The possible adverse effects of penicillamine can include allergic rashes, itching, nausea, vomiting, abdominal pain, loss of taste, blood disorders, and impaired kidney function.
– although lead-containing paints are no longer used for items that children may be in contact with.
Acute poisonings are rare. Clinical features include metallic taste, abdominal pain, vomiting, diarrhoea, ANOREXIA, fatigue, muscle weakness and SHOCK. Neurological effects may include headache, drowsiness, CONVULSIONS and COMA. Inhalation results in severe respiratory-tract irritation and systemic symptoms as above.
Chronic poisonings cause gastrointestinal disturbances and constipation. Other effects are ANAEMIA, weakness, pallor, anorexia, insomnia, renal HYPERTENSION and mental fatigue. There may be a bluish ‘lead line’ on the gums, although this is rarely seen. Neuromuscular dysfunction may result in motor weakness and paralysis of the extensor muscles of the wrist and ankles. ENCEPHALOPATHY and nephropathy are severe effects. Chronic low-level exposures in children are linked with reduced intelligence and behavioural and learning disorders.
Treatment Management of patients who have been poisoned is supportive, with removal from source, gastric decontamination if required, and X-RAYS to monitor the passage of metallic lead through the gut if ingested. It is essential to ensure adequate hydration and renal function. Concentrations of lead in the blood should be monitored; where these are found to be toxic, chelation therapy should be started. Several CHELATING AGENTS are now available, such as DMSA (Meso-2,3dimercaptosuccinic acid), sodium calcium edetate (see EDTA) and PENICILLAMINE. (See also POISONS.)... lead poisoning
Causes There is a major immunogenetic predisposition to rheumatoid arthritis in people carrying the HLA-DR4 antigen (see HLA SYSTEM). Other minor immunogenetic factors have also been implicated. In addition, there is a degree of familial clustering which suggests other unidenti?ed genetic factors. Genetic factors cannot alone explain aetiology, and environmental and chance factors must be important, but these have yet to be identi?ed.
Epidemiology Rheumatoid arthritis more commonly occurs in women from the age of 30 onwards, the sex ratio being approximately 4:1. Typical rheumatoid arthritis may occur in adolescence, but in childhood chronic SYNOVITIS usually takes one of a number of di?erent patterns, classi?ed under juvenile chronic arthritis.
Pathology The primary lesion is an in?ammation of the synovial membrane of joints. The synovial ?uid becomes diluted with in?ammatory exudate: if this persists for months it leads to progressive destruction of articular CARTILAGE and BONE. Cartilage is replaced by in?ammatory tissue known as pannus; a similar tissue invades bone to form erosions. Synovitis also affects tendon sheaths, and may lead to adhesion ?brosis or attrition and rupture of tendons. Subcutaneous and other bursae may be involved. Necrobiotic nodules also occur at sites outside synovium, including the subcutaneous tissues, the lungs, the pericardium and the pleura.
Clinical features Rheumatoid arthritis varies from the very mild to the severely disabling. Many mild cases probably go undiagnosed. At least 50 per cent of patients continue to lead a reasonably normal life; around 25 per cent are signi?cantly disabled in terms of work and leisure activities; and a minority become markedly disabled and are limited in their independence. There is often an early acute phase, followed by substantial remission, but in other patients gradual step-wise deterioration may occur, with progressive involvement of an increasing number of joints.
The diagnosis of rheumatoid arthritis is largely based on clinical symptoms and signs. Approximately 70 per cent of patients have rheumatoid factor ANTIBODIES in the SERUM but, because of the large number of false positives and false negatives, this test has very little value in clinical practice. It may be a useful pointer to a worse prognosis in early cases if the level is high. X-RAYS may help in diagnosing early cases and are particularly helpful when considering surgery or possible complications such as pathological fracture. Patients commonly develop ANAEMIA, which may be partly due to gastrointestinal blood loss from antiin?ammatory drug treatment (see below).
Treatment involves physical, pharmacological, and surgical measures, together with psychological and social support tailored to the individual patient’s needs. Regular activity should be maintained. Resting of certain joints such as the wrist with splints may be helpful at night or to assist prolonged manual activities. Sound footwear is important. Early use of antirheumatic drugs reduces long-term disability. Drug treatment includes simple ANALGESICS, NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS), and slow-acting drugs including GOLD SALTS (in the form of SODIUM AUROTHIOMALATE), PENICILLAMINE, SULFASALAZINE, METHOTREXATE and AZATHIOPRINE.
The non-steroidal agents are largely e?ective in reducing pain and early-morning sti?ness, and have no e?ect on the chronic in?ammatory process. It is important, especially in the elderly, to explain to patients the adverse effects of NSAIDs, the dosage of which can be cut by prescribing paracetamol at the same time. Combinations of anti-rheumatic drugs seem better than single agents. The slow-acting drugs take approximately three months to act but have a more global e?ect on chronic in?ammation, with a greater reduction in swelling and an associated fall in erythrocyte sedimentation rate (ESR) and rise in the level of HAEMOGLOBIN. Local CORTICOSTEROIDS are useful, given into individual joints. Systemic corticosteroids carry serious problems if continued long term, but may be useful under special circumstances. Much research is currently going on into the use of tumour necrosis factor antagonists such as INFLIXIMAB and etanercept, but their precise role remains uncertain.... rheumatoid arthritis
Antirheumatic drugs affect the disease process and may limit joint damage, unlike nonsteroidal anti-inflammatory drugs, which only relieve pain and stiffness.
