Anemia (/əˈniːmiə/; also spelled anaemia and anæmia; from Ancient Greek: ἀναιμία anaimia, meaning lack of blood) is a decrease in number of red blood cells (RBCs) or less than the normal quantity of hemoglobin in the blood.^[1][2] However, it can include decreased oxygen-binding ability of each hemoglobin molecule due to deformity or lack in numerical development as in some other types of hemoglobin deficiency.

Because hemoglobin (found inside RBCs) normally carries oxygen from the lungs to the tissues, anemia leads to hypoxia (lack of oxygen) in organs. Since all human cells depend on oxygen for survival, varying degrees of anemia can have a wide range of clinical consequences.

Anemia is the most common disorder of the blood. There are several kinds of anemia, produced by a variety of underlying causes. Anemia can be classified in a variety of ways, based on the morphology of RBCs, underlying etiologic mechanisms, and discernible clinical spectra, to mention a few. The three main classes of anemia include excessive blood loss (acutely such as a hemorrhage or chronically through low-volume loss), excessive blood cell destruction (hemolysis) or deficient red blood cell production (ineffective hematopoiesis).

There are two major approaches to diagnosis: the "kinetic" approach which involves evaluating production, destruction and loss,^[3] and the "morphologic" approach which groups anemia by red blood cell size. The morphologic approach uses a quickly available and low cost lab test as its starting point (the MCV). On the other hand, focusing early on the question of production may allow the clinician to expose cases more rapidly where multiple causes of anemia coexist.

Signs and symptoms[link]

Main symptoms that may appear in anemia.^[4]

Anemia goes undetermined in many people, and symptoms can be minor or vague. The signs and symptoms can be related to the anemia itself, or the underlying cause.

Most commonly, people with anemia report non-specific symptoms of a feeling of weakness, or fatigue, general malaise and sometimes poor concentration. They may also report dyspnea (shortness of breath) on exertion. In very severe anemia, the body may compensate for the lack of oxygen-carrying capability of the blood by increasing cardiac output. The patient may have symptoms related to this, such as palpitations, angina (if preexisting heart disease is present), intermittent claudication of the legs, and symptoms of heart failure.

On examination, the signs exhibited may include pallor (pale skin, mucosal linings and nail beds) but this is not a reliable sign. There may be signs of specific causes of anemia, e.g., koilonychia (in iron deficiency), jaundice (when anemia results from abnormal break down of red blood cells — in hemolytic anemia), bone deformities (found in thalassemia major) or leg ulcers (seen in sickle-cell disease).

In severe anemia, there may be signs of a hyperdynamic circulation: tachycardia (a fast heart rate), bounding pulse, flow murmurs, and cardiac ventricular hypertrophy (enlargement). There may be signs of heart failure.

Pica, the consumption of non-food based items such as dirt, paper, wax, grass, ice, and hair, may be a symptom of iron deficiency, although it occurs often in those who have normal levels of hemoglobin.

Chronic anemia may result in behavioral disturbances in children as a direct result of impaired neurological development in infants, and reduced scholastic performance in children of school age.

Restless legs syndrome is more common in those with iron-deficiency anemia.

Less common symptoms may include swelling of the legs or arms, chronic heartburn, vague bruises, vomiting, increased sweating, and blood in stool.

Diagnosis[link]

Peripheral blood smear microscopy of a patient with iron-deficiency anemia.

Anemia is typically diagnosed on a complete blood count. Apart from reporting the number of red blood cells and the hemoglobin level, the automatic counters also measure the size of the red blood cells by flow cytometry, which is an important tool in distinguishing between the causes of anemia. Examination of a stained blood smear using a microscope can also be helpful, and is sometimes a necessity in regions of the world where automated analysis is less accessible.

In modern counters, four parameters (RBC count, hemoglobin concentration, MCV and RDW) are measured, allowing others (hematocrit, MCH and MCHC) to be calculated, and compared to values adjusted for age and sex. Some counters estimate hematocrit from direct measurements.

Reticulocyte counts, and the "kinetic" approach to anemia, have become more common than in the past in the large medical centers of the United States and some other wealthy nations, in part because some automatic counters now have the capacity to include reticulocyte counts. A reticulocyte count is a quantitative measure of the bone marrow's production of new red blood cells. The reticulocyte production index is a calculation of the ratio between the level of anemia and the extent to which the reticulocyte count has risen in response. If the degree of anemia is significant, even a "normal" reticulocyte count actually may reflect an inadequate response.

If an automated count is not available, a reticulocyte count can be done manually following special staining of the blood film. In manual examination, activity of the bone marrow can also be gauged qualitatively by subtle changes in the numbers and the morphology of young RBCs by examination under a microscope. Newly formed RBCs are usually slightly larger than older RBCs and show polychromasia. Even where the source of blood loss is obvious, evaluation of erythropoiesis can help assess whether the bone marrow will be able to compensate for the loss, and at what rate.

