SUMMARY We report on a patient with systemic lupus erythematosus (SLE) who suffered catastrophic haemorrhage following rupture of an intrahepatic aneurysm. The association between hepatic artery aneurysm and SLE has not been recorded previously, but we have found evidence from the literature that there may be an association between autoaggressive disorders and this surgical emergency.Aneurysm of the hepatic artery is not common. When intrahepatic, it is associated with systemic disorders. In this report we describe a patient with systemic lupus erythematosus in whom rupture of an intrahepatic artery aneurysm occurred and led to ife-threatening haemorrhage.Case report An Asian women of 33 presented in 1965 with arthritis and joint swelling. She was anaemic and pyrexial with thinning head hair and pubic hair. A diagnosis of systemic lupus erythematosus (SLE) was made on the basis of marked anaemia, thrombocytopenia, a raised erythrocyte sedimentation rate, raised plasma gammaglobulins, and a positive LE cell preparation. The patient responded to treatment with 6-mercaptopurine and betamethasone.Ten years later she was admitted to hospital with arthralgia, pleuritic chest pain, and dependent oedema. X-rays showed bilateral pleural effusions, and an electrocardiogram suggested pericarditis. Further investigations showed antinuclear antibody (positive to 1/50) and raised DNA binding, confirming the diagnosis of SLE. Renal involvement produced proteinuria and diminished function (creatinine clearance 34 ml/min). Frusemide 120 mg with dexamethasone 4 mg was prescribed daily.
Black Death, caused by Yersinia pestis, originally had a 40–75% mortality rate, with a risk of the disease maturing into the pneumonic and septicaemic phases. With current threats of using Y. pestis as an agent of biological warfare, studying how the virulency of the disease is important as the bubonic plague could be a potent weapon. A recently discovered potential treatment would inhibit the omptin (outer‐membrane protease) Pla, which cleaves the R561–V562 bond in the amino acid sequence of plasminogen, converting it to plasmin: an enzyme that degrades proteins in blood plasma such as fibrin. This leads to a lack of clotting, thus enabling the bacteria to gain entry into the host organism. Y. pestis injects toxins in immune cells, killing these cells. The result is a depressed immune response. However, if Pla is inhibited, then the mortality rate decreases as there is no progression to the pneumonic phase (quantized by the lack of change of fluid in the lungs). A lack of Pla would mean that the plague would not spread into other areas of the body, localizing the disease and making it possible to treat. Because the bubonic plague is a disease that kills in 2–7 days, inhibiting Pla would increase the window for treatment. The Torrey Pines SMART Team (Students Modeling A Research Topic) modeled the Pla protein using 3D printing technology. Supported by a grant from the HHMI Pre‐ College Program.
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