Sporadic Health Dictionary

(Singhalese: beri = extreme weakness.) Formerly a major health problem in many Asian countries, beriberi is a nutritional de?ciency disease resulting from prolonged de?ciency of the water-soluble vitamin, THIAMINE (vitamin B1). It is often associated with de?ciencies of other members of the the vitamin B complex (see APPENDIX 5: VITAMINS). A major public-health problem in countries where highly polished rice constitutes the staple diet, beriberi also occurs sporadically in alcoholics (see WERNICKE’S ENCEPHALOPATHY) and in people suffering from chronic malabsorptive states. Clinical symptoms include weakness, paralysis – involving especially the hands and feet (associated with sensory loss, particularly in the legs) – and ‘burning sensations’ in the feet (dry beriberi). Alternatively, it is accompanied by oedema, palpitations and a dilated heart (wet beriberi). Death usually results from cardiac failure. Thiamine de?ciency can be con?rmed by estimating erythrocyte transketolase concentration; blood and urine thiamine levels can be measured by high-pressure liquid chromatography.

Treatment consists of large doses of vitamin B1 – orally or intramuscularly; a diet containing other vitamins of the B group; and rest.

Infantile beriberi This is the result of maternal thiamine de?ciency; although the mother is not necessarily affected, the breast-fed baby may develop typical signs (see above). Optic and third cranial, and recurrent laryngeal nerves may be affected; encephalopathy can result in convulsions, coma and death.... beriberi

A rapidly progressive, fatal, degenerative disease in humans caused by an abnormal PRION protein. There are three aetiological forms of CJD: sporadic, IATROGENIC, and inherited. Sporadic CJD occurs randomly in all countries and has an annual incidence of one per million. Iatrogenic CJD is caused by accidental exposure to human prions through medical and surgical procedures (and cannibalism in the case of the human prion disease known as kuru that occurs in a tribe in New Guinea, where it is called the trembling disease). Inherited or familial CJD accounts for 15 per cent of human prion disease and is caused by a MUTATION in the prion protein gene. In recent years a new variant of CJD has been identi?ed that is caused by BOVINE SPONGIFORM ENCEPHALOPATHY (BSE), called variant CJD. The incubation period for the acquired varieties ranges from four years to 40 years, with an average of 10–15 years. The symptoms of CJD are dementia, seizures, focal signs in the central nervous system, MYOCLONUS, and visual disturbances.

Abnormal prion proteins accumulate in the brain and the spinal cord, damaging neurones (see NEURON(E)) and producing small cavities. Diagnosis can be made by tonsil (see TONSILS) biopsy, although work is under way to develop a diagnostic blood test. Abnormal prion proteins are unusually resistant to inactivation by chemicals, heat, X-RAYS or ULTRAVIOLET RAYS (UVR). They are resistant to cellular degradation and can convert normal prion proteins into abnormal forms. Human prion diseases, along with scrapie in sheep and BSE in cattle, belong to a group of disorders known as transmissible spongiform encephalopathies. Abnormal prion proteins can transfer from one animal species to another, and variant CJD has occurred as a result of consumption of meat from cattle infected with BSE.

From 1995 to 1999, a scienti?c study of tonsils and appendixes removed at operation suggested that the prevalence of prion carriage may be as high as 120 per million. It is not known what percentage of these might go on to develop disease.

One precaution is that, since 2003, all surgical instruments used in brain biopsies have had to be quarantined and disposable instruments are now used in tonsillectomy.

Measures have also been introduced to reduce the risk of transmission of CJD from transfusion of blood products.

In the past, CJD has also been acquired from intramuscular injections of human cadaveric pituitary-derived growth hormone and corneal transplantation.

The most common form of CJD remains the sporadic variety, although the eventual incidence of variant CJD may not be known for many years.... creutzfeldt-jakob disease (cjd)

Known colloquially as ‘mad cow disease’, this is a fatal and untreatable disease. Along with scrapie in sheep and CREUTZFELDT-JACOB DISEASE (CJD) in humans, BSE belongs to a class of unusual degenerative diseases of the brain known as transmissible spongiform encephalopathies. The disease is caused by abnormal PRION proteins, which are resistant to cellular degradation. These abnormal prion proteins accumulate in and eventually cause the death of nerve cells, both in the spinal cord and the brain. The rare human disease CJD occurs throughout the world and is of three types: sporadic, iatrogenic (see IATROGENIC DISEASE) and inherited.

