[Acute pancreatitis and AIDS]. / Pancreatite acuta e AIDS.

It's well known that patients was acquired immunodeficiency syndrome (AIDS) can develop various kinds of hepatobiliopancreatic diseases, for causes related to AIDS and for causes not related to HIV infection. The authors describe a case to their attention due to a suspected acute pancreatitis. The patient presented with abdominal pain, increased serum alkaline phosphatase and amylase levels. Serological test and stool concentration didn't show any opportunistic infection (Cytomegalovirus, Cryptosporidium). Abdominal ultrasonography showed enlargement of the head of the pancreas, gallbladder with biliary sludge, and a little dilatation of the biliary tree. The patient didn't feel better despite the medical treatment, so considering the probability of the migration of calculus, the patient underwent cholecystectomy. After the operation the patient felt better quickly. This case confirms the presence in HIV patients of pancreatitis for causes unrelated to AIDS like cholelithiasis as we showed, alcoholism, hypercalcemia, and the importance of an opportune surgical treatment that was resolutive.

[Necrotizing fasciitis: case reports and review of the literature] / Fascite necrotizzante: descrizione di casi clinici e rassegna della letteratura.

Necrotizing fasciitis is a rare, rapidly progressing infection affecting the superficial fascia and the subcutaneous tissue, accompanied by severe systemic toxicity and multiorgan failure. It is caused by aerobic and anaerobic bacteria, occasionally in a synergistic polymicrobial combination (Type I Necrotizing Fasciitis); in other cases group A -haemolitic Streptoccoccus is the organism responsible for the infection (Type II Necrotizing Fasciitis). The infection often originates from small traumatic injuries or operative wounds and rapidly spreads especially in individuals with identifiable risk factors or immunocompromised patients. Sometimes necrotizing fasciitis occurs when no known portal of entry for bacteria is present. The increasing incidence of necrotizing fasciitis observed may reflect a resurgence of highly virulent mutant strains of group A beta-haemolitic Streptococcus. The pathogenesis, clinical features and treatment of the disease have been reviewed in the light of recent literature. We also report clinical data for four patients with necrotizing fasciitis. They show the importance of early diagnosis and rapid, aggressive and radical surgical intervention. High-dose broad-spectrum antibiotic therapy and intensive medical support are also required to avoid a fatal outcome.

Biphasic and dose-dependent accumulation of INSP3 in Trypanosoma cruzi stimulated by a synthetic peptide carrying a chicken alpha D-globin fragment.

A synthetic peptide corresponding to residues 1 to 40 of chicken alpha D-globin stimulated the accumulation of inositol phosphates (InsPs) in Trypanosoma cruzi epimastigotes. This accumulation was shown to be biphasic and dose-dependent. The enhanced inositol trisphosphate (InsP3) accumulation occurred at the third minute with a subsequent increase which is not transient, but sustained over a much longer period. Another peptide carrying residues 35 to 73 was less active. These results evidenced the activation of the phosphoinositide phospholipase C activity in response to peptides that bind specifically to T. cruzi epimastigote cells.

Binding of nicotinic ligands to and nicotine-induced calcium signaling in Trypanosoma cruzi.

This work provides evidence that nicotine (1 x 10(-5) M) can cause changes in the intracellular calcium concentration of Trypanosoma cruzi epimastigotes, which can be blocked by alpha-bungarotoxin but not by atropine. Moreover, parasite membranes also bind such nicotinic acetylcholine receptor antagonist as well as agonists such as carbamylcholine (IC(50): 7.6 x 10(-7) M) and nicotine (IC(50): 1 x 10(-7) M). Results suggest that there is a molecular species in the surface of the parasite able to bind nicotinic ligands; therefore, nicotine interaction could lead to the activation of the mechanisms involved in intracellular calcium concentration increase in the parasite.

Carbachol stimulates inositol phosphate formation transiently in Trypanosoma cruzi.

The effect of carbachol on Trypanosoma cruzi epimastigote forms was studied. Suspension of epimastigote cells prelabelled with myo[3H]-inositol were incubated at 28 degrees C in the presence of carbachol. The levels of inositol phosphate after the challenge of carbachol were determined to see if the accumulation of inositol phosphate was time-dependent. In the presence of Li+ the levels of IP3 and IP4 were significantly increased during the 3 min. with a peak at 1 min. after the carbachol challenge. This effect was suppressed by atropine. The results show that carbachol influences rapid changes in phosphoinositide metabolism and they are time-dependent involving second-messenger systems associated with the generation of IP3. In addition they would suggest that this IP3 generation is through a receptor-mediated process linked to phospholipase C by a G-protein.

[False positive reactions to the fluorescence test (FTA-ABS) in skin disease patients]. / False reazioni positive al test di fluorescenza (FTA-ABS) in dermopazienti.

False positive reactions to the fluorescence test (FTA-ABS) were found in a group of dermatological patients compared to another group, made up of healthy subjects and blood-donors. Reactivity to FTA-ABS test was particularly evident in patients suffering from Herpes simplex genitalis, allergic diseases and collagenoses. Practical and theoretical aspects of this finding are discussed.