These infections respond to antibiotics but can recur upon discontinuation of antibiotics. Bronchiectasis can develop when severe recurrent pulmonary infections are left untreated. In addition to infections, people with CVID can develop complications. These include:

Autoimmune manifestations, e.g. pernicious anemia, autoimmune haemolytic anemia (AHA), idiopathic thrombocytopenic purpura (ITP), psoriasis, vitiligo, rheumatoid arthritis, primary hypothyroidism, atrophic gastritis. Autoimmunity is the main complication in people with CVID, appearing in some form in up to 50% of individuals;
Malignancies, particularly non-Hodgkins lymphoma and gastric carcinoma;
Enteropathy, which manifests with a blunting of intestinal villi and inflammation, and is usually accompanied by symptoms such as abdominal cramps, diarrhea, constipation, and in some cases malabsorption and weight loss. Symptoms of CVID enteropathy are similar to those of celiac disease, but do not respond to a gluten-free diet. Infectious causes must be excluded before a diagnosis of enteropathy can be made, as people with CVID are more susceptible to intestinal infections, e.g. by Giardia lamblia;
Lymphocytic infiltration of tissues, which can cause enlargement of lymph nodes (lymphadenopathy), of the spleen (plenomegaly) and of the liver (hepatomegaly), as well as the formation of granulomas. In the lung this is known as granulomatous–lymphocytic interstitial lung disease.Anxiety and depression can occur as a result of dealing with the other symptoms.CVID patients generally complain of severe fatigue.As with any antibody deficiency, the most common types of infections and illnesses involve the ears, sinuses, nose, and lungs. Common infections include:

Pneumonia
Ear infections
Sinusitis
Chronic coughing (lasting from a few weeks to many months)
Gastrointestinal infectionsGastrovascular infections or inflammation are very common for those with CVID.
The underlying causes of CVID are largely obscure. Genetic mutations can be identified as the cause of disease in about 10% of people, while familial inheritance accounts for 10–25% of cases. Rather than arising from a single genetic mutation, CVID seems to result from variety of mutations that all contribute to a failure in antibody production. Mutations in the genes encoding ICOS, TACI, CD19, CD20, CD21, CD80 and BAFFR have been identified as causative of CVID. Susceptibility to CVID may also be linked to the major histocompatibility complex (MHC) of the genome, particularly to DR-DQ haplotypes. A mutation in the NFKB2 gene has recently been shown to cause CVID-like symptoms in a murine model. The frequency of this NFKB2 mutation in the CVID population is, however, yet to be established. Diagnosis
According to a European registry study, the mean age at onset of symptoms was 26.3 years old. As per the criteria laid out by ESID (European Society for Immunodeficiencies) and PAGID (Pan-American Group for Immunodeficiency), CVID is diagnosed if:
the person presents with a marked decrease of serum IgG levels (<4.5 g/L) and a marked decrease below the lower limit of normal for age in at least one of the isotypes IgM or IgA;
the person is four years of age or older;
the person lacks antibody immune response to protein antigens or immunization.Diagnosis is chiefly by exclusion, i.e. alternative causes of hypogammaglobulinemia, such as X-linked agammaglobulinemia, must be excluded before a diagnosis of CVID can be made.