The main antirheumatic drugs are corticosteroid drugs, immunosuppressant drugs, chloroquine, gold, penicillamine, and sulfasalazine.
Many of these drugs can have serious side effects, and treatment must be under specialist supervision.... antirheumatic drugs
Thiamine plays a role in the activities of various enzymes involved in the utilization of carbohydrates and thus in the functioning of nerves, muscles, and the heart. Sources include whole-grain cereals, wholemeal breads, brown rice, pasta, liver, kidney, pork, fish, beans, nuts, and eggs.
Those susceptible to deficiency include elderly people on a poor diet, and people who have hyperthyroidism, malabsorption, or severe alcohol dependence. Deficiency may also occur as a result of severe illness, surgery, or injury.
Mild deficiency may cause tiredness, irritability, and loss of appetite. Severe deficiency may cause abdominal pain, constipation, depression, memory impairment, and beriberi; in alcoholics, it may cause Wernicke–Korsakoff syndrome. Excessive intake is not known to cause harmful effects.
Riboflavin is necessary for the activities of various enzymes involved in the breakdown and utilization of carbohydrates, fats, and proteins; the production of energy in cells; the utilization of other B vitamins; and hormone production by the adrenal glands. Liver, whole grains, milk, eggs, and brewer’s yeast are good sources. People who are susceptible to riboflavin deficiency include those taking phenothiazine antipsychotic drugs, tricyclic antidepressant drugs, or oestrogen-containing oral contraceptives, and those with malabsorption or severe alcohol dependence. Riboflavin deficiency may also occur as a result of serious illness, surgery, or injury.
Prolonged deficiency may cause soreness of the tongue and the corners of the mouth, and eye disorders such as amblyopia and photophobia.
Excessive intake of riboflavin is not known to have any harmful effects.
Niacin plays an essential role in the activities of various enzymes involved in the metabolism of carbohydrates and fats, the functioning of the nervous and digestive systems, the manufacture of sex hormones, and the maintenance of healthy skin. The main dietary sources are liver, lean meat, fish, nuts, and dried beans. Niacin can be made in the body from tryptophan (an amino acid). Most cases of deficiency are due to malabsorption disorders or to severe alcohol dependence. Prolonged niacin deficiency causes pellagra. Excessive intake is not known to cause harmful effects.
Pantothenic acid is essential for the activities of various enzymes involved in the metabolism of carbohydrates and fats, the manufacture of corticosteroids and sex hormones, the utilization of other vitamins, the functioning of the nervous system and adrenal glands, and growth and development. It is present in almost all vegetables, cereals, and animal foods. Deficiency of pantothenic acid usually occurs as a result of malabsorption or alcoholism, but may also occur after severe illness, surgery, or injury. The effects include fatigue, headache, nausea, abdominal pain, numbness and tingling, muscle cramps, and susceptibility to respiratory infections. In severe cases, a peptic ulcer may develop. Excessive intake has no known harmful effects.Pyridoxine aids the activities of various enzymes and hormones involved in the utilization of carbohydrates, fats, and proteins, in the manufacture of red blood cells and antibodies, in the functioning of the digestive and nervous systems, and in the maintenance of healthy skin. Dietary sources are liver, chicken, pork, fish, whole grains, wheatgerm, bananas, potatoes, and dried beans. Pyridoxine is also manufactured by intestinal bacteria. People who are susceptible to pyridoxine deficiency include elderly people who have a poor diet, those with malabsorption or severe alcohol dependence, or those who are taking certain drugs (including penicillamine and isoniazid). Deficiency may cause weakness, irritability, depression, skin disorders, inflammation of the mouth and tongue, anaemia, and, in infants, seizures. In very large amounts, pyridoxine may cause neuritis.
Biotin is essential for the activities of various enzymes involved in the breakdown of fatty acids and carbohydrates and for the excretion of the waste products of protein breakdown. It is present in many foods, especially liver, peanuts, dried beans, egg yolk, mushrooms, bananas, grapefruit, and watermelon. Biotin is also manufactured by bacteria in the intestines. Deficiency may occur during prolonged treatment with antibiotics or sulphonamide drugs. Symptoms are weakness, tiredness, poor appetite, hair loss, depression, inflammation of the tongue, and eczema. Excessive intake has no known harmful effects.
Folic acid is vital for various enzymes involved in the manufacture of nucleic acids and consequently for growth and reproduction, the production of red blood cells, and the functioning of the nervous system. Sources include green vegetables, mushrooms, liver, nuts, dried beans, peas, egg yolk, and wholemeal bread. Mild deficiency is common, but can usually be corrected by increasing dietary intake. More severe deficiency may occur during pregnancy or breastfeeding, in premature or low-birthweight infants, in people undergoing dialysis, in people with certain blood disorders, psoriasis, malabsorption, or alcohol dependence, and in people taking certain drugs. The main effects include anaemia, sores around the mouth, and, in children, poor growth. Folic acid supplements taken just before conception, and for the first 12 weeks of pregnancy, have been shown to reduce the risk of a neural tube defect.... vitamin b complex
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