P Couture1, P Moguelet2, F Chasset3, A Barbaud3, P Senet3, J-B Monfort3. 1. Médecine, Sorbonne université, 75013 Paris 06, France; Service de dermatologie, UF de dermatologie vasculaire, hôpital Tenon, AP-HP, 4, rue de la Chine, 75020 Paris, France. Electronic address: couture.priscille@gmail.com. 2. Médecine, Sorbonne université, 75013 Paris 06, France; Service d'anatomopathologie, hôpital Tenon, AP-HP, 4, rue de la Chine, 75020 Paris, France. 3. Médecine, Sorbonne université, 75013 Paris 06, France; Service de dermatologie, UF de dermatologie vasculaire, hôpital Tenon, AP-HP, 4, rue de la Chine, 75020 Paris, France.
Abstract
BACKGROUND: Chilblains are inflammatory dermal lesions associated with hypersensitivity to cold, and they occur on the extremities bilaterally and symmetrically. Their onset during the course of pro-thermogenic and autoimmune diseases has been widely reported, but the association with predisposing locoregional causes is not well known. PATIENTS AND METHODS: Case 1: a 57-year-old man, who smoked 80 packets per year, presenting a deficit of the levator muscles in his right foot following lumbar sciatica with paralysis of L5, consulted for unilateral necrotic lesions of the toes recurring each winter in the paralysed limb only. Case 2: a 60-year-old man had a previous history of liposarcoma of the right side treated with radiotherapy and surgery, resulting in sequelae of monoparesis and radiation-induced arteritis. Each winter, he presented recurring unilateral purpuric macules of the toes on his right foot, with no necrotic progression. In both cases, clinical examination, disease progression over time, histology and laboratory tests confirmed the diagnosis of idiopathic chilblains. CONCLUSION: The physiopathological hypotheses posited to account for the unilateral appearance of chilblains in the event of paralysis include decreased blood flow to the paralysed limb, imbalance in neuromodulators, dysfunction of the autonomous nervous system, cutaneous atrophy with hypertrophy of underlying soft tissues, and finally, hypoesthesia aggravating the trophic disorders.
BACKGROUND: Chilblains are inflammatory dermal lesions associated with hypersensitivity to cold, and they occur on the extremities bilaterally and symmetrically. Their onset during the course of pro-thermogenic and autoimmune diseases has been widely reported, but the association with predisposing locoregional causes is not well known. PATIENTS AND METHODS: Case 1: a 57-year-old man, who smoked 80 packets per year, presenting a deficit of the levator muscles in his right foot following lumbar sciatica with paralysis of L5, consulted for unilateral necrotic lesions of the toes recurring each winter in the paralysed limb only. Case 2: a 60-year-old man had a previous history of liposarcoma of the right side treated with radiotherapy and surgery, resulting in sequelae of monoparesis and radiation-induced arteritis. Each winter, he presented recurring unilateral purpuric macules of the toes on his right foot, with no necrotic progression. In both cases, clinical examination, disease progression over time, histology and laboratory tests confirmed the diagnosis of idiopathic chilblains. CONCLUSION: The physiopathological hypotheses posited to account for the unilateral appearance of chilblains in the event of paralysis include decreased blood flow to the paralysed limb, imbalance in neuromodulators, dysfunction of the autonomous nervous system, cutaneous atrophy with hypertrophy of underlying soft tissues, and finally, hypoesthesia aggravating the trophic disorders.