Pigmentation Health Dictionary

Increased pigmentation with light brown patches on the skin, especially in pregnancy where it appears as blotches on the face. Adrenal insufficiency. A side-effect of the contraceptive pill. Treatment. Echinacea, Ginseng, Liquorice, Sarsaparilla, Wild Yam. (A. Warren-Davis FNIMH) Tinctures. Formula. Ginseng 2; Wild Yam 1. Liquorice quarter; One 5ml teaspoon in water thrice daily. Topical. Distilled Extract Witch Hazel. Cider vinegar.

Supplementation. Vitamin A, B-complex. PABA. ... chloasma

A disease causing failure of adrenal gland function, in particular deficiency of adrenal cortical hormones, mainly cortisol and aldosterone. Commonest causes are tuberculosis and auto- immune disease.

Symptoms: (acute) abdominal pain, muscle weakness, vomiting, low blood pressure due to dehydration, tiredness, mental confusion, loss of weight and appetite. Vomiting, dizzy spells. Increased dark pigmentation around genitals, nipples, palms and inside mouth. Persistent low blood pressure with occasional low blood sugar. Crisis is treated by increased salt intake. Research project revealed a craving for liquorice sweets in twenty five per cent of patients.

Herbs with an affinity for the adrenal glands: Parsley, Sarsaparilla, Wild Yam, Borage, Liquorice, Ginseng, Chaparral. Where steroid therapy is unavoidable, supplementation with Liquorice and Ginseng is believed to sustain function of the glands. Ginseng is supportive when glands are exhausted by prolonged stress. BHP (1983) recommends: Liquorice, Dandelion leaf.

Alternatives. Teas. Gotu Kola, Parsley, Liquorice root, Borage, Ginseng, Balm.

Tea formula. Combine equal parts: Balm and Gotu Kola. Preparation of teas and tea mixture: 1 heaped teaspoon to each cup boiling water: infuse 5-10 minutes; 1 cup 2 to 3 times daily.

Tablets/capsules. Ginseng, Seaweed and Sarsaparilla, Wild Yam, Liquorice. Dosage as on bottle. Formula. Combine: Gotu Kola 3; Sarsaparilla 2; Ginseng 1; Liquorice quarter. Doses. Powders: 500mg (two 00 capsules or one-third teaspoon). Liquid extracts: 30-60 drops. Tinctures: 1-2 teaspoons 2 to 3 times daily.

Formula. Alternative. Tinctures 1:5. Echinacea 20ml; Yellow Dock 10ml; Barberry 10ml; Sarsaparilla 10ml; Liquorice (liquid extract) 5ml. Dose: 1-2 teaspoons thrice daily.

Supplementation. Cod liver oil. Extra salt. B-Vitamins. Folic acid. ... addison’s disease

The cause of Addison’s disease (also called chronic adrenal insu?ciency and hypocortisolism) is a de?ciency of the adrenocortical hormones CORTISOL, ALDOSTERONE and androgens (see ANDROGEN) due to destruction of the adrenal cortex (see ADRENAL GLANDS). It occurs in about 1 in 25,000 of the population. In the past, destruction of the adrenal cortex was due to TUBERCULOSIS (TB), but nowadays fewer than 20 per cent of patients have TB while 70 per cent suffer from autoimmune damage. Rare causes of Addison’s disease include metastases (see METASTASIS) from CARCINOMA, usually of the bronchus; granulomata (see GRANULOMA); and HAEMOCHROMATOSIS. It can also occur as a result of surgery for cancer of the PITUITARY GLAND destroying the cells which produce ACTH (ADRENOCORTICOTROPHIC HORMONE)

– the hormone which provokes the adrenal cortex into action.

Symptoms The clinical symptoms appear slowly and depend upon the severity of the underlying disease process. The patient usually complains of appetite and weight loss, nausea, weakness and fatigue. The skin becomes pigmented due to the increased production of ACTH. Faintness, especially on standing, is due to postural HYPOTENSION secondary to aldosterone de?ciency. Women lose their axillary hair and both sexes are liable to develop mental symptoms such as DEPRESSION. Acute episodes – Addisonian crises – may occur, brought on by infection, injury or other stressful events; they are caused by a fall in aldosterone levels, leading to abnormal loss of sodium and water via the kidneys, dehydration, low blood pressure and confusion. Patients may develop increased tanning of the skin from extra pigmentation, with black or blue discoloration of the skin, lips, mouth, rectum and vagina occurring. ANOREXIA, nausea and vomiting are common and the sufferer may feel cold.

Diagnosis This depends on demonstrating impaired serum levels of cortisol and inability of these levels to rise after an injection of ACTH.

Treatment consists in replacement of the de?cient hormones. HYDROCORTISONE tablets are commonly used; some patients also require the salt-retaining hormone, ?udrocortisone. Treatment enables them to lead a completely normal life and to enjoy a normal life expectancy. Before surgery, or if the patient is pregnant and unable to take tablets, injectable hydrocortisone may be needed. Rarely, treated patients may have a crisis, perhaps because they have not been taking their medication or have been vomiting it. Emergency resuscitation is needed with ?uids, salt and sugar. Because of this, all patients should carry a card detailing their condition and necessary management. Treatment of any complicating infections such as tuberculosis is essential. Sometimes DIABETES MELLITUS coexists with Addison’s disease and must be treated.

Secondary adrenal insu?ciency may occur in panhypopituitarism (see PITUITARY GLAND), in patients treated with CORTICOSTEROIDS or after such patients have stopped treatment.... addison’s disease

An inherited condition, the adrenogenital syndrome – also known as congenital adrenal hyperplasia – is an uncommon disorder affecting about 1 baby in 7,500. The condition is present from birth and causes various ENZYME defects as well as blocking the production of HYDROCORTISONE and ALDOSTERONE by the ADRENAL GLANDS. In girls the syndrome often produces VIRILISATION of the genital tract, often with gross enlargement of the clitoris and fusion of the labia so that the genitalia may be mistaken for a malformed penis. The metabolism of salt and water may be disturbed, causing dehydration, low blood pressure and weight loss; this can produce collapse at a few days or weeks of age. Enlargement of the adrenal glands occurs and the affected individual may also develop excessive pigmentation in the skin.

When virilisation is noted at birth, great care must be taken to determine genetic sex by karyotyping: parents should be reassured as to the baby’s sex (never ‘in between’). Blood levels of adrenal hormones are measured to obtain a precise diagnosis. Traditionally, doctors have advised parents to ‘choose’ their child’s gender on the basis of discussing the likely condition of the genitalia after puberty. Thus, where the phallus is likely to be inadequate as a male organ, it may be preferred to rear the child as female. Surgery is usually advised in the ?rst two years to deal with clitoromegaly but parent/ patient pressure groups, especially in the US, have declared it wrong to consider surgery until the children are competent to make their own decision.

Other treatment requires replacement of the missing hormones which, if started early, may lead to normal sexual development. There is still controversy surrounding the ethics of gender reassignment.

