Suppurative corneal ulceration in Bangladesh

Suppurative keratitis is an important preventable cause of blindness, particularly in the developing world. This study analyses 142 cases of suppurative keratitis referred to Chittagong Eye Infirmary, Bangladesh. Some 53.5% of cases were bacterial and 35.9% were fungal. The five most common pathogens were: Pseudomonas sp. 24%, Streptococcus pneumoniae 17%, Aspergillus sp. 13%, Fusarium sp. 7% and Curvularia sp. 6%. Gram stain and culture results were consistent in 62.6% of cases. Previous antibiotic treatment was a significant factor for failure of culture isolation and less so for Gram stain failure. On Gram stain, 55.9% of pseudomonal cases were missed, but only 2% of fungal cases were missed. Over all, Gram stain had a sensitivity of 62% and positive predictive value of 84% for bacterial cases, and 98% and 94% for fungal cases, respectively. Fungal ulcers were typically filamentous, but an antecedent history of trauma was not common. The most frequent injury was due to rice grains, but the inoculum appeared to be introduced during eye washing with contaminated water. Pseudomonal ulcers occurred most frequently in the monsoon season, and Fusarium cases were seen only in the hot, dry season.     

Mineral balance in adult men: effect of four refined fibers

Eleven men consumed a basal diet alone and with cellulose (Na-carboxymethylcellulose, locust bean gum, or karaya gum) added at 7.5 g fiber per 1000 calories for 4 wk each. Food, urine, and fecal composites were collected during the last 8 d of each feeding period. Bowel transit time was not significantly affected; however, total dry fecal weight was significantly increased after the refined fibers compared with that after the basal diet. Adding refined fibers to the basal diet did not significantly affect apparent mineral balance of calcium, magnesium, manganese, iron, copper, or zinc, with the exception of a negative mineral balance for manganese with carboxymethylcellulose. Karaya gum had a mean positive balance for all minerals tested. These results indicate that the hypocholesterolemic effect of the fibers that form gels occurs without compromising mineral balance in those subjects consuming Recommended Dietary Allowance levels of the minerals studied.     

Nonheme iron in sickle erythrocyte membranes: association with phospholipids and potential role in lipid peroxidation

Previous studies documented the abnormal association of heme and heme proteins with the sickle RBC membrane. We have now examined RBC ghosts and inside-out membranes (IOM) for the presence of nonheme iron as detected by its formation of a colored complex with ferrozine. Sickle ghosts have 33.8 +/- 18.2 nmol nonheme iron/mg membrane protein, and sickle IOM have 4.3 +/- 3.0 nmol/mg. In contrast, normal RBC ghosts and IOM have no detectable nonheme iron. The combination of heme and nonheme iron in sickle IOM averages nine times the amount of membrane- associated iron in normal IOM. Kinetics of the ferrozine reaction show that some of this nonheme iron on IOM reacts slowly and is probably in the form of ferritin, but most (72% +/- 18%) reacts rapidly and is in the form of some other biologic chelate. The latter iron compartment is removed by deferoxamine and by treatment of IOM with phospholipase D, which suggests that it represents an abnormal association of iron with polar head groups of aminophospholipids. The biologic feasibility of such a chelate was demonstrated by using an admixture of iron with model liposomes. Even in the presence of tenfold excess adenosine diphosphate, iron partitions readily into phosphatidylserine liposomes; there is no detectable association with phosphatidylcholine liposomes. To examine the bioavailability of membrane iron, we admixed membranes and t-butylhydroperoxide and found that sickle membranes show a tenfold greater peroxidation response than do normal membranes. This is not due simply to a deficiency of vitamin E, and this is profoundly inhibited by deferoxamine. Thus, while thiol oxidation in sickle membranes previously was shown to correlate with heme iron, the present data suggest that lipid peroxidation is related to nonheme iron. In control studies, we did not find this pathologic association of nonferritin, nonheme iron with IOM prepared from sickle trait, high-reticulocyte, postsplenectomy, or iron-overloaded individuals. These data provide additional support for the concept that iron decompartmentalization is a characteristic of sickle RBCs.     

Nerve conduction studies in adrenomyeloneuropathy.

OBJECTIVE--Adrenomyeloneuropathy (AMN) is an X linked metabolic disorder presenting with progressive spastic paraparesis in the third to fifth decade of life. Although peripheral neuropathy is also present in most patients, prominent pyramidal signs may make its clinical recognition difficult. The objective was to characterise the peripheral neuropathy in patients with AMN by nerve conduction studies. METHODS--Nerve conduction studies were performed in 99 men known to have AMN and in 38 heterozygous women, all of whom had neurological disabilities. RESULTS--Of the 13 variables obtained, at least one was abnormal in 82% of patients. The abnormalities were more common in men than in women (87% v 67%); in legs than in arms (77% v 38%); in motor than in sensory conduction (80% v 39%); and in latency (distal and F wave) and velocity compared with amplitude (80% v 29%). Twenty six patients had at least one nerve variable value in the demyelinating range. Four variables (sural velocity, peroneal amplitude, peroneal velocity, and peroneal F wave) were correlated with the expanded disability status scale; five variables (peroneal velocity, tibial H reflex, median distal latency, median conduction velocity, and median F wave latency) were correlated with serum very long chain fatty acids (VLCFAs); and two variables (sural amplitude and peroneal distal latency) were more likely to be abnormal in patients with normal adrenal function than in patients with Addison's disease. CONCLUSIONS--Nerve conduction studies in patients with AMN are often abnormal and suggest a mixture of axonal loss and multifocal demyelination. Their correlation with disability status and serum VLCFAs suggests that measures from nerve conduction studies may be useful in evaluating future treatments.