Since the BSE epidemic in cattle developed in the UK in the 1980s, however, a new variant of CJD has been identi?ed and is believed to be the result of consumption of the meat of BSE-infected cattle. Studies in transgenic mice have con?rmed that BSE caused variant CJD. The new variant has affected younger people and may have a shorter incubation period. If this incubation period turns out to be the same as for the other types of CJD, however, it could be 2005– 2010 before the peak of this outbreak is reached. Over 148 people had died, or were dying, from variant CJD in the UK by the year 2005.

The appearance of BSE in cattle is believed to have been caused by a gene mutation (see GENETIC DISORDERS), although whether this mutation ?rst occurred in cattle or in some other animal remains uncertain. Although the ?rst case of BSE was o?cially reported in 1985, the ?rst cattle are thought to have been infected in the 1970s. BSE spread to epidemic proportions because cattle were fed meat and bone meal, made from the o?al of cattle suffering from or incubating the disease. Mother-to-calf transfer is another likely route of transmission, although meat and bone meal in cattle feed were the main cause of the epidemic. The epidemic reached its peak in 1992 when the incidence of newly diagnosed cases in cattle was 37,545.

A two-year UK government inquiry into the BSE epidemic concluded that BSE had caused a ‘harrowing fatal disease in humans’, and criticised o?cials for misleading the public over the risk to humans from BSE. Consequently, a compensation package for patients and relatives was made available. Meanwhile, a ban on the export of UK beef and restrictions on the type of meat and products made from beef that can be sold to the public were put in place. Although initially thought to be a problem primarily con?ned to the UK, several other countries – notably France, Germany, Spain, Switzerland and the United States – have also discovered BSE in their cattle.... encephalopathy (bse)

Painful, sporadic and drop-by-drop urination, caused by the presence of kidney stones, chronic inflammation such as interstitial cystitis, or urethral scar tissue. This is not a specific disease, but a symptom, like nausea or a sore joint.... strangury

Roxb.

Family: Guttiferae; Clusiaceae.

Habitat: Forests of northeast Bengal, sporadic in NEFA, Manipur and upper Assam

Ayurvedic: Amlavetasa. Vetasaamla.

Folk: Thaikala (Bengal).

Action: Antiscorbutic, astringent, cooling, cardiotonic, emollient. Used in anorexia, dyspepsia, colic, liver and spleen diseases difficult micturition. Cough and other respiratory disorders, ulcers and skin diseases.

Dry fruits (pericarp) contain the benzophenones, pedunculol, garcinol and cambogin.

The heartwood gave benzophenone and xanthone.

Dosage: Fruit—5-10 ml juice. (CCRAS.)... garcinia pedunculata

A condition resulting from environmental temperatures which are too high for compensation by the body’s thermo-regulatory mechanism(s). It is characterised by hyperpyrexia, nausea, headache, thirst, confusion, and dry skin. If untreated, COMA and death ensue. The occurrence of heat stroke is sporadic: whereas a single individual may be affected (occasionally with fatal consequences), his or her colleagues may remain unaffected. Predisposing factors include unsatisfactory living or working conditions, inadequate acclimatisation to tropical conditions, unsuitable clothing, underlying poor health, and possibly dietetic or alcoholic indiscretions. The condition can be a major problem during pilgrimages – for example, the Muslim Hadj. Four clinical syndromes are recognised:

Heat collapse is characterised by fatigue, giddiness, and temporary loss of consciousness. It is accompanied by HYPOTENSION and BRADYCARDIA; there may also be vomiting and muscular cramps. Urinary volume is diminished. Recovery is usual.

Heat exhaustion is characterised by increasing weakness, dizziness and insomnia. In the majority of sufferers, sweating is defective; there are few, if any, signs of dehydration. Pulse rate is normal, and urinary output good. Body temperature is usually 37·8–38·3 °C.

Heat cramps (usually in the legs, arms or back, and occasionally involving the abdominal muscles) are associated with hard physical work at a high temperature. Sweating, pallor, headache, giddiness and intense anxiety are present. Body temperature is only mildly raised.

Heat hyperpyrexia is heralded by energy loss and irritability; this is followed by mental confusion and diminution of sweating. The individual rapidly becomes restless, then comatose; body temperature rises to 41–42 °C or even higher. The condition is fatal unless expertly treated as a matter of urgency.

