Background: Hepatitis B virus infection has become a global public health problem. In Nigeria, several studies from different parts of the country have confirmed the endemicity of the infection. This study seeks examine the seroprevalence of Hepatitis B viral infection among patients attending Aminu Kano Teaching Hospital in Kano metropolis.Method: This is a retrospective study in which patients tested for hepatitis B virus using hepatitis B surface antigen (HBsAg) as a marker were reviewed over 3 years.

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INTRODUCTION: Severe Gestational Hypertriglyceridemia (HTG) is a rare but potentially life-threatening condition, which can lead to devastating complications, including acute pancreatitis (AP), hyperviscosity syndrome, preeclampsia, maternal & fetal morbidity & mortality. CASE PRESENTATION:A 33-year-old female G3P1þ1 at 37-week gestation, presented with acute abdominal pain nausea & vomiting. She admitted consuming a high fat high carb diet for a few weeks before presentation. Family history significant for her mother was diagnosed with familial Chylomirconemia & AP in pregnancy due to HTG. On presentation her vital signs were stable, physical exam consistent with early labor & negative for eruptive xanthomas. Labs showed Lipase 1,106 U/L, Amylase 750 U/L, TG 5,531 mg/dl, Cholesterol 702 mg/dl, ALP 163 U/L & glucose 82 mg/dl. She underwent C-section after which she was admitted to ICU for treatment of AP with aggressive fluid resuscitation, insulin drip with dextrose infusion & Gemfibrozil. Abdominal US revealed no biliary stones with CT abdomen revealing edematous pancreas & a region of hypoattenuation suspicious for necrotizing pancreatitis & was started on IV antibiotics. Insulin Drip was stopped once TG were less than 700 mg/ dl & symptoms resolved. She was discharged on Gemfibrozil & fish Oil.DISCUSSION: Plasma TG level normally increases 2-4 folds in pregnancy secondary to hormonally driven changes in the liver & adipose tissue with the most profound increase in the 3rd trimester as high estrogen enhances hepatic TG synthesis. Concomitantly, insulin resistance caused by human placental lactogen decreases lipoprotein lipase activity which increases adipose tissue lipolysis & free fatty acids needed for TG synthesis(1). Gestational HTG is defined as fasting plasma TG level above the age-adjusted 95th percentile for the non-pregnant population. Severe HTG defined as TG levels greater than 1000 mg/dl as it's associated with an increased risk of AP which represents a diagnostic challenge in pregnancy due to nonspecific presentation & imaging limitation(1,2). Severe Gestational HTG is typically seen in patients with underlying genetic abnormalities in TG metabolism which most likely what our patient has given her family history & poorly controlled diabetes considered the most common secondary risk factor(1). Insulin infusion is used to treat severe HTG if associated with AP or hyperglycemia. Low fat diet remains the cornerstone of maintenance management with oral administration of medium chain fatty acid or omega-3 acid ethyl esters has become part of management. Though safety for fibrates has not been well established yet; they may still be used in the later stages of gestation when benefits outweigh the risks(1,2). CONCLUSIONS:Severe gestational HTG is a rare but serious condition that can cause AP which can be challenging to diagnose & treat in pregnancy.

Ectopic adrenocorticotropic hormone (ACTH)-secreting syndrome (EAS) is a rare but often aggressive paraneoplastic syndrome. Patients with EAS typically present with high ACTH levels and rapid clinical progression in the setting of acute cortisol elevation, which can delay diagnosis due to a lack of typical Cushingoid features. High levels of ACTH have also been shown to stimulate the adrenal zona glomerulosa to oversecrete aldosterone. We present the case of a 58-year-old male presenting with new-onset hypertension and severe metabolic alkalosis with spontaneous hypokalemia, in the setting of elevated aldosterone and low renin levels, suggestive of primary aldosteronism. Subsequent biochemical testing, imaging, and pathology, however, revealed suppression of aldosterone with evidence of hypercortisolism in the setting of metastatic small cell lung cancer. This was, therefore, suggestive of pseudo primary aldosteronism in the setting of a paraneoplastic ectopic ACTH-producing syndrome. This case highlights that hypercortisolism, in the setting of EAS, can initially present with a clinical picture suggestive of hyperaldosteronism. The use of a Dexamethasone suppression test can allow the clinician to differentiate between idiopathic bilateral adrenal hyperplasia and ectopic ACTH syndrome.