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IntroductionUp-to-date statistics on prostate cancer incidence and causative risk factors are essential for the primary prevention of this disease. However, the incidence of Prostate cancer (ICD-10 code C61) (PCa), or cancers in general, are poorly documented in Eritrea. This study analyses the data available to produce an estimate of the incidence of PCa in Eritrea.MethodsWe conducted a retrospective study by identifying all incident cases of PCa captured between 2011-2018 in the National Health Laboratory pathology database (Polytech 8.37.C); Urology departments of Orotta Referral Hospital and Sembel Hospital. Crude incidence rates (CIRs), age-adjusted rates per 100,000 person years and associated trends were subsequently calculated. Joinpoint Regression Program, V.4.5.0.1 was employed in these analyses.ResultsA total of 1721 cases were reported, of which 1593 (92.5%) were benign prostatic hypertrophy cases and 128 (7.5%) were PCa cases. The mean (±SD) age of the patients with PCa was 73.49 (± 8.9), confidence interval (CI) (54-98) and the minimum and maximum ages were 54 and 98, respectively. The median age interquartile ranges (IQR) was 73 (13) years. The highest and lowest PCa incidence rates were in 2017 (4.51 per 100 000) and 2014 (2.69 per 100 000), respectively. The age standardised rates (ASIR) (World) over the study period (2011-2018) was 30.26 per 100 000. The annualized ASIR values over the study period was 3.78 per 100 000. The associated average annual percentage change (APC) (CI) over the study period was 5.4 (-1.4-12.7), P-value = 0.100, showing a static trend over the study period.ConclusionThis study suggests that previous reports have under-estimated the incidence of PCa in Eritrea. The study provides ample evidence on the need for research targeted at uncovering the true burden of PCa in Eritrea. Potential solutions will require the establishment of high-quality population-based cancer registries (PBCRs) and long-term commitment to improvements in research, training, screening, diagnosis, and the overall management of PCa in the country.

Rarely, zoonotic Taenia species other than Taenia solium cause human cysticercosis. The larval stages are morphologically often indistinguishable. We therefore investigated 12 samples of suspected human cysticercosis cases at the molecular level and surprisingly identified one Taenia crassiceps and one Taenia serialis (coenurosis) infection, which were caused by tapeworm larvae normally infecting rodents and sheep via eggs released from foxes and dogs.

We have reviewed our experience with conversion to tacrolimus after 435 liver transplantations. Tacrolimus was administered as a rescue agent in 33 patients until October 1993. Indications for rescue therapy were: cholestatic forms of severe, steroid-resistant cellular rejection (n = 8), OKT3-resistant cellular rejections (n = 6), cellular rejections in patients suffering from cyclosporin malabsorption (n = 4), late onset cellular rejections (n = 4), early chronic rejections (n = 3), and chronic vascular or ductopenic rejections (n = 8). Response was evident in 29 of the 33 patients (88%), whereas 4 patients (12%) were nonresponsive. Patient and graft survival were 76% and 70%, respectively. Graft loss with or without patient death occurred in three of eight patients suffering from severe, steroid-resistant cellular rejection, in two of six patients with OKT3-resistant cellular rejections, and in five of eight patients undergoing chronic rejection. In severe steroid-resistant cellular rejection, successful tacrolimus rescue therapy corresponded to a significantly lower total serum bilirubin than unsuccessful therapy (12.0 +/- 5.6 mg% vs 29.7 +/- 5.9 mg%, P0.05). We conclude that tacrolimus rescue therapy is a safe and efficient alternative for high-risk cases that do not respond to conservative treatment. In severe, steroid-resistant cellular rejection and in chronic ductopenic rejection, conversion to tacrolimus is beneficial only in a limited number of cases. A predictive parameter, which total serum bilirubin may prove to be in severe, steroid-resistant cellular rejection, is needed to select those cases that might benefit more from retransplantation than from conversion to tacrolimus.

Eradication of Helicobacter pylori usually consists of a 7-day course of triple therapy including metronidazole or amoxicillin plus clarithromycin plus a proton pump inhibitor. We report about a rare adverse event of Hp eradication in a patient with moderate chronic and moderate active pangastritis. Shortly after the end of treatment cholestatic hepatitis occurred which was most likely related to clarithromycin, perhaps enhanced by amoxicillin. Since liver dysfunction was self-limited, no further treatment was required. In summary, clinicians should be aware about the presented rare adverse event of Helicobacter pylori eradication treatment for a close monitoring of those patients and rapid management of acute liver failure.