See www.baps.org.uk... adrenogenital syndrome

Alopecia areata is a common form of reversible hair loss which may be patchy, total on the scalp, eyebrows or eyelashes, or universal on the body. The onset is sudden at any age and the affected scalp-skin looks normal. The hair follicles remain intact but ‘switched o?’ and usually hair growth recovers spontaneously. No consistently e?ective treatment is available but injections of CORTICOSTEROIDS, given with a spray gun into the scalp, may be useful. The regrown hair may be white at ?rst but pigmentation recovers later.... alopecia areata

A CYTOTOXIC antibiotic, obtained from Streptomyces verticillus, used to treat solid cancerous tumours of the upper part of the gut and genital tract, and lymphomas. Like other cytotoxic drugs it can have serious side-effects, and bleomycin may cause pulmonary ?brosis and skin pigmentation.... bleomycin

Also called hypo-pigmentation, this congenital or acquired disorder is one in which the skin loses its pigmentation because of reduced MELANIN production. It can be classi?ed into three groups: VITILIGO, ALBINISM and post-in?ammatory hypopigmentation.... depigmentation

A rare disease in which areas of bone are replaced by ?brous tissue (see CONNECTIVE TISSUE). This renders the bone fragile and liable to fracture. It may involve only one bone – usually the thigh bone or FEMUR – or several bones. This latter form of the disease may be accompanied by pigmentation of the skin and the early onset of PUBERTY.... fibrous dysplasia

A disease in which cirrhosis of the liver (see LIVER, DISEASES OF), enlargement of the SPLEEN, pigmentation of the skin, and DIABETES MELLITUS are associated with the abnormal and excessive deposit in the organs of the body of the iron-containing pigment, haemosiderin. It is caused by an increase in the amount of iron absorbed from the gastrointestinal tract.... haemochromatosis

1. Beta carotene: Carrots are a rich source of this powerful antioxidant, which, among other vital uses, can be converted into vitamin A in the body to help maintain healthy skin. 2. Digestion: Carrots increase saliva and supply essential minerals, vitamins and enzymes that aid in digestion. Eating carrots regularly may help prevent gastric ulcers and other digestive disorders. 3. Alkaline elements: Carrots are rich in alkaline elements, which purify and revitalize the blood while balancing the acid/alkaline ratio of the body. 4. Potassium: Carrots are a good source of potassium, which can help maintain healthy sodium levels in the body, thereby helping to reduce elevated blood pressure levels. 5. Dental Health: Carrots kill harmful germs in the mouth and help prevent tooth decay. 6. Wounds: Raw or grated carrots can be used to help heal wounds, cuts and inflammation. 7. Phytonutrients: Among the many beneficial phytochemicals that carrots contain is a phytonutrient called falcarinol, which may reduce the risk of colon cancer and help promote overall colon health. 8. Carotenoids: Carrots are rich in carotenoids, which our bodies can use to help regulate blood sugar. 9. Fiber: Carrots are high in soluble fiber, which may reduce cholesterol by binding the LDL form (the kind we don’t want) and increasing the HDL form (the kind our body needs) to help reduce blood clots and prevent heart disease. 10. Eyes, hair, nails and more! The nutrients in carrots can improve the health of your eyes, skin, hair, nails and more through helping to detoxify your system and build new cells! 11. Improves vision There’s some truth in the old wisdom that carrots are good for your eyes. Carrots are rich in beta-carotene, which is converted into vitamin A in the liver. Vitamin A is transformed in the retina, to rhodopsin, a purple pigment necessary for night vision. Beta-carotene has also been shown to protect against macular degeneration and senile cataracts. A study found that people who eat large amounts of beta-carotene had a 40 percent lower risk of macular degeneration than those who consumed little. 12. Helps prevent cancer Studies have shown carrots reduce the risk of lung cancer, breast cancer and colon cancer. Falcarinol is a natural pesticide produced by the carrot that protects its roots from fungal diseases. Carrots are one of the only common sources of this compound. A study showed 1/3 lower cancer risk by carrot-eating rats. 13. Slows down aging The high level of beta-carotene in carrots acts as an antioxidant to cell damage done to the body through regular metabolism. It help slows down the aging of cells. 14. Promotes healthier skin Vitamin A and antioxidants protect the skin from sun damage. Deficiencies of vitamin A cause dryness to the skin, hair and nails. Vitamin A prevents premature wrinkling, acne, dry skin, pigmentation, blemishes and uneven skin tone. 15. Helps prevent infection Carrots are known by herbalists to prevent infection. They can be used on cuts—shredded raw or boiled and mashed. 16. Promotes healthier skin (from the outside) Carrots are used as an inexpensive and very convenient facial mask. Just mix grated carrot with a bit of honey. See the full recipe here: carrot face mask. 17. Prevents heart disease Studies show that diets high in carotenoids are associated with a lower risk of heart disease. Carrots have not only beta-carotene but also alpha-carotene and lutein. The regular consumption of carrots also reduces cholesterol levels because the soluble fibers in carrots bind with bile acids. 18. Cleanses the body Vitamin A assists the liver in flushing out the toxins from the body. It reduces the bile and fat in the liver. The fiber present in carrots helps clean out the colon and hasten waste movement. 19. Protects teeth and gums It’s all in the crunch! Carrots clean your teeth and mouth. They scrape off plaque and food particles just like toothbrushes or toothpaste. Carrots stimulate gums and trigger a lot of saliva, which, being alkaline, balances out the acid-forming, cavity-forming bacteria. The minerals in carrots prevent tooth damage. 20. Prevents stroke From all the above benefits it’s no surprise that in a Harvard University study, people who ate five or more carrots a week were less likely to suffer a stroke than those who ate only one carrot a month or less.... amazing health benefits of carrots

Diseases affecting the kidneys can be broadly classi?ed into congenital and genetic disorders; autoimmune disorders; malfunctions caused by impaired blood supply; infections; metabolic disorders; and tumours of the kidney. Outside factors may cause functional disturbances – for example, obstruction in the urinary tract preventing normal urinary ?ow may result in hydronephrosis (see below), and the CRUSH SYNDROME, which releases proteins into the blood as a result of seriously damaged muscles (rhabdomyolosis), can result in impaired kidney function. Another outside factor, medicinal drugs, can also be hazardous to the kidney. Large quantities of ANALGESICS taken over a long time damage the kidneys and acute tubular NECROSIS can result from certain antibiotics.

K

Diagram of glomerulus (Malpighian corpuscle).

Fortunately the body has two kidneys and, as most people can survive on one, there is a good ‘functional reserve’ of kidney tissue.

Symptoms Many patients with kidney disorders do not have any symptoms, even when the condition is quite advanced. However,

others experience loin pain associated with obstruction (renal colic) or due to infection; fevers; swelling (oedema), usually of the legs but occasionally including the face and arms; blood in the urine (haematuria); and excess quantities of urine (polyuria), including at night (nocturia), due to failure of normal mechanisms in the kidney for concentrating urine. Patients with chronic renal failure often have very di?use symptoms including nausea and vomiting, tiredness due to ANAEMIA, shortness of breath, skin irritation, pins and needles (paraesthesia) due to damage of the peripheral nerves (peripheral neuropathy), and eventually (rarely seen nowadays) clouding of consciousness and death.

