For 10 weeks a 25-year-old man had been suffering from tiredness, fatigue, nausea and a 16 kg weight loss. Erythrocyte sedimentation rate (83/133 mm), serum C-reactive protein (5.5 mg/dl) and creatinine (5.05 mg/dl) were all elevated. He also had proteinuria (1120 mg daily), sterile leukocytosis and a creatinine clearance of 10 ml/min. Renal biopsy showed interstitial nephritis and bone marrow biopsy revealed non-caseous epithelioid-cell granulomas. 14 days after admission he developed acute iritis in the right eye. Other causes having been excluded, the diagnosis of tubulo-intestinal nephritis with uveitis (TINU syndrome) was made. The clinical symptoms and laboratory findings improved within a few days of the start of glucocorticoid treatment (initially, 100 mg prednisone daily, reduced to 5 mg within 30 days). The patient was discharged after 8 days in good general condition.

Subacute meningitis caused by Candida albicans was confirmed by culture and immunoserologically in a 19-year-old girl. Combined administration of amphotericin B and flucytosine only slowly affected the course of the disease despite impressive improvement in clinical symptoms. Pleocytosis (1000/mm3) in cerebrospinal fluid persisted. Falling Candida antibody titre in serum and CSF, however, pointed to an improvement in the acute infection. Treatment had to be discontinued after 42 days because of side-effects such as rigor, fever and polyuria with low concentration. Under serial clinical observations with occasional CSF punctures complete cure occurred with normal CSF findings. There was an additional and unusual neurological-otological condition of intermittent inner-ear deafness, left more than right, before treatment. Recording of early auditory evoked potentials pointed to an involvement of the cranial nerves as part of the inflammatory process.

Grundproblematik und Fragestellung: Patienten und Methodik: Ergebnisse: P P Folgerung: Aim of study: Patients and methods: Results: P P Conclusion:

A 43-year-old woman with a solitary renal cyst developed polycythaemia. 21 well documented cases of this type have been previously published. In the majority of them a causal connection could be assumed between the renal cyst and polycythaemia: in 13 of the 15 cases (as in the reported one), the polycythaemia disappeared after surgical removal of the cyst. Measurement of serum erythropoietin can help in the differential diagnosis, but exclusion of polycythaemia vera may be difficult in the individual case.

Neurologic manifestations were the sole symptoms of disease in three patients with systemic lupus erythematodes (SLE): one case presented with Brown-Séquard's syndrome, a second with spinal ataxia and polyneuropathy, and a third with polyneuropathy. In all three patients there was a considerable delay in making the diagnosis after onset of neurological symptoms. The diagnosis was established either by demonstration of antinuclear antibodies in combination with antibodies against dsDNA or by the demonstration of antibodies against dsDNA alone. In two patients perivascular deposits of IgG and C3 were seen in skin-muscle biopsies from the calf region.

Fourteen days after renal transplantation, at first gave with good transplant function, a 36-year-old woman developed neurogenic dysfunction of bladder emptying. This was treated with baclofen, 5 mg three times daily by mouth. Between the 7th and 10th treatment day she progressively developed an organic psychotic syndrome and increasing respiratory paralysis after the onset of renal failure, associated with rejection of the transplanted kidney which required dialysis. Plasma concentration of baclofen was 565 ng/ml (therapeutic range 80-400 ng/ml). After discontinuing the drug and renewed haemodialysis the baclofen level rapidly fell and the symptoms receded. In a second case, a 57-year-old man on dialysis developed a thalamic pain syndrome after an intracerebral haemorrhage in the region of the basal ganglia. He was given four times 10 mg baclofen by mouth over 24 hours. 24 hours after the first dose he became deeply unconscious with respiratory failure. Plasma concentration of baclofen after the first haemodialysis period was 480 ng/ml. After 48 hours of artificial ventilation it was possible to extubate; a symptomatic transitory psychotic syndrome disappeared within 4 days. Both patients had pre-existing cerebral damage in addition to the chronic renal failure (in the first patient, meningoencephalitis 30 years previously with persisting focal lesions in the computed tomogram CT]; in the second one, residual lesions in the CT after intracerebral haemorrhage). It is emphasized that in patients who are in renal failure baclofen treatment should be undertaken cautiously: toxic signs can quickly develop especially if there is pre-existing cerebral damage.

Drug Prescribing for Patients with Chronic Kidney Disease in General Practice: a Cross-Sectional Study

In a 36-year-old patient an acute onset of psychosis occurred, probably due to HIV infection. For one year HIV-infection with reduced T4/T8 ratio had been known without clinical manifestation (stage IV B of the CDC-classification). He developed chronic delusional hallucinations, which persisted for more than one year in spite of adequate psychoactive drug therapy. So far AIDS-related dementia has not become evident. Focal lesions caused by opportunistic infections or tumour were excluded by computed tomography and magnetic resonance imaging. The latter revealed several small lesions and the brain scan showed a nonhomogeneous pattern of cerebral blood flow. CSF-examination disclosed a mild lymphocytosis and raised protein concentration. A classification as an organic, HIV-induced delusional hallucination seems to be justified.

