Patients with portal hypertension of varying etiology may develop pulmonary artery hypertension. In the present autopsy study, pulmonary and hepatic tissue was studied in 12 patients in whom pulmonary and portal hypertension coexisted. Plexogenic pulmonary arteriopathy was present in 10 patients, 7 of whom had coexistent thromboembolic lesions. One patient had isolated medial hypertrophy, which may be an early stage in the plexogenic category, whereas isolated thromboembolic pulmonary vascular disease was observed in one subject. Hepatic disease was consistent with alcoholic cirrhosis in seven patients, cryptogenic cirrhosis in four and extrahepatic portal hypertension without cirrhosis in one. Thrombocytopenia was present in all 10 patients whose platelet count was determined. This study suggests that pulmonary hypertension associated with portal hypertension commonly has a plexogenic appearance on histologic examination. However, thrombosis (whether embolic or in situ) may also contribute to vascular obstruction.

Candida species have been often considered but infrequently documented as a credible cause of diarrhea. Evaluations of the colon in patients who have diarrhea and for whom Candida organisms have been isolated from stool have not shown invasive fungal lesions, and the mechanisms by which Candida species may induce diarrhea remain undefined. However, symptoms ascribed to Candida-associated diarrhea in the literature include prolonged secretory diarrhea with abdominal pain and cramping but without blood, mucus, fever, nausea, or vomiting. A critical review literature review showed a strong between the abatement of diarrheal symptoms in patients for whom a significant growth of Candida was found in their stools and treatment with specific topical antifungal agents. Most of the patients had received antibacterial therapy before the onset of symptoms. On the basis of these data, we conclude that Candida species may cause diarrhea in selective clinical settings.

We report simultaneous infections with Clostridium difficile and methicillin-resistant Staphylococcus aureus (MRSA) in a patient with discrete colonic pseudomembranes typical of C. difficile infection, as well as confluent, loosely adherent pseudomembranes in the small bowel. Identification of MRSA in the small bowel pseudomembrane by polymerase chain reaction supports S. aureus as an enteric pathogen.

Diverse lines of evidence indicate that pre-fibrillar, diffusible assemblies of the amyloid β-protein play an important role in Alzheimer’s disease pathogenesis. Although the precise molecular identity of these soluble toxins remains unsettled, recent experiments suggest that SDS-stable amyloid β-protein dimers may be the basic building blocks of Alzheimer’s disease-associated synaptotoxic assemblies and as such present an attractive target for therapeutic intervention. In the absence of sufficient amounts of highly pure cerebral amyloid β-protein dimers, we have used synthetic disulfide cross-linked dimers (free of Aβ monomer or fibrils) to generate conformation-specific monoclonal antibodies. These dimers aggregate to form kinetically trapped protofibrils, but do not readily form fibrils. We identified two antibodies, 3C6 and 4B5, which preferentially bind assemblies formed from covalent Aβ dimers, but do not bind to amyloid β-protein monomer, amyloid precursor protein, or aggregates formed by other amyloidogenic proteins. Monoclonal antibody 3C6, but not an IgM isotype-matched control antibody, ameliorated the plasticity-disrupting effects of Aβ extracted from the aqueous phase of Alzheimer’s disease brain, thus suggesting that 3C6 targets pathogenically relevant amyloid β-protein assemblies. These data prove the usefulness of covalent dimers and their assemblies as immunogens and recommend further investigation of the therapeutic and diagnostic utility of monoclonal antibodies raised to such assemblies.