Posts Tagged ‘retaining water’

itraconazole An orally active antifungal agent used in the treatment of vulvovaginal candidiasis, pityriasis and tinea infections. Dose: 200 mg twice a day for the I -day treatment of vulvovaginal infections; 200 nig daily for 7 days in pityriasis, 100nig daily for 15-30 days in tinea infections. Side-effects are nausea and abdominal pain. Liver disease is a contraindication. Combined treatment with astiniazole or ierfenadine should be avoided. (Sporonox).
ivermeclin A fungal derivative effective against the microfilaria causing ‘river blindness. It does not kill either the adult worms or their larvae, but prevents the growth of the latter, and treatment must be continued until the adult worms die out. Dose: 150. (Mectizan).
kanamycin An aminoglycoside antibiotic now used mainly in gentamicin-resistant infections.
Dose: I g daily by i.m. injection; 15-30 rng/ kg daily by i.v. infusion. (Kannasyn).
kaolin Aluminium silicate. Used as an absorbent in diarrhoea, colitis, food poisoning, etc., often as Kaolin and Morphine Mixture.
Dose: 10-20 nil as required. It is also used externally as Kaolin Poultice to relieve the pain of sprains, etc.
kelocyanor A specific antidote for cyanide poisoning. See dicobalt edetate.
ketamine A short-acting i.v. anaesthetic with analgesic properties.
Dose: 1-2 mg/kg i.v. over I minute, repeated as required; 4-10 nig/kg by deep Lin. injection. It is used mainly in paediatric anaesthesia, and its analgesic action is also of value in neurodiagnostic procedures, and other painful investigations. Hallucinations may occur during the recovery period. (Ketalar).
ketoconazole A broad-spectrum, orally active antifungal agent. It is of value in systemic and deep mycoses, and in severe and resistant mycoses of the gastrointestinal tract and the vagina. It is also effective in severe mycoses of the skin, but it should be used only for superficial fungal infections not responding to other treatment.
Dose: 200 mg daily with ft)od, up to a maximum of 4tH) mg daily. Side-effects include nausea, rash and pruritus. It may cause hepatitis; liver function tests may be necessary if given for more than 14 (lays. (Ki-zoral).
ketoprofen A non-steroidal anti-inflammatory and analgesic agent of the ibuprofen type. It is of value in rheumatoid arthritis, gout, spondylitis and related conditions, and in dysmenorrhoea.
Dose: 100-200 mg daily with food;
100 Ing by suppository at night, 50-100 mg by deep Lin. injection 4-hourly. Care is necessary in peptic ulcer and hepatic disease. May increase the action of anticoagulants and other drugs bound to plasma protein. (AlrheLiniat; OrUdis; Orivail). See page 165 and Table 29.
ketorolacV A potent analgesic used for the short-term reliefofacute postoperative pain.
Dose: tO mg 4-6-hourly up to 40 ing daily for not more than 7 days; dose by deep i.m. or slow i.v. injection. 10 mg initially, then 30 mg 4-6-hourly up to 90 mg daily for not more than 2 days. Side-effects are numerous; see data sheet. (Toradol). Also used as eye drops (0.51)/0 to reduce pain and inflammation after ocular surgery. (Acular).
keftotifen An antihistamine that may also have some of the properties ofsodium cromoglycate. It is used in the prophylactic treatment of asthma.
Dose: 4 mg daily with food, continued lor ,sine weeks. Other anti-asthmatic therapy should be continued for at least 2 weeks to ensure maintenance of control. Side-
effects include sedation and dryness of the mouth. (Zadi(en). See page 110 and Table 2.
Kogenate A recombinant form of the human blood Factor Vill, given i.v, as replacement therapy in the treatment of haemophilia A.

labetalol A beta - adrenocepior blocking agent with some alpha-blocking activity. Like related drugs, labetalol is indicated in all types of hypertension, including that following myocardial infarction.
