Minimal criteria include five factors:  the presence of asthma and/or cystic fibrosis, a positive skin test to Aspergillus sp., total serum IgE > 416 IU/mL (or kU/L), an increased Aspergillus species–specific IgE and IgG antibodies, and the presence of infiltrates on a chest X-ray.ABPA should be suspected in patients with a predisposing lung disease—most commonly asthma or cystic fibrosis— and is often associated with chronic airway limitation (CAL). Patients generally present with symptoms of recurrent infection such as fever, but do not respond to conventional antibiotic therapy. Poorly-controlled asthma is a common finding, with a case series only finding 19% of ABPA patients with well-controlled asthma. Wheezing and hemoptysis (coughing up blood) are common features, and mucus plugging is seen in 31–69% of patients. Blood tests and serology
The first stage involves exposing the skin to Aspergillus fumigatus antigens; an immediate reaction is hallmark of ABPA. The test should be performed first by skin prick testing, and if negative followed with an intradermal injection. The overall sensitivity of the procedure is around 90%, though up to 40% of asthmatic patients without ABPA can still show some sensitivity to Aspergillus antigens (a phenomenon likely linked to a less severe form of ABPA termed severe asthma with fungal sensitization (SAFS)).Serum blood tests are an important marker of disease severity and are also useful for the primary diagnosis of ABPA. When serum IgE is normal (and patients are not being treated by glucocorticoid medications), ABPA is excluded as the cause of symptoms.
Once identified, parents of infants who carry mutant aldolase B alleles leading to HFI, or older individuals who have clinical histories compatible with HFI can be identified and counselled with regard to preventive therapy: dietary exclusion of foods containing fructose, sucrose, or sorbitol. If possible, individuals who suspect they might have HFI should avoid testing via fructose challenge as the results are non-conclusive for individuals with HFI, and even if the diagnostic administration of fructose is properly controlled, profound hypoglycemia and its sequelae can threaten the patients well-being. Treatment
Treatment of HFI depends on the stage of the disease, and the severity of the symptoms. Stable patients without acute intoxication events are treated by careful dietary planning that avoids fructose and its metabolic precursors. Fructose is replaced in the diet by glucose, maltose or other sugars. Management of patients with HFI often involves dietitians who have a thorough knowledge of what foods are acceptable. See also
Fructose malabsorption

References


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