ObjectiveTo characterize the care flow and the primary diagnoses of an Adolescent Medicine Clinic.MethodsA retrospective descriptive study, with analysis of clinical processes of adolescents (10-18 years) seen at the Adolescent Medicine Clinic, from January 2006 to December 2013. The following variables were analyzed: sex, age, number of visits, referring service and primary diagnoses according to the International Statistical Classification of Diseases and Related Health Problems. As to the variable age, the adolescents were divided into two groups: Group I comprised those aged 10-14 years, and Group II, 15-18 years.ResultsA total of 7,692 visits were carried out, in that, 1,659 first visits (22%), with an annual growth rate of 6%. The mean age was 14.2 years, and 55% of patients were female. The group of endocrine, nutritional and metabolic diseases was the most representative in our sample (34%), with obesity being the most frequent diagnosis in both sexes and age groups (23%), with a higher prevalence in males (13% male versus 10% female, p<0.001) and younger adolescents (18% in Group I versus 5% in Group II p<0.001). The group of mental and behavioral disorders was the second most prevalent (32%), affecting mainly females (39% female versus 22% male, p<0.001) and the older age group (39% Group II versus 27% Group I, p<0.001). Social problems were the primary diagnosis in 8% of visits.ConclusionMost diseases diagnosed have a strong behavioral and social component, particularly mental disorders and obesity. This specific type of diagnoses reinforces the need for a global approach for adolescents and specialized adolescent medicine units/clinics.

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Maturity Onset Diabetes of the Young (MODY) includes a clinically and genetically heterogeneous group of diabetes subtypes with MODY-2 being the second most prevalent form. We report 2 cases of MODY-2 identified during the investigation of asymptomatic hyperglycemia. A 12-year-old girl with a familiar history of diabetes (mother, maternal aunt, and maternal grandfather) was referred due to hypercholesterolemia, abnormal fasting glucose (114 mg/dL), and increased levels of glycated haemoglobin (HbA1c) (6%) presenting with negative β-cell antibodies. A glucokinase (GCK) heterozygous missense mutation c.364C>T (p.Leu122Phe) in exon 4 was identified in the index patient and in the 3 family members. An obese 9-year-old boy was investigated for elevated fasting glycemic levels (99–126 mg/dL), HbA1c rise (6.6%–7.6%), and negative β-cell antibodies. The patient’s father, paternal aunt, and paternal grandfather had a history of diabetes during their childhood. A GCK heterozygous missense mutation c.698G>A (p.Cys233Tyr) in exon 7 was identified in the index patient. This variant was only described in another family strongly affected by both MODY and classic autoimmune mediated diabetes, contrary to our case. MODY-2 should be suspected in the presence of early onset of persistent mild fasting hyperglycemia and negative β-cell antibodies associated with a positive family history of diabetes. These cases illustrate the challenging aspects of MODY diagnosis due to possible phenotypic overlap with other types of diabetes. The diagnosis requires a high level of suspicion and GCK genetic screening should be performed in the presence of compatible features. An early diagnosis allows for appropriate management, genetic counselling, and the identification of affected family members.

A 4-year-old boy, previously healthy, had a 7-month history of a lesion on his face. He also had left-sided cervical adenopathy, with a diameter of 3.5 × 2.5 cm, which was not painful nor adherent to the overlying skin. Despite several courses of antibiotic therapy (erythromycin, amoxicillin-clavulanic acid, and cefaclor), there was no improvement. Surgical drainage of the lymphadenitis, undertaken after 14 days of illness, led to a chronic draining fistulous tract. Subsequently, he presented with 2 skin lesions, the largest being 2.5 × 2.5 cm (Figure). Tuberculin skin test was positive with an induration of 25 mm. Lymph node biopsy showed granulomatous inflammation and caseation necrosis. The exudate culture was positive for Mycobacterium tuberculosis. Radiography of the chest, computed tomography of the chest, and laboratory results were all normal. Serologic testing for the human immunodeficiency virus was negative. A 75-yearold relative with pulmonary tuberculosis was identified as the source of contagion, which had occurred approximately 6 weeks before clinical onset.Following completion of a 2-month course of isoniazid, rifampin, and pyrazinamide followed by isoniazid and rifampin for 4 months, there was a gradual improvement of all lesions. Five years later, the patient was noted to have only a residual scar of the tuberculous adenopathy.Scrofula, the popular name for cervical tuberculous lymphadenitis (CTA), is the most frequent presentation of extrapulmonary tuberculosis in childhood 1,2 but is rare in developed countries. 3 It seems to occur as a result of previous infection involving the Waldeyer ring. 1 Ulceration, fistula, or abscess formation are frequent complications of CTA. 1 Scrofula may cause a form of cutaneous tuberculosis called scrofuloderma, from contiguous spread of the infection, as seen in our case. 3,4 CTA and cutaneous tuberculosis often have delayed diagnosis, leading to serious morbidity. [2][3][4] Diagnosis is made through biopsy for histopathology examination with acid-fast bacilli smear and culture for Mycobacterium tuberculosis, which remains the gold standard. 1,4 Concurrent pulmonary tuberculosis must be excluded. 1,4 Incision of the adenopathy increases the risk for cutaneous fistulous tract. 2 Spontaneous healing, although possible, is rare and takes years to achieve. 3,4 Scrofula and scrofuloderma respond well to antimycobacterial regimens for tuberculosis and have a good prognosis. 4 ■

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