When the cause is not obvious, clinicians use other tests: ESR, ferritin, serum iron, transferrin, RBC folate level, serum vitamin B₁₂, hemoglobin electrophoresis, renal function tests (e.g. serum creatinine).

When the diagnosis remains difficult, a bone marrow examination allows direct examination of the precursors to red cells.

Classification[link]

Red blood cell size[link]

In the morphological approach, anemia is classified by the size of red blood cells; this is either done automatically or on microscopic examination of a peripheral blood smear. The size is reflected in the mean corpuscular volume (MCV). If the cells are smaller than normal (under 80 fl), the anemia is said to be microcytic; if they are normal size (80–100 fl), normocytic; and if they are larger than normal (over 100 fl), the anemia is classified as macrocytic. This scheme quickly exposes some of the most common causes of anemia; for instance, a microcytic anemia is often the result of iron deficiency. In clinical workup, the MCV will be one of the first pieces of information available; so even among clinicians who consider the "kinetic" approach more useful philosophically, morphology will remain an important element of classification and diagnosis.

Production vs. destruction or loss[link]

The "kinetic" approach to anemia yields what many argue is the most clinically relevant classification of anemia. This classification depends on evaluation of several hematological parameters, particularly the blood reticulocyte (precursor of mature RBCs) count. This then yields the classification of defects by decreased RBC production versus increased RBC destruction and/or loss. Clinical signs of loss or destruction include abnormal peripheral blood smear with signs of hemolysis; elevated LDH suggesting cell destruction; or clinical signs of bleeding, such as guaiac-positive stool, radiographic findings, or frank bleeding.

The following is a simplified schematic of this approach:

* For instance, sickle cell anemia with superimposed iron deficiency; chronic gastric bleeding with B₁₂ and folate deficiency; and other instances of anemia with more than one cause.
** Confirm by repeating reticulocyte count: ongoing combination of low reticulocyte production index, normal MCV and hemolysis or loss may be seen in bone marrow failure or anemia of chronic disease, with superimposed or related hemolysis or blood loss.

Here is a schematic representation of how to consider anemia with MCV as the starting point:

Other characteristics visible on the peripheral smear may provide valuable clues about a more specific diagnosis; for example, abnormal white blood cells may point to a cause in the bone marrow.

Microcytic[link]

Microcytic anemia is primarily a result of hemoglobin synthesis failure/insufficiency, which could be caused by several etiologies:

• Heme synthesis defect
  • Iron deficiency anemia
  • Anemia of chronic disease (more commonly presenting as normocytic anemia)
• Globin synthesis defect
  • alpha-, and beta-thalassemia
  • HbE syndrome
  • HbC syndrome
  • and various other unstable hemoglobin diseases
• Sideroblastic defect
  • Hereditary sideroblastic anemia
  • Acquired sideroblastic anemia, including lead toxicity
  • Reversible sideroblastic anemia

Iron deficiency anemia is the most common type of anemia overall and it has many causes. RBCs often appear hypochromic (paler than usual) and microcytic (smaller than usual) when viewed with a microscope.

• Iron deficiency anemia is due to insufficient dietary intake or absorption of iron to meet the body's needs. Infants, toddlers, and pregnant women have higher than average needs. Increased iron intake is also needed to offset blood losses due to digestive tract issues, frequent blood donations, or heavy menstrual periods.^[6] Iron is an essential part of hemoglobin, and low iron levels result in decreased incorporation of hemoglobin into red blood cells. In the United States, 12% of all women of childbearing age have iron deficiency, compared with only 2% of adult men. The incidence is as high as 20% among African and Mexican American women.^[7] Studies have shown that iron deficiency without anemia causes poor school performance and lower IQ in teenage girls, although this may be due to socioeconomic factors.^[8][9] Iron deficiency is the most prevalent deficiency state on a worldwide basis. Iron deficiency is sometimes the cause of abnormal fissuring of the angular (corner) sections of the lips (angular stomatitis).
• In the United States, the most common cause of iron deficiency is bleeding or blood loss, usually from the gastrointestinal tract. Fecal occult blood testing, upper endoscopy and lower endoscopy should be performed to identify bleeding lesions. In older men and women the chances are higher that bleeding from the gastrointestinal tract could be due to colon polyp or colorectal cancer.
• Worldwide, the most common cause of iron deficiency anemia is parasitic infestation (hookworm, amebiasis, schistosomiasis and whipworm).^[10]

Macrocytic[link]

