Table 1.

Clinical characteristics of acquired cutis laxa[1,2,3,4,5]

	Type 1 or generalised acquired elastolysis	Type 2 or Marshall’s syndrome
Etiology	• Drugs (isoniazid, penicillin)	Post-inflammatory elastolysis after Sweet’s syndrome or Sweet’s syndrome like inflammatory dermatoses
	• Malignancies (multiple myeloma, lymphoma)
	• Infections (Toxocara canis, Borrelia burgdorferi, Treponema pallidum, Onchocerca volvulus)
	• Connective tissue diseases (rheumatoid arthritis, systemic lupus erythematosus)
	• Inflammatory (dermatitis herpetiformis, interstitial granulomatous dermatitis, sarcoidosis, celiac disease, acute generalised exanthematous pustulosis)
	• Miscellaneous (nephrotic syndrome, alpha-1 antitrypsin deficiency, mastocytosis, amyloidosis)
Age group	Usually in adults	• Children (when associated with Sweet’s syndrome)
		• Young adults (when associated with Sweet’s syndrome like inflammatory dermatoses)
Progression	Starts in head and neck region and expands peripherally in a cranio-caudal fashion	Starts in head and neck region and expands peripherally in a cranio-caudal fashion.
Clinical presentation	Generalised or circumscribed (in interstitial granulomatous dermatitis), with or without preceding inflammatory lesions	• Eruptive phase: Appearance of bright red papules and plaques with or without associated fever. It can persist for months to years
		• Elastolysis phase: Clinical lesions fade and signs of post-inflammatory elastolysis appear
Systemic involvement	Pulmonary emphysema, pneumothorax, vascular dilatations, gastrointestinal diverticulae, cor-pulmonale, and hernia.	Cardiovascular involvement, Takayasu arteritis