To the Editor:

Journal of Pediatric Gastroenterology and NutritionVolume 29, Issue 4 p. 490-490 Abstracts: Annual Meeting of the North American Society for Pediatric Gastroenterology and Nutrition; Denver, October 21-24, 1999 AZATHIOPRINE CAN MODULATE IMMUNOSUPPRESSION THROUGH AN IL-10 MEDIATED MECHANISM I J Fuss, I J Fuss Mucosal Immunity Section, NIH, Bethesda, MD Laboratory of Immunology, University of Mainz, GermanySearch for more papers by this authorJ F Schlaak, J F Schlaak Mucosal Immunity Section, NIH, Bethesda, MD Laboratory of Immunology, University of Mainz, GermanySearch for more papers by this authorK H Meyer Zum Buschenfelde, K H Meyer Zum Buschenfelde Mucosal Immunity Section, NIH, Bethesda, MD Laboratory of Immunology, University of Mainz, GermanySearch for more papers by this authorW Strober, W Strober Mucosal Immunity Section, NIH, Bethesda, MD Laboratory of Immunology, University of Mainz, GermanySearch for more papers by this authorM F Neurath, M F Neurath Mucosal Immunity Section, NIH, Bethesda, MD Laboratory of Immunology, University of Mainz, GermanySearch for more papers by this author I J Fuss, I J Fuss Mucosal Immunity Section, NIH, Bethesda, MD Laboratory of Immunology, University of Mainz, GermanySearch for more papers by this authorJ F Schlaak, J F Schlaak Mucosal Immunity Section, NIH, Bethesda, MD Laboratory of Immunology, University of Mainz, GermanySearch for more papers by this authorK H Meyer Zum Buschenfelde, K H Meyer Zum Buschenfelde Mucosal Immunity Section, NIH, Bethesda, MD Laboratory of Immunology, University of Mainz, GermanySearch for more papers by this authorW Strober, W Strober Mucosal Immunity Section, NIH, Bethesda, MD Laboratory of Immunology, University of Mainz, GermanySearch for more papers by this authorM F Neurath, M F Neurath Mucosal Immunity Section, NIH, Bethesda, MD Laboratory of Immunology, University of Mainz, GermanySearch for more papers by this author First published: 01 October 1999 https://doi.org/10.1002/j.1536-4801.1999.tb02503.xRead the full textAbout ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume29, Issue4October 1999Pages 490-490 RelatedInformation

BACKGROUND Crohn’s disease is a chronic inflammatory disease of the alimentary tract. Azathioprine is an effective agent in the management of chronic active Crohn’s disease leading to long term remission of disease activity. Such treatment leads to limited efficacy or side effects in a small subset of patients. AIMS To compare efficacy and side effects of treatment with azathioprine plus corticosteroids versus mycophenolate mofetil (MMF) plus corticosteroids in patients with chronic active Crohn’s disease. METHODS Seventy patients with chronic active Crohn’s disease (Crohn’s disease activity index (CDAI) greater than 150) were randomised for treatment with azathioprine/cortisone or MMF/cortisone. Corticosteroid dosage was tapered according to a standard protocol. Disease activity was monitored by clinical scores after one, two, three, and six months. RESULTS Treatment of patients with moderately active (CDAI 150–300) Crohn’s disease with MMF/cortisone led to a significant reduction in clinical activity scores comparable to treatment with azathioprine/cortisone. Treatment of patients with highly active Crohn’s disease (CDAI greater than 300) with MMF/cortisone caused significant suppression of clinical activity earlier than azathioprine/cortisone treatment. Treatment with MMF/cortisone was associated with few adverse effects. CONCLUSION Treatment of chronic active Crohn’s disease with MMF plus cortisone appears to be effective and well tolerated and should be considered in patients allergic to azathioprine or in whom azathioprine has failed.

History and clinical findings: Since the age of 19 a now 22-year-old man had complained of intermittent abdominal pain, irregular stools and paroxysmal tachycardia. The only preceding illness had been a single episode of iron-deficiency anemia. A laparoscopy, done 8 months after the onset of symptoms, had revealed an inflamed Meckel's diverticulum which was surgically removed. After transient improvement the symptoms recurred 5 month postoperatively. On admission to clarify the cause of the symptoms he had discrete abdominal pain on pressure, but physical examination was otherwise unremarkable.Investigations: Routine biochemical tests and endoscopy were normal. Abdominal computed tomography was suspicious of severe narrowing of the left renal artery by a crossing superior mesenteric artery. As a result the left testicular vein and the peripelvic Venous network were markedly dilated by retrograde congestion, strongly suggesting the,,nutcracker syndrome" of obstruction of the left renal vein. This diagnosis was confirmed by selective renal phlebography and pressure measurement.Treatment and course: The vascular anomaly was corrected surgically by reimplanting the left renal vein into the inferior vena cava 3-4cm further caudally. The patients has been completely symptom-free since then.Conclusions: The nutcracker-syndrome is a rare cause of hematuria. The coexistence of this anomaly with gastrointestinal symptoms has not been previously described, but it is likely that congestion of the splanchnic veins by obstruction of the left renal vein was at least partly responsible for them, in view of the postoperative relief.