Signs of kidney disease include loin tenderness, enlarged kidneys, signs of ?uid retention, high blood pressure and, in patients with end-stage renal failure, pallor, pigmentation and a variety of neurological signs including absent re?exes, reduced sensation, and a coarse ?apping tremor (asterixis) due to severe disturbance of the body’s normal metabolism.

Renal failure Serious kidney disease may lead to impairment or failure of the kidney’s ability to ?lter waste products from the blood and excrete them in the urine – a process that controls the body’s water and salt balance and helps to maintain a stable blood pressure. Failure of this process causes URAEMIA – an increase in urea and other metabolic waste products – as well as other metabolic upsets in the blood and tissues, all of which produce varying symptoms. Failure can be sudden or develop more slowly (chronic). In the former, function usually returns to normal once the underlying cause has been treated. Chronic failure, however, usually irreparably reduces or stops normal function.

Acute failure commonly results from physiological shock following a bad injury or major illness. Serious bleeding or burns can reduce blood volume and pressure to the point where blood-supply to the kidney is greatly reduced. Acute myocardial infarction (see HEART, DISEASES OF) or pancreatitis (see PANCREAS, DISORDERS OF) may produce a similar result. A mismatched blood transfusion can produce acute failure. Obstruction to the urine-?ow by a stone (calculus) in the urinary tract, a bladder tumour or an enlarged prostate can also cause acute renal failure, as can glomerulonephritis (see below) and the haemolytic-uraemia syndrome.

HYPERTENSION, DIABETES MELLITUS, polycystic kidney disease (see below) or AMYLOIDOSIS are among conditions that cause chronic renal failure. Others include stone, tumour, prostatic enlargement and overuse of analgesic drugs. Chronic failure may eventually lead to end-stage renal failure, a life-threatening situation that will need DIALYSIS or a renal transplant (see TRANSPLANTATION).

Familial renal disorders include autosomal dominant inherited polycystic kidney disease and sex-linked familial nephropathy. Polycystic kidney disease is an important cause of renal failure in the UK. Patients, usually aged 30–50, present with HAEMATURIA, loin or abdominal discomfort or, rarely, urinary-tract infection, hypertension and enlarged kidneys. Diagnosis is based on ultrasound examination of the abdomen. Complications include renal failure, hepatic cysts and, rarely, SUBARACHNOID HAEMORRHAGE. No speci?c treatment is available. Familial nephropathy occurs more often in boys than in girls and commonly presents as Alport’s syndrome (familial nephritis with nerve DEAFNESS) with PROTEINURIA, haematuria, progressing to renal failure and deafness. The cause of the disease lies in an absence of a speci?c ANTIGEN in a part of the glomerulus. The treatment is conservative, with most patients eventually requiring dialysis or transplantation.

Acute glomerulonephritis is an immune-complex disorder due to entrapment within glomerular capillaries of ANTIGEN (usually derived from B haemolytic streptococci – see STREPTOCOCCUS) antibody complexes initiating an acute in?ammatory response (see IMMUNITY). The disease affects children and young adults, and classically presents with a sore throat followed two weeks later by a fall in urine output (oliguria), haematuria, hypertension and mildly abnormal renal function. The disease is self-limiting with 90 per cent of patients spontaneously recovering. Treatment consists of control of blood pressure, reduced ?uid and salt intake, and occasional DIURETICS and ANTIBIOTICS.

Chronic glomerulonephritis is also due to immunological renal problems and is also classi?ed by taking a renal biopsy. It may be subdivided into various histological varieties as determined by renal biospy. Proteinuria of various degrees is present in all these conditions but the clinical presentations vary, as do their treatments. Some resolve spontaneously; others are treated with steroids or even the cytotoxic drug CYCLOPHOSPHAMIDE or the immunosuppressant cyclosporin. Prognoses are generally satisfactory but some patients may require renal dialysis or kidney transplantation – an operation with a good success rate.

Hydronephrosis A chronic disease in which the kidney becomes greatly distended with ?uid. It is caused by obstruction to the ?ow of urine at the pelvi-ureteric junction (see KIDNEYS – Structure). If the ureter is obstructed, the ureter proximal to the obstruction will dilate and pressure will be transmitted back to the kidney to cause hydronephrosis. Obstruction may occur at the bladder neck or in the urethra itself. Enlargement of the prostate is a common cause of bladder-neck obstruction; this would give rise to hypertrophy of the bladder muscle and both dilatation of the ureter and hydronephrosis. If the obstruction is not relieved, progressive destruction of renal tissue will occur. As a result of the stagnation of the urine, infection is probable and CYSTITIS and PYELONEPHRITIS may occur.

Impaired blood supply may be the outcome of diabetes mellitus and physiological shock, which lowers the blood pressure, also affecting the blood supply. The result can be acute tubular necrosis. POLYARTERITIS NODOSA and SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) may damage the large blood vessels in the kidney. Treatment is of the underlying condition.

Infection of the kidney is called pyelonephritis, a key predisposing factor being obstruction of urine ?ow through the urinary tract. This causes stagnation and provides a fertile ground for bacterial growth. Acute pyelonephritis is more common in women, especially during pregnancy when bladder infection (CYSTITIS) spreads up the ureters to the kidney. Symptoms are fever, malaise and backache. Antibiotics and high ?uid intake are the most e?ective treatment. Chronic pyelonephritis may start in childhood as a result of congenital deformities that permit urine to ?ow up from the bladder to the kidney (re?ux). Persistent re?ux leads to recurrent infections causing permanent damage to the kidney. Specialist investigations are usually required as possible complications include hypertension and kidney failure.

Tumours of the kidney are fortunately rare. Non-malignant ones commonly do not cause symptoms, and even malignant tumours (renal cell carcinoma) may be asymptomatic for many years. As soon as symptoms appear – haematuria, back pain, nausea, malaise, sometimes secondary growths in the lungs, bones or liver, and weight loss – urgent treatment including surgery, radiotherapy and chemotherapy is necessary. This cancer occurs mostly in adults over 40 and has a hereditary element. The prognosis is not good unless diagnosed early. In young children a rare cancer called nephroblastoma (Wilm’s tumour) can occur; treatment is with surgery, radiotherapy and chemotherapy. It may grow to a substantial size before being diagnosed.

