Aldehyde dehydrogenase 2 polymorphism: possibly a predisposing factor to hepatocellular carcinoma in hepatitis C cirrhotics?

Hepatocellular carcinoma [HCC] is considered as a long term multistage disease with multiple genetic alteration. Aldehyde dehydrogenase 2 [ALDH2] polymorphism may modify the risk of HCC. The aim of the present work was to evaluate the role of ALDH2 polymorphism as a predisposing factor for HCC in chronic hepatitis C virus [HCV] infected patients with cirrhosis for early detection. This study included fifty five subjects divided into three groups; twenty chronic hepatitis C patients with cirrhosis [group A], twenty chronic hepatitis C patients with cirrhosis and HCC [group B] and fifteen control subjects [group C]. The included patients were subjected to history taking, clinical examination, abdominal ultrasonography and liver biopsy [whenever possible]. All the subjects enrolled in this study were analysed for ALDH2 gene polymorphism. Genomic DNA prepared from leucocytes were used for polymerase chain reaction-restriction fragment length polymorphism [PCR-RFLP] technique. In addition, mitöchondrial ALDH activity was estimated in leucocytes. Of all fifty five subjects included in this study, six were heterozygous for ALDH2 gene mutation [ALDH2*1/*2] representing 10.9%, and the others were homozygous for the normal allele [ALDH2*11*1]. Non was detected to have homozygous mutant allele. The distribution among the patients groups was the same; three patients out of twenty in each group were heterozogous for the mutant gene [15%]. All the control subjects had normal homnozygous gene [ALDH2*1/*1]. The two patients' groups showed significantly higher percent of heterozygous mutant; ALDH2*1/*2 [X[2]=11.92,P=0.0027] and lower mitochondrial ALDH activity towards acetaldehyde [F=24.32, P=0.0002] in comparison to control group. However, non significant changes in both parameters were observed between the two patients' groups [P>0.05]. ALDH2 gene mutation could not be considered as a possible predictor for HCC in non alcoholic HCV-cirrhotic patients. However, these data did not exclude completely the relation to HCV infection and/or cirrhosis. Follow-up large scale studies are needed to investigate the exact link between ALDH2 mutation and cancer

Pulse methylprednisolone therapy in children with resistant nephrotic syndrome

This study was conducted on 26 children with steroid-resistant idiopathic nephrotic syndrome [NS], 14 males and 12 females, ranging in age at the start of pulse methylprednisolone therapy from 14/12 to 9 10/12 years, admitted to Alexandria University Children's Hospital starting from 1-4-1996. All cases of idiopathic NS admitted during this period were treated by prednisone 2 mg/kg/day divided into 3-4 doses. If the child continues to have proteinuria [2+ or greater] after one month of this treatment, the nephrosis was considered steroid-resistant and renal biopsy was indicated to determine the precise etiology of the disease. All the 26 cases were still edematous with nephrotic proteinuria after one month of prednisone therapy. The diagnoses were: minimal-change disease [MCD], 8 cases, diffuse mesangial proliferation [DMP], 12 cases, and focal segmental glomerulosclerosis [FSGS], 6 cases. All cases received multiple infusions of high dose intravenous methylprednisolone as described by Mendoza and Tune. Many of the children also received cyclophosphamide according to the criteria of the previous authors. The period of follow up [from the start of therapy till 30-6-99] ranged from 4 to 38 months. At the last follow up, the results were as follows: In MCD, all cases responded with disappearance of edema and nephrotic-range proteinuria, 50% with complete remission and 50% with non-nephrotic proteinuria [partial response]. All maintained normal GFR. In DMP, normal GFR was maintained in 75% [9 cases]. Complete remission was found in 7 cases and partial response in 2 cases. End-stage renal failure [ESRF] occurred in one case and 2 cases died [one from septicemia and one from thromboembolic complications]. In FSGS, GFR was normal in 50% [3 cases], two cases with complete remission and one case with partial response. GFR was decreased in one case and ESRF developed in one case. One case died from septicemia. We concluded that pulse methyl prednisolone therapy with or without cyclophosphamide has better results than those reported for cyclophosphamide alone or cyclosporine. However, newer protocols are still needed to achieve better results

role of endobrush in diagnosis of endometrial pathology in perimenopausal uterine bleeding

The value of the Endobrush endometrial cell sampling device in the cytological assessment of the endometrium was compared with dilatation and curettage. 100 women presenting with perimenopausal uterine bleeding were studied by both endometrial cytology and histopathology. The Endobrush sampling procedure caused no pain in 94% and slight pain in 6%. There was no incidence of failed insertion among the 100 cases examined. None of the women developed complications from the use of the instrument. The smears yielded specimens with abundant cells in 76% and moderate number of cells in 24%. None of the smears were acellular. In the 100 patients, 6 [6%] had a histopathological diagnosis of endometrial adenocarcinoma, and 78 [78%] had a histopathological diagnosis of endometrial hyperplasia. The cytology samples obtained with this device were diagnostic of endometrial adenocarcinoma in 5 [83.3%] of these 6 patients and 66 [84.6%] of the patients with endometrial hyperplasia. To lower these false negative results, the combination of office sampling with vaginal ultrasonography is proposed. A negative sampling in the presence of a thickened sonographic endometrial lining warrants additional investigation. The Endobrush cytology sampler is considered a safe and effective screening tool for endometrial adenocarcinoma and hyperplasia. The method is simple, quick and painless and therefore well acceptable to patients and suitable for clinical use

Transit time, bacterial growth and electron microscope study of the small intestine in schistosomal hepatic fibrosis with portal pressure chances

Transit time, bacterial growth together with both light and electron microscopy of small intestine were studied in relation to different portal pressure levels in 23 patients with schistosomal hepatic fibrosis Schistosomal patients were divided into two groups: the first included those without ascites or elevated portal pressure [100-150 mm H[2]0] while the second group comprised patients with ascites and a portal pressure varying between 180 and 400 mm H[2]0. Although all findings were within normal in the first group patients, yet those of the second group showed delayed intestinal transit time[80%], small bowel bacterial overgrowth whether aerobic or anaerobic [80%] along with mild, moderate or marked light and electron microscopic pathological changes which seemed to depend on the extent of rise of the portal pressure. In spite of the fact that all studied parameters seem to be of importance, yet further attempts should be made in order to clarify the role and sequence of event, each of these factors play, in induction of altered intestinal functions in hepatic schistosomiasis patients

Chronic diabetes mellitus: osteotic and mineral changes in human beings and rats

Clinical examination and Laboratory investigations done to IS male type I chronic diabetic patients [insulin dependent more than 5 years] and to an age mached group of 10 normal male volunteers revealed normocalcaemia and normomagnesaemia with significant hyperphosphataemia. Estimation of serum level of parathormone showed significant hypoparathyroidism. An addition, significant hypercalcuria, hyperphosphaturia and hpermagnes uria were also detected. Histopathological examination of trabecular bone biopsies from both groups revealed marked osteoportic changes among the diabetic patients. Biochemical analysis of similar bone samples supported the microscopic findings by demonstrating significant decrease of calcium contents of the bone in the diabetic group. In the chronic rats [7 weeks after streptozotecin induction] significant hypercalcaemia, hyperphosphataemia and normomagnesaemia were found. Their sera showed significant hypoparathyroidism. In addition, significant hypermagnesuria. Histopathological examination of the rat's right tibiae revealed advanced rachitic changes. Biochemical analysis of the left tibias approved the microscopic findings by showing significant decrease in bone calcium contents