Although the occurrence of a seizure in a child without a provocative stimulus such as high fever is often considered a harbinger of a chronic seizure disorder or epilepsy, less than half of these children go on to develop a 2nd seizure. A careful history is warranted to ascertain a potential family history of epilepsy, a prior neurologic disorder, or history of seizure with fever, which may increase the likelihood of recurrence. Laboratory testing of serum electrolytes, toxicology screening, or urine and serum metabolic testing should be chosen based on individual clinical circumstances rather than on a routine basis. Serum glucose should be evaluated with the 1st afebrile seizure. In the child with a 1st nonfebrile seizure, a lumbar puncture is of limited value and should be used primarily when there is concern about possible meningitis, encephalitis, sepsis, subarachnoid hemorrhage, or a demyelinating disorder. An EEG is recommended as part of the neurodiagnostic evaluation of the child with an apparent 1st unprovoked seizure because it is useful for diagnosis of the event, prediction of recurrence risk, and identification of specific focal abnormalities and/or epileptic syndromes. Neuroimaging is generally not recommended after a 1st unprovoked seizure unless there is an indication for it on neurologic examination (focal neurologic deficits). If it is obtained, however, MRI of the brain is recommended over CT scanning. Anticonvulsant medication is generally not recommended after a single seizure. MRI may also be indicated in infants and adolescents with their 1st seizure
RECURRENT SEIZURES.
Two unprovoked seizures >24 hr apart suggest the presence of an epileptic disorder within the brain that will lead to future recurrences. It is important to perform a careful evaluation to look for the cause of the seizures as well as to assess the need for treatment with antiepileptic drugs and estimate the potential for response to treatment and remission of seizures in the future.
The history can provide important information about the type of seizures. Some parents can precisely act out or recreate a seizure. Children who have a propensity to develop epilepsy may experience the 1st convulsion in association with a viral illness or a low-grade fever. Seizures that occur during the early morning hours or with drowsiness, particularly during the initial phase of sleep, are common in childhood epilepsy. In retrospect, irritability, mood swings, headache, and subtle personality changes may precede a seizure by several days. Some parents can accurately predict the timing of the next seizure on the basis of changes in the child's disposition. The physical portrayal of the convulsion by the parent or caregiver is often surprisingly similar to the actual convulsion and is much more accurate than the verbal description
CLASSIFICATION OF SEIZURES.
It is important to classify the type of seizure ( Table 593-2 ). The seizure type may provide a clue to the cause of the seizure disorder. Precise delineation of the seizure may allow a firm basis for making a prognosis and choosing the most appropriate treatment. Anticonvulsants may readily control generalized tonic-clonic epilepsy in a child, but a patient with multiple seizure types or partial seizures may fare less well with the same type of therapy. Infants with benign myoclonic epilepsy have a more favorable outlook than patients with infantile spasms. Similarly, a school-aged child who has benign partial epilepsy with centrotemporal spikes (rolandic epilepsy) has an excellent prognosis and is unlikely to require a prolonged course of anticonvulsants. Clinical classification of seizures may be difficult because the manifestations of different seizure types may be similar. The clinical features of a child with absence seizures may be almost identical to those of another patient with complex partial epilepsy. An EEG is a useful adjunct to the classification of epilepsy because of the variability of seizure expressivity in this age group
TABLE 593-2 -- International Classification of Epileptic Seizures
PARTIAL SEIZURES
Simple partial (consciousness retained)
Motor
Sensory
Autonomic
Psychic
Complex partial (consciousness impaired)
Simple partial, followed by impaired consciousness
Consciousness impaired at onset
Partial seizures with secondary generalization
GENERALIZED SEIZURES
Absences
Typical
Atypical
Generalized tonic-clonic
Tonic
Clonic
Myoclonic
Atonic
Infantile spasms
UNCLASSIFIED SEIZURES
2.1. A seizure is considered generalized when clinical
symptomatology provides no indication of an
anatomic localization and no clinical evidence of
focal onset. When possible, three main seizure subtypes
may be categorized:
Generalized convulsive seizures with predominantly
tonic, clonic, or tonicoclonic features
Generalized nonconvulsive seizures represented
by absence seizures
Myoclonic seizures
In patients who have experienced several types
of generalized seizure each seizure type must be
categorized.