Dose: 200 mg daily initially, with food, slowly increased up to a maximum of 2.4 g daily; by i.v. injection 50 mg repeated as required; for the rapid control of the hypertension of pregnancy 20-160 ing by i.v. infusion hourly. It should be used with care in asthma and heart block. Side-effects include weakness, nausea, bradycardia and postural hypotension. Liver damage has been reported. (Trandate). See page 148 and `fable 21.
lacidipine A calcium channel blocking agent with the actions and uses of nifedipine. In hypertension it is given as a single morning dose of 2 nig with food, increased up to 6 mg as the response develops over 3-4 weeks. Half doses in hepatic impairment and the elderly. Early chest pain is an indication that the drug should be withdrawn. (Motens). See page 148 and Table 21.
lactilol A semi-synthetic sugar that is not absorbed orally, and acts as an osmotic laxative by retaining water in the intestinal tract. Also inhibits ammonia-producing organisms, and is of value in hepatic encephalopathy.
Dose: as laxative 20 mg daily mixed with food, together with 2 glasses of water. Dose in hepatic encephalopathy, 500700 inglkl; daily.
lactulose An osmotic laxative. See lactilol.
laevulose Fructose. A sugar sometimes given i.v. as an alternative to glucose.
in the brain by inhibiting the influx of sodium ions. It is used both as primary treatment and as additional therapy (often with sodium valproate) for seizures not fully controlled by other drugs.
Dose: 25 ing daily initially for 14 (lays, slowly rising to 100-200 nig daily. See data sheet for details of combined therapy. (Limictal). See page 136 and Table 15.
lanolin See wool fat.
lansoprazole An inhibitor of the enzyme 11, K’-AI’Pase (the proton pump) used in the treatment of peptic ulcer.
Dose: 30 ing daily for 4-8 weeks. (Luton). See orneprazole, page 162 and Table 27.
Lasser’s paste A stiffointment containing zinc oxide, starch and white soft paraffin with 2% salicylic acid. Used as protective in eczema.
latanoprost A prostaglandin alpha-analogue used once daily as eye drops (0.00596) in glaucoma. It increases the outflow of the aqueous humour, whereas other agents reduce its secretion. Continued use may cause changes in eye colour. (Xalantan). See page 138.
lenograstimV A recombinant form of the granulocyte colony stimulating factor (G–GSF) that governs the production of neutrophils. It is used as supplementary treatment in cancer chemotherapy to stimulate neutrophil production in drug induced neutropenia.
Dose: under expert supervision by s.,:. injection, in daily doses of 150 pg/m2 Until neutrophil count is satisfactory. Also used i.v. after hone narrow transplantation. (Granocyte). See filgrastim and rinolgraniostirn. See page 122 and Table 8.
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lamivudine An antiviral agent that acts like zidovudine by inhibiting reverse transcriptase, an enzyme essential for DNA formation and viral replication. It is used in HIV infections.
Dose: 300 ing daily, preferably with food, and combined with a protease inhibitor. (Epivir). See page 144 and Table 19.
lamotrigine\” An anti-epileptic that alleviates the imbalance of neurotransmitters
letrozoleV A non-steroid inhibitor of aromatase, the enzyme that controls the conversion of testosterone to oestrogen. It acts as an anti-oestrogen and is used in advanced breast cancer that has not responded to tamoxifen or similar therapy. Dose: 2.5 mg once daily. Side-effects include musculoskeletal pain, arthralgia and hot flushes. (Fernara). See page 122 and Table 8.
leucovorin See folinic acid.

leuprorelin A synthetic hormone that indiandrogen and oestrogen production by inhibiting gonadotrophin activity. It is used in endonietriosis and
advanced prostatic cancer.