• Megaloblastic anemia, the most common cause of macrocytic anemia, is due to a deficiency of either vitamin B₁₂, folic acid (or both). Deficiency in folate and/or vitamin B₁₂ can be due either to inadequate intake or insufficient absorption. Folate deficiency normally does not produce neurological symptoms, while B₁₂ deficiency does.
  • Pernicious anemia is caused by a lack of intrinsic factor. Intrinsic factor is required to absorb vitamin B₁₂ from food. A lack of intrinsic factor may arise from an autoimmune condition targeting the parietal cells (atrophic gastritis) that produce intrinsic factor or against intrinsic factor itself. These lead to poor absorption of vitamin B₁₂.
  • Macrocytic anemia can also be caused by removal of the functional portion of the stomach, such as during gastric bypass surgery, leading to reduced vitamin B₁₂/folate absorption. Therefore one must always be aware of anemia following this procedure.
• Hypothyroidism
• Alcoholism commonly causes a macrocytosis, although not specifically anemia. Other types of liver disease can also cause macrocytosis.
• Methotrexate, zidovudine, and other drugs that inhibit DNA replication.

Macrocytic anemia can be further divided into "megaloblastic anemia" or "non-megaloblastic macrocytic anemia". The cause of megaloblastic anemia is primarily a failure of DNA synthesis with preserved RNA synthesis, which result in restricted cell division of the progenitor cells. The megaloblastic anemias often present with neutrophil hypersegmentation (6–10 lobes). The non-megaloblastic macrocytic anemias have different etiologies (i.e. there is unimpaired DNA globin synthesis,) which occur, for example in alcoholism.

In addition to the non-specific symptoms of anemia, specific features of vitamin B₁₂ deficiency include peripheral neuropathy and subacute combined degeneration of the cord with resulting balance difficulties from posterior column spinal cord pathology.^[11] Other features may include a smooth, red tongue and glossitis.

The treatment for vitamin B₁₂-deficient anemia was first devised by William Murphy who bled dogs to make them anemic and then fed them various substances to see what (if anything) would make them healthy again. He discovered that ingesting large amounts of liver seemed to cure the disease. George Minot and George Whipple then set about to isolate the curative substance chemically and ultimately were able to isolate the vitamin B₁₂ from the liver. All three shared the 1934 Nobel Prize in Medicine.^[12]

Normocytic[link]

Normocytic anemia occurs when the overall hemoglobin levels are decreased, but the red blood cell size (mean corpuscular volume) remains normal. Causes include:

• Acute blood loss
• Anemia of chronic disease
• Aplastic anemia (bone marrow failure)
• Hemolytic anemia

Dimorphic[link]

When two or more causes of anemia act simultaneously, e.g., macrocytic hypochromic, due to hookworm infestation leading to deficiency of both iron and vitamin B₁₂ or folic acid ^[13] or following a blood transfusion more than one abnormality of red cell indices may be seen. Evidence for multiple causes appears with an elevated RBC distribution width (RDW), which suggests a wider-than-normal range of red cell sizes.

Heinz body anemia[link]

Heinz bodies form in the cytoplasm of RBCs and appear like small dark dots under the microscope. There are many causes of Heinz body anemia, and some forms can be drug induced. It is triggered in cats by eating onions^[14] or acetaminophen (paracetamol). It can be triggered in dogs by ingesting onions or zinc, and in horses by ingesting dry red maple leaves.

Hyperanemia[link]

Hyperanemia is a severe form of anemia, in which the hematocrit is below 10%.

Refractory anemia[link]

Refractory anemia is an anemia which does not respond to treatment.^[15] It is often seen secondary to myelodysplastic syndromes.^[16]

Iron deficiency anemia may also be refractory as a clinical manifestation of gastrointestinal problems which disrupt iron metabolism. ^[17]

Grading[link]

WHO Grading of anemia:^[18][19]

• Grade 1 (Mild Anemia): 10 g/dl - cutoff point for ages
• Grade 2 (Moderate Anemia): 7-10 g/dl
• Grade 3 (Severe Anemia): below 7 g/dl

National Cancer Institute Grading of Anemia:^[20]

• Grade 0 (within normal limits) 12.0–16.0 g/dl for women and 14.0–18.0 g/ dl for men
• Grade 1 (Mild) 10 g/dl to levels within normal limits
• Grade 2 (Moderate) 8.0–10.0 g/dl
• Grade 3 (Severe) 6.5–7.9 g/dl
• Grade 4 (Life threatening) <6.5 g/dl

Causes[link]

Broadly, causes of anemia may be classified as impaired red blood cell (RBC) production, increased RBC destruction (hemolytic anemias), blood loss and fluid overload (hypervolemia). Several of these may interplay to cause anemia eventually. Indeed, the most common cause of anemia is blood loss, but this usually doesn't cause any lasting symptoms unless a relatively impaired RBC production develops, in turn most commonly by iron deficiency.^[21] (See Iron deficiency anemia)

Impaired production[link]

• Disturbance of proliferation and differentiation of stem cells.
  • Pure red cell aplasia^[22]
  • Aplastic anemia,^[22] affecting all kinds of blood cells. Fanconi anemia is a hereditary disorder or defect featuring aplastic anemia and various other abnormalities.
  • Anemia of renal failure,^[22] by insufficient erythropoietin production
  • Anemia of endocrine disorders