2.2. A seizure should be classified as partial when
there is evidence of a clinical partial onset, regardless
of whether the seizure is secondarily generalized.
The first clinical signs of a seizure, designated
for too long by the misleading term of “aura,” have
a highly localizing value and result from the anatomic
or functional neuronal activation of part of
one hemisphere.
When alertness and ability to interact appropriately
with the environment is maintained, the seizure
is classified as a simple partial seizure.
When impairment of consciousness, amnesia, or
confusion during or after a seizure is reported, the
seizure is classified as a complex partial seizure.
When the distinction between simple and complex
partial seizure cannot be made, from information
provided by history or medical records, the
seizure is classified as partial epileptic seizure of
unknown type.
When a patient has several types of partial seizure,
each should be separately categorized.
When a seizure becomes secondarily generalized,
the seizure is classified as partial seizure, secondarily
generalized (simple or complex).
miércoles, 16 de junio de 2010
lunes, 14 de junio de 2010
Idiopathic Short Stature - Williams and NEJM Review
IGF deficiency: GH deficiency
a deficiency of IGF levels and concomitant alterations in serum concentrations of IGFBPs suggests an abnormality of GH secretion or activity and makes necessary a thorough evaluation of hypothalamic-pituitary-IGF function.
Thus, even in children below the 5th percentile in height (which, obviously, applies to 5% of the normal population), documentation of a normal height velocity (above the 25th percentile for several years) makes the diagnosis of IGF deficiency and GHD highly unlikely.
Stimulation tests have often been divided into “screening tests” (exercise, fasting, levodopa, clonidine), which are characterized by ease of administration, low toxicity, low risk, and low specificity) and “definitive tests” (arginine, insulin, glucagon).
It is generally accepted that a child must “fail” provocative tests with at least two separate stimuli to be considered as having GHD.
Despite the many problems with GH measurements described above, there continues to be a value in determination of GH secretory capacity in the diagnostic evaluation of a child with IGF deficiency. Documentation of normal (or increased) GH levels is necessary in discriminating between primary and secondary IGF deficiency. The documented presence of GH deficiency should alert the clinician to the possibility of other pituitary deficiencies.
An alternative means of diagnosing GHD is the assessment of IGF-I and -II and their binding proteins. [261] [262] [264] [290] GHD then becomes part of the differential diagnosis of IGF deficiency, which includes hypothalamic dysfunction, pituitary insufficiency, and GHI. With the development of sensitive and specific assays for IGF-I, IGF-II, and the IGFBPs, it has become clear that these peptides accurately reflect integrated GH status of pediatric patients. Furthermore, IGF-I and -II normally circulate in serum in sufficiently high levels that assay sensitivity is not an issue. Serum levels of both peptides are relatively constant during the day so that provocative testing or multiple sampling is not necessary. Even when these caveats are considered, the correlation between serum IGF-I levels and provocative or spontaneous GH measurements is imperfect. In a group of children younger than 10 years of age, IGF-I levels were below -2 SD in only 8/15 children with a diagnosis of GHD based upon provocative testing (53.3% sensitivity), and normal in 47/48 children with a normal GH response (97.9% specificity).[
The utility of IGFBP-3 assays in the diagnosis of GHD was evaluated by Blum and colleagues,[488] who found that serum IGFBP-3 levels were below the 5th percentile for age in 128/132 of children (97%) diagnosed with GHD by conventional criteria (height less than 3rd percentile, height velocity less than 10th percentile, and peak serum GH less than 10 μg/L.
