Vogt-Koyanagi-Harada syndrome (VKH syndrome) is a condition seen in humans and dogs involving various melanocyte-containing organs, characterized by uveitis (inflammation of the inside of the eye), poliosis (whitening of hair), vitiligo (loss of pigment in the skin), and meningitis, although dogs with this syndrome rarely develop meningitis. It is also known as uveodermatologic syndrome.

VKH syndrome is an immune-mediated disease. The mechanism of the disease is thought to be T helper cell mediated autoimmune attack of melanocytes in the skin and uvea of dogs and humans, and in the central nervous system and inner ear of humans.[1]

In humans there is a higher rate of VKH syndrome in people of Asian, Latin, and Mediterranean descent.[2]

In dogs VKH syndrome (often called VKH-like syndrome) most commonly affects young animals and is seen most commonly in the Akita Inu, but also in the Siberian Husky and Samoyed.[2] Uveitis usually occurs first and is often severe enough to cause blindness. VKH syndrome can also cause retinal detachment, cataracts, and glaucoma. Pigment partly disappears from the retinal pigment epithelium and iris. Skin lesions include loss of pigment and hair on the eyelids, nose, and lips. Symptoms and biopsy will confirm the diagnosis. Treatment is with immunosuppressive drugs such as prednisone and azathioprine. The prognosis is guarded.[2]

It is named for Alfred Vogt, Yoshizo Koyanagi, and Einosuke Harada.[3][4][5][6]

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Vitiligo (pronounced /v?t?’la?go?/) or leukoderma is a chronic skin disease that causes loss of pigment, resulting in irregular pale patches of skin. It occurs when the melanocytes, cells responsible for skin pigmentation, die or are unable to function. The precise cause of vitiligo is complex and not fully understood. There is some evidence suggesting it is caused by a combination of auto-immune, genetic, and environmental factors. The population incidence worldwide is considered to be between 1% and 2%.[1]

According to Diseases Database: “A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached.”

Half of people with vitiligo develop patches of de-pigmented skin appearing on extremities before their 20s. The patches may grow, shrink, or remain constant in size. Patches often occur symmetrically across both sides on the body. Occasionally small areas may repigment as they are recolonised by melanocytes. The location of vitiligo affected skin changes over time, with some patches re-pigmenting and others becoming affected.

Vitiligo may also be caused by stress that affects the immune system, leading the body to react and start eliminating skin pigment.

Vitiligo on the scalp may affect the color of the hair (though not always), leaving white patches or streaks. It will similarly affect facial and body hair.

Some symptoms are:

Vitiligo can have a significant effect on the psychological well being of the patient.[2] This is especially true for darker skinned patients as the contrast between pigmented and depigmented skin can be quite drastic.

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B12 deficiency is a reduction in vitamin B12 from inadequate dietary intake or impaired absorption. The condition is commonly asymptomatic, but can also present as anemia characterized by enlarged blood corpuscles, so-called megaloblastic anemia. However in serious cases deficiency can potentially cause severe and irreversible damage to the nervous system, including subacute combined degeneration of spinal cord.

The anemia is thought to be due to problems in DNA synthesis, specifically in the synthesis of thymine, which is dependent on products of the MTR reaction. Other cell lines such as white blood cells and platelets are often also low. Bone marrow examination may show megaloblastic hemopoiesis. The anemia is easy to cure with vitamin B12.

Early and even fairly pronounced deficiency does not always cause distinct or specific symptoms. Common early symptoms are tiredness or a decreased mental work capacity, decreased concentration and decreased memory, irritability and depression.

Sleep disturbances may occur, because B12 may be involved in the regulation of the sleep wake cycle by the pineal gland (through melatonin)[1].

Neurological signs of B12 deficiency, which can occur without anemia, include sensory disturbances due to damage to peripheral nerves caused by demyelination and irreversible nerve cell death. Symptoms include numbness, tingling of the extremities, disturbed coordination and, if not treated in time, an ataxic gait, a syndrome known as subacute combined degeneration of spinal cord.

B-12 deficiency can also cause symptoms of mania and psychosis.[2][3]

Recent studies have devalued a possible connection between B12 deficiency and Alzheimer’s dementia, and such a correlation is unlikely as of June 2007.[4]

Studies showing a relationship between clinical depression levels and deficient B12 blood levels in elderly people are documented in the clinical literature.[5] and 2002 [6]

Bipolar disorder appears to genetically co-segregate with the hereditary B12-deficiency disorder pernicious anemia [7][8].

