Background: Little information is available on leptin concentrations in individuals with IGT. This study aims to determine and correlate leptin levels to anthropometric measures of obesity in prediabetic, (IFG and IGT), type 2 diabetic and normoglycaemic Saudis.
Vanishing bile duct syndrome (VBDS) is a condition resulting from severe bile duct injury, progressive destruction, and disappearance of intrahepatic bile ducts (ductopenia) leading to cholestasis, biliary cirrhosis, and liver failure. VBDS can be associated with a variety of disorders, including Hodgkin's lymphoma (HL). We describe a 33-year-old male patient who presented with lymphadenopathy and jaundice, and was diagnosed to have HL. Serum bilirubin worsened progressively despite chemotherapy, with a cholestatic pattern of liver enzymes. Diagnosis of VBDS was established on liver biopsy. Although remission from HL was achieved, the patient died of liver failure. Presence of jaundice in HL patients should raise the possibility of VBDS. This report discusses the difficulties of delivering chemotherapy in patients with liver dysfunction. HL-associated VBDS carries a high mortality but lymphoma remission can be achieved in some patients. Therefore, liver transplantation should be considered early in these patients.
Patient: Male, 58Final Diagnosis: Acute lymphoblastic leukemiaSymptoms: Chest pain • fatigue • loss of appetite • shortness of breathMedication: —Clinical Procedure: Liver biopsy and bone marrow biopsySpecialty: HematologyObjective:Rare diseaseBackground:Type-B lactic acidosis is a rare complication of solid tumors and hematological malignancies. It occurs secondary to Warburg effect, when glucose metabolism in cancer cells switches from the oxidative pathway to the glycolytic pathway. Malignant lactic acidosis is a life-threatening condition if not promptly diagnosed and treated urgently.Case Report:We report the case of a 58-year-old male patient who presented with severe chest pain, dyspnea, systemic symptoms, leukopenia, normocytic anemia, and severe lactic acidosis. He was admitted with a possible diagnosis of acute pericarditis and lactic acidosis. Sodium bicarbonate replacement did not improve the lactic acidosis. Liver biopsy was performed because of persistently elevated alkaline phosphatase and gamma-glutamyl transferase; the biopsy showed atypical lymphoblasts and bone marrow biopsy confirmed the diagnosis of precursor B acute lymphoblastic leukemia. Lactic acidosis normalized after initiation of chemotherapy.Conclusions:Cancer, particularly hematological malignancy, should be considered as an etiology and differential diagnosis of type-B lactic acidosis. Prompt recognition and urgent initiation of specific therapy to control the underlying malignancy are critical to manage this serious metabolic complication.
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