The American College of Obstetricians and Gynecologists recommends all people thinking of becoming pregnant be tested to see if they have thalassemia. Genetic counseling and genetic testing are recommended for families who carry a thalassemia trait.

A screening policy exists in Cyprus to reduce the rate of thalassemia, which, since the program's implementation in the 1970s (which also includes prenatal screening and abortion), has reduced the number of children born with the disease from one of every 158 births to almost zero.

In Iran as a premarital screening, the man's red cell indices are checked first, if he has microcytosis (mean cell hemoglobin < 27 pg or mean red cell volume < 80 fl), the woman is tested. When both are microcytic, their hemoglobin A2 concentrations are measured. If both have a concentration above 3.5% (diagnostic of thalassemia trait) they are referred to the local designated health post for genetic counseling.

Large scale awareness campaigns are being organized in India both by government and non-government organizations in favor of voluntary premarital screening to detect carriers of thalassemia and marriage between both carriers are strongly discouraged.

Mild thalassemia: people with thalassemia traits do not require medical or follow-up care after the initial diagnosis is made. People with β-thalassemia trait should be warned that their condition can be misdiagnosed as the more common iron deficiency anemia. They should avoid routine use of iron supplements; iron deficiency can develop, though, during pregnancy or from chronic bleeding. Counseling is indicated in all persons with genetic disorders, especially when the family is at risk of a severe form of disease that may be prevented.

Overall, hemoglobin C disease is one of the more benign hemoglobinopathies. Mild-to-moderate reduction in RBC lifespan may accompany from mild hemolytic anemia. Individuals with hemoglobin C disease have sporadic episodes of musculoskeletal (joint) pain. People with hemoglobin C disease can expect to lead a normal life.

Usually no treatment is needed. Folic acid supplementation may help produce normal red blood cells and improve the symptoms of anemia

Hemoglobinopathy is a kind of genetic defect that results in abnormal structure of one of the globin chains of the hemoglobin molecule. Hemoglobinopathies are inherited single-gene disorders; in most cases, they are inherited as autosomal co-dominant traits. Common hemoglobinopathies include sickle-cell disease. It is estimated that 7% of world's population (420 million) are carriers, with 60% of total and 70% pathological being in Africa. Hemoglobinopathies are most common in populations from Africa, the Mediterranean basin and Southeast Asia.

Hemoglobinopathies imply structural abnormalities in the globin proteins themselves. Thalassemias, in contrast, usually result in underproduction of normal globin proteins, often through mutations in regulatory genes. The two conditions may overlap, however, since some conditions which cause abnormalities in globin proteins (hemoglobinopathy) also affect their production (thalassemia). Thus, some hemoglobinopathies are also thalassemias, but most are not.

Either hemoglobinopathy or thalassemia, or both, may cause anemia. Some well-known hemoglobin variants such as sickle-cell anemia and congenital dyserythropoietic anemia are responsible for diseases, and are considered hemoglobinopathies. However, many hemoglobin variants do not cause pathology or anemia, and thus are often not classed as hemoglobinopathies, because they are not considered pathologies. Hemoglobin variants are a part of the normal embryonic and fetal development, but may also be pathologic mutant forms of hemoglobin in a population, caused by variations in genetics. Other variants cause no detectable pathology, and are thus considered non-pathological variants.

In general on alkaline electrophoresis in order of increasing mobility are hemoglobins A2, E=O=C, G=D=S=Lepore, F, A, K, J, Bart's, N, I, and H.

In general a sickling test (sodium bisulfite) is performed on abnormal hemoglobins migrating in the S location to see if the red cells precipitate in solution.

In persons with sickle cell disease, high levels of fetal hemoglobin as found in a newborn or as found abnormally in persons with hereditary persistence of fetal hemoglobin, the HbF causes the sickle cell disease to be less severe. In essence the HbF inhibits polymerization of HbS. A similar mechanism occurs with persons who have sickle cell "trait". Approximately 40% of the hemoglobin is in the HbS form while the rest is in normal HbA form. The HbA form interferes with HbS polymerization.

Basically classified by causative mechanism, types of congenital hemolytic anemia include:

- Genetic conditions of RBC Membrane

- Hereditary spherocytosis

- Hereditary elliptocytosis

- Genetic conditions of RBC metabolism (enzyme defects). This group is sometimes called "congenital nonspherocytic (hemolytic) anemia", which is a term for a congenital hemolytic anemia without spherocytosis, and usually excluding hemoglobin abnormalities as well, but rather encompassing defects of glycolysis in the erythrocyte.