• Disturbance of proliferation and maturation of erythroblasts
  • Pernicious anemia^[22] is a form of megaloblastic anemia due to vitamin B₁₂ deficiency dependent on impaired absorption of vitamin B₁₂.
  • Anemia of folic acid deficiency.^[22] As with vitamin B₁₂, it causes megaloblastic anemia
  • Anemia of prematurity, by diminished erythropoietin response to declining hematocrit levels, combined with blood loss from laboratory testing. It generally occurs in premature infants at 2 to 6 weeks of age.
  • Iron deficiency anemia, resulting in deficient heme synthesis^[22]
  • thalassemias, causing deficient globin synthesis^[22]
  • Congenital dyserythropoietic anemias, causing ineffective erythropoiesis
  • Anemia of renal failure^[22] (also causing stem cell dysfunction)

• Other mechanisms of impaired RBC production
  • Myelophthisic anemia^[22] or myelophthisis is a severe type of anemia resulting from the replacement of bone marrow by other materials, such as malignant tumors or granulomas.
  • Myelodysplastic syndrome^[22]
  • anemia of chronic inflammation^[22]

Increased destruction[link]

Anemias of increased red blood cell destruction are generally classified as hemolytic anemias. These are generally featuring jaundice and elevated LDH levels.

• Intrinsic (intracorpuscular) abnormalities,^[22] where there the red blood cells have defects that cause premature destruction. All of these, except paroxysmal nocturnal hemoglobinuria, are hereditary genetic disorders.^[23]
  • Hereditary spherocytosis^[22] is a hereditary defect that results in defects in the RBC cell membrane, causing the erythrocytes to be sequestered and destroyed by the spleen.
  • Hereditary elliptocytosis,^[22] another defect in membrane skeleton proteins
  • Abetalipoproteinemia,^[22] causing defects in membrane lipids
  • Enzyme deficiencies
    • Pyruvate kinase and hexokinase deficiencies,^[22] causing defect glycolysis
    • Glucose-6-phosphate dehydrogenase deficiency and glutathione synthetase deficiency,^[22] causing increased oxidative stress
  • Hemoglobinopathies
    • Sickle cell anemia^[22]
    • Hemoglobinopathies causing unstable hemoglobins^[22]
  • Paroxysmal nocturnal hemoglobinuria^[22]

• Extrinsic (extracorpuscular) abnormalities
  • Antibody-mediated
    • Warm autoimmune hemolytic anemia is an anemia caused by autoimmune attack against red blood cells, primarily by IgG. It is the most common of the autoimmune hemolytic diseases.^[24] It can be idiopathic, that is, without any known cause, drug-associated or secondary to another disease such as systemic lupus erythematosus, or a malignancy, such as chronic lymphocytic leukemia (CLL)^[25][25]
    • Cold agglutinin hemolytic anemia is primarily mediated by IgM. It can be idiopathic^[26] or result from an underlying condition.
    • Rh disease,^[22] one of the causes of hemolytic disease of the newborn
    • Transfusion reaction to blood transfusions^[22]
  • Mechanical trauma to red cells
    • Microangiopathic hemolytic anemias, including thrombotic thrombocytopenic purpura and disseminated intravascular coagulation^[22]
    • Infections, including malaria^[22]
    • heart surgery

Blood loss[link]

• Anemia of prematurity from frequent blood sampling for laboratory testing, combined with insufficient RBC production.
• Trauma^[22] or surgery, causing acute blood loss
• Gastrointestinal tract lesions,^[22] causing a rather chronic blood loss
• Gynecologic disturbances,^[22] also generally causing chronic blood loss
• From menstruation, mostly among young women

Fluid overload[link]

Fluid overload (hypervolemia) causes decreased hemoglobin concentration and apparent anemia:

• General causes of hypervolemia include excessive sodium or fluid intake, sodium or water retention and fluid shift into the intravascular space.^[27]
• Anemia of pregnancy is anemia that is induced by blood volume expansion experienced in pregnancy.

Treatments[link]

Treatments for anemia depend on severity and cause.

Iron deficiency from nutritional causes is rare in men and post-menopausal women. The diagnosis of iron deficiency mandates a search for potential sources of loss such as gastrointestinal bleeding from ulcers or colon cancer. Mild to moderate iron-deficiency anemia is treated by oral iron supplementation with ferrous sulfate, ferrous fumarate, or ferrous gluconate. When taking iron supplements, it is very common to experience stomach upset and/or darkening of the feces. The stomach upset can be alleviated by taking the iron with food; however, this decreases the amount of iron absorbed. Vitamin C aids in the body's ability to absorb iron, so taking oral iron supplements with orange juice is of benefit.

