Autosomal dominant polycystic kidney disease is a hereditary disease, characterized by the development of cysts in the renal parenchyma with extra-renal manifestations. Liver damage is rarely a source of complications. A Budd-Chiari syndrome could occur following the compression of the supra-hepatic veins by the cysts. It is an exceptional mechanical complication. We present a case of a 54 year old woman, with a diagnostic of an asymptomatic autosomal dominat polycystic kidney disease since childhood was admitted to our hospital due to significantly increased abdominal girth. The physical examination showed grade III ascites. A paracentesis for relief at admission disclosed an exudative fluid. A abdominal computed tomographic scan showed multiples cystic lesions in the kidneys and liver, with a large hepatic cyst responsible for compression of the suprahepatic veins and the inferior vena cava resulting in chronic Budd-Chiari syndrome. The treatment was radiological drainage followed by percutaneous sclerosis of cysts to alleviation of the compression. Unfortunately, the patient died a few days after an intraperitoneal cystic rupture.

The incidence of extramammary Paget’s disease (EMPD) is very low. It is very important to distinguish between primary Paget’s disease and secondary process. An 85-year-old man was consulted for the presence of an erythematous plaque located in the anal and gluteal area, confirming Paget cells in the biopsy.

Hepatitis B (HBV) and C (HCV) are two other forms of infections for which co-infection in HIV has been associated with alteration of the immune response, increased risk of progression to liver diseases, and increased risk of hepatotoxicity associated with antiretroviral therapy. This study aimed to establish the prevalence of hepatitis B surface antigen (HBsAg) and hepatitis C antibody (HCVAb) among HIV patients, evaluate response to treatment between the different categories and identify the possible risk factors associated with this burden of hepatitis B/C among HIV patients and the resulting responses to HAART in Kumba Health, in the South West Region of Cameroon. Method: We performed a systematic screening using Rapid Diagnostic Test, for HBsAg and HCVAb among 299 HIV patients enrolled at the treatment centers in Kumba Health District (District hospital Kumba, Kumba Town Sub-Divisional hospital, and the Apostolic hospital Banga Bakundu), with all positives for HBV or HCV confirmed by the ELISA and results analyzed using SPSS version 20. Out of the 299 participants, 52 HIV patients, 36 HIV/HBV, and 12 HIV/HCV patients were involved in the prospective cohort study for 24 months which permitted monitored the immune response (CD4 counts and viral load test), as well as variation of biochemical parameters (ALAT/ASAT, albumin, bilirubine, creatinine) and weights of the studied participants. Result: Out of the 100 HIV patients involved in the prospective cohort, 36 and 12 were hepatitis B and C virus-positive respectively. Following the analysis of the viral load and CD4 cell counts, there were differences in response to HAART after 24 months between the mono-infected and co-infected patients, taking into consideration the, CD4 cell counts (HIV: 930.846 cells/mm3, HIV/HBV: 595.139 cells/mm3 and HIV/HCV: 678.500cells/mm3), and viral load (HIV: 1777.85copies/ml, HIV/HBV: 2232.61copies/ml and HIV/HCV: 750.83copies/ml). There were variations in biomarkers of the liver (ALAT/ASAT, bilirubin, and albumine) and renal function (creatinine) for both patients. There were also variations of the different biomarkers linked to the infection status of the different participants. Conclusion: There were positive variations in viral load and CD4 cell counts among the studied participants, with a more rapid response to the mono-infected HIV patients compared to the co-infected patients. Similar strength was observed in the variation of the different biomarkers and such variation indicates that co-infection of HIV patients with either hepatitis B or C virus can affect rapid response to HAART and the variations in the level of Biochemical markers among the different categories are linked to the alteration of the functions of the respective organs and so this result could be used for health decisions regarding co-infections.

I have observed what seems to be a rare but novel symptom that has not been documented in the medical literature, in a subject that I have been studying. The observation was a worsening of flatus and stool odor in this subject, a few days after the subject started an unphysiologically high dose of dietary molybdenum.