- Glucose-6-phosphate dehydrogenase deficiency (G6PD or favism)

- Pyruvate kinase deficiency

- Aldolase A deficiency

- Hemoglobinopathies/genetic conditions of hemoglobin

- Sickle cell anemia

- Congenital dyserythropoietic anemia

- Thalassemia

Congenital hemolytic anemia (or hereditary hemolytic anemia) refers to hemolytic anemia which is primarily due to congenital disorders.

Hereditary persistence of fetal hemoglobin (HPFH, BrE: "Hereditary persistence of foetal haemoglobin") is a benign condition in which significant fetal hemoglobin (hemoglobin F) production continues well into adulthood, disregarding the normal shutoff point after which only adult-type hemoglobin should be produced.

The cause of TEC is unknown, but it thought to be triggered by a viral infection. While rare cases have been attributed to infection with Parvovirus B19, the majority of cases are not related to Parvovirus infection. This is in contrast to transient aplastic crisis, seen in patients with hemoglobinopathies such as sickle cell disease, which is usually caused by Parvovirus infection.

Most patients recover completely within 1–2 months.

However many reported cases have lasted 18–24 months and longer.

There is no treatment that directly interferes with the disease process, although dietary restriction of calcium has been tried with limited results. For excessive areas of skin, plastic surgery may be needed. For the growth of abnormal blood vessels in the retina, laser photocoagulation and photodynamic therapy may be used; injections with triamcinolone have shown limited effect. Antiangiogenic drugs such as bevacizumab (Avastin) and ranibizumab (Lucentis) have been effective, similar to its efficacy in age-related macular degeneration. Cardiovascular disease is treated as in individuals without PXE. Some recommend avoidance of nonsteroidal anti-inflammatory drugs (NSAIDS) that increase bleeding risk, such as aspirin, and ibuprofen.

Pseudoxanthoma elasticum (PXE), also known as Grönblad–Strandberg syndrome, is a genetic disease that causes fragmentation and mineralization of elastic fibers in some tissues. The most common problems arise in the skin and eyes, and later in blood vessels in the form of premature atherosclerosis. PXE is caused by autosomal recessive mutations in the "ABCC6" gene on the short arm of chromosome 16 (16p13.1).

Splenic infarction can be induced for the treatment of such conditions as portal hypertension or splenic injury. It can also be used prior to splenectomy for the prevention of blood loss.

In 1985 the UAE established a national program to prevent transmission of acquired immune deficiency syndrome (AIDS) and to control its entry into the country. According to World Health Organization estimates, in 2002−3 fewer than 1,000 people in the UAE were living with human immunodeficiency virus (HIV)/AIDS.

In 2009, 119 genetic disorders were identified among Emiratis and 241 among Arab citizens and expatriates combined in the UAE. This is the second-highest incidence of genetic disorders in the Arab world (after Oman). Autosomal recessive disorders are common in the UAE. Hemoglobinopathies are one of the most common disorders among the UAE nationals. Beta-thalassemia constitutes a major public health problem in the UAE. During 1989-2004, more than 850 patients have been registered at the Dubai Genetics and Thalassemia Center. Surveys have shown that the UAE exhibits one of the highest carrier frequencies of β-thalassemia in the Persian Gulf region which is 8.5%. Pre-marital medical examinations in the UAE, excluding the HAAD, include blood group tests, sickle cell anaemia, hepatitis B and C, German measles, haemoglobin variance, HIV/AIDS, thalassaemia, and syphilis.

The Health Authority – Abu Dhabi introduced premarital screening and counselling in 2011. 56,226 men and women preparing for marriage were tested for genetic and infectious disorders were tested between 2011 and the end of 2014. in 2014 16,247 people were tested, 342 were Beta-thalassaemia carriers, 8 had sickle-cell anaemia, 205 were sickle-cell anaemia carriers, 36 had syphilis and 140 had hepatitis B.

Splenic infarction is a condition in which oxygen supply to the spleen is interrupted, leading to partial or complete infarction (tissue death due to oxygen shortage) in the organ.

Splenic infarction occurs when the splenic artery or one of its branches are occluded, for example by a blood clot. Although it can occur asymptomatically, the typical symptom is severe pain in the left upper quadrant of the abdomen, sometimes radiating to the left shoulder. Fever and chills develop in some cases. It has to be differentiated from other causes of acute abdomen.

An abdominal CT scan is the most commonly used modality to confirm the diagnosis, although abdominal ultrasound can also contribute.

There is no specific treatment, except treating the underlying disorder and providing adequate pain relief. Surgical removal of the spleen (splenectomy) is only required if complications ensue; surgical removal predisposes to overwhelming post-splenectomy infections.

In one series of 59 patients, mortality amounted to 5%. Complications include a ruptured spleen, bleeding, an abscess of the spleen (for example, if the underlying cause is infective endocarditis) or pseudocyst formation. Splenectomy may be warranted for persistent pseudocysts due to the high risk of subsequent rupture.