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The real problem in interpreting these data involves the techniques used to diagnose mycoplasma infections. PCR for children uses nasopharyngeal aspiration or nasal lavage fluid samples, and rates of positivity vary in children with asthma or pneumonia. This rate would probably be higher if the PCR were performed on bronchoalveolar lavage fluid samples, but it is difficult to routinely obtain such samples from children. All of the investigators who tested serologic samples obtained from children for the presence of M. pneumoniae report that, in 20% of patients, initial serum samples yield negative results, and only serum samples obtained 2–3 weeks after the initial onset of symptoms are positive for IgM [ 3 , 19 , 25 , 26 ]. PCR was positive for M. pneumoniae in only 12 (41%) of the 29 patients with positive serologic test results who underwent PCR. Hardy et al. [ 27 ] found that PCR of nasopharyngeal swab specimens that were obtained from children with community-acquired pneumonia and with serologic test results positive for M. pneumoniae were positive in only 9 (43%) of 21 children. Reliable serologic testing is therefore essential for this diagnosis; for that reason, the diagnosis of acute M. pneumoniae infection in our study was based solely on the presence of IgM and elevated levels of IgG and was not simply based on a positive PCR result. The different serologic techniques are not equivalent, but the kit used here gives fewer false-positive results than do the others [ 28 ]. Because we considered only the patients who were IgM positive and who clearly had elevated levels of IgG, it is highly probable that we accurately diagnosed the acute infections. In this series, the differences between the 3 groups of children in term of serologic testing for M. pneumoniae were very significant, and IgM was observed in only 5% of the children with stable asthma (whom we used as a control group). According to our data, mycoplasma infections play a major role in exacerbations of known asthma and in first asthma attacks.

The role of M. pneumoniae in inflammation and bronchial hyperreactivity has been observed clinically in adults [ 29 ] and has been demonstrated experimentally in animals. Hardy et al. [ 17 ] showed in a mouse model that acute mycoplasma infection increases bronchial resistance and elevates cytokine production. Similar experimental results were reported by Martin et al. [ 18 ] in mice that were first sensitized to ovalbumin and then exposed to the allergen before the experimental induction of infection. In other words, in mice at risk for asthma, M. pneumoniae caused serious bronchial events and increased airway resistance. The clinical data of the study we report here support these conclusions. The first asthma attacks during mycoplasma infection occurred largely among predisposed children with a personal or family history of allergy and with high levels of IgE, and this asthma recurred following the infection, especially when treatment did not control it. All the children who did not receive macrolides initially and were infected with mycoplasma had very serious new asthma attacks. Among the subjects with a first asthma attack, those with M. pneumoniae or C. pneumoniae infection differed significantly in one respect from the other patients: 30% of them had IgE levels of ⩾200 IU/mL, compared with 68% of the other patients ( P < .05), and 7% of them had atopic dermatitis, versus 55% of the other patients ( P < .05). Mycoplasma infection thus plays a major role in the inception of asthma.

Although word-finding is central to normal communication, word-finding difficulty should not be equated with aphasia. Problems with word-finding may develop in the setting of otherwise normal language as a result of a problem in another cognitive domain. A major goal of clinical assessment, therefore, is to decide whether word-finding difficulty reflects a primary language disorder, or whether the problem is secondary to other non-linguistic cognitive deficits. Primary word-finding difficulty may occur as an isolated language disturbance or may occur as part of a more extensive cognitive or behavioural syndrome. Secondary word-finding difficulty occurs when a deficit within another cognitive domain interferes with the function of a more or less intact language system. For example, a patient in whom failure to name household objects on bedside testing is accompanied by a failure to locate or correctly use the same items may have a primary visual perceptual problem, patients who participate less in conversations may be deaf, while difficulty remembering the names of acquaintances or in delivering messages may indicate a more general problem with episodic memory. Conversely, patients with a primary word-finding difficulty and their carers often describe their symptoms in terms of memory failure (they may say that they ‘forget’ the names of people or things) or a perceptual defect (impaired speech comprehension is not uncommonly ascribed to ‘deafness’ by the patient's family). It is also important to recognize the wide spectrum of normal variation in word-finding ability, and the potential effects of fatigue, anxiety or mood disorders. The evaluation of word-finding ability therefore requires both an objective assessment of performance, and an awareness of the wider context in which the problem has developed and its impact on the patient's daily life.