Recommendations by the GH Research Society (GRS)[1276] for defining GHD recognize no “gold standard” for that diagnosis and propose that in a child with slow growth, whose history and auxology suggest GHD ( Table 23-9 ), testing for GH/IGF-I deficiency requires the measurement of IGF-I and IGFBP-3 levels as well as GH provocation tests (after hypothyroidism has been excluded).
Some patients with auxology suggestive of GHD, however, may have IGF-I and/or IGFBP-3 levels below the normal range on repeated tests but GH responses in provocation tests above the “cutoff” level. Such children do not have classical GHD but nonetheless may have an abnormality of the GH-IGF axis and, after the exclusion of systemic disorders affecting the synthesis or action of IGF-I, could be considered for GH treatment.
TABLE 23-9 -- KEY HISTORY AND PHYSICAL EXAMINATION FINDINGS THAT MAY INDICATE THAT GROWTH HORMONE DEFICIENCY COULD BE PRESENT (THE GRS 2000 CRITERIA[1276])
|
Children with Turner's syndrome and short stature should not be required to undergo GH testing to qualify for GH therapy, because such treatment is not predicated on abnormal GH secretion.
The diagnosis of GHD in a newborn is especially challenging. The presence of micropenis in a male newborn should always lead to an evaluation of the GH-IGF axis
There remains a large cadre of short children in whom the cause of their diminished stature is unknown or “idiopathic.” Many children and early adolescents are short (<3rd>. Such children usually have normal GH secretory dynamics, although provocative tests may be blunted under some circumstances. GH-dependent peptides are frequently (but not invariably) lower than expected on a chronologic though often not skeletal age basis. Treatment with exogenous GH usually augments linear growth. These children have often been considered variants of normal growth and, if untreated, may achieve a final adult height within the range considered acceptable for the family. It should be noted, however, that many of these children are as short as those with GHD and so cannot simply be considered “normal, short children.” The etiology of the slowed childhood growth and frequently delayed pubertal spurt has not been established in most of these children. As this is the largest group of short children, continuing efforts are underway to develop a rational categorization and to develop the means of defining these children within the possible abnormalities of the GH-IGF axis. Multiple groups of patients are included in this broad category, including those with constitutional delay of growth and maturation and so-called genetic or familial short stature. The genetic characterization of the former syndrome, with an emphasis upon the timing and tempo of pubertal onset and progression, is beyond the scope of this chapter. Familial short stature, while not usually in the range of the dramatic genetic syndromes resulting in extremely poor growth described above, generally results in an adult whose height is close to or below the bottom of the normal range, but appropriate for family. It must be noted that this should not be considered totally reassuring, because there is growing recognition of subtle genetic defects contributing to growth failure and masquerading as “benign” familial short stature. ISS is the remaining large but uncharacterized group of children. These children presumably have more subtle disorders of the hypothalamic-pituitary-IGF axis [907] [928] than those described in the discussion of primary IGFD (see Table 23-10 ). Heterozygous mutations throughout the growth system, a relatively greater preponderance of blockers of the GH-signaling cascade, such as enhanced intracellular phosphatase activity and production of such signaling factors as SOC2 and CIS, and gene-mediated alterations in patterns of GH or IGF production await to be described.
The term constitutional delay [1285] [1286] describes children with a normal variant of maturational tempo characterized by short stature but relatively normal growth rates during childhood, delayed puberty with a late and attenuated pubertal growth spurt, and attainment of normal adult height. Most children with constitutional delay begin to deviate from the normal growth curve during the early years of life and by age 2 years are at or slightly below the 5th percentile for height.[1287] During midchildhood years, height SDS may gradually drift lower, but this does not appear to affect adult height outcome.
Final height, though usually within the normal population range, is often in the lower part of the parental height target zone, [1289] [1290] [1291] with few patients exceeding that target height. The predicted final height, especially when the skeletal age is extremely delayed, is greater than that usually achieved, but is difficult to reliably anticípate.