Dose: 3.73 rig by s.c. or i.m. injection every 4 weeks. Side-effects are impotence, flushing and local irritation. There may be an initial and temporary increase in pain. The injection site should be varied. (Prostap SR). See buserelin, goserelin, page 122 and Table 8.
levamisole A single-dose (150 mg) anthelmintic of value in round worm (Ascaris). It is also effective against hookworm (Ancylostoma and Necator). Dose: 2.5-5 mg1kg daily for 2-5 days.
levobunolol A beta-blocker used as eye drops 0.5% in glaucoma. (Betagaii). See carteolol.
levocabastine An antihistamine used as drops (0.05% twice a day in the symptomatic treatment of seasonal allergic conjunctivitis and rhinitis. (Livostin).
levodopa An amino acid that is converted to dopamine in the body. It is used in the treatment of Parkinson’s disease, which is associated with a reduction in brain
dopamine levels due to degeneration in the substantia nigra, thus causing an imbalance in the neurohorinonal system of the brain. Levodopa is essentially replacement therapy, but as an oral dose is metabolized to some extent in the peripheral circulation It is often given with art enzyme inhibitor such as benserazide or carbidopa. Combined therapy permits a larger dose of active drug to reach the cerebral tissues, and at the same time reduces some of the general side-effects of levodopa.
Dose: 125-300 mg initially, increased according to need and response. Side-effects include nausea and cardiovascular disturbances, but psychiatric side- effects may be (lose limiting. Close angle glaucoma is a contraindication. See page 160 and ‘I able 26.
lignocaine (lidocaine) A local anaesthetic widely used for infiltration anaesthesia as a 0.25-0.5% solution, usually with adrenaline, as well as for epidural, caudal and nerve block anaesthesia. It is the local anaesthetic present in many dental cartridges. A 2-4% solution is used for
surface anaesthesia, and a 2% gel is used to relieve the pain and discomfort of catheterization, but rapid absorption may cause side-effects. Lignocaine is also the drug of choice in the control of ventricular tachycardia following myocardial infarction. Dose: 100 mg as an i.v. bolus, followed by a dose of 4 mg/min by i.v. infusion for 3(t minutes, with subsequent doses of 2 inghnin. Side-effects include confusion, convulsions, bradycardia and I p hy oten- sion. (Xylocard). Emla cream contains lignocaine and prilocaine. It is used for local anaesthesia and to relieve the pain associated with injections, especially in children. It is applied under an occlusive dressing 1-2 hours before the injection.
lindane A pesticide used as a 1% solution for the treatment of scabies.
liothyronine (tri-iodothyronine) A thyroid hormone with it rapid action, an(] probably a precursor of thyroxine. It is given orally in severe hypothyroid conditions when a rapid action is necessary, and by injection in hypothyroid coma. Dose: 20-60 fag daily; 5-20 pg i.v.
0 ertroxin).
liquid paraffin A lubricant laxative and faecal softener.
Dose: la-mj, nil. Its extensive use is now
discouraged, as it may cause granulomatous reactions and reduce the absorption of fat-soluble vitamins.
lisinopril An ACE inhibitor similar to enalapril, but with it longer action that permits the use of a single daily dose. Dose: in the treatment of hypertension, (loses of 2.5 rig daily initially, slowly increased according to response up to 10-20 mg daily, occasionally up to 40 mg. In patients receiving diuretics, such Ilierapy should be withdrawn for 2-3 days before lisinopril therapy and resumed later if necessary. (Carace; Zesiril). See
page 148 and Table 21.
lithium carbonate Lithium carbonate and itratearc used for their mood-regulating action in the prophylaxis and treatment of mania and depressive illness, but the mode of action is not known. The therapeutic/ toxic range of lithium is very narrow, and continuous control of the plasma/lithium level is essential to avoid the many side-effects and hazards of therapy.

Atopic eczema
A Greek word meaning ‘to boil over’ or ‘to erupt’ is the source of the medical term ‘eczema’. It refers, of course, to the way in which the skin erupts into a rash, but it could equally well describe the eruption of controversy around this disease. No other allergic disease is quite such a cauldron of dissent - indeed, even the question of whether it is an allergic disease remains unresolved. These controversies directly affect the treatment of atopic eczema, so it is useful to understand them if you or your child have eczema.
The disagreement begins with the question of what causes atopic eczema.
Let’s start with the one point that everyone agrees on: dry skin plays a fundamental role. Those with atopic eczema have dry skin, not just in the eczematous areas, but in other parts as well, sometimes all over the body. The skin cells are less efficient than normal skin cells at retaining water.