Treatment With the ?rst two syndromes, the affected individual must be removed immediately to a cool place, and isotonic saline administered – intravenously in a severe case. The fourth syndrome is a medical emergency. The patient should be placed in the shade, stripped, and drenched with water; fanning should be instigated. He or she should be wrapped in a sheet soaked in cool water and fanning continued. When rectal temperature has fallen to 39 °C, the patient is wrapped in a dry blanket. Immediately after consciousness returns, normal saline should be given orally; this usually provokes sweating. The risk of circulatory collapse exists. Convalescence may be protracted and the patient should be repatriated to a cool climate. Prophylactically, personnel intended for work in a tropical climate must be very carefully selected. Adequate acclimatisation is also essential; severe physical exertion must be avoided for several weeks, and light clothes should be worn. The diet should be light but nourishing, and ?uid intake adequate. Those performing hard physical work at a very high ambient temperature should receive sodium chloride supplements. Attention to ventilation and air-conditioning is essential; fans are also of value.... heat stroke

Trichinosis, or trichiniasis, is a disease caused by eating meat infected with the parasitic nematode worm, Trichinella spiralis. Although it infects more than 100 animal species, this nematode usually infects humans via pig meat in which the immature spiralis is encysted. The full-grown female worm, which inhabits the intestine, is 3 mm in length, and the larvae, to whose movements the disease is due, are much smaller. The disease is acquired by eating raw or underdone pork from pigs that have been infected with the worm. When such a piece of meat is eaten, the embryos contained in it are set free and develop into full-grown trichinellae; from each pair of these, 1,000 or more new embryos may arise in a few weeks. These burrow through the walls of the gut, spread throughout the body and settle in voluntary muscle.

Prevention is based on thorough inspection of meat in slaughterhouses; even cooking, unless the meat is in slices, is not an e?cient protection. Pigs should not be fed on unboiled garbage. Rats may be a source of sporadic outbreaks, as infected rats have been found near piggeries. The disease is widely distributed throughout the Americas, Asia, Africa and the Arctic. Sporadic cases and epidemics occur and outbreaks also appear in Europe, although rarely in Britain.

Treatment Thiabendazole or mebendazole are usually e?ective, while STEROID treatment helps patients with systemic illness and muscle tenderness.... trichinosis

The disease (caseous lymphadenitis) attacks the lymphatic system and may spread to sheep and humans. Breaks out sporadically in goats imported from abroad. Those in close contact with infected animals are at risk.

Symptoms: loss of weight, wasting illness, skin abscesses.

Treatment. Tea: Aniseed 1; Senna leaf 1; Nettles 2. 2 teaspoons to each cup boiling water; infuse 10-15 minutes in covered vessel. 1 cup thrice daily. Add to each dose: 30 drops Tincture Echinacea. ... goat disease

An epidemic form of encephalitis.

There have been no major outbreaks since the 1920s, but rare sporadic cases still occur.

Many people who survived the initial illness during the major epidemics developed post-encephalitic Parkinson’s disease.... encephalitis lethargica

n. a fungus (Claviceps purpurea) that grows on rye. It produces several important alkaloids, chemically related to LSD, including *ergotamine and *ergometrine, which are used in medicine in the treatment of migraine and in childbirth. Eating bread made with rye infected with the fungus has led to sporadic outbreaks of *ergotism over the centuries.... ergot

These are caused when there are mutations or other abnormalities which disrupt the code of a gene or set of GENES. These are divided into autosomal (one of the 44 CHROMOSOMES which are not sex-linked), dominant, autosomal recessive, sex-linked and polygenic disorders.

Dominant genes A dominant characteristic is an e?ect which is produced whenever a gene or gene defect is present. If a disease is due to a dominant gene, those affected are heterozygous – that is, they only carry a fault in the gene on one of the pair of chromosomes concerned. A?ected people married to normal individuals transmit the gene directly to one-half of the children, although this is a random event just like tossing a coin. HUNTINGTON’S CHOREA is due to the inheritance of a dominant gene, as is neuro?bromatosis (see VON RECKLINGHAUSEN’S DISEASE) and familial adenomatous POLYPOSIS of the COLON. ACHONDROPLASIA is an example of a disorder in which there is a high frequency of a new dominant mutation, for the majority of affected people have normal parents and siblings. However, the chances of the children of a parent with the condition being affected are one in two, as with any other dominant characteristic. Other diseases inherited as dominant characteristics include spherocytosis, haemorrhagic telangiectasia and adult polycystic kidney disease.