Vitamin supplements given orally (folic acid) or intramuscularly (vitamin B-12) will replace specific deficiencies.

In anemia of chronic disease, anemia associated with chemotherapy, or anemia associated with renal disease, some clinicians prescribe recombinant erythropoietin, epoetin alfa, to stimulate red-cell production.

In severe cases of anemia, or with ongoing blood loss, a blood transfusion may be necessary.

Blood transfusions[link]

Doctors attempt to avoid blood transfusion in general, since multiple lines of evidence point to increased adverse patient clinical outcomes with more intensive transfusion strategies. The physiological principle that reduction of oxygen delivery associated with anemia leads to adverse clinical outcomes is balanced by the finding that transfusion does not necessarily mitigate these adverse clinical outcomes.

In severe, acute bleeding, transfusions of donated blood are often lifesaving. Improvements in battlefield casualty survival is attributable, at least in part, to the recent improvements in blood banking and transfusion techniques.^{[citation needed]}

Transfusion of the stable but anemic hospitalized patient has been the subject of numerous clinical trials.

Four randomized controlled clinical trials have been conducted to evaluate aggressive versus conservative transfusion strategies in critically ill patients. All four of these studies failed to find a benefit with more aggressive transfusion strategies.^{[28][29][30][31]}

In addition, at least two retrospective studies have shown increases in adverse clinical outcomes in critically ill patients that underwent more aggressive transfusion strategies.^[32][33]

Hyperbaric oxygen[link]

Treatment of exceptional blood loss (anemia) is recognized as an indication for hyperbaric oxygen (HBO) by the Undersea and Hyperbaric Medical Society.^[34][35] The use of HBO is indicated when oxygen delivery to tissue is not sufficient in patients who cannot be transfused for medical or religious reasons. HBO may be used for medical reasons when threat of blood product incompatibility or concern for transmissible disease are factors.^[34] The beliefs of some religions (ex: Jehovah's Witnesses) may require they use the HBO method.^[34]

In 2002, Van Meter reviewed the publications surrounding the use of HBO in severe anemia and found that all publications report a positive result.^[36]

References[link]

External links[link]

• National Anemia Action Council (USA)

This article is about the philanthropist. For institutions named after him, see Johns Hopkins University and Johns Hopkins Hospital.

Johns Hopkins
Born	(1795-05-19)May 19, 1795 Anne Arundel County, Maryland, US
Died	December 24, 1873(1873-12-24) (aged 78) Baltimore, Maryland, US
Occupation	Entrepreneur, investor, philanthropist, abolitionist
Net worth	USD $10 million at the time of his death (approximately 1/944th of US GNP)[1]
Religion	Quaker

Johns Hopkins (May 19, 1795^[2] – December 24, 1873) was an American entrepreneur, abolitionist and philanthropist of 19th-century Baltimore, Maryland.

His bequests founded numerous institutions bearing his name, including Johns Hopkins Hospital, Johns Hopkins University, Johns Hopkins School of Nursing, Johns Hopkins School of Medicine, and Johns Hopkins Bloomberg School of Public Health.

A biography entitled Johns Hopkins: A Silhouette written by his cousin, Helen Hopkins Thom, was published in 1929 by the Johns Hopkins University Press.

Early life[link]

Johns Hopkins was born on May 19, 1795, to Samuel Hopkins (1759–1814) of Anne Arundel County, Maryland, and Hannah Janney (1774–1864), of Loudoun County, Virginia. Home was Whitehall, a 500-acre (two km²) tobacco plantation in Anne Arundel County.^[3] His first name derives from a maternal great-grandmother, Margaret Johns, who passed it on to her son.

The Hopkins family were members of the Society of Friends (Quakers). In 1807 they emancipated their slaves in accordance with their local Society decree, which called for freeing the able-bodied and caring for the others, who would remain at the plantation and provide labor as they could.^[4] The second eldest of eleven children, 12 year-old Johns was required to work on the farm, interrupting his formal education. From 1806 to 1809, he likely attended The Free School of Anne Arundel County, which was located in today's Davidsonville, Maryland.

In 1812, at the age of 17, Hopkins left the plantation to work in his uncle Gerard Hopkins' Baltimore wholesale grocery business. While living with his uncle's family, Johns and his cousin, Elizabeth, fell in love; however, the Quaker taboo against marriage of first cousins was especially strong, and neither Johns nor Elizabeth ever married.^[3]

As he became able, Hopkins provided for his extended family, both during his life and posthumously through his will. He bequeathed a home for Elizabeth, where she lived until her death in 1889.

Whitehall Plantation is located in today's Crofton, Maryland. Its home, since restored and modified, is on Johns Hopkins Road, adjacent to Reidel Road. The heavily landscaped property is surrounded by Walden Golf Course, and bears a historic marker.

