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This is a benign condition causing an orange-yellow coloration of the skin of the palms, soles, forearms, and the region of the nose. It is partly due to the consumption of large amounts of foods rich in carotenoids, especially carrots, tomatoes, and the green outer leaves of vegetables.


Weakness of specific muscle groups is common and is due to severe protein-energy malnutrition. There is a 'proximal' myopathy, affecting the musculature of the pelvic girdle and the shoulder girdle. The patient first notices an increasing difficulty in climbing stairs. Weakness may also affect the muscles of the head and neck. When the patient is asked to rise from a sitting position, she will tend to push herself up using her hands and arms. She also has difficulty in rising unaided from a squatting position.(88)

There are no characteristic abnormalities in blood chemistry, although creatine kinase and liver enzymes may be elevated and the activity of enzyme carnosinase may be reduced. Myopathic changes are consistently present in muscle biopsy specimens. Histology reveals the 'chequerboard' distribution of muscle fibres but with a selective type 2 fibre atrophy. Electron microscopy reveals the presence of strikingly abundant glycogen granules between the myofibrils and under the sarcolemma.(88>

The detection of myopathy is a clear indication for the patient's admission to hospital and a refeeding programme. After a weight gain of a few kilograms her muscle strength will begin to return and a complete recovery is the rule.


A high proportion of patients with anorexia nervosa risk developing osteoporosis and consequent pathological fractures. Significant reduction in bone mineral density of the femoral neck was found in all 20 patients with anorexia nervosa of 6 years or more duration.(89) The favourite method of measuring bone density in the lumbar spine and hip is by dual-energy X-ray absorptiometry. A measurement for all patients with anorexia nervosa of 2 years duration or more is recommended. (99 It is difficult to disentangle the harmful effect of the nutritional deficiency itself from the associated oestrogen deficiency. It is likely that the pathogenesis of osteoporosis in anorexia nervosa differs from that in postmenopausal women. In anorexia nervosa the nutritional deficiency (often including a lack of calcium and vitamin D) leads to a low rate of the recycling of bone through bone formation and resorption, but the balance is disturbed by a relative increase in bone resorption.

On the whole the evidence favours the likelihood of improvement of bone density with nutritional recovery and resumption of menstruation. (89) There is much uncertainty about the best treatment. Although patients are often automatically prescribed oestrogen replacement, the only controlled trial undertaken so far indicated that oestrogen was only effective in severely underweight anorexic patients.(91) Indeed, it has been argued that oestrogen replacement could be harmful in some patients (children with premenarchal onset) and unnecessary in others with an illness of less than 3 years duration. (90) Instead the emphasis should be on encouraging weight gain, with the possible addition of calcium and vitamin D. There is a wider acceptance that patients with a poor prognosis (e.g. who have been ill over 10 years) might benefit from oestrogen replacement.

Disturbed temperature regulation

Disturbances in the control of temperature are evident from clinical observations; the patients frequently complain of feeling cold, and in the winter they have cold and blue extremities and suffer from chilblains. In the severely malnourished patient hypothermia may be a cause of death. Severe malnutrition is accompanied by a low central body temperature, presumably because of a low metabolic rate. Ingestion of a high-calorie meal can cause a significant increase in the central body temperature(92> which causes some patients to complain of heat in the periphery and sweating after food.

Haematological changes

Anorexic patients may develop a significantly lowered haemoglobin level and a reduced haematocrit and white cell count, with a relative decrease in neutrophil leucocytes and an increase in lymphocytes.(93) The anaemia is usually moderate and is normocytic normochromic in type. The mechanism is that of starvation-induced bone marrow hypoplasia. Only occasionally is there an iron deficiency. The anaemia gradually becomes corrected with weight gain. A low platelet count in the blood has also been observed and there may be an associated thrombocytopenic purpura.

Complications arising during rapid refeeding

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