|Year : 1995 | Volume
| Issue : 3 | Page : 173-175
Cutaneous vasculitis with peripheral neuropathy
RA Joshi, VA Phadke, SL Wadhwa
R A Joshi
a 40-year-old male patient presented with cutaneous vasculitis affecting both lower legs without any evidence of systemic involvement and a bilateral sensory neuropathy affecting both lateral popliteal nerves. Treatment with oral prednisolone resulted in healing of the cutaneous lesions but the sensory loss persisted.
|How to cite this article:|
Joshi R A, Phadke V A, Wadhwa S L. Cutaneous vasculitis with peripheral neuropathy.Indian J Dermatol Venereol Leprol 1995;61:173-175
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Joshi R A, Phadke V A, Wadhwa S L. Cutaneous vasculitis with peripheral neuropathy. Indian J Dermatol Venereol Leprol [serial online] 1995 [cited 2019 Jul 17 ];61:173-175
Available from: http://www.ijdvl.com/text.asp?1995/61/3/173/4194
Peripheral neuropathy is a very common complication in systemic vasculitides like periarteritis nodosa, lupus erythematosus and rheumatoid vaseulitis. It is however a rare occurrence in localized cutaneous vasculitis. Localized cutaneous vasculitis is often a hypersensitivity vasculitis where the inflammatory process affects mainly the capillaries and small venules of the skin and nerve affliction is distinctly uncommon. We report the rare occurrence of localized cutaneous vasculitis complicated by bilateral sensory neuropathy of both lateral popliteal nerves.
A 40-year-old male patient presented with a 2 month history of painful ulcerating skin lesions over both lower legs. The lesions initially began on the left lower leg as a single painful erythematous papule following an insect bite which soon ulcerated and was followed within 15 days by crops of similar lesions on both lower legs. The erythematous papules used to ulcerate and get covered by a black eschar. There were several crops of similar lesions in the 2 months prior to presentation. He also complained of numbness and paraesthesias over both lower legs and dorsae of both the feet. There was no history suggestive of any systemic involvement. The medical, personal and family histories were non-contributory.
On examination the vital parameters were normal. Blood pressure was 110/80 mm Hg in the supine position and general examination was normal except for bilateral pitting pedal oedema. Cutaneous examination revealed multiple ulcers 0.5-1 cm in size [Figure:l] with irregular margins with several of them showing a black eschar, situated over both lower legs. Also seen were a few tender erythematous papulonodules over the same sites. Sensory loss to light touch and pinprick was present over the lateral aspect of both lower legs and the dorsa of the left foot. The examination of the motor system and deep reflexes was normal. Systemic examination did not reveal any abnormality. Investigations showed a TC:9600, DC:P70, L28, E2, haemoglobin : 13 gm%, ESR: 25 mm/hour. Routine urine and stool examinations were normal. Blood sugar, BUN, serum creatinine, bilirubin, SGOT, SGPT, were within normal limits. VDRL test and Elisa for HIV were negative. A swab from the ulcers grew Staph. aureus sensitive to erythromycin and cloxacillin. Tests for Australia antigen, anti nuclear antibodies, RA factor and cryoglobulins were negative. Serum immunoglobulins were normal. Mantoux was 6x6 mm at 48 hours and the X-ray chest was normal. Doppler studies demonstrated normal arterial blood flow in both lower limbs.
Biopsy from an early non-ulcerated papulo-nodule revealed necrotizing vasculitis with prominent fibrinoid degeneration of the vessel walls and pronounced leucocytoclasia affecting the upper and mid dermal vessels [Figure:2] A biopsy of the left sural nerve did not reveal vasculitis. EMG/nerve conduction studies showed a bilateral sensory neuropathy affecting both lateral popliteal nerves with decreased sensory amplitudes and lowered conduction velocities. No muscle affection was evident.
The patient was started on oral erythromycin followed by cloxacillin and 40 mg of prednisolone. Most skin lesions had healed at the end on one month of therapy when steroids were gradually tapered. At 3 months all skin lesions had healed with no new lesions appearing but the sensory loss persisted.
Henoch-Schonlein purpura and serum sickness are distinctive syndromes within the category of hypersensitivity vasculitis in which the skin is the predominant organ involved and neuropathy may occasionally be seen. The relative roles of vascular damage, direct immune attack and nerve oedema and compression in the pathogenesis of neuropathy are unknown. Serum sickness is historically important because of its contributions to early ideas about the pathogenesis of vasculitis. Peripheral nerve is rarely involved in hypersensitivity vasculitis and very few cases of hypersensitivity vasculitis with peripheral neuropathy have been reported.
Stafford et al reported a drug addict who developed a rapidly progressive mononeuritis multiplex as a complication of IV amphitamine with involvement of the right occulomotor, radial and peroneal nerves, which responded to oral steroids. Their findings including a biopsy were typical of hypersensitivity angiitis. Ritter et al reported a case of peripheral neuropathy complicating anaphylactoid purpura in a young girl where the left common peroneal palsy was attributed to oedema and compression of the nerve due to marked swelling of the left knee joint. Both cases had predominant motor involvement which improved partially after a period of time unlike our case where only sensory affection was noted which failed to improve even after 3 months of oral steroids. The cause of the neuropathy in our case is unknown as neither there was marked oedema of the lower limbs nor vasculitis demonstrated in the left sural nerve biopsy.
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