Business years[link]

Hopkins' early experiences and successes in business came when he was put in charge of the store while his uncle was away during the War of 1812. After seven years with his uncle, Hopkins went into business together with Benjamin Moore, a fellow Quaker. The business partnership was later dissolved with Moore purporting Hopkins' penchant for capital accumulation as the cause for the divide.^[3]

After Moore's withdrawal, Hopkins partnered with three of his brothers and established Hopkins & Brothers. The company prospered by selling various wares in the Shenandoah Valley from Conestoga wagons, sometimes in exchange for corn whiskey, which was then sold in Baltimore as "Hopkins' Best". The bulk of Hopkins' fortune however was made by his judicious investments in a myriad of ventures, most notably the Baltimore and Ohio Railroad (B&O), of which he became a Director in 1847 and Chairman of the Finance Committee in 1855. He was also President of Merchants' Bank as well as director of a number of other organizations.^[5]

A charitable individual, Hopkins put up his own money more than once to not only aid Baltimore City during times of financial crises, but also to twice bail the railroad out of debt, in 1857 and 1873.^[6] In 1996, Johns Hopkins ranked 69th in "The Wealthy 100: From Benjamin Franklin to Bill Gates - A Ranking of the Richest Americans, Past and Present."^[7]

Civil War[link]

One of the first campaigns of the American Civil War was planned at Johns Hopkins' summer estate, Clifton, where he had also entertained a number of foreign dignitaries including the future King Edward VII.^[8] Hopkins was a strong supporter of the Union, unlike most Marylanders, who sympathized with and often supported the South and the Confederacy.^[9] During the Civil War, Clifton became a frequent meeting place for local Union sympathizers, and federal officials.

Hopkins' support of Abraham Lincoln also often put him at odds with some of Maryland's most prominent people, particularly Supreme Court Justice Roger B. Taney, who continually opposed Lincoln's presidential decisions, such as his policies of limiting habeas corpus and stationing troops in Maryland. In 1862 Hopkins wrote a letter to Lincoln requesting the President not to heed the detractors' calls and continue to keep soldiers stationed in Maryland. Hopkins also pledged financial and logistic support to Lincoln, in particular the free use of the B&O railway system.^[10][11]

Abolitionism[link]

Johns Hopkins is described as being an "abolitionist before the word was even invented", having been represented as such both prior to the Civil War period, as well as during the Civil War and Reconstruction Era.^[12][13][14] There are several accounts that describe the abolitionist influence Hopkins was privy to as a 12 year old participant in his parents' emancipation of their family's slaves in 1807.^[3] Prior to the Civil War Johns Hopkins worked closely with two of America's most famous abolitionists, Myrtilla Miner^[15] and Henry Ward Beecher.^[16] During the Civil War Johns Hopkins, being a staunch supporter of Lincoln and the Union, was instrumental in bringing fruition to Lincoln's emancipatory vision.^[17][18]

After the Civil War and during Reconstruction, Johns Hopkins' stance on abolitionism infuriated many prominent people in Baltimore.^[19][20] During the American Reconstruction period to his death ^[21] his abolitionism was expressed in the documents founding the Johns Hopkins Institutions, and reported in newspaper articles before, during, and after the founding of these institutions. Before the war, there was significant written opposition to his support for Myrtilla Miner's founding of a school for African American females^[22] (now the University of the District of Columbia). Similarly, opposition (and some support) was expressed during Reconstruction, such as in 1867, the same year he filed papers incorporating the Johns Hopkins Institutions, when he attempted unsuccessfully to stop the convening of the Constitutional Convention where the Democratic Party came into power and where a new Constitution, the Constitution still in effect, was voted to replace the Constitution of the Radical Republicans previously in power.^[23]

Apparent also in the literature of the times was opposition, and support for, the various other ways he expressed opposition to the racial practices that were beginning to emerge, and re-emerge as well, in the city of Baltimore, the state of Maryland, the nation and in the posthumously constructed and founded institutions that would carry his name,^[24] A Baltimore American journalist praised Hopkins for founding three institutions, a university, a hospital and an orphan asylum, specifically for colored children, adding that Hopkins was a "man (beyond his times) who knew no race" citing his provisions for both blacks and whites in the plans for his hospital. The reporter also pointed to similarities between Benjamin Franklin's and Johns Hopkins' views on hospital care and construction, such as their shared interest in free hospitals and the availability of emergency services without prejudice. This article, first published in 1870, also accompanied Hopkins' obituary in the Baltimore American as a tribute in 1873. Cited in many of the newspaper articles on him during his lifetime and immediately after his death were his provisions of scholarships for the poor, and quality health services for the underserved, the poor without regard to their age, sex and color, the colored children asylum and other orphanages, the mentally ill and convalescents.

Philanthropy[link]

Living his entire adult life in Baltimore, Hopkins made many friends among the city's social elite, many of them Quakers. One of these friends was George Peabody, who was also born in 1795, and who in 1857 founded the Peabody Institute in Baltimore. Other examples of public giving were evident in the city, as public buildings housing free libraries, schools and foundations sprang up along the city's widening streets. On the advice of Peabody, some believe, Hopkins determined to use his great wealth for the public good.