TABLE 23-11 -- CRITERIA FOR PRESUMPTIVE DIAGNOSIS OF CONSTITUTIONAL DELAY OF GROWTH AND MATURATION
|
Genetic (Familial) Short Stature
Nonetheless, a constellation of clinical findings describes a normal variant referred to as genetic short stature (GSS) (or familial short stature) that differs from the syndrome of constitutional delay of growth and maturation discussed above. In GSS, childhood growth is at or below the 5th percentile, but the velocity is generally normal. The onset and progression of puberty are normal or even slightly early and more rapid than normal so that skeletal age is concordant with chronologic age. Parental height is short (both parents are often below the 10th percentile) and pubertal maturation is normal. Final heights in these individuals are short and in the target zone for the family.[1291] The GH-IGF system is normal, but exogenous GH therapy during middle childhood years may increase linear growth velocity substantially without disproportionate augmentation of skeletal maturation. Whether long-term GH treatment enhances final height outcome, however, is not clear.
Growth hormone in idiopatic short stature
Growth Hormone Therapy
Gains in Height
Available data suggest that growth hormone therapy increases adult height between 3 and 6 cm in children with idiopathic short stature, but such growth requires long-term therapy. In studies demonstrating the efficacy of growth hormone therapy for this indication, the mean duration of therapy was four to seven years.6,8,9,29 A meta-analysis of the efficacy of growth hormone
therapy in children with idiopathic short stature identified only four controlled studies and six uncontrolled studies with data regarding adult height.6 After growth hormone therapy (at doses
of 0.25 to 0.40 mg per kilogram of body weight per week) or observation for a mean of 5.3 years
in 118 patients in controlled studies, the adult height in the group that was treated with growth
hormone was 5 to 6 cm greater than that of the untreated controls and 3.6 to 4.6 cm greater than the height predicted at baseline. In the eight uncontrolled studies with data regarding adult height for 246 patients, growth hormone treatment (at a dose of 0.14 to 0.33 mg per kilogram per week) for a mean of 4.7 years resulted in a gain of 3.8 to 4.5 cm in adult height above the height predicted at baseline. Higher doses of growth hormone may confer a greater benefit. A European study compared adult heights of 17 patients treated with growth hormone that was administered six times a week at a mean dose of 0.37 mg per kilogram per week for 7.0 years to that of 17 patients treated with a dose of 0.24 mg per kilogram per week for 6.1 years.9 In comparison with their baseline predicted adult height, the children who were treated with
the higher dose had a significantly greater gain in adult height (7.2 cm, as compared with 5.4 cm for the group that received a lower dose). Moreover, daily administration of growth hormone has been shown to be more efficacious than administration three times per week.
A recent economic analysis, based on the approved dosing guidelines and published efficacy data regarding adult height, calculated that the current cost of growth hormone therapy for five years is $52,000 per incremental inch of height gained.50 Because of the exorbitant cost and the large number of children whose height falls below the 1.2 percentile who theoretically qualify for therapy, the use of growth hormone in idiopathic short stature generates questions about the equitable distribution of health care resources and the economic effect on the health care system
domingo, 13 de junio de 2010
HEMANGIOMAS
Clues:
The 95% porcent involve at 9 years
If the aspect is not benign, or if it's ulcerated: prednisolone 2-3mg/kg/day
If it's something abnormal in the clinical review, emphasize with more studies.
Hemangiomas are proliferative hamartomas of vascular endothelium that may be present at birth or, more commonly, become apparent in the 1st 2 mo of life, predictably enlarge, and then spontaneously involute. Hemangiomas are the most common tumor of infancy, occurring in 1–2% of newborns and 10% of white infants in the 1st yr of life.
Girls are affected more often than boys. Favored sites are the face, scalp, back, and anterior chest.
The lesions are cystic, firm, or compressible, and the overlying skin may appear normal in color or have a bluish hue.
Hemangiomas undergo a phase of rapid expansion, followed by a stationary period and finally by spontaneous involution.
Regression may be anticipated when the lesion develops blanched or pale gray areas that indicate fibrosis. The course of a particular lesion is unpredictable, but ≈60% of these lesions reach maximal involution by 5 yr of age, with 90–95% by age 9.