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A ventricular septal defect (VSD) is a defect in the ventricular septum, the wall dividing the left and right ventricles of the heart.

The ventricular septum consists of an inferior muscular and superior membranous portion and is extensively innervated with conducting cardiomyocytes. The membranous portion, which is close to the atrioventricular node, is most commonly affected in adults and older children.[1][2]

Congenital VSDs are collectively the most common congenital heart defects.[3]

A VSD can be detected by cardiac auscultation. Classically, a VSD causes a pathognomonic holo- or pansystolic murmur. Auscultation is generally considered sufficient for detecting a significant VSD. The murmur depends on the abnormal flow of blood from the left ventricle, through the VSD, to the right ventricle. If there is not much difference in pressure between the left and right ventricles, then the flow of blood through the VSD will not be very great and the VSD may be silent. This situation occurs a) in the fetus (when the right and left ventricular pressures are essentially equal), b) for a short time after birth (before the right ventricular pressure has decreased), and c) as a late complication of unrepaired VSD. Confirmation of cardiac auscultation can be obtained by non-invasive cardiac ultrasound (echocardiography). To more accurately measure ventricular pressures, cardiac catheterization, can be performed.

During ventricular contraction, or systole, some of the blood from the left ventricle leaks into the right ventricle, passes through the lungs and reenters the left ventricle via the pulmonary veins and left atrium. This has two net effects. First, the circuitous refluxing of blood causes volume overload on the left ventricle. Second, because the left ventricle normally has a much higher systolic pressure (~120 mm Hg) than the right ventricle (~20 mm Hg), the leakage of blood into the right ventricle therefore elevates right ventricular pressure and volume, causing pulmonary hypertension with its associated symptoms. This effect is more noticeable in patients with larger defects, who may present with breathlessness, poor feeding and failure to thrive in infancy. Patients with smaller defects may be asymptomatic.

Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth.

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Variegate porphyria is an autosomal dominant porphyria[1] that can have acute (severe but usually not long-lasting) symptoms along with symptoms that affect the skin. The disorder results from low levels of the enzyme responsible for the seventh step in heme production. Heme is a vital molecule for all of the body’s organs. It is a component of hemoglobin, the molecule that carries oxygen in the blood.

Many people with this disorder never experience symptoms. When symptoms occur, they can include acute attacks (similar to acute intermittent porphyria), skin damage, or both. Acute attacks usually begin in adulthood and cause abdominal pain, vomiting, diarrhea and constipation. During an attack, a person may also experience muscle weakness, seizures, and mental changes such as anxiety and hallucinations. These signs and symptoms are triggered by nongenetic factors such as certain drugs, dieting or fasting, certain hormones and stress.

Some people with variegate porphyria have skin that is overly sensitive to sunlight. Areas of skin exposed to the sun develop severe blistering, scarring, changes in pigmentation, and increased hair growth. Exposed skin becomes fragile and is easily damaged.

Rarely, the signs and symptoms of variegate porphyria can begin in infancy or early childhood. In such cases, the signs and symptoms are usually more severe than those starting later in life. In addition to the health problems described above, children with this disorder may have mental retardation and grow more slowly than other children.

This type of porphyria is most common in the white population of South Africa; about 3 per 1,000 people in this population are diagnosed each year. The disorder occurs much less frequently in other parts of the world.

When it does occur in other populations (such as Switzerland), it can be with different mutations than in South Africa.[2]

It is also found in Argentina[3] and Sweden.[4]

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VATER syndrome or VACTERL association is a nonrandom association of birth defects. The reason it is called an association, rather than a syndrome is that while all of the birth defects are linked, it is still unknown which genes or sets of genes cause these birth defects to occur.

Each child with this condition can be truly unique, with defects being different from any other child. At present this condition is treated after birth with issues being approached one at a time.

VACTERL association can be linked to other similar conditions such as, Klippel Feil and Goldenhar Syndrome including crossovers of conditions.

No specific genetic or chromosome problem has been identified with VACTERL association. VACTERL can be seen with some chromosomal defects such as Trisomy 18 and is more frequently seen in babies of diabetic mothers. VACTERL association, however, is most likely caused by multiple factors.

VACTERL association specifically refers to the abnormalities in structures derived from the embryonic mesoderm.