Molybdenum is a trace mineral needed in small quantities by most life forms. In living organisms, a molybdenum atom is found within molybdenum-dependent enzymes or molybdoenzymes. Molybdoenzymes catalyze reactions in carbon, sulfur, and nitrogen metabolism. Only four molbdoenzymes have been identified in humans. Most of the known molybdoenzymes are found in bacteria. Dietary molybdenum can be administrated to humans, to treat Wilson disease and tungsten poisoning; and it may be useful in arthritis. Sulfur-reducing bacteria are the bacterial group that reduces certain sulfur molecules to hydrogen sulfide. These bacteria can inhabit anaerobic parts of the gastrointestinal tract of mammals and are the predominant producer of hydrogen sulfide in the human colon. Hydrogen sulfide plays a major role in the malodor of human flatus. Some individuals have reported an increase in foul odoriferous gases from the colon after molybdenum supplementation. The underlying mechanism as to how this occurs is currently not known. Possible bacteria that are involved could be sulfur-reducing bacteria and methionine dissimilating bacteria. Supplementing sheep with molybdenum and with sulfur exclusively in the form of methionine can stimulate the growth of sulfur-reducing bacteria and increase the level of sulfides in the rumen. The molybdoenzyme, thiosulfate reductase, is found in sulfur-reducing bacteria and catalyzes the reduction of thiosulfate to hydrogen sulfide. The source of thiosulfate could be from ruminal epithelial cells detoxifying methanethiol, produced by methionine dissimilating bacteria, degrading the dietary methionine to methanethiol. Therefore, the molybdenum could be activating thiosulfate reductases of sulfur-reducing bacteria in the rumen of these animals. The human colon can also harbor sulfur-reducing bacteria, and dietary molybdenum and methionine can reach this organ. Therefore, dietary molybdenum may be stimulating the growth of sulfur-reducing bacteria in some individuals. Sulfides in the human colon could have beneficial and detrimental effects on health. Such effects could include the already mentioned malodor of flatus, the stabilizing of the microbiome-mucosa interface in an intestinal dysbiosis, the treatment of hypertension and the promotion of inflammation in ulcerative colitis.

Caecum volvulus is, in frequency, the second part of the colon concerned by volvulus after the sigmoid and before the transverse colon. This pathology occurs in the cecum with abnormal mobility The mechanism of volvulus can be summarized in 2 either by torsion or tilting. The clinical picture is that of an acute intestinal occlusion by strangulation. The abdomen without preparation (ASP) and the abdominal CT are the radiological examinations of the first choice for the diagnosis. It is a surgical emergency, the conduct of which is to make a resection of the cecum and the terminal ileum. We report the case of a cecal volvulus admitted to the emergency room with an acute intestinal obstruction, the diagnosis was confirmed by an abdominopelvic CT scan and the treatment consisted of an ileocecal resection with immediate restoration of continuity, the postoperative follow-up was simple.

Background: Cholelithiasis is a chronic recurrent disease of the hepatobiliary system and cholecystectomy is one of the commonly performed surgeries. This study intends to evaluate the demographic of patients with cholelithiasis, its various mode of presentation, surgical intervention, and its outcome. Methods: This was a quantitative retrospective cross-sectional study conducted in the College of Medical Sciences- a Superspeciality Tertiary Care Teaching Hospital in Bharatpur, Chitwan in central Nepal. All patients undergoing laparoscopic or open cholecystectomy in the department of GI and General Surgery at the College of Medical Sciences from 1st May 2017 to April 30, 2021were included in the study. Study tools were records of the patients retrieved from the medical record section. Results: A total of 355 patients data were analyzed. The mean age of the study samples was 46.43 +/- 16.47 years. Female predominance was seen at 76.18% with M: F ratio of 1:3.18. The most common presenting symptoms were pain abdomen (70.4%), bloating of the abdomen (63.9%), and fatty dyspepsia (46.8%). Acute cholecystitis was seen in 14.36%, biliary pancreatitis in 6.2%, and gallbladder perforation in 2.25% cases. Laparoscopic cholecystectomy was done in 269(83.94%), open cholecystectomy in 57(16.05%), and laparoscopic converted into open cholecystectomy 29 in (9.73%). Intra-operative complications like gallbladder perforation and controlled bleeding were seen in 10.14% and 4.23% of cases. Post-operative complications like bile leak and major bile duct injury were seen in 6.19% and 1.40% of cases. Regarding management of bile leak, conservative management was successfully done in 54.54% of cases while they were managed with ERCP in 27.27%, hepaticojejunostomy in 13.63%, and with T-tube repair in 4.5% cases. The overall mortality was 0.8%.