Liver transplantation for advanced hepatocellular carcinoma is often followed by early tumour recurrence and death. At the beginning of the liver transplantation programme at Berlin Virchow we decided to offer liver transplantation only to patients with solitary tumours not exceeding a maximum diameter of 5 cm or to patients with two or three tumour nodes with a maximum diameter of 4 cm. From September 1988 to October 1993 435 liver transplants were performed in 403 patients. Of these, 32 patients (8%) had a histologically confirmed hepatocellular carcinoma (29 males, 3 females, median age 56 years). The overall actuarial survival according to Kaplan-Meier for the whole series of 32 patients with hepatocellular carcinoma was 82%, 78%, and 78% at 1, 2 and 3 years, respectively. Tumour size alone did not seem to be a relevant factor when comparing patients with tumours up to or larger than 3 cm in diameter. Patients with solitary tumours had a better prognosis than patients with multiple tumours. The largest difference was found between patients with stage I-III (UICC) tumours and those with stage IVA tumours: 1-, 2- and 3-year survival rates were 89% throughout in the former group, while the corresponding figures for patients with stage IVA tumours were 63%, 47% and 47%. Efforts should be made to identify stage IVA tumours preoperatively in order to use the precious resource of scarce donor livers in an optimal way.

Hereditary hemorrhagic teleangiectasia, or M. Osler (Osler-Weber-Rendu disease), is an autosomal dominant, systemic fibrovascular dysplasia. This may lead to increased liver blood flow from arteriovenous fistulas. A 45-year-old woman with a known M. Osler was admitted for liver transplantation. On admission, exertional dyspnea was the predominant symptom. Radiological investigations revealed multiple intrahepatic arteriovenous fistulas and consecutive high-output heart failure. Laboratory findings revealed remarkably elevated bilirubin and alkaline phosphatase. To alleviate the high-output cardiac failure, the hepatic artery was ligated. Fourteen months later, the patient presented again with increased levels of bilirubin and recurrent bleeding episodes from esophageal varices grade IV. The patient underwent liver transplantation and post-transplant recovery was excellent. A hyperdynamic circulatory state due to a hepatic M. Osler has been treated in several cases by ligation or embolization of the hepatic artery. This procedure, however, is recommended only for patients with normal liver function and carries a considerable risk of bile duct necrosis.

Recurrence-free survival (RFS) in patients with small hepatocellular carcinoma (HCC) after orthotopic liver transplantation (OLT) was analyzed. From 1988 until 1996, 725 OLTs were performed in 669 patients. In 52 adults, HCC was confirmed histologically. OLT was limited to patients with small (< 5 cm) HCC with a maximum number of three nodules. Actuarial survival for these 52 patients at 1 and 5 years is 88 % and 71 %. RFS was defined as time until death without recurrence, time until follow up with a diagnosis of recurrence, or, in patients without recurrence, time of last follow up. Overall, the 5-year RFS was 60 %. Five-year RFS was less for bilobar compared to unilobar tumors (36 % vs 70 %), less for stage IVa tumors (UICC) compared to stage I–III tumors (17 % vs 71 %), and less for multiple compared to solitary tumors (54 % vs 67 %). In conclusion, potential cure may be achieved in more than 50 % of all transplanted patients.