Everyone would also agree that there is inflammation of the skin – a reaction that is produced by the immune system. But when it comes to the question of what starts off the inflammation there are huge differences of opinion among specialists treating atopic eczema – these specialists include dermatologists, allergists and paediatricians.
Since people with atopic eczema are atopic (allergy-prone), and most have
huge amounts of the allergy antibody, IgE, going round in their blood, it might
seem plausible that an allergic reaction to some external item kicks off the
inflammation. And when skin-prick tests (see p. 91) to common allergens such
as house-dust mite are tried, there are usually a large number of positive results.
But many of these turn out to be false positives – when tested more directly,
the allergen concerned does not actually play a part in causing the skin symptoms.
This has led some specialists working with eczema, mainly dermatologists, to
What the words mean
Eczema is not a disease in itself. The word refers to a certain type of reddish rash — a rash which can be caused in a variety of ways. The type of eczema that affects people of an allergic disposition (atopics), is called either atopic eczema or atopic dermatitis.
The word dermatitis just means inflammation of the skin. Most doctors consider it to be synonymous with eczema, but some give it a slightly broader meaning.
believe that allergic reactions play little part in either initiating or perpetuating atopic eczema. In their view, the basic cause of atopic eczema is dry skin and a generally overwrought immune system, not specific allergic reactions.
To some of these doctors, positive skin-prick tests are all false positives in atopic eczema – that is, irrelevant to the disease process. A positive skin-test result, in their opinion, simply indicates that the skin of atopic eczema sufferers is in a highly sensitive state, not that the allergen concerned plays any causative role.
Allergists tend to take a different view of this, as you might expect. And recent research shows that they are correct – allergens often do play a significant part in provoking atopic eczema.
Research using direct challenge tests (see p. 90) has identified some of the things that could provoke such sensitivity reactions:
• house-dust mites, pollen or moulds
• cats, dogs, rabbits and other furry pets
• cow’s milk or other food – a prime suspect in babies and young children (see p. 68). The response to food is usually delayed, occurring some hours after the item is consumed.
With mite, pollen and pet allergens, the eczema symptoms can be provoked either by allergens falling on the skin, or by direct contact (e.g. mite allergens in the bed, skin contact with pets, or lying on grass for those with grass-pollen allergy).
The rash tends to occur on skin not covered by clothes, as you would expect. But it can sometimes occur only on particular exposed areas – usually the most sensitive areas of skin. For example, there are people who react to house-dust mite but have eczema on the eyelids only.
Additionally, experiments show that even when an airborne allergen is only inhaled it can sometimes provoke eczema symptoms. The allergen probably reaches the skin in the bloodstream. (Alternatively, it might provoke an immune reaction in the airways which generates chemical messages of the kind that promote inflammation – these then reach the skin in the blood.) This means that the skin reaction could occur anywhere on the body, not just on exposed skin.
In the case of food, the molecules of food that cause the trouble are probably being absorbed from the stomach without being completely broken down. They then reach the skin via the blood to provoke a reaction there. (Or, again, it could be an inflammatory messenger chemical travelling from the gut to the skin in the blood.)
When food gets directly onto the skin – which it frequently does with small children, of course – it can provoke a reaction that way too. This may be a slow eczema-causing reaction, or a much faster reaction known as contact urticaria (see pp. 50-51). Reacting to food with contact urticaria is quite common in children with atopic eczema – but the same food doesn’t necessarily provoke atopic eczema when it is eaten. (However, eating these foods can sometimes trigger anaphylaxis – see pp. 58-9. They should therefore be treated with great caution.)
At the same time as all this research – which shows for sure that allergens play a part in atopic eczema – others have been asking what actually happens when skin reacts to an allergen. Their studies have turned the accepted understanding of allergies upside-down. They show that when something like egg or pollen provokes atopic eczema, what is occurring isn’t necessarily an allergic reaction of the usual sort, with IgE and mast cells (see
box on p.12). Instead, other immune cells are causing the trouble. Sometimes IgE is involved, but without mast cells. Sometimes neither is involved. These revolutionary discoveries are described in more detail on pp. 18-19. One interesting realisation from this research is that in different eczema sufferers, different immune reactions may be producing the rash – even if they are reacting to the same allergen! This helps to explain why the results of skin tests are so inconsistent and puzzling.
