Agoraphobia without a history of panic disorder (also called primary agoraphobia) is an anxiety disorder where the individual with the diagnosis does not meet the DSM-5 criteria for panic disorder. Agoraphobia typically develops as a result of having panic disorder. In a small minority of cases, however, agoraphobia can develop by itself without being triggered by the onset of panic attacks. Agoraphobia can be caused by traumatic experiences, such as bullying or abuse. Historically, there has been debate over whether agoraphobia without panic genuinely existed, or whether it was simply a manifestation of other disorders such as panic disorder, generalized anxiety disorder, avoidant personality disorder and social phobia. One researcher said: "out of 41 agoraphobics seen (at a clinic) during a period of 1 year, only 1 fit the diagnosis of agoraphobia without panic attacks, and even this particular classification was questionable...Do not expect to see too many agoraphobics without panic". In spite of this earlier skepticism, current thinking is that agoraphobia without panic disorder is indeed a valid, unique illness which has gone largely unnoticed, since those with the condition are far less likely to seek clinical treatment. Diagnostic criteria (DSM-IV-TR)
According to the DSM-IV-TR, a widely used manual for diagnosing mental disorders, the condition is diagnosed when agoraphobia is present without panic disorder where symptoms are not caused by or are unreasonable to an underlying medical problem or pharmacological influence. See also
Panic disorder
Agoraphobia

References
Spiti Raffaello, Scarpato Maria Alessandra, Spiti Alessandra (2011). "Primary agoraphobia specific symptoms: from natural information to mental representations".
Later pediatric endocrinologist Aaron Hanukoglu reported that there are two independent forms of PHA with different inheritance patterns: A renal form with autosomal dominant inheritance exhibiting salt loss mainly from the kidneys, and a multi-system form with autosomal recessive form exhibiting salt loss from kidney, lung, and sweat and salivary glands.The hereditary lack of responsiveness to aldosterone could be due to at least two possibilities: 1. A mutation in the mineralocorticoid receptor that binds aldosterone, or 2. A mutation in a gene that is regulated by aldosterone. Linkage analysis on patients with the severe form of PHA excluded the possibility of linkage of the disease with the mineralocorticoid receptor gene region. Later, the severe form of PHA was discovered to be due to mutations in the genes SCNN1A, SCNN1B, and SCNN1G that code for the epithelial sodium channel subunits, α, β, and γ, respectively.A stop mutation in the SCNN1A gene has been shown to be associated with female infertility. See also
Hyperchloremic acidosis
Pseudohyperaldosteronism

References
External links
GeneReviews/NCBI/NIH/UW entry on Pseudohypoaldosteronism Type II