Respiratory Health

Liver & Kidney Health, Respiratory Health

Alpha-1-Antitrypsin level may be increased in normal pregnancy and in several diseases including chronic pulmonary disease; hereditary angioedema; renal, gastric, liver and pancreatic diseases; diabetes; carcinomas and rheumatoid diseases. Alpha-1-Antitrypsin may be decreased in emphysema, hepatic cirrhosis, respiratory distress syndrome of the newborn, nephrosis, malnutrition and cachexia. If a deficiency is present, aat phenotyping may be considered to confirm heterozygous versus homozygous deficiencies.

Infectious Diseases, Respiratory Health

A positive result indicates prior exposure toMycoplasma. A single positive IgG result may be present in the absence of any clinical symptoms as specific IgG antibodies may remain elevated for up to one year after the initial infection. Recent or acute infection can only be documented by a positiveMycoplasmaIgM result and/or a significant increase in the IgG value between sera drawn two to four weeks apart. In some individuals,MycoplasmaIgG levels decline to undetectable levels after four to six months.

Infectious Diseases, Respiratory Health

Low positive results (770-950 units/mL) are presumptive evidence of acute or recent infection. It is recommended that the test be repeated on a fresh specimen one to two weeks later to assure reactivity. Specific IgM may persist for several months after initial infection or be absent during reinfection.

Infectious Diseases, Respiratory Health

This test allows rapid diagnosis of the presence of respiratory syncytial virus. It avoids the necessity of obtaining acute and convalescent specimens over a two-week period. It may be particularly useful in children younger than six months old, whose antibody response to infection may not be diagnostic.

Infectious Diseases, Respiratory Health

Offered as part of multiple lab tests

Respiratory Health, Allergy Testing

Hypersensitivity pneumonitis (HP) is an interstitial lung disease that is characterized by a complex immunological reaction of the lung parenchyma in response to repetitive inhalation and subsequent sensitization to a wide variety of inhaled organic dusts.1-7HP is associated with progressive pulmonary disability, irreversible lung damage, and mortality in some cases. HP can be classified as Acute/Inflammatory (symptoms less than six months) and Chronic/Fibrotic (symptoms more than six months) based on clinical, radiologic and pathologic characteristics.8The name previously used for this condition, extrinsic allergic alveolitis, has been largely abandoned because inflammation involves more than just the alveoli and can extend to the bronchioles as well. The severity of the disease and clinical presentation varies depending on the quantity and type of inhaled antigen causing the condition. Numerous antigens have been found to cause HP.Diagnosis of HP can be challenging and requires a combination of detailed history, radiologic evaluation, pathological examination and laboratory testing. Acute exposures to inciting antigens typically cause abrupt onset of nonproductive cough, dyspnea, and chills with arthralgias or malaise within a few hours of heavy exposure to a specific antigen.1-4,8Symptoms usually resolve within a few days of avoiding exposure. Coughing is a predominant symptom due to airway-centered nature of inflammation.Patients also report shortness of breath, malaise, weight loss. No single laboratory testis diagnostic for hypersensitivity pneumonitis.1,6-8Double diffusion (Ouchterlony) assays are used to determine antigen-specific IgG antibodies. The appearance of precipitin arcs confirms the presence of precipitating antibodies to specific antigens.A number of antigens have been found to cause HP but only a small proportion of the people who are exposed to these antigens develop HP.1-6,8,9Exposures to the causative antigens can be associated with specific occupations or hobbies but can also occur in the home and general environment.Bird or Pigeon Fancier’s Lung: Globally, this is the most commonly reported form of HP and is caused by exposure to organic antigens in bird (particularly pigeon) excreta.1,10,11Indirect exposure from feather bedding or down comforters have also been reported to cause disease. Avian antigen can exist in the indoor environment regardless of antigen avoidance.12The presence of avian antigen in the indoor environment can be attributed to wild birds found outdoors.12Farmer’s Lung: Caused by exposure to moldy hay, compost or grain stored in conditions of high humidity in the agricultural workplace.2,13IgG precipitins commonly associated with Farmer’s Lung includingAspergillus fumigatus, Thermoactinomyces sacchari, Thermoactinomyces vulgarisandSaccharopolyspora rectivirgula(formerly calledMicropolyspora faeni).Humidifier/Sauna Taker’s Lung: HP secondary to occupational exposure to moldy water from heating/ventilation/air-conditioning systems has been described in adults.14-16Non-occupational exposure to molds includingAspergillus fumigatusandaureobasidium pullulansvia home saunas or water damage has also been shown to cause HP.17-20Early diagnosis of HP is critical to avoid the development of extensive pulmonary fibrosis or restrictive lung disease has occurred.1Identification of the offending agentis critical in diagnosing HP and implementing preventive measures.5,7If diagnosed early enough, complete avoidance of inciting antigen results in total recovery of lung function in the majority of patients. If not promptly diagnosed and treated, HP can progress to pulmonary fibrosis and progressive respiratory failure. Presence of fibrosis and honeycombing have been associated with higher mortality. Primary prevention should aim to reduce exposure to known organic antigens.