Hepatitis B virus (HBV) infection of the liver graft is a major complication after orthotopic liver transplantation (OLT) for HBV-related cirrhosis. A high viral load before OLT is a known risk factor, whereas the relevance of precore mutants of HBV is a subject of controversy. The aim of this study was to correlate the pretransplantation viral load and a pretransplantation infection with precore mutant HBV (pmHBV) or wildtype HBV (wtHBV) with allograft damage, graft failure, and survival after OLT. Sixty-nine patients with HBV cirrhosis underwent OLT under high dose immunoprophylaxis with anti-hepatitis B surface (HBs) hyperimmunoglobulins (HBIg). A pretransplantation infection with pmHBV and wtHBV was detected by polymerase chain reaction (PCR) and direct sequencing in 30 patients each (pmHBV and wtHBV group). Nine of 69 patients were PCR-negative (noHBV group). Median pretransplantation levels of HBV DNA assessed by hybridization assay were 42 pg/mL for pmHBV and 54 pg/mL for wtHBV patients. HBV recurred in 17 of 30 (57%) of pmHBV and in 14 of 30 (47%) of wtHBV patients and graft failure occurred in 6 of 30 (20%) of pmHBV and 7 of 30 (23%) of wtHBV patients. Neither HBV recurrence nor graft failure occurred in patients in whom no HBV DNA could be detected by PCR using primers flanking the HBV precore region (noHBV) patients. Allograft damage assessed by histology activity index (HAI) scoring was median 6 for pmHBV and 7 for wtHBV patients. Cumulative survival after 5 years was 72% for pmHBV, 74% for wtHBV, and 100% for noHBV patients. In this study, we provide evidence that pretransplantation viral load, but not infection with pmHBV, determines the outcome after OLT in patients on high dose HBIg prophylaxis.

The pathogenesis of hepatitis C virus (HCV) infection is likely to be associated with viral replication in vivo, but little is known concerning the dynamics of HCV turnover. We performed serial measurements of serum HCV-RNA levels following orthotopic liver transplantation (OLT) in nine patients with HCV-positive cirrhosis. Serum HCV-RNA levels were determined by quantitative polymerase chain reaction before, immediately after, and for up to 1 month after OLT. There was a rapid decline in HCV-RNA levels from 3.1 +/- 1.3 x 105 copies/ mL (mean +/- SEM) preoperatively to 0.15 +/- 0.6 x 105 copies/mL on the first and 0.16 +/- 0.6 x 105 copies/mL on the second postoperative day (mean viral half-life, 4.0 +/- 0.5 h). Thereafter, HCV-RNA levels increased in all but one patient, and by postoperative day 8 reached 3.6 +/- 1.3 x 105 copies/mL, exceeding the preoperative levels irrespective of the use or not of rescue immunosuppressive therapy including steroid bolus administration. In most patients, serum virions continued to increase averaging 11.6 +/- 2.8 x 105 copies/mL on the 30th postoperative day. These findings indicate that the half- life of HCV is quite short, and that extrahepatic viral replication contributes little to the total virus pool in serum. Furthermore, the marked HCV replication beginning as early as the third postoperative day strongly suggests that the liver graft is rapidly reinfected by HCV after OLT. (Hepatology 1996 Dec;24(6):1351-4)

A 54-year-old male patient with end-stage liver failure from Budd-Chiari syndrome due to paroxysmal nocturnal hemoglobinuria (PNH) underwent liver transplantation (OLT) in 1989. Retransplantation became necessary 1 year later when thrombotic occlusion of the portal vein and common hepatic artery led to graft loss after withdrawal of anticoagulation therapy because of several gastrointestinal bleeding episodes. The patient is now alive 3 years after the first OLT. To the best of our knowledge and according to the literature, this is, to date, the longest that any PNH patient has survived after liver transplantation. Although the course of this patient was complicated in a way similar to that reported for other cases in the literature, patients with PNH should not, in principle, be excluded from liver transplantation. Lifelong anticoagulation with coumarin and the use of steroids together with cyclosporin reduce the risk of recurrent thrombosis and PNH crises.

Overexpression of p170 glycoprotein, the product of the multiple drug resistance (mdr) gene, has been associated with resistance to various cytotoxic drugs used in the treatment of human neoplasms. Normal renal epithelial cells express p170 as a function of their secretory capacity. Because renal cell carcinomas (RCC) respond poorly to chemotherapeutic regimens, p170 expression was studied in primary RCC. Such expression was measured in 40 human RCC and normal kidney tissues using immunohistochemical staining with the monoclonal antibody C-219. Staining intensities of the whole tumor and of different areas of the cryostat sections were transformed into digital numbers using an algorithm designed for this purpose. In most tumors, an inhomogeneous staining pattern and a correlation between grade of differentiation and C-219 immunoreactivity was observed. A comparison of the tumors according to their histopathologic subtypes showed clear differences. The means (range) of the staining intensities of the different types of RCC: clear cell carcinoma Grade 1 (n = 3), 2.0 (2.0 to 2.0); clear cell carcinoma Grade 2 (n = 19), 0.8 (0.0 to 2.9); clear cell carcinoma Grade 3 (n = 5), 0.1 (0.0 to 0.2); tubular carcinoma (n = 4), 2.0 (2.0 to 3.0); anaplastic carcinoma (n = 8), 0.05 (0.0 to 0.2); oncocytoma (n = 1), 0.0 (0.0 to 0.0); and normal kidney (n = 40), 0.5 (0.0 to 2.0). The differences between anaplastic, clear cell, and tubular carcinoma were significant (P less than 0.001 by Kruskal-Wallis test). In addition, the difference between the three subgroups of clear cell carcinoma was significant (P less than 0.01). It was concluded that the histopathologic subtypes of RCC correlate with the degree of mdr gene expression, as determined by staining with the C-219 monoclonal antibody.