Hemangiomas in a “beard” distribution may be associated with upper airway or subglottic involvement.
In the usual patient who has no serious complications or extensive growth that results in tissue destruction and severe disfigurement, treatment consists of expectant observation. Because almost all lesions regress spontaneously, therapy is rarely indicated and may cause further harm.
In the rare case in which intervention is required, if the lesion is very superficial, early therapy with PDL may be beneficial in decreasing growth of the hemangioma. PDL is also useful for the treatment of small (<4–5>
Syndromes associated with hemangiomas include PHACES (posterior fossa defects such as Dandy-Walker malformation or cerebellar hypoplasia, large plaquelike facial hemangioma, arterial abnormalities such as aneurysms and stroke, coarctation of the aorta, eye abnormalities, and sternal raphe defects such as pits or scars)
ACNE - NEJM REVIEW
Clues:
In mild Acne: benzoyl peroxide (2.5-5%) plus (clindamicine or adapalene) in topical use twice daily
In moderate acne: benzoyl peroxide plus oral Doxicicline 100mg twice daily
In severe Acne: Isotretinoine 40 mg once dailyplus oral doxicicline 100mg twice daily (if it's women, add hormonal therapy)
Acne is a follicular disease, the principal abnormality of which is impaction and distention
of the pilosebaceous unit. The cause of the hyperproliferation of keratinocytes
and the abnormalities of differentiation and desquamation are unknown. It is likely that
hyperresponsiveness to the stimulation of sebocytes and follicular keratinocytes by
androgens leads to the hyperplasia of the sebaceous glands and the seborrhea that
characterize acne.
7-9
Propionibacterium acnes colonizes the follicular duct and proliferates in teenagers with
acne.10
This organism probably contributes to the development of inflammation. With
this combination of factors present, the follicular epithelium is invaded by lymphocytes;
it ruptures, and sebum, microorganisms, and keratin are released into the dermis.
Neutrophils, lymphocytes, and foreign-body giant cells accumulate and produce the
erythematous papules, pustules, and nodular swellings characteristic of inflammatory
acne
The diagnosis of acne is usually readily made. Acne is characterized by open and closed
comedones (blackheads and whiteheads), which are present either alone or, more
commonly, with pustules and erythematous papules concentrated on the face and
upper trunk. Many systems for grading the severity of disease have been used. The severity
of acne is generally assessed by the number, type, and distribution of lesions.
For the mild, primarily comedonal, types of acne (Fig. 1), topical retinoids may be used alone, where as for patients with more severe acne, the use of these products in combination with topical or oral antimicrobial agents is appropriate. Randomized, double-blind, multicenter comparative studies have shown a reduction of 38 to 71 percent in noninflammatory and inflammatory lesion counts. Direct comparisons of topical retinoids have indicated that tazarotene in a 0.1 percent gel is more efficacious than 0.1 percent tretinoin or 0.1 percent adapalene, 14,15 although tazarotene also tends to be the most irritating. The maximum therapeutic response to topical retinoids occurs over approximately 12 weeks.
Antimicrobials
Topical antimicrobial agents are effective in the treatment of inflammatory disease.
24 Benzoyl peroxide is a bactericide and is an excellent first-line
medication. The response to this agent is rapid, with improvement noted as early as five days after treatment has begun, but irritation is common. Water-based products, as compared with alcoholbased products, when used at low peroxide concentrations (2.5 to 5 percent) will help to limit this problem and have an efficacy similar to that of other products in this class. Topical clindamycin or erythromycin also may be useful, but, as documented in many randomized,
clinical trials, these agents are most effective when used in combination with benzoyl peroxide or
topical retinoids
Oral Antibiotics
Oral antibiotics are indicated for moderate-tosevere disease, for the treatment of acne on the
chest, back, or shoulders, and in patients with inflammatory disease in whom topical combinations have failed or are not tolerated.
