Early anion gap metabolic acidosis in acetaminophen overdose.

PURPOSE: The study aimed to determine the incidence and clinical significance of early high (>15 mEq/L) anion gap metabolic acidosis in acetaminophen (APAP) overdose. METHODS: A retrospective review of a cohort of 74 patients presenting within 24 hours of APAP overdose was conducted. RESULTS: Early high anion gap metabolic acidosis was present in 41% of patients on admission and persisted for 1.5 ± 0.1 days. The anion gap was associated with an elevated lactate level (4.5 ± 1 mmol/L) (r(2) = 0.66, P < .05), which persisted for 1 day. The lactate level increased in proportion to the APAP concentration (r(2) = 0.75, P < .05). Patients with increased anion gap had a higher incidence of confusion (48% vs 3%; P < .001) and lethargy (39% vs 6%; P = .003). Early high anion gap metabolic acidosis was found in the absence of shock or liver failure. All patients were treated with N-acetylcysteine and, despite the early high anion gap metabolic acidosis, none developed hepatic failure or hypoglycemia. CONCLUSION: Early high anion gap metabolic acidosis in patients with APAP overdose is self-limited and does not predict clinical or laboratory outcomes. Persistent or late metabolic acidosis in the absence of liver failure is not likely due to APAP and should prompt a search for other causes of metabolic acidosis. Finally, APAP overdose should be considered in patients presenting to the emergency department with altered mental status, as this is a treatable condition when detected early.

Portal hypertension and variceal hemorrhage.

Portal hypertension, a major hallmark of cirrhosis, is defined as a portal pressure gradient exceeding 5 mm Hg. In portal hypertension, porto-systemic collaterals decompress the portal circulation and give rise to varices. Successful management of portal hypertension and its complications requires knowledge of the underlying pathophysiology, the pertinent anatomy, and the natural history of the collateral circulation, particularly the gastroesophageal varices.

Menetrier's Disease.

Menetrier's disease is a rare acquired disorder of the fundus and body of the stomach (ie, oxyntic mucosa) characterized by giant hyperplastic folds, protein-losing gastropathy, hypoalbuminemia, increased mucus secretion, and hypochlorhydria. Recent research implicates overproduction of transforming growth factor-alpha with increased signaling of the epidermal growth factor receptor (EGFR) in the pathogenesis. Activation of the EGFR, a transmembrane receptor with tyrosine kinase activity, triggers a cascade of downstream, intracellular signaling pathways that leads to expansion of the proliferative compartment within the isthmus of the oxyntic gland. The diagnosis of Menetrier's disease is based upon characteristic histologic changes, including foveolar hyperplasia, cystic dilation of pits, and reduced numbers of parietal and chief cells. The best treatment for Menetrier's disease is not clear. It seems reasonable to test and treat for cytomegalovirus and Helicobacter pylori, as 1) in children, evidence exists that the disease may be due to cytomegalovirus infection in up to one third of patients; and 2) in adults, there are anecdotal reports of resolution upon H. pylori eradication. More recently, therapies targeting increased signaling of the EGFR have shown promise, including somatostatin analogues and monoclonal antibodies (eg, cetuximab) directed against the EGFR. In refractory cases, gastrectomy is curative.

Cough and spontaneous rupture of a normal spleen.

Rupture of the spleen is a relatively common complication of trauma and many systemic disorders affecting the reticuloendothelial system, including infections and neoplasias. A rare subtype of rupture occurring spontaneously and arising from a normal spleen was recognized as a distinct clinicopathologic entity. The pathogenesis is debated in the absence of external trauma or predisposing disease. It has been reported in association with apparently trivial insults such as vomiting. We report a case of a patient with spontaneous rupture of a normal spleen. Interestingly, it was observed after severe coughing.

Remission of natural-killer cell lymphoma of the liver with anti-hepatitis C therapy.

Non-Hodgkin lymphomas (NHL) consist of a diverse group of lymphoproliferative neoplasms with unique patterns of biology, behavior, and differing responses to therapy. A rare subtype of malignancy arising from cells of putative natural killer (NK) origin is being recognized as a distinct clinicopathological entity. Viruses including hepatitis C have been reported in association with various types of NHL but not the NK-cell subtype. We hereby report a unique case of a patient with hepatitis C who developed hepatic NK-cell lymphoma and chronic NK-cell leukemia. Interestingly, we observed clinical and radiologic remission of the neoplasm following treatment with anti-hepatitis C therapy.