Metabolic dysfunction-associated steatohepatitis (MASH) is one of the major risk factors for chronic liver disease and hepatocellular carcinoma (HCC). The incidence of MASH in Western countries continues to rise, driving HCC as the third cause of cancer-related death worldwide. HCC has become a major global health challenge, partly from the obesity epidemic promoting metabolic cellular disturbances but also from the paucity of biomarkers for its early detection. Over 50% of HCC cases are clinically present at a late stage, where curative measures are no longer beneficial. Currently, there is a paucity of both specific and sensitive biological markers for the early-stage detection of HCC. The search for biological markers in the diagnosis of early HCC in high-risk populations is intense. We described the potential role of surrogates for a liver biopsy in the screening and monitoring of patients at risk for nesting HCC.

Autoimmune hepatitis (AIH) is an extremely rare cause of chronic liver disease (CLD) in sub-Saharan Africa—there have only been 3 reported cases of AIH in Nigeria, a country of about 200 million people. We report the first case of AIH in a male patient in Nigeria and highlight its unusual presentation. A 41-year-old man with jaundice and malaise for 3 months was referred for evaluation after investigations revealed deranged liver enzymes and a cirrhotic liver. Laboratory evaluation revealed high serum immunoglobulin G, but there was also marked elevation of serum ferritin and transferrin saturation, resulting in a diagnostic dilemma between AIH and an iron overload condition such as hemochromatosis. A liver biopsy was crucial in providing a definitive diagnosis of AIH. Despite its rarity, clinicians should maintain a high index of suspicion for AIH in sub-Saharan Africa and should proceed to a liver biopsy when the cause of CLD is unclear.

Propofol-related infusion syndrome (PRIS) is an uncommon complication resulting from prolonged propofol use. Common clinical presentations include metabolic acidosis, cardiac arrhythmias, and renal complications. The mortality rate is high if it is not recognized in time. There is no antidote to propofol. Initial treatment involves discontinuing ongoing propofol use and providing supportive measures. The reversal of clinical and laboratory features upon discontinuation of propofol provides a basis for retrospective diagnosis or PRIS. In severe cases, ultrafiltration may be utilized.

Hemosuccus pancreaticus (HP) is a rare cause of upper gastrointestinal bleeding. It was described by Lawal and Farrel in 1931. This disorder has also been referred to as pseudohemobilia or wirsungorrhagia, caused by bleeding into the pancreatic duct. The rarity of this condition can pose a diagnostic challenge. HP is life-threatening and requires immediate attention. The commonly used treatment modality is coil embolization. Surgery is considered in the case of failed embolization or uncontrolled bleeding. Described below, is a case of a 72-year-old female with a history of chronic pancreatitis who presented with anemia secondary to bleeding peripancreatic varices.

Hepatocyte nuclear factor-1 beta (HNF1B) gene is predominantly expressed in the liver, kidney, lung, genitourinary tract, and pancreas. It is an important transcription factor that regulates pancreas development. Mutation or absence of this gene is rare and can cause incomplete pancreatic development known as the agenesis of the dorsal pancreas. This rare genetic abnormality is associated with other disorders like maturity-onset diabetes of the young, abnormal liver function tests, genitourinary tract malformation, pancreatitis, and renal cysts. Diagnosing this genetic abnormality is difficult, especially in patients presenting with symptoms specific to only one system. Management is based on disease manifestation and involves a multidisciplinary approach. Our case describes a 51-year-old female with poorly controlled diabetes mellitus and Mullerian duct anomalies who presented with abdominal pain, fatigue, dizziness, and electrolyte derangement. Contrast-enhanced computed tomography (CECT) of the abdomen showed a multicystic kidney and a pancreatic head with a missing body and tail. Further workup revealed an HNF1B mutation.

Background: The inflammation and repair of the intestinal mucosa in inflammatory bowel disease (IBD) involve a complex interplay between innate, adaptive immune responses, and hormones. This may explain the relapsing clinical course of the disease.Methods: We present the first reported case of a patient presenting their initial flare of ulcerative colitis immediately after discontinuing growth hormone (GH) therapy, suggesting treatment with GH or growth factors may prevent the development of IBD.Results: This is a case of a 13-year-old female with a history of GH deficiency, presenting with an 8-week history of abdominal pain, blood-stained diarrhea, and fecal calprotectin greater than 8000 mcg/g, 2 weeks after discontinuing GH therapy. The patient subsequently underwent an esophagoduodenoscopy and colonoscopy with biopsies showing histological features consistent with ulcerative colitis.Conclusions: The finding of withdrawing GH or growth factors therapy potentially unmasking IBD in this patient raises a question of whether growth factors can inhibit the development of IBD and suggests beneficial effects of treatment with GH or growth factors as adjuvant therapy for IBD.