The Civil War had taken its toll on Baltimore, however, as did the yellow fever and cholera epidemics that repeatedly ravaged the nation's cities, killing 853 in Baltimore in the summer of 1832 alone. Hopkins was keenly aware of the city's need for medical facilities, particularly in light of the medical advances made during the war, and in 1870 he made a will setting aside seven million dollars - mostly in B&O stock - for the incorporation of a free hospital and affiliated medical and nurse's training colleges, as well as an orphanage for colored children and a university. Many board members were on both boards. The hospital and orphan asylum would each be overseen by the 12-member hospital board of trustees, and the university by the 12-member university board of trustees. Johns Hopkins' bequest was used to posthumously found the Johns Hopkins Colored Children Orphan Asylum ^[25] first as he requested, in 1875; the Johns Hopkins University in 1876; the Johns Hopkins Press, the longest continuously operating academic press in America, in 1878; the Johns Hopkins Hospital and the Johns Hopkins School of Nursing in 1889; the Johns Hopkins University School of Medicine 1893; and the Johns Hopkins School of Hygiene and Public Health in 1916.

Johns Hopkins' views on his bequests, and on the duties and responsibilities of the two board of trustees, especially the hospital board of trustees led by his friend and fellow Quaker Francis King, were formally stated primarily in four documents, the incorporation papers filed in 1867, his instruction letter to the hospital trustees dated March 12, 1873, his will, which was quoted from extensively in his Baltimore Sun obituary,^[26] and in his will's two codicils, one dated 1870 and the other dated 1873.^[27]

In these documents, Hopkins also made provisions for scholarships to be provided for poor youths in the states where Johns Hopkins had made his wealth, as well as assistance to orphanages other than the one for African American children, to members of his family, to those he employed, black and white, his cousin Elizabeth, and, again, to other institutions for the care and education of youths regardless of color and the care of the elderly, and the ill, including the mentally ill, and convalescents.

John Rudolph Niernsee, one of the most famous architects of the time, designed the orphan asylum and helped to design the Johns Hopkins Hospital. The original site for the Johns Hopkins University had been chosen personally by Hopkins. According to his will, it was to be located at his summer estate, Clifton. However, a decision was made not to found the university there. The property, now owned by the city of Baltimore, is the site of a golf course and a park named Clifton Park. While the Johns Hopkins Colored Children Orphan Asylum was founded by the hospital trustees, the other institutions that carry the name of "Johns Hopkins" were founded under the administration of the first president of the Johns Hopkins University and Johns Hopkins Hospital, Daniel Coit Gilman and his successors.

Colored Children Orphan Asylum[link]

As per Johns Hopkins' instruction letter, the Johns Hopkins Colored Children Orphan Asylum (JHCCOA)^[28] was founded first, in 1875, a year before Gilman's inauguration, now the founding date of the university. The construction of the asylum, including its educational and living facilities, was praised by The Nation and the Baltimore American, the latter stating that the orphan asylum was a place where "nothing was wanting that could benefit science and humanity". As was done for other Johns Hopkins Institutions, it was planned after visits and correspondence with similar institutions in Europe and America.

The Johns Hopkins Orphan Asylum opened with 24 boys and girls. Under Gilman and his successors, this orphanage was later changed to serve as an orphanage and training school for black female orphans principally as domestic workers, and next as an "orthopedic convalescent" home and school for "colored crippled" children and orphans. The asylum was eventually closed in 1924 nearly fifty years after it opened, and was never reopened.

Hospital, University, Press, and Schools of Nursing and Medicine[link]

As per Hopkins' March 1873 Instruction Letter, the School of Nursing was founded alongside the Hospital in 1889 by the hospital board of trustees in consultation with Florence Nightingale. Both the nursing school and the hospital were founded over a decade after the founding of the orphan asylum in 1875 and the university in 1876. Hopkins' instruction letter explicitly stated his vision for the hospital; first, to provide assistance to the poor of "all races", no matter the indigent patient's "age, sex or color"; second, that wealthier patients would pay for services and thereby subsidize the care provided to the indigent; third, that the hospital would be the administrative unit for the orphan asylum for African American children which was to receive $25,000 in annual support out of the hospital's half of the endowment; and fourth, that the hospital and orphan asylum should serve 400 patients and 400 children respectively, fifth, that the hospital should be part of the university, and, sixth, that religion but not sectarianism should be an influence in the hospital.

