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SUMMARY Hormonal dysfunction involving the hypothalamic-pituitary-adrenal (HPA) axis, prolactin (PRL) secretion and sex hormone status has been supposed to contribute to the development or persistence of rheumatoid arthritis (RA). In addition, a reduced number of glucocorticoid receptors on circulating lymphocytes has been found in patients with RA. However, so far most studies have been performed in pre-treated patients. A combined test for total anterior pituitary reserve was performed in 10 patients with newly diagnosed untreated RA. Before and after stimulation with the respective hypothalamic releasing hormones, RA patients showed no difference in plasma concentrations of adrenocorticotrophic hormone (ACTH), cortisol, prolactin (PRL) and thyroid-stimulating hormone (TSH) when compared to healthy controls. In contrast, the growth hormone (GH) response to growth hormone-releasing hormone (GHRH) was blunted in RA patients. The hypothalamic-pituitary-thyroid/gonadal and adrenal axes seem to be unaltered in RA. However, if one considers the presence of chronic inflammation, normal plasma ACTH and cortisol concentrations must be considered as inappropriately low. The observed blunted GH release could be mediated by cytokines (e.g. IL-1), which are known to be elevated in RA. [ABSTRACT FROM PUBLISHER]

In a 64 year old man sigma cancer was diagnosed unexpectedly during an operation for retroperitoneal fibrosis (histologically benign fibrosis), that had caused unilateral hydronephrosis. In the following hemicolectomy this tumor of the colon turned out to be a medium high grade adenocarcinoma (tumor staging pT2, pN1, DUKES C). Chemotherapy with 450 mg/m2 5-FU once a week and a concomitant therapy with laevamisol was added for 6 months. Computer-tomography revealed a significant reduction of the retroperitoneal masses already before induction of chemotherapy. One year after termination of chemotherapy retroperitoneal fibrosis was no longer detectable. The course of events makes us assume that the retroperitoneal fibrosis of our patient was paraneoplastic and therefore completely reversible by successful removal of the underlying tumor.

We present the case of a 79-year-old female patient with criteria typical for Ménétrier's disease, i.e. enlargement of the gastric folds due to foveolar hyperplasia associated with severe protein-loss along with epigastric pain, nausea, vomiting and weight loss. Gastrin levels were within the normal range, but elevated Helicobacter pylori antibody titers (83 microg/ml) were indicative of a recent infection. Histologic examination of a gastric polyp, which was removed in toto, revealed the presence of early gastric cancer of the mucosal type. After initiation of antibiotic treatment with clarithromycin (3 x 250 mg/day) and metronidazole (2 x 500 mg/day) in combination with lansoprazole (30 mg/day), the patient's condition improved rapidly along with abrogation of protein loss. Under maintenance treatment as indicated above, the patient has been free of symptoms now for a period of more than 2 years. On repetitive endoscopic follow-up, there was no change in gastric mucosa morphology either endoscopically or histologically, and also no evidence of recurrence of a malignant lesion. We conclude that this therapeutic regimen represented an effective alternative to surgical intervention in this patient and should be considered in similar cases.

We report on a patient after brain injury additionally showing signs of ethylene glycol intoxication. CT-scan showed a subdural hematoma, which in spite of increasing neurological deficit didn't show any enlargement. Metabolic acidosis with an increased anion gap and osmolar gap led to the diagnosis of ethylene glycol intoxication. Then intensive hemodialysis and i.v. ethanol were administered and the intoxication could be treated successfully.

This paper tries to evaluate the importance of IFN-alpha induced thyroid dysfunction. Based on our own experience and reported data we present the results obtained in a total of 588 patients, in whom thyroid function and thyroid antibody occurrence was monitored during therapy with IFN-alpha: About 10% of these patients developed thyroid dysfunction during IFN-alpha treatment. Half of them reacted with hypothyroidism, 3% with hyperthyroidism and in 2% a biphasic (hyperthyroidism followed by hypothyroidism) pattern of reaction was observed. The frequency of these thyroid dysfunctions was increased in female patients and in patients with preexisting thyroid antibodies. The risk to develop thyroid dysfunction is reduced to 7% in patients with no pretherapeutic thyroid antibodies. The evolution of the thyroid ailment is variable and therefore unpredictable. In many patients there is no need to stop treatment with IFN-alpha nor to treat the thyroid dysfunction specifically. IFN-alpha induced autoimmune- phenomena seem to be etiologically important for the development of thyroid disease during IFN-alpha. The reported data allow in our view some basic recommendations for the clinician: thyroid function and thyroid antibodies should be evaluated before the start of treatment with IFN-alpha. During therapy with IFN-alpha these parameters should be regularly (eg every 4 months) monitored. In patients with thyroid autoantibodies or dysfunction already before IFN-alpha the control intervals should not be longer than every two months.

Renal transplantation is frequently accompanied by systemic hypertension. In the present study we evaluated the effect of 2.5 mg lisinopril in 12 hypertensive and proteinuric renal graft recipients with stable graft function over 3 months. Only patients with absence of renal artery stenosis, at least as judged by technetium-scan imaging, were included. Lisinopril was effective in lowering systemic blood pressure. Mean arterial pressure was unchanged despite reduction of concomitant antihypertensive medication. Mean serum creatinine was unchanged during the study (1.95 +/- 0.8 mg/dl in the pretreatment period vs. 1.77 +/- 0.76 mg/dl in the intervention period, n.s.). Glomerular filtration rate remained stable (62.75 +/- 21.96 vs. 60.17 +/- 18.27 ml/min/1.73 m2, n.s.) whereas renal plasma flow increased (224.75 +/- 91.66 vs. 244.92 +/- 94.13 ml/min/1.73m2, P < 0.01), leading to a drop in filtration fraction (31.4 +/- 12.4 vs. 26.8 +/- 8.6, n.s.). Renal vascular resistance was significantly reduced following angiotensin-converting enzyme (ACE) inhibitor therapy (26,447 +/- 14,574 vs. 23,425 +/- 12,430 dyne sec cm-5/1.73 m2, P < 0.01). Mean daily proteinuric decreased significantly (2.98 +/- 2.06 vs. 2.06 +/- 2.29 g, P < 0.01) whereas in a group of patients with comparable blood pressure but without ACE inhibitor therapy and similar degree of proteinuria, 24-hr proteinuria remained stable. No severe side effects were observed--in particular, mean serum potassium showed only a slight increase and no clinically significant hyperkalemic condition was observed. When lisinopril therapy was withdrawn after 3 months, blood pressure increased in all patients, requiring reinstitution of additional antihypertensive medication. Renal hemodynamic parameters and daily proteinuria returned to baseline values. We conclude that 2.5 mg lisinopril daily was safe and effective in this group of renal transplant recipients and showed a good antihypertensive as well as antiproteinuric effect.