Recessive genes If a disease is due to a recessive gene, those affected must have the faulty gene on both copies of the chromosome pair (i.e. be homozygous). The possession of a single recessive gene does not result in overt disease, and the bearer usually carries this potentially unfavourable gene without knowing it. If that person marries another carrier of the same recessive gene, there is a one-in-four chance that their children will receive the gene in a double dose, and so have the disease. If an individual sufferer from a recessive disease marries an apparently normal person who is a heterozygous carrier of the same gene, one-half of the children will be affected and the other half will be carriers of the disease. The commonest of such recessive conditions in Britain is CYSTIC FIBROSIS, which affects about one child in 2,000. Approximately 5 per cent of the population carry a faulty copy of the gene. Most of the inborn errors of metabolism, such as PHENYLKETONURIA, GALACTOSAEMIA and congenital adrenal hyperplasia (see ADRENOGENITAL SYNDROME), are due to recessive genes.

There are characteristics which may be incompletely recessive – that is, neither completely dominant nor completely recessive – and the heterozygotus person, who bears the gene in a single dose, may have a slight defect whilst the homozygotus, with a double dose of the gene, has a severe illness. The sickle-cell trait is a result of the sickle-cell gene in single dose, and sickle-cell ANAEMIA is the consequence of a double dose.

Sex-linked genes If a condition is sex-linked, affected males are homozygous for the mutated gene as they carry it on their single X chromosome. The X chromosome carries many genes, while the Y chromosome bears few genes, if any, other than those determining masculinity. The genes on the X chromosome of the male are thus not matched by corresponding genes on the Y chromosome, so that there is no chance of the Y chromosome neutralising any recessive trait on the X chromosome. A recessive gene can therefore produce disease, since it will not be suppressed by the normal gene of the homologous chromosome. The same recessive gene on the X chromosome of the female will be suppressed by the normal gene on the other X chromosome. Such sex-linked conditions include HAEMOPHILIA, CHRISTMAS DISEASE, DUCHENNE MUSCULAR

DYSTROPHY (see also MUSCLES, DISORDERS OF – Myopathy) and nephrogenic DIABETES INSIPIDUS.

If the mother of an affected child has another male relative affected, she is a heterozygote carrier; half her sons will have the disease and half her daughters will be carriers. The sister of a haemophiliac thus has a 50 per cent chance of being a carrier. An affected male cannot transmit the gene to his son because the X chromosome of the son must come from the mother; all his daughters, however, will be carriers as the X chromosome for the father must be transmitted to all his daughters. Hence sex-linked recessive characteristics cannot be passed from father to son. Sporadic cases may be the result of a new mutation, in which case the mother is not the carrier and is not likely to have further affected children. It is probable that one-third of haemophiliacs arise as a result of fresh mutations, and these patients will be the ?rst in the families to be affected. Sometimes the carrier of a sex-linked recessive gene can be identi?ed. The sex-linked variety of retinitis pigmentosa (see EYE, DISORDERS OF) can often be detected by ophthalmoscopic examination.

A few rare disorders are due to dominant genes carried on the X chromosome. An example of such a condition is familial hypophosphataemia with vitamin-D-resistant RICKETS.

Polygenic inheritance In many inherited conditions, the disease is due to the combined action of several genes; the genetic element is then called multi-factorial or polygenic. In this situation there would be an increased incidence of the disease in the families concerned, but it will not follow the Mendelian (see MENDELISM; GENETIC CODE) ratio. The greater the number of independent genes involved in determining a certain disease, the more complicated will be the pattern of inheritance. Furthermore, many inherited disorders are the result of a combination of genetic and environmental in?uences. DIABETES MELLITUS is the most familiar of such multi-factorial inheritance. The predisposition to develop diabetes is an inherited characteristic, although the gene is not always able to express itself: this is called incomplete penetrance. Whether or not the individual with a genetic predisposition towards the disease actually develops diabetes will also depend on environmental factors. Diabetes is more common in the relatives of diabetic patients, and even more so amongst identical twins. Non-genetic factors which are important in precipitating overt disease are obesity, excessive intake of carbohydrate foods, and pregnancy.