Cystinuria is an inherited metabolic defect in the renal tubular reabsorption of cystine, ornithine, lysine and arginine. Cystine precipitates in an alkaline urine to form cystine stones. Triple phosphate stones are associated with infection and may develop into a very large branching calculi (staghorn calculi). Stones present as renal or ureteric pain, or as an infection. Treatment has undergone considerable change with the introduction of MINIMALLY INVASIVE SURGERY (MIS) and the destruction of stone by sound waves (LITHOTRIPSY).... kidneys, diseases of

Irregularly shaped areas of bluish-black pigmentation found occasionally on the buttocks, lower back or upper arms in newborn infants of African, Chinese and Japanese parentage, and sometimes in the babies of black-haired Europeans. They measure from one to several centimetres in diameter, and usually disappear in a few months. They are commonly mistaken for bruises.... mongolian blue spots

(body louse) di?ers from the head and crab louse in that it lives in clothing and only goes on to the body to feed. Infestation is found in vagabonds, armies in the ?eld, or prisoners in conditions where even minimal hygiene is impossible. The lice are found in the seams of clothing together with multiple eggs. Typically excoriation and pigmentation are seen on the back of the infested person. Replacement of clothing or autoclaving or hot ironing of the clothes is curative.... pediculus humanus var. corporis

Pale patches on skin due to loss of pigmentation. May follow a skin disease or from handling chemicals. Vitiligo is a modified form of the disease. There is no known cure, although Dr Wm Burton (Ellingwood) found Butternut useful. Seeds of Psoralea corylifolia appear to be indicated. (Indian Journal of Pharmacy 26:141.1964)

See entry: HIMALAYAN COW PARSLEY. ... leukoderma

Linn.

Family: Cyperaceae.

Habitat: Throughout India, as a weed upto 2,000 m.

English: Nut Grass.

Ayurvedic: Musta, Mustaa, Mus- taka, Abda, Ambuda, Ambhoda, Ambodhara, Bhadra, Bhadraa, Bhadramusta, Bhadramustaa, Bhadramustaka, Ghana, Jalada, Jaldhara, Meghaahvaa, Nirada, Vaarida, Vaarivaaha, Payoda, Balaahaka. Ganda-Duurvaa (var.).

Unani: Naagarmothaa, Saad-e-Kufi.

Siddha/Tamil: Koraikkizhangu.

Folk: Mothaa.

Action: Carminative, astringent, anti-inflammatory, antirheumat- ic, hepatoprotective, diuretic, antipyretic, analgesic, hypoten- sive, emmenagogue and nervine tonic.

Used for intestinal problems, indigestion, sprue, diarrhoea, dysentery, vomiting and fever; also as a hypoc- holesterolaemic drug and in obesity.

Along with other therapeutic applications, The Ayurvedic Pharmacopoeia of India indicated the use of the rhizome in rheumatism, inflammations, dysuria, puerperal diseases and obesity.

The tuber is rich in Cu, Fe, Mg and Ni. Beta-sitosterol, isolated from the tubers, exhibits significant anti- inflammatory activity against carra- geenan- and cotton pellet-induced oedema in rats; the activity is comparable to hydrocortisone and phenylbutazone when administered intraperi- toneally.

The alcoholic and aqueous extracts of the tubers possess lipolytic action and reduce obesity by releasing enhanced concentrations of biogenic amines from nerve terminals of the brain which suppress the appetite centre. Presence of eudalne group of ses- quiterpenic compounds of sesquiter- pene alcohol, isocyperol is said to play an important role in lipid metabolism.

An alcoholic extract of the plant exhibits liver-protective activity against CCL4-induced liver damage in mice.

Methanolic extract of the plant stimulates the production of melanin in cultured melanocytes. (Plant extract is used in preparations used for pigmentation of skin and hair, also in suntan gels.) Aqueous-alcoholic extract of the tuber exhibited hypotensive, diuretic, antipyretic and analgesic activities. These are attributed to a triterpenoid.

The essential oil (0.5-0.9%) from the tubers contains mainly sesquiterpenes.

C. platystilis Br. is equated with Kaivarta-mustaka.

Dosage: Rhizome—3-6 g powder; 20-30 ml decoction. (API Vol. III.)... cyperus rotundus

Diseases of the SKIN for which sunlight is partially or wholly responsible. In su?cient dosage, short-wave ultraviolet light (UVB – see ULTRAVIOLET RAYS (UVR)) always causes ERYTHEMA. Higher doses progressively cause OEDEMA and blistering; this is acute sunburn. Graduated exposure to UVB causes pigmentation (tanning). Prolonged chronic exposure to sunlight eventually accelerates ageing of the exposed skin with LENTIGO formation and loss of COLLAGEN and elastic tissue. After decades of such exposure, epidermal DYSPLASIA and CANCER may supervene.

Drugs given orally or topically may induce phototoxic reactions of various types. Thus, TETRACYCLINES exaggerate sunburn reactions. and the diuretic FRUSEMIDE may cause blistering reactions. Psoralens induce erythema and pigmentation. AMIODARONE also induces pigmentation. (See also PHOTOCHEMOTHERAPY.)

Phytophotodermatitis is a streaky, blistering photodermatosis typically seen on the limbs of children playing in grassy meadows in summer. The phototoxic reaction is caused by psoralens in weeds.

Berlocque dermatitis is a pattern of streaky pigmentation usually seen on women’s necks, caused by a reaction to psoralens in perfumes.

Certain rare metabolic diseases may lead to photosensitisation. They include the PORPHYRIAS and PELLAGRA. Other skin diseases such as lupus erythematosus (see under LUPUS) and ROSACEA may be aggravated by light exposure. Sometimes, in the absence of any of these factors, some people spontaneously develop a sensitivity to light causing various patterns of DERMATITIS or URTICARIA. The most common pattern is ‘polymorphic light eruption’ which typically appears within a day or two of arrival at a sunny holiday destination and persists until departure. Continuously exposed areas, such as the hands and face, may be ‘hardened’ and unaffected.

Treatment Appropriate clothing and headgear, sunscreen creams and lotions are the main preventative measures.... photodermatoses

The main pigment found in bile. It is produced by the breakdown of haemoglobin, the pigment in red blood cells. Excessively high levels of bilirubin cause the yellow pigmentation associated with jaundice.... bilirubin

A tiny patch of pigmentation that occurs on sun-exposed skin.

Freckles tend to become more numerous with continued exposure to sunlight.

A tendency to freckling is inherited and occurs most often in fair and red-haired people.... freckle

A rare disorder of the endocrine system that causes increased skin pigmentation. Nelson’s syndrome results from enlargement of the pituitary gland, which can follow removal of the adrenal glands (a treatment for Cushing’s syndrome).

Nelson’s syndrome is treated by hypophysectomy (removal or destruction of the pituitary gland).... nelson’s syndrome

A common disorder of skin pigmentation in which patches of skin, most commonly on the face, hands, armpits, and groin, lose their colour. Vitiligo is thought to be an autoimmune disorder. It may occur at any age but usually develops in early adulthood.

Spontaneous repigmentation occurs in some cases.