Celiac disease is an immune-mediated enteropathy, caused (in genetically predisposed or susceptible individuals) by the ingestion of gluten, the complex of water-insoluble proteins found in cereal grains such as wheat, rye and barley. In terms of terminology, it is the complex natural history and extremely polymorphous clinical presentation that has created some confusion. In fact, to date, at least three different forms of celiac disease are known, in addition to the simple non-celiac gluten sensitivity, since in common clinical practice most patients do not present the classic symptoms such as malabsorptive syndrome with diarrhoea, steatorrhoea, weight loss and nutritional deficiency, but rather an anaemia, asthenia, meteorism, abdominal tension, osteoporosis and infertility, thus painting an extremely varied and complex symptomatic picture that is linked to enteric microbiota and microbiome issues. Celiac disease affects the mucosa of the small intestine, while it generally spares the submucosa, muscolaris propria and serosa; if the disease does not involve the whole of the small intestine but only part of it, it is usually more serious in the proximal than the distal tract. The simultaneous presence of shortened villi, crypt hyperplasia, the abnormal cytological appearance of the absorbent surface and increased lamina propria cells is required for the diagnosis of celiac disease. Based on these findings, several forms of celiac disease have been identified in the clinic: typical, atypical (and in turn silent, latent, and potential), and sensitive non-celiac. Based on these considerations a specific diagnostic scheme is suggested to frame the celiac universe more functionally and structurally (so-called Diagnostic Scheme for Celiac Disease and Nonceliac Gluten Sensitivity, DSCNC), identifying at least eight clinical hypotheses based on the serological, genetic, bioptic and allergological tests suggested). From a pharmacological and integrative point of view, the protocols shared by the scientific community remain in place: gluten-free diet, vitamin and salt supplementation if appropriate, pharmacological therapy (antibiotics, antihistamines, corticosteroids and immunosuppressants) if necessary, also in the future with the majority orientation oriented towards oral glutenase able to counteract the effects of gliadin in sensitive subjects, the use of larazotide acetate to remedy the increase in intestinal permeability and tTG inhibitors to reduce the toxic effects of gluten intake. The state of the art on celiac disease is not yet able to explain the precise aetiology and atypical forms of the disease, as well as the real impact of genetic predisposition on clinical manifestations. Research continues and seems to point the way to a complete resolution of this enteropathy that has been so prevalent over the last two decades.

Background: Atrophy of the gastric mucosa and intestinal metaplasia is considered malignant precursor lesions of gastric cancer, which is considered the fifth most common neoplasm in the world and the third cause of death from cancer. The main risk factor is the infection by Helicobacter pylori (H. pylori), which increases up to six times the risk of gastric cancer, through gastritis, atrophy, and hypochlorhydria, consequences of the infection. Other risk factors are also worth noting, like smoking and a family history of gastric cancer. Objective: To investigate the prevalence of malignant precursor lesions and their associated factors in patients who underwent upper gastrointestinal endoscopy. Methods: A descriptive, observational study was performed based on an analysis of endoscopic gastric biopsies performed in two affiliated private laboratories to the Unified Health System (Sistema Único de Saúde [SUS]) in a city in Paraná state. Patients were assessed for age, sex, active or recent smoking, family history of gastric cancer, and previous treatment for H. pylori. The samples were evaluated for the presence of glandular atrophy, intestinal metaplasia, dysplasia, and H. pylori infection. Results: A total of 1,549 medical records and patient reports were evaluated and 945 were eligible, the average age was 52.2 (±14.3) years old and most patients (73.3%) were female. The prevalence of H. pylori infection was 47.5% (n= 449) and the highest percentage was between 30-39 years (58.7%). Among H. pylori-positive (+) patients who had developed intestinal metaplasia, there is more risk of having incomplete than complete metaplasia (OR: 4.34; 1.1–17.1; 95%CI). Patients who smoke are more increase the risk to developed glandular atrophy (OR: 1.91; 1.09-3.33; 95%CI) and intestinal metaplasia (OR: 1.93; 0.72-5.11; 95%CI). Conclusion: The study reinforces risk factors such as smoking and H. pylori infection as precursors for developing pre-neoplastic lesions in a population in southern Brazil, highlighting the importance of smoking cessation and prevention of H. pylori infection and the treatment of infected patients.

A 39-year-old man with newly diagnosed and well controlled hypertension was in his usual state of good health. He was diagnosed with a retroperitoneal tumor during a health check-up, which was suspicious of adrenal tumor by abdominal computed tomography.