SCHIZOPHRENIA is another example of the combined effects of genetic and environmental in?uences in precipitating disease. The risk of schizophrenia in a child, one of whose parents has the disease, is one in ten, but this ?gure is modi?ed by the early environment of the child.... genetic disorders

a condition in which sudden rapid destruction of red blood cells (see haemolysis) causes acute renal failure due partly to obstruction of small arteries in the kidneys. The haemolysis also causes a reduction in the number of platelets, which can lead to severe haemorrhage. The syndrome may occur as a result of septicaemia following a respiratory or gastrointestinal infection (especially by pathogenic *Escherichia coli), eclamptic fits in pregnancy (see eclampsia), or as a reaction to certain drugs. There may also be small sporadic outbreaks of the condition without any obvious cause.... haemolytic uraemic syndrome

Though the Black Death is supposed to have passed into medical history, occasional cases are recorded which give rise to the question: “Could it really come again?”

In an atomic age the collapse of medical services provided by governments is not far removed from the bounds of possibility. Wars come and go, medical fashions change, what is regarded as scientific today, may be neglected to tomorrow’s superstition. It is possible this book may be consulted long after 20th century medicine has had its day.

The preventative remedy of history is Garlic. It was given to workers on the Great Pyramid of Cheops as a known antiseptic and prophylactic against infection. A riot ensued when supplies ran out. During the Great Plague under Charles II a colony of people escaped death, living to reveal their secret – all were in the habit of eating Garlic. It was later confirmed that the plague was not found in houses in which Garlic had been consumed.

The disease is spread by fleas from the black rat by the organism: bacillus pestis. Incubation period is two to five days, followed by severe headache, shivering, dizziness, fever and rapid pulse. Before delirium, the patient may have the ‘staggers’ and confused speech.

Glands of the body enlarge and may suppurate. Suppuration is a welcome sign indicating speedy elimination of pus. Haemorrhagic spots break out on the skin.

The most dangerous type is that which affects the lungs, known as ‘pneumonic’ and which is highly infectious; characterised by cyanosis (blueness of the face).

Occasionally there are human cases of Bubonic Plague in California and the West but today they seldom prove fatal. Public health officials point out that the incidence of the disease in China and Vietnam is lower than for centuries because of vaccine therapy. Wild animals still spread sporadic cases of the Plague.

Treatment: Health Authorities to be notified immediately and patient isolated. All bedding and personal effects to be destroyed or disinfected. Specialised nursing necessary. If hospital care is not available, the patient should receive treatment for collapse (Capsicum, Ginger or other circulatory stimulants).

In the absence of streptomycin and tetracycline, to which the organism yersinia is sensitive, powerful alternatives may assist: Echinacea, Wild Indigo, Poke root, Queen’s Delight, Sarsaparilla, Yellow Parilla, Goldenseal, Prickly Ash.

Topical. Poultice of Slippery Elm, Marshmallow, or both combined to promote suppuration. History records pulped fresh Plantain leaves.

To be treated by general medical practitioner or Infectious Diseases consultant. ... bubonic plague

Any of a group of infectious diseases with similar symptoms that are caused by rickettsiae and are spread by insects or similar animals.

Except in some highland areas of tropical Africa and South America, epidemic typhus is rare today. Endemic typhus, also called murine typhus, is a disease of rats that is occasionally spread to humans by fleas; sporadic cases occur in North and Central America. Scrub typhus is spread by mites and occurs in India and Southeast Asia.

The symptoms and complications of all types of typhus are similar. Severe headache, back and limb pain, coughing, and constipation develop suddenly and are followed by high fever, a measles-like rash, confusion, and prostration. Left untreated, the condition may be fatal, especially in elderly or debilitated people.

A diagnosis is made by blood tests, and treatment is with antibiotic drugs and supportive treatment.... typhus

the most common form of *dementia, occurring in middle age or later. It is characterized by memory impairment and, as the disease progresses, language difficulties, *apraxia, and visuospatial problems, leading to a loss of judgment and the inability to carry out even basic functions. At post mortem there are excess deposits of *amyloid protein and *neurofibrillary tangles in the brain. In rare cases of familial Alzheimer’s, mutations in three genes have so far been detected; patients with these genes usually have early-onset dementia. The cause of the common sporadic form is not known although genetic factors can significantly increase the risk of developing the disease. Mutations in four other genes have been implicated in the more common late-onset form of the disease. The demonstration of damage to the cholinergic pathways has led to the development of *acetylcholinesterase inhibitors, which have been shown to slow disease progression. Ethical problems in the care of someone who has been used to making their own decisions (but now cannot) include respecting what *autonomy remains, how to gain valid *consent for treatment, and how to allow the patient proper *dignity. [A. Alzheimer (1864–1915), German physician]