A course of phototherapy using PUVA can also induce repigmentation of the skin, and creams containing corticosteroid drugs may help.... vitiligo

n. the inherited absence of pigmentation in the skin, hair, and eyes, resulting in white hair and pink skin and eyes. The pink colour is produced by blood in underlying blood vessels, which are normally masked by pigment. Ocular signs are reduced visual acuity, sensitivity to light (see photophobia), and involuntary side-to-side eye movements.... albinism

(argyrosis) n. the deposition of silver in the skin and other tissues, either resulting from industrial exposure or following ingestion or long-term administration of silver salts. A slate-grey pigmentation develops slowly; this is accentuated in areas exposed to light. Deposition of silver in the conjunctiva, corneal epithelium, stroma, and Descemet’s membrane is usually due to chronic exposure to silver compounds or instillation of eye drops containing silver.... argyria

Ammi majus

Apiaceae

Importance: Greater Ammi, also known as Bishop’s weed or Honey plant is an annual or biennial herb which is extensively used in the treatment of leucoderma (vitiligo) and psoriasis. The compounds responsible for this are reported to be furocoumarins like ammoidin (xanthotoxin), ammidin (imperatorin) and majudin (bergapten) present in the seed. Xanthotoxin is marketed under the trade name “Ox soralen” which is administered orally in doses of 50 mg t.d. or applied externally as 1% liniment followed by exposure of affected areas to sunlight or UV light for 2 hours. It is also used in “Suntan lotion”. Meladinine is a by-product of Ammi majus processing, containing both xanthotoxin and imperatorin sold in various formulations increases pigmentation of normal skin and induces repigmentation in vitiligo. Imperatorin has antitumour activity. Fruit or seed causes photosensitization in fouls and sheep.

Distribution: The plant is indigenous to Egypt and it grows in the Nile Valley, especially in Behira and Fayoom. It is also found in the basin of the Mediterranean Sea, in Syria, Palestine, Abyssinia, West Africa, in some regions of Iran and the mountains of Kohaz (Ramadan, 1982). It grows wild in the wild state in Abbottabad, Mainwali, Mahran and is cultivated in Pakistan. The crop was introduced to India in the Forest Research Institute, Dehra Dun, in 1955 through the courtesy of UNESCO. Since then, the crop has been grown for its medicinal fruit in several places in Uttar Pradesh, Gujarat, Kashmir and Tamil Nadu.

Botany: Ammi majus Linn. belongs to the family Apiaceae (Umbelliferae). A. visnaga is another related species of medicinal importance. A. majus is an annual or beinnial herb growing to a height of 80 to 120 cm. It has a long tap root, solid erect stem, decompound leaves, light green alternate, variously pinnately divided, having lanceolate to oval segments. Inflorescence is axillary and terminal compound umbels with white flowers. The fruits are ribbed, ellipsoid, green to greenish brown when immature, turning reddish brown at maturity and having a characteristic terebinthinate odour becoming strong on crushing with extremely pungent and slightly bitter taste.

Agrotechnology: Ammi is relatively cold loving and it comes up well under subtropical and temperate conditions. It does not prefer heavy rainfall. Though the plant is biennial it behaves as an annual under cultivation in India. A mild cool climate in the early stages of crop growth and a warm dry weather at maturity is ideal. It is cultivated as a winter annual crop in rabi season. A wide variety of soils from sandy loam to clay loam are suitable. However, a well drained loamy soil is the best. Waterlogged soils are not good. Being a hardy crop, it thrives on poor and degraded soils.

The plant is seed propagated. Seeds germinate within 10-12 days of sowing. The best time of sowing is October and the crop duration is 160-170 days in north India. Crop sown later gives lower yield. The crop can be raised either by direct sowing of seed or by raising a nursery and then transplanting the crop. Seed rate is 2 kg/ha. The land is brought to a fine tilth by repeated ploughing and harrowing. Ridges and furrows are then formed at 45-60 cm spacing. Well decomposed FYM at 10-15 t/ha and basal fertilisers are incorporated in the furrows. Seeds being very small are mixed with fine sand or soil, sown in furrows and covered lightly with a thin layer of soil. A fertilizer dose of 80:30:30 kg N, P2O5 and K2O/ha is generally recommended for the crop while 150:40:40 kg/ha is suggested in poor soils for better yields. The furocoumarin content of Ammi majus is increased by N fertiliser and the N use efficiency increases with split application of N at sowing, branching and at flowering. For obtaining high yields it is essential to give one or two hoeings during November to February which keeps down the weeds. If winter rains fail, one irrigation is essential during November to January. As the harvesting season is spread over a long period of time, two irrigations during March and April meets the requirements of the crop (Chadha and Gupta, 1995).

White ants and cut worms are reported to attack the crop which can be controlled by spraying the crop with 40g carbaryl in 10 l of water. Damping off and powdery mildew are the common diseases of the crop. Seed treatment with organomercuric compounds is recommended for damping off. To control powdery mildew the crop is to be sprayed with 30g wettable sulphur in 10 l of water whenever noticed.

The crop flowers in February. Flowering and maturity of seed is spread over a long period of two months. The primary umbels and the early maturing secondary umbels are the major contributors to yield. A little delay in harvesting results in the shattering of the seed which is the main constraint in the commercial cultivation of the crop and the main reason for low yields in India. Sobti et al (1978) have reported increased yield by 50 - 60% by the application of planofix at 5 ppm at flower initiation and fruit formation stages. The optimum time of harvest is the mature green stage of the fruit in view of the reduced losses due to shattering and maximum contents of furocoumarins. The primary umbels mature first within 35-45 days. These are harvested at an interval of 2-4 days. Later, the early appearing secondary umbels are harvested. Afterwards, the entire crop is harvested, stored for a couple of days and then threshed to separate the seeds. The seed yield is 900-1200 kg/ha.

Postharvest technology: The processing of seed involves solvent extraction of powdered seeds, followed by chilling and liquid extraction and chromatographic separation after treatment with alcoholic HCl. Bergapten, xanthotoxin and xanthotoxol can be separated. Xanthotoxol can be methylated and the total xanthotoxin can be purified by charcoal treatment in acetone or alcohol.

Properties and activity: Ammi majus fruit contains amorphous glucoside 1%, tannin 0.45%, oleoresin 4.76%, acrid oil 3.2%, fixed oil 12.92%, proteins 13.83% and cellulose 22.4%. This is one of the richest sources of linear furocoumarins. Ivie (1978) evaluated the furocoumarin chemistry of taxa Ammi majus and reported the presence of xanthotoxin, bergapten, imperatorin, oxypencedanin, heraclenin, sexalin, pabulenol and many other compounds. Furocoumarins have bactericidal, fungicidal, insecticidal, larvicidal, moluscicidal, nematicidal, ovicidal, viricidal and herbicidal activities (Duke, 1988).... greater ammi

(dysplastic naevus syndrome) a condition in which patients have numerous moles, some of which are relatively large and irregular in shape or pigmentation. There may be a family history of this syndrome or of malignant *melanoma.... atypical mole syndrome

combining form denoting staining or pigmentation.... chromasia

In?ammation of the LIVER which damages liver cells and may ultimately kill them. Acute injury of the liver is usually followed by complete recovery, but prolonged in?ammation after injury may result in FIBROSIS and CIRRHOSIS. Excluding trauma, hepatitis has several causes:

Viral infections by any of hepatitis A, B, C, D, or E viruses and also CYTOMEGALOVIRUS (CMV), EPSTEIN BARR VIRUS, and HERPES SIMPLEX.

