Factors influencing the prognosis were studied in 165 patients with polyarteritis nodosa (PAN) and Churg-Strauss angiitis. One hundred and forty-seven of the patients fulfilled histological and/or arteriographic diagnostic criteria, and in 18 patients the diagnosis was based on clinical criteria. The patients' mean age on diagnosis was 48.4 +/- 16.4 years. The main symptoms were fever (69%), weight loss (66%), arthritis (44%), mononeuritis multiplex (67%), cutaneous signs (46%), renal involvement (26%), gastrointestinal symptoms (31%), asthma (29%), hypertension (31%) and cardiac failure (18%). Ninety-two per cent of the patients survived for at least 1 year after diagnosis of the disease, 79% for 2 years, and 63% for 5 years. The immediate causes of death were gastrointestinal bleeding or peritonitis in 11 cases, pancreatitis in two, renal insufficiency in six, cardiac failure in five, infectious complications in four, stroke in three and other causes in 11. We studied the prognosis of necrotizing angiitis in relation to clinical symptoms and laboratory findings. The association of four conditions were associated with a poor prognosis: age over 50, gastrointestinal problems, cardiomyopathy and renal signs. The survival rates in patients with these conditions were: for gastrointestinal problems, 55% 5-year survival (versus 67%); and for age over 50, 68% 3-year survival (versus 78%; p less than 0.09). One hundred and fifty-nine patients were treated with steroids for at least 18 months. Forty-eight also received cytotoxic agents (27%) and 46 plasma exchange. Patients who were treated with plasma exchange and prednisone were randomly assigned to additional treatment with cyclophosphamide. Survival rates were comparable in both groups.

With the current tendency of increasing minimally invasive cosmetic surgeries, some rare but disastrous complications of facial filler injections come into sight, such as visual loss. The study aims to investigate the possible route that the injected droplet accesses the ophthalmic artery to explain and prevent such devastating complications. We searched the National Library of Medicine’s PubMed database for cases of visual loss secondary to cosmetic facial filler injection, and reviewed relevant case reports/surveys, as well as accompanying references. Data obtained were analyzed, with special interest in injected sites and filler material, and clinical features of visual loss. Based on the anatomy of facial vessels, we inferred the possible route of injected droplet migrating from injection sites to ophthalmic artery. Most physicians propose a retrograde embolic mechanism, but the culprit artery when injecting different sites is not determined. We consider accidentally breaking into supraorbital artery or supratrochlear artery may cause occlusion of ophthalmic artery when injecting into glabella or forehead region. Speaking of the nasolabial fold and nasal dorsum region, any injections in the anastomosis of the dorsal nasal artery, angular artery, and lateral nasal artery can lead to retrograde embolism. Similarly, in the temporal region, we believe there is abnormal anastomosis between frontal branch of superficial temporal artery from external carotid artery and supraorbital artery from ophthalmic artery. In our hypothesis, we can explain the accompanying brain infarction after iatrogenic visual loss. If the injecting pressure is forceful enough, it may push the embolic materials into middle cerebral artery. Although iatrogenic ophthalmic artery occlusion is a rare complication after the facial filler injection surgery, it is usually devastating. Both the patient and the surgeon should be aware of the risk of irreversible blindness. Ideally, the injection sites should avoid the small vessels nearby, the injecting force and velocity should be as gentle and slow as possible.

Objective-To determine the factors associated with the occurrence of Pneumocystis carinil pneumonia (PCP) in Wegener's granulomatosis (WG). Methods (PCP) is one of the most frequent and opportunistic, often resulting in death.3 It is therefore important to identify patients with WG who are at risk of PCP in order that they receive primary antipneumocystis prophylaxis. To determine the factors associated with the occurrence of PCP in WG, we compared retrospectively a group of 12 patients with both WG and PCP, with all patients suffering from WG, but without PCP, followed in the same units over the same period.

We adapted an immunoblotting technique for the immunochemical characterization of cryoglobulins. We first compared the results from 157 samples with results obtained by immunofixation and immunoelectrophoresis and then with clinical observations in 125 cases. Full identification was possible in 98% of the cases by immunoblotting, in 54% by immunofixation, and in 28% by immunoelectrophoresis. Novel microheterogeneity aspects were observed by immunoblotting and immunofixation in 13% and 6% of the cases studied, respectively. Our results confirm the frequency of autoimmune and infectious diseases associated with mixed cryoglobulinemias, whereas a lymphoproliferative syndrome was observed only in cases of cryoglobulinemia with a monoclonal constituent or a microheterogeneity aspect, which was not always revealed by immunofixation or immunoelectrophoresis. The pathophysiological importance and classification of microheterogeneity aspects is not clear. These observations justify using a sensitive and specific method for identifying cryoglobulins, even when present at low concentrations, and call for long-term studies of these patients.