The wandering rash
For a baby with atopic eczema, the face, and especially the cheeks, are commonly affected, but there may be a rash all over the legs, the backs of the arms, and the back. As the months go by, the rash settles on the lower legs, and spreads to the fold of the elbow, and then the fold at the back of the knees — by about three years of age, this flexure eczema is the main problem for most children.
In adults, eczema is often found in quite restricted areas, such as the hands, scalp, lips, eyelids or chest. It may be located around the nipples — a sensitive spot where rubbing by clothing is enough to initiate a rash.
Atopic eczema is always in a process of change, and different parts of the body may display different stages of the rash:
• The rash is red and usually dry at first, and there may be not a great deal to see. In this early stage the visible signs may be minimal, while the itchiness can be colossal. Sometimes there is oozing of clear fluid.
• Occasionally the first phase is more marked, with dense patches of small red bumps or tiny blisters. On the hands, these may merge to form larger blisters.
• Infections tend to change the appearance of the rash (see p. 44).
• With time the skin becomes thicker, paler and scaly. It may form leathery patches (called lichenification), especially if there is habitual scratching or rubbing. This is chronic eczema.
• When the eczema clears, there may be an area of skin that is lighter in colour, or darker, than the surrounding skin.
The next step
Whatever causes atopic eczema, it provokes the most horrendous itching, as every eczema sufferer knows. The itch cries out to be scratched, and scratching is the major cause of the visible rash. If left untouched, the skin does not erupt into eczema, although it may well turn red, and there are still distinct changes in the skin that can be seen with a microscope.
Once eczema has erupted, the skin is no longer an intact protective layer that neatly separates ‘in-here’ from ‘out-there’. The skin becomes more permeable and loses its own natural moisture far more readily, so the dryness gets worse. At the same time allergens and irritants penetrate far more easily, causing yet more inflammation.
Something else compounds the damage: once atopic eczema is established, the immune system starts making IgE antibodies to the body’s own proteins, especially those found in skin cells. This helps explain why atopic eczema can become so severe and so entrenched.
Infections — another vicious circle
When eczema erupts and the skin barrier is breached, infections often become a problem. A regular source of trouble is the bacterium Staphylococcus aureus, a cause of the infection impetigo. This microbe invades eczematous skin far more readily than healthy skin, causing a prolific ooze with golden-yellow crusting.
Staphylococcus aureus produces a toxin known as a ’super-antigen’ which revs up the immune system to even more furious effort. This effort does not, unfortunately, oust the bacteria, but it does make the skin inflammation even worse. To add to their woes, many who are afflicted with atopic eczema start making IgE antibodies against Staphylococcus aureus toxins.
Infection with fungi (yeasts and moulds) is also a problem in atopic eczema (see p. 49), and there may be sensitivity reactions to these fungi.
The herpes virus, responsible for causing cold sores, can also invade eczematous skin, though this is much rarer. It worsens the eczema and produces fever and general weakness. There may also be flocks of small red bumps, each with a tiny dimple or blister at the centre. Any symptoms of this kind indicate that the patient needs urgent treatment.
Irritants and stress
People with atopic eczema are far more susceptible to everyday irritants such as wool and rough synthetic fabrics, soap, and traces of detergent left behind in clothes. Chlorinated water, either in swimming pools or from the tap, can also aggravate the skin, and even ‘hard’ water (found in areas with chalk or limestone bedrock) may be a factor.
Some air pollutants may play a part in atopic eczema. Researchers in Germany have found that children living close to busy trunk roads, or in homes with a gas cooker and no extraction hood (see pp. 128-9), were more likely to develop eczema. Formaldehyde fumes, often found in modern houses (see p. 129), are sometimes a factor when eczema affects the face and hands.