Autoimmune disorders such as autoimmune chronic hepatitis, toxins, alcohol and certain drugs – ISONIAZID, RIFAMPICIN, HALOTHANE and CHLORPROMAZINE.

WILSON’S DISEASE.

Acute viral hepatitis causes damage throughout the liver and in severe infections may destroy whole lobules (see below).

Chronic hepatitis is typi?ed by an invasion of the portal tract by white blood cells (mild hepatitis). If these mononuclear in?ammatory cells invade the body (parenchyma) of the liver tissue, ?brosis and then chronic disease or cirrhosis can develop. Cirrhosis may develop at any age and commonly results in prolonged ill health. It is an important cause of premature death, with excessive alcohol consumption commonly the triggering factor. Sometimes, cirrhosis may be asymptomatic, but common symptoms are weakness, tiredness, poor appetite, weight loss, nausea, vomiting, abdominal discomfort and production of abnormal amounts of wind. Initially, the liver may enlarge, but later it becomes hard and shrunken, though rarely causing pain. Skin pigmentation may occur along with jaundice, the result of failure to excrete the liver product BILIRUBIN. Routine liver-function tests on blood are used to help diagnose the disease and to monitor its progress. Spider telangiectasia (caused by damage to blood vessels – see TELANGIECTASIS) usually develop, and these are a signi?cant pointer to liver disease. ENDOCRINE changes occur, especially in men, who lose their typical hair distribution and suffer from atrophy of their testicles. Bruising and nosebleeds occur increasingly as the cirrhosis worsens, and portal hypertension (high pressure of venous blood circulation through the liver) develops due to abnormal vascular resistance. ASCITES and HEPATIC ENCEPHALOPATHY are indications of advanced cirrhosis.

Treatment of cirrhosis is to tackle the underlying cause, to maintain the patient’s nutrition (advising him or her to avoid alcohol), and to treat any complications. The disorder can also be treated by liver transplantation; indeed, 75 per cent of liver transplants are done for cirrhosis. The overall prognosis of cirrhosis, however, is not good, especially as many patients attend for medical care late in the course of the disease. Overall, only 25 per cent of patients live for ?ve years after diagnosis, though patients who have a liver transplant and survive for a year (80 per cent do) have a good prognosis.

Autoimmune hepatitis is a type that most commonly occurs in women between 20 and 40 years of age. The cause is unknown and it has been suggested that the disease has several immunological subtypes. Symptoms are similar to other viral hepatitis infections, with painful joints and AMENORRHOEA as additional symptoms. Jaundice and signs of chronic liver disease usually occur. Treatment with CORTICOSTEROIDS is life-saving in autoimmune hepatitis, and maintenance treatment may be needed for two years or more. Remissions and exacerbations are typical, and most patients eventually develop cirrhosis, with 50 per cent of victims dying of liver failure if not treated. This ?gure falls to 10 per cent in treated patients.

Viral hepatitis The ?ve hepatic viruses (A to E) all cause acute primary liver disease, though each belongs to a separate group of viruses.

•Hepatitis A virus (HAV) is an ENTEROVIRUS

which is very infectious, spreading by faecal contamination from patients suffering from (or incubating) the infection; victims excrete viruses into the faeces for around ?ve weeks during incubation and development of the disease. Overcrowding and poor sanitation help to spread hepatitis A, which fortunately usually causes only mild disease.

Hepatitis B (HBV) is caused by a hepadna virus, and humans are the only reservoir of infection, with blood the main agent for transferring it. Transfusions of infected blood or blood products, and injections using contaminated needles (common among habitual drug abusers), are common modes of transfer. Tattooing and ACUPUNCTURE may spread hepatitis B unless high standards of sterilisation are maintained. Sexual intercourse, particularly between male homosexuals, is a signi?cant infection route.

Hepatitis C (HCV) is a ?avivirus whose source of infection is usually via blood contacts. E?ective screening of blood donors and heat treatment of blood factors should prevent the spread of this infection, which becomes chronic in about 75 per cent of those infected, lasting for life. Although most carriers do not suffer an acute illness, they must practise life-long preventive measures.

Hepatitis D (HDV) cannot survive independently, needing HBV to replicate, so its sources and methods of spread are similar to the B virus. HDV can infect people at the same time as HBV, but it is capable of superinfecting those who are already chronic carriers of the B virus. Acute and chronic infection of HDV can occur, depending on individual circumstances, and parenteral drug abuse spreads the infection. The disease occurs worldwide, being endemic in Africa, South America and the Mediterranean littoral.

Hepatitis E virus (HEV) is excreted in the stools, spreading via the faeco-oral route. It causes large epidemics of water-borne hepatitis and ?ourishes wherever there is poor sanitation. It resembles acute HAV infection and the patient usually recovers. HEV does not cause chronic infection. The clinical characteristics of the ?ve hepatic

viruses are broadly similar. The initial symptoms last for up to two weeks (comprising temperature, headache and malaise), and JAUNDICE then develops, with anorexia, nausea, vomiting and diarrhoea common manifestations. Upper abdominal pain and a tender enlarged liver margin, accompanied by enlarged cervical lymph glands, are usual.

As well as blood tests to assess liver function, there are speci?c virological tests to identify the ?ve infective agents, and these are important contributions to diagnosis. However, there is no speci?c treatment of any of these infections. The more seriously ill patients may require hospital care, mainly to enable doctors to spot at an early stage those developing acute liver failure. If vomiting is a problem, intravenous ?uid and glucose can be given. Therapeutic drugs – especially sedatives and hypnotics – should be avoided, and alcohol must not be taken during the acute phase. Interferon is the only licensed drug for the treatment of chronic hepatitis B, but this is used with care.

Otherwise-?t patients under 40 with acute viral hepatitis have a mortality rate of around

0.5 per cent; for those over 60, this ?gure is around 3 per cent. Up to 95 per cent of adults with acute HBV infection recover fully but the rest may develop life-long chronic hepatitis, particularly those who are immunode?cient (see IMMUNODEFICIENCY).

Infection is best prevented by good living conditions. HVA and HVB can be prevented by active immunisation with vaccines. There is no vaccine available for viruses C, D and E, although HDV is e?ectively prevented by immunisation against HBV. At-risk groups who should be vaccinated against HBV include:

Parenteral drug abusers.

Close contacts of infected individuals such as regular sexual partners and infants of infected mothers.

Men who have sex with men.

Patients undergoing regular haemodialysis.

Selected health professionals, including laboratory sta? dealing with blood samples and products.... hepatitis

The mucous membrane of the mouth can indicate the health of the individual and internal organs. For example, pallor or pigmentation may indicate ANAEMIA, JAUNDICE or ADDISON’S DISEASE.

