lpsilaterally and contralaterally recorded auditory brain stem responses to 80 dB nHL clicks were recorded from 37 infants, aged 2 weeks to 20 mo and from six adults, all with normal auditory function. With increasing age, contralateral waves A, B, C, and D and ipsilateral waves 111 and V decreased in latency, with the contralateral morphology more closely resembling the ipsilateral morphology as age increased, especially after the age of 9 mo. The mean latencies and their change with age for waves A and B resembled those of ipsilateral waves 111 and Ill', respectively; both waves C and D demonstrated similarities with wave V. Large waveform changes were seen with maturation in the latency region of contralateral waves C and D. In 42 of 43 subjects, wave V latency occurred after wave C and before wave D. Peak to peak amplitudes of contralateral waves A-B and D-E' increased with age, but were smaller than those of ipsilateral 1'-111 and V-V', respectively. The smaller contralateral responses make their use for threshold estimation problematic, especially before the age of 9 months. The contralateral response, however, may help to select wave V in ambiguous cases, and to determine response laterality (Ear Hear 12 3: 167-173).
Streptococcus agalactiae
is well known to be a potential etiology of bacterial meningitis in neonates. Invasive
S. agalactiae
has been also reported in nonpregnant adults. Among adults, the incidence of invasive group B Streptococcus (GBS) has been increasing 2–4 times in the past 2 decades. Chronic medical disease was suspected to increase the susceptibility for invasive GBS, especially diabetes mellitus. There was only one case reported to have GBS meningitis from acute otitis media infection in otherwise healthy individual. Hereby, we are reporting the second invasive GBS meningitis from acute otitis media infection with mastoiditis.
Angiotensin converting enzyme inhibitors (ACE-Is) have long been associated with angioedema and cough. These complications are thought to be related to an increase in bradykinin levels. Angiotensin receptor blockers (ARBs) such as losartan, however, are not known to increase bradykinin levels and, therefore, this complication is not as widely recognized. However, there is a significant proportion of patients who develop angioedema on ARB medications after previous episodes of angioedema on ACE-I. Though there is increasing literature to support that the patients may develop angioedema while taking ARBs such as losartan, a dose-dependent nature has not been well documented. We present a patient with a 20-year history of losartan use who developed angioedema suddenly after an increase in dosage. A dose-dependent relationship between ARBs and angioedema has not been well documented and this is the first documented case of angioedema presenting in a dose-dependent manner with losartan use. We hope that our case will bring awareness to the potential dose-dependent relationship between losartan and angioedema in order to aid clinicians when titrating ARB medications in order to expediently diagnose the fatal side-effect of angioedema and to encourage further research.
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