Unrelieved upper airway obstruction from highly prevalent adenotonsillar hypertrophy (ATH) has the potential of producing structural remodelling of the pulmonary vascular bed with resultant pulmonary hypertension (PH) and cor pulmonale. This cross-sectional study aimed to determine the local prevalence of PH and examine its clinical and radiological pointers among children with ATH. The airway obstruction was evaluated clinically by grading the nocturnal and daytime symptoms of ATH. A Brodsky scale and adenoid-nasopharynx ratio (AN ratio) were used to categorize tonsil and adenoid size, respectively. Mean pulmonary artery pressure (mPAP), was measured noninvasively for each child using Doppler echocardiography and PH was defined by mPAP ≥25 mmHg. Comparison of symptom scores, tonsil and adenoid size and demographic factors was made between children with mPAP ≥25 mmHg and those mPAP <25 mmHg using univariate and multivariate analysis. There was 22.8 % (18/79) prevalence of PH among the 26 children with only adenoid hypertrophy and 53 with ATH. Significant risk factors identified by logistic regression analysis associated with PH were daytime mouth breathing, daytime stertor, and AN ratio >0.75 (P = 0.002, 0.018, and 0.04, respectively), with more than sixfold and fourfold increase risk for daytime mouth breathing and daytime stertor, respectively. Obstructive breathing during sleep was significant only on univariate analysis. Prolonged symptom duration ≥24 months, large tonsils (grades 3 and 4), snoring and mouth breathing during sleep were not significant. This study demonstrated that pulmonary hypertension remains prevalent in children with ATH. Daytime mouth breathing and stertor as well as AN ratio >0.75 are the prime predictors of pulmonary hypertension, with an AN ratio cut-off point of 0.73 on ROC analysis.
Malignancies occurred in 63.8% of HIV patients and 65% of the negative group (p = 0.87). While non-Hodgkin's lymphoma (NHL), squamous cell carcinoma (SCC), and Hodgkin's lymphoma (HL) constituted 40%, 27%, and 17% of malignancies in HIV patients, respectively; in the HIV-negative group, it was 53%, 13%, and 2% for SCC, NHL, and HL, respectively (p = 0.039, 0.017, and 0.035, respectively). Reactive lymphoid proliferation accounted for 82.4% of the benign masses in the HIV positive group. Malignant tumours were recorded more in younger patient in the HIV positive than the negative group (p = 0.001).
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