A woman with severe immunosuppression provoked by the acquired immunodeficiency syndrome developed a disseminated cytomegalovirus infection of the genital tract. Using in situ hybridization and the AP

Surgical strategies in the therapy of hilar cholangiocarcinoma afford patients the best chance for significant survival. Radical resections are currently considered as optimal treatment, but

Lysine-specific cleavage of β 2 -microglobulin in amyloid deposits associated with hemodialysis. Amyloid fibrils isolated from bone and carpal synovia of seven patients on long-term hemodialysis were further characterized biochemically. In addition, renal amyloid stones of three dialyzed patients were examined. All deposits and stones were of beta 2 -microglobulin-origin (AB-amyloid) by immunohistochemical and immunochemical evaluation. Amyloid fibril extracts were dissolved in 80% formic acid and separated by high performance liquid chromatography in 60% formic acid and 20% 2-propanol. Three major retarded fractions with molecular weights of approximately 24, 12 and 7 to 10 kD were recovered. N-terminal amino acid sequence analysis documented beta 2 -microglobulin (β 2 m) as the principal polypeptide in all investigated cases. In addition to proteins with intact N-termini, one fragment commencing with isoleucine in position 7 was found in osseous or synovial amyloid. In renal amyloid stones, one additional fragment was found beginning with serine in position 20. Generally, these data point to proteolytic cleavage carboxyterminal to a lysine residue and establish that not only intact β 2 m but also at least one β 2 m fragment is present in β 2 m-derived amyloid deposits of patients with long-term hemodialysis. The fragmentation pattern is consistent with the action of lysine-specific protease(s) and underscores a potentially important role of limited proteolysis in the pathogenesis of AB-amyloid deposits.

The optimal immunosuppressive regimen in patients transplanted for hepatitis C (HCV) is still under discussion. High immunosuppression may promote viral replication and recurrent graft hepatitis. But acute and chronic rejection frequently seen in conjunction with HCV recurrence may require some rescue therapy. One hundred and thirty-seven patients transplanted for HCV cirrhosis, who were HCV-RNA positive prior to transplantation, were analyzed. Seventy-nine patients received CSA-based immunosuppression and 58 patients FK506-based immunosuppression. One-month patient survival was 100 % in both groups. Three month and 1-year survival rates and the cumulative 1–5-year patient survival was similar in CsA-treated [67/79 (84.8 %)] and FK506-treated patients [50/58 (86.2 %)]. Retransplantations for HCV recurrence were performed in 5.1 % of CsA-treated patients and 6.9 % of FK506-treated patients; it was successful in 50 % and 75 % of patients, respectively. Conversion from CsA to FK506 and vice versa was high with 25 out of 79 patients (31.6 %) converting in the CsA group and 8 out of 58 patients (13.8 %) converting in the FK506 group. Conversion to FK506 was performed due to acute and chronic rejection and to CsA because of toxicity and HCV recurrence. In both groups, 25 % of converted patients died. Five patients of the CsA group and 9 of the FK506 group received OKT3; more than one-third of each group died. Five patients in the CsA group and 6 in the FK506 group received mycophenolate mofetil (MMF) for HCV recurrence or acute and chronic rejection in conjunction with HCV recurrence. All patients of this critical group are alive with good graft function. In conclusion, survival rates of HCV patients were similar to those seen for other indications. Conversion from CsA to FK506 and vice versa was high and reflects a critical group concerning patient survival. OKT3 treatment should be avoided. A promising therapeutic option for critical patients experiencing acute or chronic rejection in conjunction with HCV recurrence may be treatment with MMF.