High blood pressure. Causes, symptoms, treatments

Mechanisms of action of mycophenolate mofetil in preventing acute and chronic allograft rejection.


Open-label, nonrandomized study.

A deceased-donor kidney transplant recipient developed purulent pericarditis caused by Nocardia despite trimethoprim-sulfamethoxazole (TMP-SMX) prophylaxis for Pneumocystis jirovecii. She was treated empirically with ceftriaxone and amikacin and subsequently underwent sternotomy with drainage of an intrapericardial abscess. Culture and susceptibility data demonstrated Nocardia farcinica, which was susceptible to SMX and amikacin, although resistant to ceftriaxone. Nocardia asteroides, the more common human pathogen, is generally susceptible to third-generation cephalosporins and TMP-SMX. N. farcinica is rare in the United States, more virulent and resistant than N. asteroides, and is more likely to cause disseminated disease. Successful therapy of disseminated Nocardia infections is dependent upon choice of appropriate empiric antibiotics in addition to surgical drainage of purulent fluid collections. TMP-SMX prophylaxis may not be sufficient to prevent infections due to Nocardia species in all immunosuppressed transplant recipients. Here, a rare complication of this unusual pathogen is discussed.

Trimethoprim-sulfamethoxazole (TMP-SMX) and nitrofurantoin were until recently the two drugs recommended in clinical guidelines in Israel for empiric treatment of uncomplicated urinary tract infection (UTI) in women.

A crystal nephropathy, characterized by serum creatinine elevation, loss of concentrating ability of the kidney, leukocyturia, and renal parenchymal image abnormalities, is a frequent complication of indinavir therapy. Identification of individuals at risk, particularly those with low body mass index or receiving TMP-SMX prophylaxis, may help the decision to initiate indinavir or chose an alternative protease inhibitor in order to minimize renal and urinary tract adverse events.

5 donkeys, 5 mules, and 3 horses.

Mice infected with Brucella melitensis were treated with streptomycin, co-trimoxazole, ciprofloxacin, doxycycline, and rifampin intraperitoneally and with ciprofloxacin, ofloxacin, pefloxacin, doxycycline, and rifampin orally for 14 to 21 days. Doxycycline- and rifampin-treated animals (either route) demonstrated a cure rate significantly better than that of controls. Longer therapy periods were associated with a significantly better outcome. Therapy failure was observed in all mice treated with ciprofloxacin, ofloxacin, and pefloxacin administered orally as well as in mice treated intraperitoneally with ciprofloxacin. Our findings demonstrate that treatment of experimental brucellosis in mice with doxycycline and rifampin yields therapeutic results that are superior to those yielded by treatment with quinolones.

To improve knowledge on the etiology of gastroenteritis and diarrhea in our patient population, stool specimens from 150 children under 5 years of age suffering from acute gastroenteritis were investigated for various common bacterial enteropathogens by conventional and molecular techniques.

Nocardiosis is an infectious actinomycetic disease with a variable clinical spectrum that makes it difficult to diagnose. It mainly affects immunosuppressed individuals. Advances in molecular genomic technology have helped in identifying new pathogenic Nocardia species. This has made identification of their specific antimicrobial sensitivity possible.

Without treatment, Pneumocystis carinii pneumonitis is almost always fatal in the immunocompromised host. Here, Walter Hughes discusses proven and potential treatments, and methods of chemoprophylaxis in high-risk patients. Two drugs, pentamidine isethionate and trimethoprimsulfamethoxazole, are equally effective therapeutically - permitting the recovery of approximately 75% of patients - but the latter drug combination is preferred because of its lower toxicity and fewer adverse effects. The pneumonitis can be prevented by prophylactic administration of trimethoprim-sulfamethoxazole. Other drugs with proven efficacy or under study include Fansidar, dapsone, trimetrexate and difluoromethylornithine.

Out of 134 RCTs identified in the search, 5 RCTs involving 287 patients were included in the analysis. There were no differences between patients with ABECB treated with SSPs and those treated with trimethoprim, alone or in combination with a sulfonamide, in treatment success (intention-to-treat patients: n = 262, odds ratio [OR] 1.68, 95% confidence interval [CI] 0.91-3.09; clinically evaluable patients: n = 246, OR 1.59, 95% CI 0.79-3.20) or number of drug-related adverse events in general (n = 186 patients, OR 0.37, 95% CI 0.11-1.24), frequency of diarrhea or skin rashes, or number of withdrawals due to adverse events (n = 179 patients, OR 0.27, 95% CI 0.07-1.03).

Atovaquone was compared to trimethoprim-sulfamethoxazole (TMP-SMZ) for the relationship of time receiving therapy, plasma drug concentrations, and incidence of adverse reactions in patients with AIDS-associated Pneumocystis carinii pneumonia. Treatment-limiting adverse events occurred in 9% of atovaquone-treated patients and 24% of TMP-SMZ-treated patients. Adverse events usually did not occur before day 7 for either treatment. Only the incidence of rash increased with increasing plasma concentrations of atovaquone. The incidence of anemia, neutropenia, and azotemia increased with increasing trimethoprim plasma concentration, while other adverse events (gastrointestinal disorders, rash, fever, and liver function abnormalities) were independent of plasma drug concentration.