Normally, the palmar fascia consists of collagen type I, but in Dupuytren patients, the collagen changes to collagen type III, which is significantly thicker than collagen type I. Related conditions
People with severe involvement often show lumps on the back of their finger joints (called "Garrods pads", "knuckle pads", or "dorsal Dupuytren nodules"), and lumps in the arch of the feet (plantar fibromatosis or Ledderhose disease). In severe cases, the area where the palm meets the wrist may develop lumps. It is thought the condition Peyronies disease is related to Dupuytrens contracture. Risk factors
Dupuytrens contracture is a non-specific condition, but primarily affects:

Non-modifiable
People of Scandinavian or Northern European ancestry; it has been called the "Viking disease", though it is also widespread in some Mediterranean countries, e.g., Spain and Bosnia. Dupuytrens is unusual among groups such as Chinese and Africans. Men rather than women; men are more likely to develop the condition (80%)
People over the age of 50 (5% to 15% of men in that group in the US); the likelihood of getting Dupuytrens disease increases with age
People with a family history (60% to 70% of those affected have a genetic predisposition to Dupuytrens contracture)

Modifiable
Smokers, especially those who smoke 25 cigarettes or more a day
Thinner people, i.e., those with a lower-than-average body mass index.
Zieves syndrome is an acute metabolic condition that can occur during withdrawal from prolonged heavy alcohol use. It is defined by hemolytic anemia (with spur cells and acanthocytes), hyperlipoproteinaemia (excessive blood lipoprotein), jaundice (elevation of unconjugated bilirubin), and abdominal pain. The underlying cause is liver delipidization. This is distinct from alcoholic hepatitis which, however, may present simultaneously or develop later.Diagnosis of Zieves syndrome should be considered in patients with prolonged alcohol use (especially after an episode of binge drinking) with an elevation of unconjugated bilirubin and without obvious signs of gastrointestinal bleeding. Pathogenesis
The proposed mechanism of the characteristic haemolytic anaemia in Zieves syndrome is due to alteration of the red cell metabolism, namely pyruvate kinase instability leaving them susceptible to circulating hemolysin such as lysolecithin. Changes in membrane lipid compositions such as increased cholesterol and polyunsaturated fatty acid (PUFA) have been reported during the hemolytic phase. Diagnosis
The diagnosis is demonstrated by the triad of alcoholic hepatitis or cirrhosis, hemolytic anemia, and hyperlipidemia. Treatment
Definitive treatment for Zieves syndrome is alcohol cessation. Individuals with markedly elevated triglycerides, particularly with a history of pancreatitis or intracerebral hemorrhage, may require plasmapharesis to avoid complications associated with hypertriglyceridemia. History
Zieves syndrome was initially described in 1958. Dr. Leslie Zieve described patients with a combination of alcoholic liver disease, hemolytic anemia and hypertriglyceridemia. References


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