Clinical and Experimental Dermatology (1977) 2, 287.
Clinical meeting of the St John's Hospital Dermatological Society: 3 February 1977
Severe palmar keratoderma in myxoedema
O.T.TAN AND I.SARKANY Department of Dermatology, Royal Free Hospital, Pond Street, London NW3 2QG
Accepted for publication 20 March 1977
History and examination Mr G.G. a 46-year-oId foreman in the motor industry was seen in December 1976 with a 3year history of severe bilateral palmar hyperkeratosis associated with painful fissures (Fig. i). The skin changes had failed to respond to any topical therapy. On direct questioning, he admitted a gradual onset of tiredness, lethargy, an increase of 21 kg in weight and a change in his voice. On examination he seemed slow and dehberate with a croaky voice, slow speech and bilateral periorbital oedema. His pulse rate was 68/min, temperature 36 C and his ankle jerks showed the typical slow relaxation phase found in hypothyroidism. Investigations Investigations conflrnied that he was severely myxoedematous with T 4 < i o nmol/1 (normal levels 58-128) and TSH 100 /lU/ml (normal less than 5). Serum cholesterol was 115 nmol/l (normal levels 30-65). Lipoprotein electrophoresis showed type II B hyperlipidaemia. Thyroid antibodies (microsomal) were absent and parietal cell and intrinsic factor antibodies were negative. Cardiac enzymes were markedly raised: creatine kinase being t89O iu/1 (normal levels 4-50), hydroxybutyrate dehydrogenase 300 iu/1 (normal levels 4-50) and aspartate transaminase 37 iu/1 (normal levels 4-15). Chest X-ray showed a moderate cardiomegaly and the electrocardiogram bradycardia but with a normal amplitude. Serum vitamin A was 24 nmol/1 (normal levels 07-17), Waaserman reaction was negative. Serum bilirubin and all other tests were normal. Comment Palmar keratoderma of unknown aetiology is common, particularly in middle-aged adults. It usually responds, at least partially and temporarily, to treatment with topical steroids and keratolytic agents. In the patient described here, both the severity of the condition and its resistance to therapy were marked. 287
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Figure i. Severe palmar keratoderma prior to treatment with Thyroxine. Figure 2. Striking improvement in previously resistant palmar keratoderma lo days after treatment with Thyroxine.
The findings of severe myxoedema in our case made us wonder whether the association of the two conditions was more than coincidental. Shaw et al. (1952) described a single case in which the myxoedema and palmar hyperkeratosis appeared to be associated. Their patient's palmar keratoderma also cleared when the myxoedema was treated. When our patient was started on Thyroxine, there was rapid improvement not only in his myxoedematous state, but there was dramatic improvement in the palmar keratoderma within 10 days of starting therapy (Figs t and 2). Palmar keratoderma and myxoedema appeared to be associated directly in both our patient and the one described by Shaw et al (1952), as shown by the striking response of the skin changes to treatment of the myxoedema. It would seem worthwhile considering the possibility of myxoedema in cases of long standing keratoderma, although at present we have no reason to believe that such an association might be common. Reference J W.M., MASONJ E.H. & KALZ, E.G. (1952) Hypothyroid, liver damage and vitamin A deficiency as factors in hyperkeratosis. American Medical Association Archives of Dermatology and Syphilology, 66, t97-203.
Clinical meeting of the St John's Hospital Dermatological Society: 3 February 1977
Severe palmar keratoderma in myxoedema
O.T.TAN AND I.SARKANY Department of Dermatology, Royal Free Hospital, Pond Street, London NW3 2QG
Accepted for publication 20 March 1977
History and examination Mr G.G. a 46-year-oId foreman in the motor industry was seen in December 1976 with a 3year history of severe bilateral palmar hyperkeratosis associated with painful fissures (Fig. i). The skin changes had failed to respond to any topical therapy. On direct questioning, he admitted a gradual onset of tiredness, lethargy, an increase of 21 kg in weight and a change in his voice. On examination he seemed slow and dehberate with a croaky voice, slow speech and bilateral periorbital oedema. His pulse rate was 68/min, temperature 36 C and his ankle jerks showed the typical slow relaxation phase found in hypothyroidism. Investigations Investigations conflrnied that he was severely myxoedematous with T 4 < i o nmol/1 (normal levels 58-128) and TSH 100 /lU/ml (normal less than 5). Serum cholesterol was 115 nmol/l (normal levels 30-65). Lipoprotein electrophoresis showed type II B hyperlipidaemia. Thyroid antibodies (microsomal) were absent and parietal cell and intrinsic factor antibodies were negative. Cardiac enzymes were markedly raised: creatine kinase being t89O iu/1 (normal levels 4-50), hydroxybutyrate dehydrogenase 300 iu/1 (normal levels 4-50) and aspartate transaminase 37 iu/1 (normal levels 4-15). Chest X-ray showed a moderate cardiomegaly and the electrocardiogram bradycardia but with a normal amplitude. Serum vitamin A was 24 nmol/1 (normal levels 07-17), Waaserman reaction was negative. Serum bilirubin and all other tests were normal. Comment Palmar keratoderma of unknown aetiology is common, particularly in middle-aged adults. It usually responds, at least partially and temporarily, to treatment with topical steroids and keratolytic agents. In the patient described here, both the severity of the condition and its resistance to therapy were marked. 287
288
O.T.Tan and I.Sarkany
Figure i. Severe palmar keratoderma prior to treatment with Thyroxine. Figure 2. Striking improvement in previously resistant palmar keratoderma lo days after treatment with Thyroxine.
The findings of severe myxoedema in our case made us wonder whether the association of the two conditions was more than coincidental. Shaw et al. (1952) described a single case in which the myxoedema and palmar hyperkeratosis appeared to be associated. Their patient's palmar keratoderma also cleared when the myxoedema was treated. When our patient was started on Thyroxine, there was rapid improvement not only in his myxoedematous state, but there was dramatic improvement in the palmar keratoderma within 10 days of starting therapy (Figs t and 2). Palmar keratoderma and myxoedema appeared to be associated directly in both our patient and the one described by Shaw et al (1952), as shown by the striking response of the skin changes to treatment of the myxoedema. It would seem worthwhile considering the possibility of myxoedema in cases of long standing keratoderma, although at present we have no reason to believe that such an association might be common. Reference J W.M., MASONJ E.H. & KALZ, E.G. (1952) Hypothyroid, liver damage and vitamin A deficiency as factors in hyperkeratosis. American Medical Association Archives of Dermatology and Syphilology, 66, t97-203.
