gms | German Medical Science

A 44-year-old female was referred to us from a community hospital. She presented with rapid deterioration of her general state of health and progressive colic type abdominal cramps which were not dependent on food intake. The bowel movement showed no diarrhea. The patient complained about difficulties swallowing and a non productive cough. Intermittently a fever developed. Within the last month she had lost approximately 10 kilograms of body weight.

The patient’s medical history consisted of a systemic lupus erythematodes (SLE) which was first diagnosed 13 years before. Renal involvement in form of lupus nephritis type IV had been confirmed via kidney biopsy in 2002. In the year 2004 a bolus therapy with cyclophosphamide had been initiated. Since 2007 a mono therapy with mycophenolate mofetil had been performed. Due to an acute progression of the lupus activity, the patient had been in our medical care about three months prior to the current admittance. A kidney biopsy had been performed and showed a membranous lupus nephritis Typ V with severe tubulus atrophy and approximately 70% interstitial fibrosis. Nevertheless, to try to save some of the kidney function and because of the suspected cerebral vasculitis, a corticoisteroide pulse therapy (1mg/kg) and a therapy with rituximab had been initiated. Four single doses of rituximab of each 375mg/m2 had been administered over the course of four weeks. Under this therapy regimen the neurological symptoms had been regressive. Unfortunately the renal function showed no lasting recovery so that dialysis therapy had to be continued.

On resent admission the blood work showed increased inflammation markers (CRP 43 mg/l (normal <5 mg/l), leukocytes 16,4/nl (normal 3,5-10/nl), procalcitonin 2,3 ng/ml (normal <0,5 ng/ml)). The white blood cell imaging count showed the elevated leukocytes with 16,4/nl with an elevated neutrophil percentage of 90,9% (normal 43-75%), the eosinophil count was negative. Hemoglobin (Hb) concentration was low with 8,8 g/dl (normal 12-16 g/dl) depicting a normochrome, normocytic anemia. The platelet count was low with 98/nl (normal 150-360/nl). Though the LDH concentration was increased with 370 U/l (normal <245 U/l), there were no signs of hemolysis. Following liver enzymes were slightly increased. There were no serological hints for lupus activity.

Because of the elevated inflammation markers and fever in this immune compromised state an empiric antibiotic therapy was rapidly established with piperacilline/tazobactam und ciprofloxacine. Regular microbiological examinations such as blood cultures and urine cultures did not lead to bacterial or fungal growth.

Due to an unexplained reduction in the patient’s vigilance a CCT was performed which ruled out an acute pathology such as intracranial hemorrhage or thrombosis. CT-Scans of the thorax and abdomen showed no pathological findings. An ultrasound of the stomach revealed increased fluid filled intestinal loops but other than that no significant findings.

Endoscopy of the sigma brought no pathologic results macroscopically and histologically. Gastric track endoscopy on the other hand showed unspecific erythema of the mucous membrane. Multiple biopsies from the stomach and duodenum were taken. The histological examination revealed signs of inflammation in the pars descendens duodeni with partial destruction of crypts.

Between the crypts lay abundant amounts of worms. In the gastric regions scattered worm eggs were detected. The microbiological work-up identified the worms as Strongyloides stercoralis larvae.

Because of the patient’s highly immunoincompetend status after treatment of an acute Lupus flare, an oral antimycotic therapy with ivermectine in combination with albendazole was immediately initiated.