Signs and symptoms
A list of the common side effects broken down by frequency.Very frequent

Abnormal gastrointestinal tract
Absent pectoral muscles
Brachydactyly (Short fingers)
Dextrocardia
Diaphragmatic hernia/defect
Humerus absent/abnormal
Liver/biliary tract anomalies
Maternal diabetes
Oligodactyly/missing fingers
Radius absent/abnormal
Rhizomelic micromelia (relatively shorter proximal segment of the limbs compared to the middle and the distal segments)
Sparsity or abnormality of axillary hair on affected side
Syndactyly of fingers (webbing)
Ulna absent/abnormal
Upper limb asymmetry
Abnormal rib
Simian crease on affected sideFrequent

Hypoplastic/absent nipples
Scapula anomalyOccasional

Agenesis/hypoplasia of kidneys
Encephalocele/exencephaly
Abnormal morphology of hypothalamic-hypophyseal axis
Abnormal function of hypothalamic-hypophyseal axis
Microcephaly
Preaxial polydactyly
Ureteric anomalies (reflux/duplex system)
Vertebral segmentation anomalyIt is usually considered a unilateral condition. Some have claimed that the term can be applied in bilateral presentation, but others recommend using alternate terminology in those cases. Causes
The cause of Poland syndrome is unknown. However, an interruption of the embryonic blood supply to the arteries that lie under the collarbone (subclavian arteries) at about the 46th day of embryonic development is the prevailing theory.The subclavian arteries normally supply blood to embryonic tissues that give rise to the chest wall and hand. Variations in the site and extent of the disruption may explain the range of signs and symptoms that occur in Poland syndrome. Abnormality of an embryonic structure called the apical ectodermal ridge, which helps direct early limb development, may also be involved in this disorder. Diagnosis
Poland syndrome is usually diagnosed at birth, based upon the physical characteristics. Imaging techniques such as a CT scan may reveal the extent to which the muscles are affected. The syndrome varies in severity and as such is often not reported until puberty, when lopsided growth becomes apparent.
Indian childhood cirrhosis is a chronic liver disease of childhood characterised by cirrhosis of the liver associated with the deposition of copper in the liver. It primarily affects children of 1–3 years of age and has a genetic predisposition. It had a very high case fatality in the past, but has eventually become preventable, treatable and is now rare.It remains a part of the differential diagnosis of Wilsons disease. See also
North American Indian childhood cirrhosis

References
Further reading

Nayak N.C.; Chitale A.R. (2013). "Indian childhood cirrhosis (ICC) & ICC-like diseases: The changing scenario of facts versus notions". Indian J. Med. Res. 137 (6): 1029–42. PMC 3734708. PMID 23852284.