When oral therapy is warranted, tetracycline is inexpensive and often effective in previously untreated cases. Clinical experience and limited data have suggested that doxycycline, minocycline, and trimethoprim– sulfamethoxazole are more effective than tetracycline.
Doxycyline and minocycline are both preferred over trimethoprim–sulfamethoxazole
because of the side-effect profile.
Starting the therapy at higher doses is recommended, since the response cannot be judged for at
least six weeks and full efficacy is not apparent for three months.
Oral antibiotic therapy generally is taken over a three-to-six-month course. Eventual discontinuance is the goal, followed by long-term topical therapy. Resistance is an increasing problem, since 60 percent of P. acnes isolates are resistant to at least one antibiotic; resistance is most common with the use of erythyromycin (50 percent of cases), clindamycin (35 percent), and tetracycline (25 percent). Tetracyclineresistant strains of P. acnes are usually also resistant
to doxycycline, so a switch to minocycline is recommended if resistance to tetracycline is suspected.
Therapy with oral contraceptives containing estrogen or with spironolactone, an androgen antagonist, is often useful in women with hyperandrogenism and in women with normal serum androgen levels. The effects on acne of injectable progestins and patch systems have not been evaluated, and progesterone-only contraceptives may make acne worse.
deep-seated nodules of the lower face and neck (Fig. 6) are part of a subset of patients in whom
hormonal treatment may be especially useful.
Patients with severe acne that does not clear with combined oral and topical therapy are candidates for treatment with oral isotretinoin Approximately 40 percent of patients remain free
of acne after one course of treatment, 40 percent have a recurrence of low severity that responds to medications to which the acne had previously been resistant, and 20 percent will need repeated treatment with isotretinoin at a future time.
Patients younger than 16 years, those with severe acne on the trunk, and adult women are more likely than others to have a relapse. The chance of a prolonged remission is greater when a total dose of 120 to 150 mg per kilogram of body weight is achieved.
Most patients can be started on 20 to 40 mg per day, with an increase
to 40 to 80 mg over several months. Isotretinoin is teratogenic, so it must be used with hormonal therapy. Isotretinoin may cause hypertriglyceridemia and, to a lesser extent, can affect cholesterol levels. Alterations in dosing or dietary interventions usually allow for the continuation of treatment. Drying of the nasal mucosa may occur, which can lead to colonization
of S. aureus , the potential complications of which include abscesses, conjunctivitis, impetigo,
cellulitis, and folliculitis. These complications may be prevented with the use of intranasal bacitracin
In mild Acne: benzoyl peroxide (2.5-5%) plus (clindamicine or adapalene) in topical use twice daily
In moderate acne: benzoyl peroxide plus oral Doxicicline 100mg twice daily
In severe Acne: Isotretinoine 40 mg once dailyplus oral doxicicline 100mg twice daily (if it's women, add hormonal therapy)
Acne is a follicular disease, the principal abnormality of which is impaction and distention
of the pilosebaceous unit. The cause of the hyperproliferation of keratinocytes
and the abnormalities of differentiation and desquamation are unknown. It is likely that
hyperresponsiveness to the stimulation of sebocytes and follicular keratinocytes by
androgens leads to the hyperplasia of the sebaceous glands and the seborrhea that
characterize acne.
7-9
Propionibacterium acnes colonizes the follicular duct and proliferates in teenagers with
acne.10
This organism probably contributes to the development of inflammation. With
this combination of factors present, the follicular epithelium is invaded by lymphocytes;
it ruptures, and sebum, microorganisms, and keratin are released into the dermis.
Neutrophils, lymphocytes, and foreign-body giant cells accumulate and produce the
erythematous papules, pustules, and nodular swellings characteristic of inflammatory
acne
The diagnosis of acne is usually readily made. Acne is characterized by open and closed
comedones (blackheads and whiteheads), which are present either alone or, more
commonly, with pustules and erythematous papules concentrated on the face and
upper trunk. Many systems for grading the severity of disease have been used. The severity
of acne is generally assessed by the number, type, and distribution of lesions.
