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Rash, abdominal pain, hematochezia, and dysuria PDF Print E-mail
AIBS teaching cases
Tuesday, 31 October 2006

A 47-year-old female patient presented with haematochezia and fatigue. She reported that she had 4 bowel motions, which were dark red in colour without mucus. 3 weeks prior to presentation she noticed a rash that begun on the lower limbs (including the soles) and was ascending in nature and eventually involved the trunk, buttocks and upper limbs as well as the palms. Arthralgias, dysuria and frequency accompanied the skin manifestations. A skin biopsy performed elsewhere, showed leukocytoclastic vasculitis but immunofluorescence was not performed. The patient was not taking any medication prior to the development of the rash. She was on a tapering dose of methylprednisolone since and was generally well, except for continuing dysuria and frequency.

Figure 1. Purpuric rash afflicting the soles.

On examination, her blood pressure was normal but she was tachycardic (114 bpm) and tachypneic (20 respirations per minute) with oxygen saturation levels on air of 95%. Her temperature was 37,3 0C. A generalized purple skin rash was evident in the aforementioned areas (Figures 1 and 2). Her abdomen was exquisitely tender in all quadrants with a degree of rebound tenderness. On rectal examination dark red blood was present. The rest of the physical examination was normal.

Significant leukocytosis (34000/mm3) was present, as were mildly elevated urea levels (56 mg/dl). Urine dipstick was positive for blood (++) and leukocytes (++) and albumin (+). On urine microscopy there were 70 leukocytes and 5 erythrocytes per high power optical field, but there were no casts. Her electrocardiogram was normal but her chest X-ray revealed moderate bilateral pleural effusions. What is the diagnosis?

With a working diagnosis of gastrointestinal involvement due to her small vessels vasculitis, she was commenced on intravenous methylprednisolone 1 mg/kg daily in three divided doses. Empirically intravenous piperacillin-tazobactam and teicoplanin were commenced, due to the severity of the abdominal complaints with possible bacterial translocation, as well as the symptoms from the urogenital system and pyuria. On the second day of her hospitalization she was already feeling much better and she underwent colonoscopy with no obvious cause of her bleeding. Her clinical condition improved and she was up and about on the fourth day of hospitalization. Proteus mirabilis was isolated from urine culture (>105/ml); based on antibiotic susceptibility results, ciprofloxacin intravenously substituted the initial antibiotic regimen.

Blood cultures and a pharyngeal culture were negative. Computed tomography of the chest and abdomen were normal. Nephrolithiasis and obstructive pathology was ruled out after a normal abdominal ultrasound. A transesophageal echocardiogram, to rule out endocarditis, was normal. Serum protein immunoelectrophoresis revealed normal levels of immunoglobulins G, M, A and no monoclonal component. No autoantibodies were detected. 24-hour urine protein estimation showed 453 mg of protein. A repeat skin biopsy was performed to evaluate additionally the pattern of immunofluorescence; it disclosed IgA depositions in the walls of small skin vessels that were more pronounced in the dermis, in addition to the findings of the leukocytoclastic vasculitis.

Teaching points
- Henoch-Schönlein purpura is a leukocytoclastic vasculitis, usually presenting in childhood 1. It is usually idiopathic, but various triggers have been reported such as infections (either viral or bacterial) and drugs. Various bacterial infections have been reported to be associated with its presentation. In a few cases treatment of the infection led to treatment of the vasculitic syndrome as well. Urinary tract infections are rarely associated with the ignition of the cascade leading to the development of the manifestations of Henoch-Schönlein disease from the skin, joints, bowel and kidneys 2. The main differential diagnosis of Henoch-Schönlein purpura is infectious purpura fulminans 3, which is associated with a variety of microorganisms that need prompt antibiotic treatment 4.

- Diagnosis is based on the constellation of clinical manifestations in addition to biopsy findings of immunoglobulin A deposition in small vessels 5. Treatment of Henoch-Schönlein purpura with steroids is indicated when the disease involves the gastrointestinal system or the kidneys. Steroids are not solely indicated for the skin manifestations. While symptomatic treatment (steroid treatment) is one facet of therapeutic management, one has to try to manage the underlying illness concurrently i.e. an infection. Our patient was found to have urinary tract infection due to Proteus mirabilis. We think that treatment of the infection at the same time with the vasculitis led to the clinical improvement of our patient.

- Various infections have been associated with Henoch-Schönlein purpura. In a comparative study of children and adults with the disease, the proportion of patients with underlying infection was not different. Probably a genetic predisposition may enhance the odds of developing Henoch-Schönlein purpura in association with an infection 6. In the table a constellation of the implicated pathogens in reported patients with Henoch-Schönlein purpura are presented 7-46. Among them, a special role is attributed to streptococcal infections. In addition, infections due to parvovirus B19 are associated with Henoch-Schönlein purpura, although not all children infected with this virus will develop the vasculitis. Specific treatment with immunoglobulin is warranted in the setting of human parvovirus infection associated with Henoch-Schönlein purpura.

- In conclusion, urinary tract infection due to Proteus mirabilis may trigger Henoch-Schönlein purpura. Cure of the infection seems to be necessary in order to manage the vasculitic component more effectively.

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Table. Pathogens associated with Henoch-Schönlein purpura.
Streptococcus pyogenes *
Streptococcus equisimilis
Streptococcus sanguis
Staphylococcus aureus *
Coagulase-negative Staphylococcus
Neisseria meningitidis
Kingella kingae
Salmonella typhi
Salmonella non-typhi
Shigella spp
Campylobacter jejuni
Morganella morganii
Yersinia spp
Pseudomonas aeruginosa
Borrelia burgdorferi
Bartonella henselae *
Ehrlichia chaffeensis
Haemophilus parainfluenzae
Clostridium difficile
Helicobacter pylori *
Legionella longbeachae
Mycoplasma pneumoniae *
Chlamydia spp
Mycobacterium tuberculosis
Mycobacterium avium-intracellulare
Human parvovirus B-19 *
Hepatitis B virus *
Human immunodeficiency virus *
Varicella-Zoster virus *
Hepatitis A virus *
Epstein Barr virus
Herpes simplex virus
Coxsackie B1 virus
Toxocara canis

* At least 5 reports were found in the literature archived in PubMed.

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