Obtaining an accurate history of word-finding difficulty ( Table 1 ) depends on interviewing both the patient and an informant who knows the patient well. A complaint of word-finding difficulty must be interpreted in light of a patient's premorbid verbal skills. Information about bilingualism (was English the first language, and if not, what level of competence was achieved?), educational attainment and literacy, occupation and any premorbid disabilities (such as developmental dyslexia) is essential. The family history may be relevant not only to the diagnosis in general but also to the interpretation of the word-finding problem in particular: an example is the emerging association of mutations in the progranulin gene with familial forms of progressive non-fluent aphasia (PNFA) (Cruts et al ., 2006 ; Mesulam et al ., 2007 ). Establishing the mode of onset and time course of the word-finding difficulty will assist in distinguishing acute processes (for example, stroke, encephalitis, delirium), chronic processes with static or fluctuating deficits (for example, head-injury or seizures) and chronic processes with progressive deficits (for example, a degenerative dementia). This information is particularly critical where the process leading to language breakdown has developed insidiously and there may be few other clinical clues to aetiology [for example, the interictal ‘pseudodementia’ of temporal lobe epilepsy: (Mayeux et al ., 1980 )]. The context in which the problem developed may be crucial. Whereas in acute disease processes, associated disturbances of alertness, perceptual and motor functions are often prominent (or may dominate the clinical presentation); in chronic disease processes, associated features may be subtle. However, the distinction between acute and chronic processes is not always clear. Patients who have sustained an acute event may present later with ongoing word-finding difficulty: accurate diagnosis then depends on establishing the degree of initial recovery and whether the word-finding deficit has evolved over time. Conversely, neurodegenerative disease can occasionally appear to present acutely following a particular event e.g. surgery (Larner, 2005 ). This may be secondary to a superimposed acute confusional state or due to the fact that mild word-finding or cognitive difficulties had previously gone unnoticed: the key to diagnosis here is to establish a background of more insidious or progressive difficulty prior to the acute presentation. The history often provides clues to the nature of the word-finding difficulty and associated cognitive, behavioural or neurological features which can then be explored systematically during the examination.

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Context:

Central precocious puberty (CPP) may have clinical implications in adulthood.

Objective:

To assess the prevalence of obesity, metabolic outcome (hyperlipidemia, diabetes, and hypertension), and malignancy rate of former CPP women between the third and fifth decades of life.

Design:

This was a case control study of a historical cohort using the computerized database of a health management organization.

Setting:

The setting was the Institute for Endocrinology and Diabetes, Schneider Children's Medical Center of Israel, and Clalit Health Services.

Participants:

The study group comprised of 142 CPP women aged 27–50 years [100 GnRH analog (GnRHa) treated; 42 untreated]. The control group comprised of 413 women randomly matched for age, year of birth, and community clinic (283 for the GnRHa treated; 130 for the untreated).

Methods:

Extracted from the database were demographic data, medical history, medications dispensed, recorded anthropometric measurements, vital signs, and laboratory data.

Results:

At young adulthood, body mass index (percentile and distribution) of treated and untreated former CPP women was comparable to that of their respective controls. Elevated body mass index at presentation was a risk factor for obesity in adulthood in the GnRHa-treated group (r = 0.257; P = .01). The prevalence of metabolic comorbidities (16 vs 13.4%; 21.4 vs 24.6%) and malignancy rate (1.0 vs 1.5%; 4.8 vs 1.5%) were similar in the former CPP women and their controls, with no significant difference between CPP groups.

Conclusion:

CPP (treated or untreated) is not associated with increased risk of obesity, metabolic derangements, or cancer morbidities in young adulthood. The finding that the health status of former CPP women is similar to that of the general population is reassuring.

Issue Section:

Central precocious puberty (CPP) in girls, defined as the appearance of secondary sex characteristics before the age of 8 years due to premature activation of the hypothalamic-pituitary-gonadal axis, is considered idiopathic for most girls ( 1 , 2 ). The goal of treatment in CPP is to prevent the unfavorable physical and emotional manifestations of premature sexual development. Since 1981, depot preparations of GnRH analogs (GnRHa) have been considered the drugs of choice for arresting pubertal progression ( 3 ). Numerous clinical trials confirmed the effectiveness and safety of these compounds in suppressing gonadal activation and the reversibility of suppression after discontinuation of treatment ( 4 ). Still, there are relatively few data on the implications of CPP on general health of former untreated and treated CPP girls in adulthood. Previous studies showed an association between early puberty or early age of menarche with higher body mass index (BMI), increased metabolic risk factors, and endocrine-related breast and reproductive tract cancers ( 5 9 ). However, these studies have limitations: the relatively small number of participants in each study, the lack of controls in most of the studies, and the rather short follow-up.

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