Thrush is characterised by the presence of white patches on the mucous membrane which bleeds if the patch is gently removed. It is caused by the growth of a parasitic mould known as Candida albicans. Antifungal agents usually suppress the growth of candida. Candidal in?ltration of the mucosa is often found in cancerous lesions.

Leukoplakia literally means a white patch. In the mouth it is often due to an area of thickened cells from the horny layer of the epithelium. It appears as a white patch of varying density and is often grooved by dense ?ssures. There are many causes, most of them of minor importance. It may be associated with smoking, SYPHILIS, chronic SEPSIS or trauma from a sharp tooth. Cancer must be excluded.

Stomatitis (in?ammation of the mouth) arises from the same causes as in?ammation elsewhere, but among the main causes are the cutting of teeth in children, sharp or broken teeth, excess alcohol, tobacco smoking and general ill-health. The mucous membrane becomes red, swollen and tender and ulcers may appear. Treatment consists mainly of preventing secondary infection supervening before the stomatitis has resolved. Antiseptic mouthwashes are usually su?cient.

Gingivitis (see TEETH, DISEASES OF) is in?ammation of the gum where it touches the tooth. It is caused by poor oral hygiene and is often associated with the production of calculus or tartar on the teeth. If it is neglected it will proceed to periodontal disease.

Ulcers of the mouth These are usually small and arise from a variety of causes. Aphthous ulcers are the most common; they last about ten days and usually heal without scarring. They may be associated with STRESS or DYSPEPSIA. There is no ideal treatment.

Herpetic ulcers (see HERPES SIMPLEX) are similar but usually there are many ulcers and the patient appears feverish and unwell. This condition is more common in children.

Calculus (a) Salivary: a calculus (stone) may develop in one of the major salivary-gland ducts. This may result in a blockage which will cause the gland to swell and be painful. It usually swells before a meal and then slowly subsides. The stone may be passed but often has to be removed in a minor operation. If the gland behind the calculus becomes infected, then an ABSCESS forms and, if this persists, the removal of the gland may be indicated. (b) Dental, also called TARTAR: this is a calci?ed material which adheres to the teeth; it often starts as the soft debris found on teeth which have not been well cleaned and is called plaque. If not removed, it will gradually destroy the periodontal membrane and result in the loss of the tooth. (See TEETH, DISORDERS OF.)

Ranula This is a cyst-like swelling found in the ?oor of the mouth. It is often caused by mild trauma to the salivary glands with the result that saliva collects in the cyst instead of discharging into the mouth. Surgery may be required.

Mumps is an acute infective disorder of the major salivary glands. It causes painful enlargement of the glands which lasts for about two weeks. (See also main entry for MUMPS.)

Tumours may occur in all parts of the mouth, and may be BENIGN or MALIGNANT. Benign tumours are common and may follow mild trauma or be an exaggerated response to irritation. Polyps are found in the cheeks and on the tongue and become a nuisance as they may be bitten frequently. They are easily excised.

A MUCOCOELE is found mainly in the lower lip.

An exostosis or bone outgrowth is often found in the mid line of the palate and on the inside of the mandible (bone of the lower jaw). This only requires removal if it becomes unduly large or pointed and easily ulcerated.

Malignant tumours within the mouth are often large before they are noticed, whereas those on the lips are usually seen early and are more easily treated. The cancer may arise from any of the tissues found in the mouth including epithelium, bone, salivary tissue and tooth-forming tissue remnants. Oral cancers represent about 5 per cent of all reported malignancies, and in England and Wales around 3,300 people are diagnosed annually as having cancer of the mouth and PHARYNX.

Cancer of the mouth is less common below the age of 40 years and is more common in men. It is often associated with chronic irritation from a broken tooth or ill-?tting denture. It is also more common in those who smoke and those who chew betel leaves. Leukoplakia (see above) may be a precursor of cancer. Spread of the cancer is by way of the lymph nodes in the neck. Early treatment by surgery, radiotherapy or chemotherapy will often be e?ective, except for the posterior of the tongue where the prognosis is very poor. Although surgery may be extensive and potentially mutilating, recent advances in repairing defects and grafting tissues from elsewhere have made treatment more acceptable to the patient.... mouth, diseases of

(chromato-) combining form denoting colour or pigmentation.... chromat

n. (pl. lentigines) a flat dark brown spot found mainly in the elderly on skin exposed to light. Lentigines have increased numbers of *melanocytes in the basal layer of the epidermis (freckles, by contrast, do not show an increase in these cells). Lentigo maligna (preinvasive or in-situ melanoma) occurs on the cheeks of the elderly and has variable pigmentation.... lentigo

a dark line down the centre of the abdomen caused by increased pigmentation in pregnancy.... linea nigra

a rare disease, occurring commonly (but not exclusively) in males, in which absorption of digested food in the intestine is reduced. As well as symptoms and signs of *malabsorption there is usually abdominal pain, skin pigmentation, and arthritis. Diagnosis is usually made by small-intestinal biopsy (duodenal or *jejunal biopsy) demonstrating the presence of PAS-positive (see periodic acid–Schiff reaction) macrophages containing the causative microorganism, Tropheryma whipplei. The disease usually responds to a prolonged course of antibiotics. [G. H. Whipple (1878–1976), US pathologist]... whipple’s disease

Hordeum distichon L. An almost perfect food. High in fibre, calcium, iron, magnesium and potassium. High in lysine, an essential amino acid. One of the best and cheapest cholesterol blockers. A grain that should have a prominent place on the dining table. This nutritive demulcent, taken as Barley- water, is still used in kidney, intestinal and bowel disorders.

Malt extract (with, or without Cod Liver oil). Green Barley. Juice of young Barley leaves harvested when 12 inches in height. A concentrate of vitamins, mineral nutrients, amino acids, enzymes and chlorophyll. Seven times richer in Vitamin C than oranges; five times richer in iron than spinach; has 25 times the potassium of wheat. High in the enzyme that slows the ageing of cells – superoxide dismutase (SOD). Said to be of value for malignancy and effective against pigmentation of the skin (melanosis, and other skin diseases). (Yoshihide Hagiwara MD, pharmacologist, Japan)

Immune system protective. Constipation. Anaemia.

Prepare in a juicer, young Barley leaves: 1 wineglassful night and morning. Green powder: (Green Barley essence) (Natural Flow) ... barley

Post phlebitis. An important fore-runner to leg ulceration without resolution of which an ulcer may reappear indefinitely. A condition due to pressure on the vascular system which causes deposition of excess fibrin in the capillaries and veins which arrests the circulation of oxygen and nutrients to the skin.

Symptoms. Those of a prelude to ulceration: eczema, pigmentation, pain.

Treatment. Aim should be (1) to reduce internal pressure on the veins and (2) to resolve deposition of fibrin.

Alternatives. Teas: Alfalfa, Nettles, Plantain. Brigham tea, Clivers, Bladderwrack.