Vertebral anomalies, or defects of the spinal column, usually consist of small (hypoplastic) vertebrae or hemivertebra where only one half of the bone is formed. About 70 percent of patients with VACTERL association will have vertebral anomalies. In early life these rarely cause any difficulties, although the presence of these defects on a chest x-ray may alert the physician to other defects associated with VACTERL. Later in life these spinal column abnormalities may put the child at risk for developing scoliosis, or curvature of the spine.

Anal atresia or imperforate anus is seen in about 55 percent of patients with VACTERL association. These anomalies are usually noted at birth and often require surgery in the first days of life. Sometimes babies will require several surgeries to fully reconstruct the intestine and anal canal.

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Parasitic melanoderma (commonly known as Vagabond’s disease, vagrant’s disease and Greenhow’s disease) is an exacerbation of body lice (scientifically referred to as Pediculosis)[1].

Its clinical features include skin abrasion (excoriations) and abnormal skin discolouration (melanoderma) at the affected site.[1]

It is caused by Phthirus pubis (crab louse) and characterized by subcutaneous hemmorrhages.[citation needed]

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Vaginismus (the Latin equivalent of the word Vaginism) is a condition which affects a woman’s ability to engage in any form of vaginal penetration, including sexual penetration, insertion of tampons, and the penetration involved in gynecological examinations. This is the result of a conditioned reflex of the pubococcygeus muscle, which is sometimes referred to as the “PC muscle”. The reflex causes the muscles in the vagina to tense suddenly, which makes any kind of vaginal penetration—including sexual penetration—either painful or impossible.

A vaginismic woman does not consciously control the spasm. The vaginismic reflex can be compared to the response of the eye shutting when an object comes towards it. The severity of vaginismus and the pain during penetration, including sexual penetration, varies from woman to woman.

The conditioned reflex can create a vicious circle for vaginismic women. One example: if a female learns that the first time she engages in penetrative sex that it will be painful, she may develop vaginismus because she expects pain. If she then attempts to engage in penetrative sex, the muscle spasm will make penetrative sex painful. This and each further attempt at sexual penetration confirms her fear of pain and may worsen the condition. Naturally, penetration may be painful without vaginismus or psychological prerequisite as well.[citation needed]

Primary vaginismus occurs when a woman has never been able to have penetrative sex or experience any kind of vaginal penetration. It is commonly discovered in teenagers and women in their early twenties, as this is when many young women in the Western world will initially attempt to use tampons, have penetrative sex, or undergo a Pap smear. Women who have vaginismus may not be aware of their condition until they attempt vaginal penetration. It may be confusing for a woman to discover she has vaginismus. She may believe that vaginal penetration should be naturally easy, or she may be unaware as to the reason for her condition.[citation needed]

Some of the things that may cause primary vaginismus are:

Secondary vaginismus occurs when a woman who has previously been able to achieve penetration develops vaginismus. This may be due to physical causes such as a yeast infection or trauma during childbirth, or it may be due to psychological causes. The treatment for secondary vaginismus is the same as for primary vaginismus, although, in these cases, previous experience with successful penetration can assist in a more rapid resolution of the condition.[citation needed]

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Vaginitis is an inflammation of the vaginal mucosa and often associated with an irritation or infection of the vulva leading to vulvovaginitis. It is a common problem.

A woman with this condition may have itching or burning and may notice a discharge. In general, these are symptoms of vaginitis:

Vulvovaginitis can affect women of all ages and is very common. Specific forms of vaginitis are:

Infectious vaginitis accounts for 90% of all cases in reproductive age women and is represented by the triad:

Other less common infections are caused by gonorrhea, chlamydia, mycoplasma, herpes, campylobacter and some parasites.[1]

Pre-pubescent girls may also have infectious vaginitis, although the causes are different than those for women:

The PH balance in girls’ bodies is not conducive to Candida albicans, so they are unlikely to contract a yeast infection.

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Van Der Woude syndrome (VDWS) consists of the following characteristics: cleft lip with or without cleft palate, isolated cleft palate, pits or mucous cysts on the lower lip, and hypodontia. It is the most common syndromic form of cleft lip and palate (CLP), accounting for 2% of all CLP cases (usually CLP is nonsyndromic). Affected individuals have normal intelligence.

It was first characterized in 1954.[1]

VDWS is an autosomal dominant or sporadic inheritance caused by mutations of the IRF6 gene, located on chromosome 1 at 1q32-q41. (Popliteal pterygium syndrome can also be caused by mutations of this gene.)

In 2002 Kondo et al. described a pair of monozygotic twins discordant for VDWS whose parents did not have the disorder.[2][3]

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