in the liver. We also remember, some of us, that if we eat too much then we feel pain or discomfort in the liver. In principle, this is gall bladder pain. The gall bladder is a neighbor to the liver and its contraction causes noises. Also, the pancreas might be involved in this pain.

The full anatomical structure of the liver organ does not allow the location of sensitive nerve fibers within the liver himself, only on the shell of the liver, which is also called the hepatic Glisson capsule. Thus the liver only hurts in unusual circumstances, when there are abscesses in the liver, when there is a large tumor or when the heart fails to collect blood and lets it accumulate, dialting the liver.

So, to sum it up, symptoms of severe liver disease usally involve other symptoms, aside from the pain. There is jaundice, there is fatigue throughout the entire body, which is to say that the liver causes the fatigue here, not the fatigue causes the liver pain. Also, the stool might be light in coloe. Severe liver diseases include many types of hepatitis, liver cancer, cirrhosis and so on. For these, looking for symptoms on google will not do you much good. If you suspect you are seriously ill, get out fo the chair and go to a doctor. Now.

The Canavan disease primarily affects children of Eastern and Central Europe Hebrew (Ashkenazi) and is an inherited neurological disorder that deteriorates the brain. The Canavan disease is caused by a deficiency of an enzyme called aspartoacilaza (ASPA).



This deficiency leads to an increased level of N-acetilaspartic (NAA) in the brain. NAA causes a chemical imbalance that destroys myelin. Myelin, known as "the white substance” in the brain protects nerves and allows you to send messages to and from the brain. If the chemical imbalance of "white substance" foam is unable to send messages, it causes Canavan disease symptoms.

Signs of Canavan disease usually appear when children are between 3 and 6 months. These include delay in development (motor slowness), the extension of the head, and loss of muscle tone, poor head control, and severe feeding problems. As the disease evolves, the Canavan disease symptoms consist of seizures, blindness, nerve damage and often eye damage, heartburn (gastrointestinal reflux) and dysphasia. Most children with Canavan disease die in the first decade of their life.

Canavan Disease is a genetic disease, an inborn neurological malformation in which the white material of the brain tissue degenerates, leading to spongiform. There is no antidote or a standard course of medical treatment. Canavan disease symptoms (occurring at an early age) include mental retardation and loss of motor skills. Death occurs at ages between 4 and 20 years. Canavan disease is one of the most common degenerative brain disease that appears in early ages. In the Ashkenazi Jewish ethnic group, about 2% of members are carriers of this hereditary disease. Of course, Canavan syndrome occurs also in other ethnic groups.

Ashkenazi Hebrew people in the group, more and more couples require genetic testing before marriage: if none or only one of the prospective parents is carrier of a gene mutation, there was a 25% chance for each pregnancy that the future child to have Canavan disease.

For this reason, DelphiTest GmbH Germany developed a new genetic test based on analysis of oral fluid samples. Customers can easily and without pain take the samples in their home. The samples are then forwarded to the laboratory in Regensburg where the gene coding region will be analyzed. The full analysis costs 400 EUR, - for each member of the couple, as described by Dr. Frank Pfannenschmid.

The Canavan disease is an autosomal recessive disorder: if the child contracted the disease, both parents must be the bearers of defect genes. The Canavan disease is a genetic disease, an inborn neurological malformation in which the white matter of brain tissue to degenerate transforming spongiform. There is no antidote or a standard course for medical treatment. From what we know, there are only two laboratories in the world that offers genetic testing for Canavan disease. These labs require their clients' blood samples to be transported very carefully, requiring high costs.

The genetic test enables the customers to check whether their genes provide increased certainty. Genetic counseling is very important in helping couples who present risks in exploring their family planning options. In America, many rabbis advise young couples to perform the Canavan test. The Canavan disease can be identified by a simple prenatal blood test that determines the absence of ASPA enzyme or mutations in the genes. A second method is measuring the NAA levels in the amniotic fluid, determining the exact NAA levels in amniotic fluid.