AMA see American Medical Association.... alzheimer’s disease

(cerebral gigantism) a rare inherited disorder resulting in excessive physical growth during the first 2–3 years of life. It presents in childhood with a characteristic facial appearance, a disproportionately large head, large hands and feet, abnormally widely spaced eyes (ocular *hypertelorism), developmental delay, and tall stature for age. Children with Sotos syndrome tend to be large at birth and taller and heavier, stabilizing after about five years to achieve normal adult height. Most cases occur sporadically, although familial cases have been reported. [J. F. Sotos (1927– ), U.S. paediatrician]... sotos syndrome

(CJD) a rapidly progressive rare neurological disease, a form of human *spongiform encephalopathy in which dementia progresses to death after a period of 3–12 months. There is no effective treatment. The causative agent is an abnormal *prion protein that accumulates in the brain and causes widespread destruction of tissue. CJD typically affects middle-aged to elderly people. Some 15% of cases are due to a form of the disease that is inherited as an autosomal *dominant trait but most cases are sporadic, susceptibility being genetically determined. A few cases of CJD are acquired: the agent is known to have been transmitted by tissue and organ transplantation and by human growth hormone injections, but the disease may take years to manifest itself. Variant Creutzfeldt–Jakob disease (vCJD) is the human form of bovine spongiform encephalopathy (BSE), which is most likely acquired by the ingestion of infected beef products. Patients are younger than those affected with sporadic CJD and present with psychiatric symptoms (e.g. depression, anxiety) and hypersensitivity to touch, which are followed after months by myoclonic jerks (see myoclonus) and dementia. [H. G. Creutzfeldt (1885–1964) and A. M. Jakob (1884–1931), German psychiatrists]... creutzfeldt–jakob disease

a virus responsible for an acute infection in humans with features similar to those of *Marburg disease. Transmission is by contact with infected blood and other body fluids and the incubation period is 2–21 days (7 days on average). The mortality rate is 53–88%, but intensive treatment (including rehydration) in the early stages of the disease can halt its rapid and usually irreversible progression to haemorrhaging of internal organs. Until recently, sporadic but short-lived outbreaks have occurred in Africa since 1976, when the virus was first identified during an outbreak in the region of the Ebola river, in Zaïre (now Democratic Republic of Congo). A major epidemic of the disease broke out in West Africa at the end of 2013 and lasted until May 2016: over 11,000 people died. An unknown species of animal – possibly a fruit bat – is assumed to act as a reservoir for the virus between outbreaks of the disease in humans.... ebola virus

n. inflammation of the brain. It may be caused by a viral or bacterial infection or it may be due to an abnormal autoimmune process, such as an allergic response to a systemic viral illness or vaccination (see encephalomyelitis), a remote response to malignancy (paraneoplastic encephalitis), or a primary antibody-mediated autoimmune disorder. Recently a number of antibody-mediated encephalitides have been described (voltage-gated potassium receptor and *NMDA-receptor antibody being the commonest) that have characteristic clinical features and are often responsive to immunosuppressive therapies. Viral encephalitis is endemic in some parts of the world; it may also occur epidemically or sporadically. One form – encephalitis lethargica – reached epidemic proportions shortly after World War I and was marked by headache and drowsiness, progressing to coma (hence its popular name – sleepy sickness). Encephalitis can cause postencephalitic *parkinsonism. Another type of encephalitis that occurs sporadically is due to the herpes simplex virus.... encephalitis

n. a swelling of the neck due to enlargement of the thyroid gland. This may be due to lack of dietary iodine, which is necessary for the production of thyroid hormone: the gland enlarges in an attempt to increase the output of hormone. This was the cause of endemic goitre, formerly common in regions where the diet lacked iodine. Sporadic goitre may be due to simple overgrowth (hyperplasia) of the gland or to a tumour. In exophthalmic goitre (Graves’ disease) the swelling is associated with overactivity of the gland and is accompanied by other symptoms (see thyrotoxicosis). Autoimmune thyroiditis can be associated with goitre (see Hashimoto’s disease).... goitre