Adji Widjaja

Autoantibody profiles in microscopic colitis.

Objective:  The etiology of microscopic colitis is unclear; an autoimmune response and pharmacological induction have been proposed as possible mechanisms. We conducted a multicentre cross‐sectional study to compare the antibody profiles of patients with collagenous and lymphocytic colitis with those of a control group.

Hepatitis C and the Leptin System: Bound Leptin Levels Are Elevated in Patients with Hepatitis C and Decrease During Antiviral Therapy

BACKGROUND Serum leptin levels are elevated in alcoholic liver cirrhosis and thus might be involved in the anorexia and hypermetabolism often seen in those patients. We hypothesized that the leptin system is modulated in patients with hepatitis C and might be affected by antiviral therapy. The aim of this study was to investigate the different leptin components in serum of patients with hepatitis C before, during and after interferon alpha and ribavirin therapy and in controls. METHODS 25 patients (11 female, 14 male) with chronic hepatitis C were compared with body mass index, gender and age-matched controls (n = 25). Patients were treated with interferon alpha alone (3 MU tiw) or in combination with ribavirin for 6-12 months. Free leptin and bound leptin levels were measured using specific radioimmunoassays before interferon therapy, at 12 weeks of therapy and after 3 months of follow-up. RESULTS Free leptin levels were higher in female than in male subjects, both for patients (P < 0.01) and controls (P < 0.05). Bound leptin levels were elevated in both female (P < 0.05) and male (P < 0.001) patients compared to controls. No alteration of free leptin levels was found during therapy, whereas bound leptin levels decreased after 3 months of therapy (P < 0.005) and re-increased to the baseline levels 3 months after therapy was stopped. Responder but not non-responder had decreased bound leptin levels (P < 0.01) comparing pre- and posttreatment levels. However, no significant correlations were determined between any of the leptin components to virus load, ALT, TNF alpha receptor levels (sTNFR-75, sTNFR-55) and histopathology at any time point. CONCLUSION Since no correlation was found between the different leptin components and any of the inflammatory markers, the decrease in bound leptin levels during antiviral therapy suggests either a direct interferon-dependent effect on the leptin system or an alteration of other leptin secretagogues.Background: Serum leptin levels are elevated in alcoholic liver cirrhosis and thus might be involved in the anorexia and hypermetabolism often seen in those patients. We hypothesized that the leptin system is modulated in patients with hepatitis C and might be affected by antiviral therapy. The aim of this study was to investigate the different leptin components in serum of patients with hepatitis C before, during and after interferon alpha and ribavirin therapy and in controls. Methods: 25 patients (11 female, 14 male) with chronic hepatitis C were compared with body mass index, gender and age-matched controls (n = 25). Patients were treated with interferon alpha alone (3 MU tiw) or in combination with ribavirin for 6-12 months. Free leptin and bound leptin levels were measured using specific radioimmunoassays before interferon therapy, at 12 weeks of therapy and after 3 months of follow-up. Results: Free leptin levels were higher in female than in male subjects, both for patients (P < 0.01) and controls (P < 0.05). Bound leptin levels were elevated in both female (P < 0.05) and male (P < 0.001) patients compared to controls. No alteration of free leptin levels was found during therapy, whereas bound leptin levels decreased after 3 months of therapy (P < 0.005) and re-increased to the baseline levels 3 months after therapy was stopped. Responder but not non-responder had decreased bound leptin levels (P < 0.01) comparing pre- and posttreatment levels. However, no significant correlations were determined between any of the leptin components to virus load, ALT, TNF alpha receptor levels (sTNFR-75, sTNFR-55) and histopathology at any time point. Conclusion: Since no correlation was found between the different leptin components and any of the inflammatory markers, the decrease in bound leptin levels during antiviral therapy suggests either a direct interferon-dependent effect on the leptin system or an alteration of other leptin secretagogues.

Uncommon Metastasis of a Glioblastoma Multiforme in Liver and Spleen

A case of a glioblastoma multiforme is presented. Craniotomy was performed with total resection of the right temporal tumor. Postoperatively, the patient received adjuvant radiotherapy, but 6 months after therapy he developed severe nausea and weight loss. Recurrence of an intracranial tumor in the right temporal region with nodules in the liver and spleen were detected by CT scan. Fine-needle biopsies of the liver confirmed the diagnosis of a glioblastoma metastasis with characteristic immunohistochemical staining for glial fibrillary acidic protein. This rare case of an intracerebral glioblastoma metastasizing to liver and spleen was managed by systemic chemotherapy.

Free and bound leptin levels during human pregnancy

Leptin is a hormone secreted from adipocytes and trophoblasts which might influence energy metabolism during gestation. In this study we evaluated the course of free and bound leptin levels in 22 healthy pregnant women and compared these values to those in non-pregnant women matched for body mass index (BMI) and age. Serum concentrations of both leptin components and plasma levels of estradiol, progesterone, insulin, non-esterified fatty acids and glucose were measured at each trimester. The BMI increased from the first to the second trimester (22.8 ± 3.1 and 24.7 ± 2.9, respectively; p < 0.05) and remained stable thereafter (third trimester 25.3 ± 2.9 kg/m2). Free leptin and bound leptin did not differ between patients and controls in the first trimester of pregnancy. Free leptin levels increased from the first (122 (60)) to the second trimester (181 (60) pmol/l; p < 0.05) and remained constant (third trimester 181 (76) pmol/l; difference between second and third trimesters, NS). Bound leptin increased from the second (0.43 (0.16)) to the third trimester (0.57 (0.21) nmol/l; p < 0.05). Only bound leptin was higher in the patient group in the third trimester compared to controls (p < 0.01). Our findings of a shift in free leptin to bound leptin in late pregnancy may indicate different physiological roles for both components. Free leptin may reflect maternal fat stores, whereas bound leptin may regulate maternal metabolism via central effects on food intake and energy expenditure.

An unusual cause of retrograde ejaculation and hypertension.

A 39-year-old man presented with a 1-year history of retrograde ejaculation and a 10-year history of drug-resistant hypertension. Diagnostic abdominal ultrasound revealed an open bladder neck during the filling phase and a retroperitoneal tumor. After surgical excision histology revealed an extra-adrenal pheochromocytoma, which should be included in the differential diagnosis of patients presenting with retrograde ejaculation and hypertension.