These symptoms can include:
Musculoskeletal Problems   
Short limbs
Shortened body trunk
Flattened bones in the spine (platyspondyly)
kyphoscoliosis
Scoliosis (Lateral curvature of the spine)
Early development of arthritis
Respiratory problems
Respiratory tract infection
Difficulty breathing
Eye problems
Severe myopia (near-sightedness)
Cataract (cloudiness in the lens of the eye)
Cranial structure may elongate the eyeball, causing a thinning of the retina, thereby predisposing retinal detachment
Hearing problems
progressive hearing loss
ear infectionsMost symptoms are chronic and will continue to worsen as the individual ages. It is essential to have regular checkups with general doctors, orthopedist, ophthalmologists, and/or otorhinolaryngologists. This will help to detect whether there are any changes that could cause concern. Genetics
Mechanism
Studies have shown that a mutated COL2A1 gene is responsible for all type II chondroldysplasias, including Kniest dysplasia. It is believed that point mutations or the alteration of splice sites in COL2A1 domains will result in Kniest Dysplasia. The COL2A1 domain typically spans between exon 12 and 24. Mutations that occur at a splice donor site results in the loss of function at that site. This leads to the skipping of the exon and deletion of amino acids. The loss of these amino acids result in an abnormal procollagen II structure. The structure is not stable like the normal procollagen II structure and is normally degraded at a faster rate. Diagnosis
Family/medical history
Kniest dysplasia is an autosomal dominant condition. This means that the person only needs to have one copy of the mutated gene in order to have the condition. People with a family history are at a higher risk of having the disease than people with no family history.
Adrenocortical adenoma is commonly described as a benign neoplasm emerging from the cells that comprise the adrenal cortex. Like most adenomas, the adrenocortical adenoma is considered a benign tumor since the majority of them are non-functioning and asymptomatic. Adrenocortical adenomas are classified as ACTH-independent disorders, and are commonly associated with conditions linked to hyperadrenalism such as Cushings syndrome (hypercortisolism) or Conns syndrome (hyperaldosteronism), which is also known as primary aldosteronism. In addition, recent case reports further support the affiliation of adrenocortical adenomas with hyperandrogenism or florid hyperandrogenism which can cause hyperandrogenic hirsutism in females. "Cushings syndrome" differs from the "Cushings disease" even though both conditions are induced by hypercortisolism. The term "Cushings disease" refers specifically to "secondary hypercortisolism" classified as "ACTH-dependent Cushings syndrome" caused by pituitary adenomas. In contrast, "Cushings syndrome" refers specifically to "primary hypercortisolism" classified as "ACTH-independent Cushings syndrome" caused by adrenal adenomas. Presentation
Adrenal adenomas are often categorized as endocrine-inactive tumors considering that majority of them are non-functioning and asymptomatic. Functional adrenocortical adenomas demonstrate symptoms consistent with mixed endocrine syndromes. In most reported cases of adrenocortical adenoma, patients have presented with one or multiple endocrine syndromes such as hyperaldosteronism/Conns Syndrome, hypercortisolism/Cushings syndrome, hyperandrogenism/feminization, virilization, or hirsutism. Some of the common symptoms associated with adrenocortical adenomas include:
Musculoskeletal

Osteopenia
Muscle weakness/muscle atrophyCardiovascular

HypertensionEndocrine and Metabolic

Obesity→More prevalent in males

virilization→More prevalent in females

Hyperandrogenism
Irregular menstrual cyclesNeuropsychological

Sleep disorders
DepressionSkin

Easy bruising
Stretch marks
Hirsutism
Acne

Cause
Study of the reported cases indicate that most adrenocortical adenomas occur due to neoplastic proliferation of adrenal cortical cells within the three distinct layers of adrenal cortex.