|Year : 1992 | Volume
| Issue : 2 | Page : 111-112
Acquired anhidrosis a case report
V Laxmi Nair, D Beena, S Manohar Ram
V Laxmi Nair
A 30-year -old man was seen for acquired anhidrosis. There was no systemic disease. Vasomotor functions were normal. Biopsy showed normal sweat glands and ducts. Intravenous injection of neostigmine could produce profuse sweating on the face, trunk and arms. The disorder is likely to be due to a peripheral dysautonomia selectively affecting the sudomotor function.
Keywords: Anhidrosis, acquired, dysautonomia, peripheral
|How to cite this article:|
Nair V L, Beena D, Ram S M. Acquired anhidrosis a case report. Indian J Dermatol Venereol Leprol 1992;58:111-2
| Introduction|| |
Anhidrosis is the inability of the body to produce and / or deliver eccrine sweat to the skin surface in response to an appropriate stimulus or environment. It may be due to changes in the eccrine sweat gland, alterations in the nervous pathway or due to metabolic, endocrine or systemic disease. Purely psychogenic anhidrosis is also known.  Occasionally it may not be possible to identify the cause. It may be localized, generalized, partial or complete.. Extensive anhidrosis may impair heat regulation and produce heat exhaustion. The following is a brief report of a patient with acquired anhidrosis.
| Case Report|| |
Mr K S, a 30-year-old healthy man, a woodcutter, came for complaints of absence of sweating and extreme intolerance to heat since 3 years. A warm environment or manual labour would lead to a burning sensation and rise of body temperature. This made him take resort to frequent showers. He also had excessive thirst and increased frequency of micturition since the onset of these symptoms. The bladder and bowel functions were preserved. He did not suffer from postural hypotension or impotence nor was there any history of preceding skin disease. 10 years ago he fell from a height of 12 feet and was unconscious for 30 minutes. He recovered without any residual symptoms or signs.
On examination, he was a man of average built and normotensive. There was no fall in the blood pressure on standing. But for minimal dryness his skin was normal. There was no evidence of any congenital ectodermal defect. Salivary, lacrimal functions and pupillary reflexes were normal. Clinically, there was no evidence of any central nervous system dysfunction. Systemic examination, routine haemogram, bone marrow studies, urinalysis, renal and hepatic functions were normal. The specific gravity of urine was 1015 after water deprivation. Serum osmolarity and X-ray of the skull were normal. Vasomotor functions was assessed to be normal by the Valsalva manoeuvre and by a normal wheal and flare on stroking the skin. His temperature was 38.4 °C.
A hot drink did not produce any visible sweating. Twenty four hours later, strenuous physical exertion in sunlight for 20 minutes produced minimal sweating over the scalp, presternal, interscapular and periumbilical regions only. The body temperature rose to 40 0 C. Starch iodine test was positive in these sites. Normal sweat glands and ducts were seen on biopsy sections from the thigh. To ascertain if there was blockage of the sweat duct in the stratum corneum it was stripped with cello tape. No sweating was observed. Neostigmine tablets 15mg four times a day failed to produce sweating but profuse sweating was seen over the face, trunk and arms following Inj. neostigmine 0.5 mg IV. His palms _and soles were dry.
| Comments|| |
Extensive anhidrosis may cause hyperpyrexia on exposure to heat. Our patient's occupation as a woodcutter would entail long hours of work in the sun and this is likely to produce profound disturbances in thermoregulation and collapse. It is not often easy to determine the cause of anhidrosis. It may be due to a systemic condition which is not clinically evident. Generalized anhidrosis may be a heralding sign of multiple myeloma and bone marrow studies are recommended in patients with acquired anhidrosis.  The sweat glands in multiple myeloma are atrophic. In our patient both the glandular structure and bone marrow studies were normal. The presence of normal sweat glands does not mean it is functioning. Autoradiography and enzyme histochemistry may help to differentiate an active from inactive gland. Moreover, there are differences in sweating in different areas with little or no sweating over the tip of the nose, elbows, patella or dorsal surfaces of the metacarpal joints.  In the absence of any abnormalities of the CNS or other evident systemic disease to account for the anhidrosis in our patient, It is likely to be due to a peripheral dysautonomia, selectively affecting the sudomotor function. The response to Inj. neostigmine is also a point in favour of such an etiology. Anhidrosis due to progressive selective sudomotor denervation with co-existing Adie's syndrome has been reported earlier.  Polydypsia is probably an attempt to offset the heat intolerance, this in turn leads to polyuria. Neostigmine did not produce palmoplantar sweating, since sweating in these areas is controlled mainly by emotional stimuli.. These patients may be managed by avoidance of factors which produce thermal stress and severely affected persons may be advised to move to cooler regions.
| References|| |
|1.||Siebert W. Ztschrf Klin, Med 1922; 94: 317 (quoted by 3) |
|2.||Shelley Y, Lehman J M. Generalized anhidrosis associated with multiple myeloma. Arch Dermatol 1961; 83: 903-9. |
|3.||Shelley W B, Horvath P N,' Pillsbury D M. Anhidrosis : an etiological interpretation. Med 1950; 29 : 195-224. |
|4.||Petajan J H, Danforth R C, D'Allesio D, et al. Progressive sudomotor denervation and Adie's syndrome. Neurol 1965; 15 : 172-6. |