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   Abstract
   Introduction
   Case Report
   Discussion
   References

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CASE REPORT
Year : 1999  |  Volume : 65  |  Issue : 2  |  Page : 79-80

Macular amyloidosis and hypothyroidism




Correspondence Address:
Adarsh Chopra


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  Abstract 

A 53 year old woman presented with extensive pruritic hyperpigmented macules in interscapular area and extremities of four years duration.She was an established case of hypothyroidism on treatment for last four years.


Keywords: Macular amyloidosis Hypothyroidism


How to cite this article:
Chopra A, Pahuja K, Chopra D. Macular amyloidosis and hypothyroidism. Indian J Dermatol Venereol Leprol 1999;65:79-80

How to cite this URL:
Chopra A, Pahuja K, Chopra D. Macular amyloidosis and hypothyroidism. Indian J Dermatol Venereol Leprol [serial online] 1999 [cited 2019 Sep 21];65:79-80. Available from: http://www.ijdvl.com/text.asp?1999/65/2/79/4767



  Introduction Top


Primary localised cutaneous amyloidosis (PLCA) is a disorder in which amyloid deposition occurs in the skin in the absence of evidence of amyloidosis in other organs.[1] PLCA comprises of macular, papular (lichen amyloidosis) and nodular (tumefactive) forms.

Macular amyloidosis is a less common variant. It is a pruritic eruption of small brownish macules distributed in a rippled, symmetrical fashion in the interscapular area but more commonly the lesions are more, extensively distributed over the back or chest. It is usually ideopathic but occasionally has been reported in association with autoimmune disease.[3]


  Case Report Top


A 53-year-old woman presented to our OPD with complaints of pruritic hyperpigmented lesions in interscapular area and extremities for the last four years. Dermatological examination revealed pruritic eruption on the back, arms and legs comprising of small brown macules which were coalescing to form plaques with rippled pattern. On further exploring she came out to be a case of hypothyroidism on treatment for last four years.

Laboratory investigations showed an elevated ESR (60mm 1st h). Full blood count and urine biochemistry were within normal limits. Thyroid function tests were highly deranged (T3 = 0.19 Ngm/ml; T4 = 1.24 mgm/dl; TSH = 110.7 ul/ml). The serum cholesterol levels were also high (323 mg%).

Ultrasonography of thyroid revealed hyperechoic lesions in right lobe which gave the impression of adenoma. There was no lymphadenopathy. Scrum calcitonin level was within normal limits.

Histopathological examination of elliptical biopsy taken from a small brown macule from the leg stained with haematoxylln and eosin showed marked pigmentary incontinence with drooping of melanin pigment in upper dermis associated with a sparse amount of lymphohistiocytic cell infiltrate in relationship to vessels of sub papillary plexus. The congo red stain revealed congo red positive areas in upper dermis confirming amyloidosis.


  Discussion Top


The patient fulfilled the criteria for being labeled as a case of hypothoyroidism.[4] The histopathological examination and dermatological examination were suggestive of the case being of macular amyloidosis. The association of hypothyroidism and macular amyloidosis has not been reported as a discrete case. The familial association of hereditary cutaneous lichen amyloidosis and MEN IIa (Multiple endocrine neoplasia IIa) have been described.[2] But the present case is a discrete case of hypothyroidism with macular amyloidosis.

 
  References Top

1.Masoliver AA. Widespread localised cutaneous amyloidosis (macular form) associated with systemic sclerosis. Br J Dermatol 1995;1:32:1:163-165.  Back to cited text no. 1    
2.Black MM, Gawkrodger DJ, Seymour CA, et al. Metabolic and nutritional disorders: Amyloid and the amyloidosis of the skin. Textbook of Dermatology. Rook A, Wilkinson DS, Ebling FJG. Blackwell Scientific Publications. 5th ed. 1992;2338.  Back to cited text no. 2    
3.Breathnach SM. The cutaneous amyloidosis. Arch Dermatol 1985;121:470-475.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Franklyn JA. Hypothyroidism. Medicine International 1997;16:20-23.  Back to cited text no. 4    




 

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