Rarely, leukocytoclastic vasculitis can result from ischemic colitis, inflammatory bowel disease, and cryoglobulinemia. There is no established standard for the treatment of leukocytoclastic vasculitis associated with gastroenterologic diseases. This paper presents three cases of leukoytoclastic vasculitis, each of which is associated with a different gastroenterologic condition: ischemic colitis, Crohn’s disease, and chronic hepatitis C. Each condition went into remission by treatment of leukocytoclastic vasculitis, regardless of the underlying disease.
Vasculitis is an uncommon disease caused by destruction, necrosis, and inflammation of vessel walls of all types and sizes, especially small vessels such as postcapillary venules. Among small vessel vasculitides, cutaneous leukocytoclastic vasculitis (LV) is the most common [
A 73-year-old male patient suffering from bloody diarrhea that had begun 3 weeks before was referred to us. He also had purpura-like rash on both lower extremities. In his history, he had been diagnosed with hypertension and pulmonary thromboembolism one year before. Our physical examination revealed widespread abdominal tenderness without defender or rebound. Stool microscopy showed an abundance of leukocytes and erythrocytes; his body temperature was 37.3°C. Laboratory test results were normal except for his C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) (Table
Vasculitis was considered in the patient due to increasing CRP (to 17 mg/dL), neutropenia, continuous fever, and purpura in the bilateral lower extremities. The skin biopsy results were compatible with leukocytoclastic vasculitis. As a secondary cause of the vasculitis, coexistence of ischemic colitis and LV was investigated. Treatment began with methyl prednisolone (40 mg/day). On the third day of the steroid therapy, the patient’s general condition improved, rashes disappeared, and the patient became afebrile, and, on the fifth day of the steroid therapy, his diarrhea was resolved. The patient was discharged on reduced steroid doses to be followed as an outpatient.
Laboratory examination of three cases.
Case |
Case |
Case |
|
---|---|---|---|
White blood cell (103/µL) | 6.57 | 25.56 | 2.63 |
Neutrocytes (%) | 80.9 | 88 | 64.6 |
Lymphocytes (%) | 12.2 | 10 | 21.7 |
Hemoglobin (g/dL) | 10.7 | 15.2 | 10.6 |
Platelets (103/µL) | 212 | 130 | 18 |
C-reactive protein (mg/dL) (0.5<) | 9.76 | 12.34 | 0.14 |
C4 (mg/dL) (10–40) | n.t. | n.t. | <1.47 |
Anti-HCV (positive > 1.0 COI) | (−) | (−) | 208.1 |
Cryoglobulin | (−) | (−) | (+) |
Skin biopsy | LV | LV | LV |
Case
Colonoscopic image.
A 28-year-old male patient had complaints of pain in his stomach and wrists for 2 weeks. His history includes no complaints except for periodic abdominal pain. Physical examination revealed widespread abdominal tenderness, plus tenderness, swelling, and limited range of motion by palpating of elbows, as well as petechial rash on bilateral lower extremities from ankle to kneecap. Selected laboratory tests results are as follows. CRP was 12.34 mg/dL (<0.5 mg/dL), white blood cell (WBC) was 25 × 103/
When the existing methyl prednisolone treatment did not reduce leukocytoclastic vasculitis-related complaints, pulse steroids (methyl prednisolone 1 g/day) were added. After three days, the rashes had regressed so that the patient’s treatment was continued with oral steroids.
A 59-year old female patient was admitted with complaints of rashes on her legs for 2 months and bleeding of the nose that had started 2 days before. In her history, the patient had been diagnosed for chronic hepatitis C (HCV), but went untreated for 2.5 years as there had been no indication to require any treatment. Physical examination was unremarkable except for petechial rashes on her bilateral lower extremities. Laboratory tests detected the following: platelet, 18 × 103/
Cutaneous leukocytoclastic rash.
Leukocytoclastic vasculitis is a pathological condition first defined in 1950 by Pearl Zeek as vasculitis of small vessels after drug intake. LV is characterized by exudates rich in neutrophils, endothelial damage, fibrin deposition, and core fragments (leukocytoclasis) in postcapillary venules of small vessels. Patients diagnosed with LV who have isolated skin involvement but no internal organ involvement are considered to have cutaneous LV [
The association between ischemic colitis and LV has not yet been reported in the literature. We wanted to present Case
Treatment of cutaneous LV is based on the degree of systemic involvement and should be appropriate to the underlying disease. Most patients have only scattered purpuric lesions and, clinically, no systemic involvement. Rashes usually restrict themselves. In the treatment of LV, if the encountering drug and antigen are eliminated, symptoms will disappear without treatment within days or weeks. Symptomatic treatment is given; bed rest is recommended. Any underlying infection should be treated. Patients who have long-standing skin manifestations, severe cutaneous involvement, and/or systemic disease should be treated with oral or parenteral corticosteroids. Prednisolone (20–60 mg daily in divided doses) will control the disease. Dosage should be gradually reduced to the lowest possible amount, and then the treatment must be terminated [
Low levels of serum complement, positive serum cryoglobulins, and high ESR may call for a diagnosis of cryoglobulinemia secondary to chronic hepatitis C [
In summary, LV cases due to ischemic colitis, Crohn’s disease, and chronic hepatitis C are rarely seen in practice and have no standard treatment. Each case may require separate treatment protocols, as did our three. Regardless of the underlying disease, however, these patients’ clinical and laboratory abnormalities resolved completely by being treated only for leukocytoclastic vasculitis.
The authors declare that there is no conflict of interests. Thanks are given to S. Delecroix for translation consultancy.