A 2016 study of over 60,000 participants from 89 countries found regional prevalence of lactose malabsorption was "64% (54–74) in Asia (except Middle East), 47% (33–61) in eastern Europe, Russia, and former Soviet Republics, 38% (CI 18–57) in Latin America, 70% (57–83) in the Middle East, 66% (45–88) in northern Africa, 42% (13–71) in northern America, 45% (19–71) in Oceania, 63% (54–72) in sub-Saharan Africa, and 28% (19–37) in northern, southern and western Europe." According to Johns Hopkins Medicine, lactose intolerance is more common in Asian Americans, African Americans, Mexican Americans, and Native Americans. Analysis of the DNA of 94 ancient skeletons in Europe and Russia concluded that the mutation for lactose tolerance appeared about 4,300 years ago and spread throughout the European population.Some human populations have developed lactase persistence, in which lactase production continues into adulthood probably as a response to the benefits of being able to digest milk from farm animals. Some have argued that this links intolerance to natural selection favoring lactase-persistent individuals, but it is also consistent with a physiological response to decrease lactase production when it is not needed in cultures in which dairy products are not an available food source. Although populations in Europe, India, Arabia, and Africa were first thought to have high rates of lactase persistence because of a single mutation, lactase persistence has been traced to a number of mutations that occurred independently.
Centrilobular necrosis occurs.Macroscopically, the liver has a pale and spotty appearance in affected areas, as stasis of the blood causes pericentral hepatocytes (liver cells surrounding the central venule of the liver) to become deoxygenated compared to the relatively better-oxygenated periportal hepatocytes adjacent to the hepatic arterioles. This retardation of the blood also occurs in lung lesions, such as chronic interstitial pneumonia, pleural effusions, and intrathoracic tumors. Diagnosis
It is diagnosed with laboratory testing, including liver function tests, and radiology imaging, including ultrasounds. Treatment
Treatment is directed largely to removing the cause, or, where that is impossible, to modifying effects of the heart failure. Thus, therapy aimed at improving right heart function will also improve congestive hepatopathy. True nutmeg liver is usually secondary to left-sided heart failure, causing congestive right heart failure, so treatment options are limited.Treatments for heart failure include medications, an intra-aortic balloon pump, a ventricular assist device, heart valve replacements, extracorporeal membrane oxygenation (if the heart failure worsens suddenly and especially if an infection was the cause), an artificial heart, or a heart transplant (from a deceased human donor, or from a pig). Some patients may need a liver transplant; an artificial liver can be used for a short period of time (about two weeks or so) as a bridge to a transplant, or until the liver recovers. See also
Ischemic hepatitis

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