Capsules: Evening Primrose oil (4 × 500mg) daily.

Tablets/capsules. Fucus (Bladderwrack). Motherwort. Chlorophyll, Rutin.

Formula. Equal parts: Dandelion and Burdock: add pinch or few drops Cayenne. Powders: half a teaspoon. Liquid Extracts: 2 teaspoons. Tinctures: 2-3 teaspoons. In water, thrice daily before meals. Topical. Graduated elastic stocking compression reduces tension on veins and prevents further deposition of fibrin. Juice, gels, or oils:– Aloe Vera, Houseleek, Evening Primrose, Comfrey, Chickweed, Zinc and Castor oil. ... lipodermatosclerosis

An uncommon genetic disorder in which an enzyme defect blocks the production of corticosteroid hormones from the adrenal glands. Excessive amounts of androgens (male sex hormones) are produced, which can result in abnormal genital development in an affected fetus. Other effects include dehydration, weight loss, low blood pressure, and hypoglycaemia. Hyperplasia (enlargement) of the adrenal glands occurs and there is excessive skin pigmentation in skin creases and around the nipples.

In severe cases, the disorder is apparent soon after birth. In milder cases, symptoms appear later, sometimes producing premature puberty in boys and delayed menstruation, hirsutism, and potential infertility in girls.

Congenital adrenal hyperplasia is confirmed by measuring corticosteroid hormones in blood and urine. Treatment is by hormone replacement. If this is started early, normal sexual development and fertility usually follow.... adrenal hyperplasia, congenital

a group of conditions affecting the *macula lutea of the eye, resulting in a reduction or loss of central vision. Age-related macular degeneration (AMD, ARMD) is the most common cause of poor vision in the elderly. Two types are commonly recognized. Atrophic (or dry) AMD results from chronic choroidal ischaemia: small blood vessels of the choroid, which lies beneath the retina, become constricted, reducing the blood supply to the macula. This gives rise to degenerative changes in the retinal pigment epithelium (RPE; see retina), clinically recognized by macular pigmentation and the deposition of *drusen. Wet AMD is associated with the growth of abnormal new blood vessels underneath the retina, derived from the choroid (see neovascularization). These can leak fluid and blood beneath the retina, which further reduces the macular function. Nutritional supplements can delay the progression of AMD in some cases. Laser surgery (see photocoagulation; photodynamic therapy) and anti-VEGF therapy (see vascular endothelial growth factor) can delay progression in cases of wet AMD.... macular degeneration

n. (pl. naevi) a birthmark: a clearly defined malformation of the skin, present at birth. There are many different types of naevi. Some, including the strawberry naevus and port-wine stain, are composed of small blood vessels (see haemangioma). The strawberry naevus (or strawberry mark) is a raised red lump usually appearing on the face and growing rapidly in the first month of life. These birthmarks slowly resolve and spontaneously disappear between the ages of five and ten. The port-wine stain (or capillary naevus) is a permanent purplish discoloration that may occur anywhere but usually appears on the upper half of the body. Laser treatment can reduce the discoloration. Occasionally a port-wine stain may be associated with a malformation of blood vessels over the brain, for example in the Sturge-Weber syndrome (see angioma).

It is not uncommon for a pale or white halo to develop around an ordinary pigmented naevus, especially on the trunk, forming a halo naevus. The pigmented naevus disappears over the course of a few months; this is followed by resolution of the pale area. A blue naevus is a small blue-grey papule appearing at birth or later in life, mainly on the extremities. Progression to malignant melanoma is very rare. A naevus of Ota is a blue-grey pigmented area on the cheek, eyelid, or forehead with similar pigmentation of the sclera of an eye. It is associated with melanomas of the uvea, orbit, and brain as well as with glaucoma of the affected eye. See also mole2.... naevus

Citrus bergamia

FAMILY: Rutaceae

SYNONYM: Citrus aurantium subsp. bergamia.

GENERAL DESCRIPTION: A small tree, about 4.5 metres high with smooth oval leaves, bearing small round fruit which ripen from green to yellow, much like a miniature orange in appearance.

DISTRIBUTION: Native to tropical Asia. Extensively cultivated in Calabria in southern Italy and also grown commercially on the Ivory Coast.

OTHER SPECIES: Not to be confused with the herb bergamot or bee balm (Monarda didyma).

HERBAL/FOLK TRADITION: Named after the Italian city of Bergamo in Lombardy, where the oil was first sold. The oil has been used in Italian folk medicine for many years, primarily for fever (including malaria) and worms; it does not feature in the folk tradition of any other countries. However, due to recent research in Italy, bergamot oil is now known to have a wide spectrum of applications, being particularly useful for mouth, skin, respiratory and urinary tract infections.

ACTIONS: Analgesic, anthelmintic, antidepressant, antiseptic (pulmonary, genito-urinary), antispasmodic, antitoxic, carminative, digestive, diuretic, deodorant, febrifuge, laxative, parasiticide, rubefacient, stimulant, stomachic, tonic, vermifuge, vulnerary.

EXTRACTION: Essential oil by cold expression of the peel of the nearly ripe fruit. (A rectified or terpeneless oil is produced by vacuum distillation or solvent extraction.)

CHARACTERISTICS: A light greenish-yellow liquid with a fresh sweet-fruity, slightly spicy-balsamic undertone. On ageing it turns a brownish-olive colour. It blends well with lavender, neroli, jasmine, cypress, geranium, lemon, chamomile, juniper, coriander and violet.

PRINCIPAL CONSTTTUENTS Known to have about 300 compounds present in the expressed oil: mainly linalyl acetate (30–60 per cent), linalol (11–22 per cent) and other alcohols, sesquiterpenes, terpenes, alkanes and furocoumarins (including bergapten, 0.30–0.39 per cent).

SAFETY DATA: Certain furocoumarins, notably bergapten, have been found to be phototoxic on human skin; that is, they cause sensitization and skin pigmentation when exposed to direct sunlight (in concentration and in dilution even after some time!). Extreme care must be taken when using the oil in dermal applications – otherwise a rectified or ‘bergapten-free’ oil should be substituted. Available information indicates it to be otherwise non-toxic and relatively non-irritant.

AROMATHERAPY/HOME: USE

Skin Care: Acne, boils, cold sores, eczema, insect repellent and insect bites, oily complexion, psoriasis, scabies, spots, varicose ulcers, wounds.

Respiratory System: Halitosis, mouth infections, sore throat, tonsillitis.

Digestive System: Flatulence, loss of appetite.

Genito-URINARY SYSTEM: Cystitis, leucorrhoea, pruritis, thrush.

Immune System: Colds, fever, ’flu, infectious diseases.

Nervous System: Anxiety, depression and stress-related conditions, having a refreshing and uplifting quality.

OTHER USES: Extensively used as a fragrance and, to a degree, a fixative in cosmetics, toiletries, suntan lotions and perfumes – it is a classic ingredient of eau-de-cologne. Widely used in most major food categories and beverages, notably Earl Grey tea.... bergamot