Disordered steroidogenesis due to cytochrome p450 oxidoreductase deficiency

Sleep-disordered breathing (SDB) in children could be resolved by adenotonsillectomy (T&A). However, incomplete results are often noted post-surgery. Because of this partial resolution, long-term follow-up is needed to monitor for reoccurrence of SDB, which may be diagnosed years later through reoccurrence of complaints or in some cases, through systematic investigations. Children undergoing T&A often have small upper airways. Genetics play a role in the fetal development of the skull, the skull base, and subsequently, the size of the upper airway. In non-syndromic children, specific genetic mutations are often unrecognized early in life and affect the craniofacial growth, altering functions such as suction, mastication, swallowing, and nasal breathing. These developmental and functional changes are associated with the development of SDB. Children without genetic mutations but with impairment of the above said functions also develop SDB. When applied early in life, techniques involved in the reeducation of these functions, such as myofunctional therapy, alter the craniofacial growth and the associated SDB. This occurs as a result of the continuous interaction between cartilages, bones and muscles involved in the growth of the base of the skull and the face. Recently collected data show the impact of the early changes in craniofacial growth patterns and how these changes lead to an impairment of the developmental functions and consequent persistence of SDB. The presence of nasal disuse and mouth breathing are abnormal functions that are easily amenable to treatment. Understanding the dynamics leading to the development of SDB and recognizing factors affecting the craniofacial growth and the resulting functional impairments, allows appropriate treatment planning which may or may not include T&A. Enlargement of lymphoid tissue may actually be a consequence as opposed to a cause of these initial dysfunctions.

Subjects who had an adenotonsillectomy, in comparison to controls, were more hyperactive on well-validated parent rating scales, inattentive on cognitive testing, sleepy on the Multiple Sleep Latency Test, and likely to have attention-deficit/hyperactivity disorder (as defined by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition) as judged by a child psychiatrist. In contrast, 1 year later, the 2 groups showed no significant differences in the same measures. Subjects who had an adenotonsillectomy had improved substantially in all measures, and control subjects improved in none. However, polysomnographic assessment of baseline SDB and its subsequent amelioration did not clearly predict either baseline neurobehavioral morbidity or improvement in any area other than sleepiness.

Enlarged tonsils and adenoids are a common cause for SDB. Surgical removal of the tonsils and adenoids (T&A) is generally considered the first line treatment for pediatric sleep disordered breathing if the symptoms are significant and the tonsils and adenoids are enlarged. Of the over 500,000 pediatric T&A procedures performed in the . each year, the majority are currently being done to treat sleep disordered breathing. Many children with sleep apnea show both short and long- term improvement in their sleep and behavior after T & A.

Not every child with snoring should undergo T&A as the procedure does have risks. Potential problems can include anesthesia or airway complications, bleeding, infection and problems with speech and swallowing.  If the SDB symptoms are mild or intermittent, academic performance and behavior is not an issue, the tonsils are small, or the child is near puberty (tonsils and adenoids often shrink at puberty), it may be recommended that a child with SDB be watched conservatively and treated surgically only if symptoms worsen.
 
Recent studies have shown that some children have persistent sleep disordered breathing after T & A. A post-operative PSG may be necessary after surgical intervention, especially in children with persistent symptoms or increased risk factors for persistent apnea after T & A such as obesity, craniofacial anomalies or neuromuscular problems. Additional treatments such as weight loss, the use of Continuous Positive Airway Pressure (CPAP) or additional surgical procedures may sometimes be required.

UARS can cause symptoms similar to those found in OSA, yet this syndrome is considerably different due to the absence of oxygen desaturation found during sleep studies. Upper airway resistance syndrome was a term first applied to patients who were found to have excessive daytime sleepiness without a clear cause on a multiple sleep latency test, which was further documented by an overnight polysomnogram. 18 These patients were often said to have idiopathic hypersomnia. After many of these patients were further tested with invasive polysomnography (including an esophageal balloon transducer and full pneumotachograph), they were found to have increased upper airway resistance. Resistance manifested as increased negative esophageal inspiratory pressure. 1

Disordered steroidogenesis due to cytochrome p450 oxidoreductase deficiency

disordered steroidogenesis due to cytochrome p450 oxidoreductase deficiency

UARS can cause symptoms similar to those found in OSA, yet this syndrome is considerably different due to the absence of oxygen desaturation found during sleep studies. Upper airway resistance syndrome was a term first applied to patients who were found to have excessive daytime sleepiness without a clear cause on a multiple sleep latency test, which was further documented by an overnight polysomnogram. 18 These patients were often said to have idiopathic hypersomnia. After many of these patients were further tested with invasive polysomnography (including an esophageal balloon transducer and full pneumotachograph), they were found to have increased upper airway resistance. Resistance manifested as increased negative esophageal inspiratory pressure. 1

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