Virushepatitiden gehören weltweit zu den wichtigsten Infektionskrankheiten. Allein über 300 Millionen chronische HBsAg-Träger und etwa die gleiche Anzahl chronischer Hepatitis-C-Virusträger werden geschätzt. Nach der Tuberkulose steht die Virushepatitis in der Statistik der infektiös bedingten Berufskrankheiten an zweiter Stelle. Insbesondere Teile Asiens, Afrikas, Lateinamerikas sowie der Mittelmeerraum und der Nahe Osten werden zu den Hochendemiegebieten der Virushepatitis gezählt. Aufgrund der immunologischen und molekularen Differenzierung sind heute die Virushepatitiden von A bis E einschließlich G weitgehend charakterisiert. Während die enteral übertragene Hepatitis A und E nur akute und in seltenen Fällen fulminante Verläufe induzieren, sind die Hepatitis B, ihre Koinfektion und Superinfektion mit Hepatitis Delta und die Hepatitis C insbesondere durch chronische Verläufe von großer medizinischer Bedeutung. Diese Erkrankungen können als Spätfolge in eine Lebercirrhose mit all ihren Komplikationen, einschließlich des primären Leberzellcarcinoms übergehen. Die für die Chirurgie besonderen Aspekte der Virushepatitis sollen diskutiert werden.

HISTORY AND CLINICAL FINDINGS:Since the age of 19 a now 22-year-old man had complained of intermittent abdominal pain, irregular stools and paroxysmal tachycardia. The only preceding illness had been a single episode of iron-deficiency anemia. A laparoscopy, done 8 months after the onset of symptoms, had revealed an inflamed Meckel's diverticulum which was surgically removed. After transient improvement the symptoms recurred 5 months postoperatively. On admission to clarify the cause of the symptoms he had discrete abdominal pain on pressure, but physical examination was otherwise unremarkable.INVESTIGATIONS:Routine biochemical tests and endoscopy were normal. Abdominal computed tomography was suspicious of severe narrowing of the left renal artery by a crossing superior mesenteric artery. As a result the left testicular vein and the peripelvic venous network were markedly dilated by retrograde congestion, strongly suggesting the "nutcracker syndrome" of obstruction of the left renal vein. This diagnosis was confirmed by selective renal phlebography and pressure measurement.TREATMENT AND COURSE:The vascular anomaly was corrected surgically by reimplanting the left renal vein into the inferior vena cava 3-4 cm further caudally. The patients has been completely symptom-free since then.CONCLUSIONS:The nutcracker-syndrome is a rare cause of hematuria. The coexistence of this anomaly with gastrointestinal symptoms has not been previously described, but it is likely that congestion of the splanchnic veins by obstruction of the left renal vein was at least partly responsible for them, in view of the postoperative relief.

Protein expression of the putative tumour-suppressor gene DCC on chromosome 18q was evaluated in a panel of 16 matched colorectal cancer and normal colonic tissue samples together with DCC mRNA expression and allelic deletions (loss of heterozygosity, LOH). Determined by a polymerase chain reaction (PCR)-LOH assay, 12 of the 16 (75%) cases were informative with LOH occurring in 2 of the 12 cases. For DCC mRNA, transcripts could be detected in all analysed normal tissues (eight out of eight) by RT-PCR, whereas 6 of the 15 tumours were negative. DCC protein expression, investigated by immunohistochemistry using the monoclonal antibody 15041 A directed against the intracellular domain, was homogeneously positive in all normal tissue samples. In tumour tissues, no DCC protein was seen in 11 out of 16 samples (69%). For the DCC codon 201, we found a loss of a wild-type codon sequence caused by mutation or LOH in at least 8 out of 15 cases (53%) compared with the corresponding normal tissue. DCC protein expression was undetectable in eight of the nine tumours missing both wild-type codons. Only one of the five tumours with retained DCC protein expression had no detectable wild-type codon 201. In addition, 9 out of 15 normal tissue specimens were mutated in codon 201. In two out of three cases with homozygous wild-type codons in peripheral blood lymphocyte (PBL) DNA, mutations were already observed in the tumour adjacent normal colonic mucosa. We conclude that DCC immunostaining should be introduced in the clinicopathological routine because of its strong correlation with the known prognostic markers 18q LOH and mutation of codon 201.

Portopulmonary venous anastomosis are a very rare complication of chronic liver diseases. We report on a patient with a cryptogenic liver cirrhosis and thrombosis of the portal vein who underwent antibiotic treatment because of recurrent pneumonias several times. Although treated successfully a pulmonal infiltrate persisted in further radiologic controls. By means of a velocity-encoded MRI a portopulmonary shunt of 30% of the cardiac output was assured. An operative correction with a distal splenorenal shunt was performed successfully. Former reports of portopulmonary anastomoses complicating chronic liver disease never were hemodynamically relevant. In the presented case, a portopulmonary anastomosis lead to recurrent pneumonias and a restrictive ventilatory disorder.