For the mild, primarily comedonal, types of acne (Fig. 1), topical retinoids may be used alone, where as for patients with more severe acne, the use of these products in combination with topical or oral antimicrobial agents is appropriate. Randomized, double-blind, multicenter comparative studies have shown a reduction of 38 to 71 percent in noninflammatory and inflammatory lesion counts. Direct comparisons of topical retinoids have indicated that tazarotene in a 0.1 percent gel is more efficacious than 0.1 percent tretinoin or 0.1 percent adapalene, 14,15 although tazarotene also tends to be the most irritating. The maximum therapeutic response to topical retinoids occurs over approximately 12 weeks.
Antimicrobials
Topical antimicrobial agents are effective in the treatment of inflammatory disease.
24 Benzoyl peroxide is a bactericide and is an excellent first-line
medication. The response to this agent is rapid, with improvement noted as early as five days after treatment has begun, but irritation is common. Water-based products, as compared with alcoholbased products, when used at low peroxide concentrations (2.5 to 5 percent) will help to limit this problem and have an efficacy similar to that of other products in this class. Topical clindamycin or erythromycin also may be useful, but, as documented in many randomized,
clinical trials, these agents are most effective when used in combination with benzoyl peroxide or
topical retinoids
Oral Antibiotics
Oral antibiotics are indicated for moderate-tosevere disease, for the treatment of acne on the
chest, back, or shoulders, and in patients with inflammatory disease in whom topical combinations have failed or are not tolerated.
When oral therapy is warranted, tetracycline is inexpensive and often effective in previously untreated cases. Clinical experience and limited data have suggested that doxycycline, minocycline, and trimethoprim– sulfamethoxazole are more effective than tetracycline.
Doxycyline and minocycline are both preferred over trimethoprim–sulfamethoxazole
because of the side-effect profile.
Starting the therapy at higher doses is recommended, since the response cannot be judged for at
least six weeks and full efficacy is not apparent for three months.
Oral antibiotic therapy generally is taken over a three-to-six-month course. Eventual discontinuance is the goal, followed by long-term topical therapy. Resistance is an increasing problem, since 60 percent of P. acnes isolates are resistant to at least one antibiotic; resistance is most common with the use of erythyromycin (50 percent of cases), clindamycin (35 percent), and tetracycline (25 percent). Tetracyclineresistant strains of P. acnes are usually also resistant
to doxycycline, so a switch to minocycline is recommended if resistance to tetracycline is suspected.
Therapy with oral contraceptives containing estrogen or with spironolactone, an androgen antagonist, is often useful in women with hyperandrogenism and in women with normal serum androgen levels. The effects on acne of injectable progestins and patch systems have not been evaluated, and progesterone-only contraceptives may make acne worse.
deep-seated nodules of the lower face and neck (Fig. 6) are part of a subset of patients in whom
hormonal treatment may be especially useful.
Patients with severe acne that does not clear with combined oral and topical therapy are candidates for treatment with oral isotretinoin Approximately 40 percent of patients remain free
of acne after one course of treatment, 40 percent have a recurrence of low severity that responds to medications to which the acne had previously been resistant, and 20 percent will need repeated treatment with isotretinoin at a future time.
Patients younger than 16 years, those with severe acne on the trunk, and adult women are more likely than others to have a relapse. The chance of a prolonged remission is greater when a total dose of 120 to 150 mg per kilogram of body weight is achieved.
Most patients can be started on 20 to 40 mg per day, with an increase
to 40 to 80 mg over several months. Isotretinoin is teratogenic, so it must be used with hormonal therapy. Isotretinoin may cause hypertriglyceridemia and, to a lesser extent, can affect cholesterol levels. Alterations in dosing or dietary interventions usually allow for the continuation of treatment. Drying of the nasal mucosa may occur, which can lead to colonization
of S. aureus , the potential complications of which include abscesses, conjunctivitis, impetigo,
cellulitis, and folliculitis. These complications may be prevented with the use of intranasal bacitracin
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