By the end of Gilman's presidency, Johns Hopkins University, Johns Hopkins Press, Johns Hopkins Hospital and Johns Hopkins School of Nursing, and Johns Hopkins School of Medicine, and Johns Hopkins Colored Children Orphan Asylum had been founded, the latter by the trustees, and the others in the order listed under the Gilman administration. "Sex" and "color" were major issues in the early history of the Johns Hopkins Institutions. The founding of the School of Nursing is usually linked to Johns Hopkins' statements in his March 1873 instruction letter to the trustees that "I desire you to establish, in connection with the hospital, a training school for female nurses. This provision will secure the services of women competent to care for those sick in the hospital wards, and will enable you to benefit the whole community by supplying it with a class of trained and experienced nurses".

Women's most well known success after the founding of the nursing school was their requirement that they be allowed to attend Johns Hopkins medical institutions after they provided funds that made possible the opening of the School of Medicine in 1893. Five African American women were among the first women enrolled in the Johns Hopkins University's undergraduate school in 1970. Furthermore Kelly Miller and Frederick Scott were the first persons of African descent to attend the Johns Hopkins University's graduate and undergraduate schools, respectively. Frederick Scott was the first graduate of African descent from Johns Hopkins University, and he, Robert Gamble, and Kenyan-born James Nabwangu were the first graduates of African descent from Johns Hopkins University's undergraduate school, and Johns Hopkins' medical schools respectively. Those employees holding jobs in the service sector are those of African descent who have the longest and most continuous history at the Johns Hopkins Institutions.

Legacy[link]

Johns Hopkins Monument

(at Johns Hopkins University)

Following Hopkins' death, the Baltimore Sun wrote a lengthy obituary which closed thus: "In the death of Johns Hopkins a career has been closed which affords a rare example of successful energy in individual accumulations, and of practical beneficence in devoting the gains thus acquired to the public." His contribution to the university that has become his greatest legacy was, by all accounts, the largest philanthropic bequest ever made to an American educational institution.

Johns Hopkins' Quaker faith and his early life experiences, in particular the 1807 emancipation, had a lasting influence throughout his life and his posthumous legacy as a businessman, railroad man, banker, investor, ship owner,^[29] philanthropist and a founder of several Institutions. From very early on, Johns Hopkins had looked upon his wealth as a trust to benefit future generations. He is said to have told his gardener that, "like the man in the parable, I have had many talents given to me and I feel they are in trust. I shall not bury them but give them to the lads who long for a wider education"; his philosophy quietly anticipated Andrew Carnegie's much publicized Gospel of Wealth by more than 25 years.^[30]

His philanthropy, banking and other business practices were founded neither on slavery nor on the separate but unequal racism of the post Civil War years of his life. In this vein, integral parts of his legacy, as an emancipator, a founder of an orphan asylum for African-American youths, a staunch advocate of abolitionism and of quality care not just for those physically ill, but also for the elderly, the poor, no matter their age, gender, or skin color, and the mentally ill, have by and large been overlooked, even in the institutions that carry his name.

In 1973 Johns Hopkins was cited prominently in the Pulitzer Prize winning book The Americans: The Democratic Experience by Daniel Boorstin, former head of the Library of Congress. From November 14, 1975 to September 6, 1976 Hopkins portrait was displayed at the National Portrait Gallery in an exhibit on the democratization of America based on Boorstin's book. In 1989, the United States Postal Service issued a $1 postage stamp in Johns Hopkins' honor, as part of the Great Americans series.^[31]

References[link]

External links[link]

	United States portal
	Maryland portal

• Genealogical Records on Marylanders
• Thom and Jacob discuss his love for his cousin and Quaker traditions
• In his 1887 memoir, Baltimore and the Nineteenth of April, 1861: A Study of the War, George William Brown cites Johns Hopkins as a wealthy Union man in Baltimore, a city with strong Confederate and Southern leanings
• In The Chronicles of Baltimore: Being a Complete History of "Baltimore Town" and Baltimore City from the Earliest Period to the Present Time published in 1874, John Thomas Scharf cited the 1873 instruction letter to the hospital trustees and a city council resolution thanking Johns Hopkins for his philanthropy. Thom's biography and New York and Maryland newspapers were sources that published parts or all of this letter
• The Institutional Records of The Johns Hopkins Hospital Colored Orphan Asylum
• Abstract Johns Hopkins Dream for a Model of its Kind: The JHH Colored Orphans Asylum", 2000 Conference International Society for the History of Medicine BY Dr. P. Reynolds
• Grave site of Johns Hopkins
• Graveside ceremony for Johns Hopkins
• Baltimore and the Nineteenth of April, 1861: A Study of the War, the memoir of George William Brown then the mayor of Baltimore city, later a member of the university board of trustees of the Johns Hopkins University
• The Chronicles of Baltimore: Being a Complete History of "Baltimore Town" and Baltimore City from the Earliest Period to the Present Time published in 1874 by John Thomas Scharf
• "If He Could See Us Now: Mr. Johns Hopkins' Legacy Strong University, Hospital Benefactor Turned 200 on May 19, 1995", Mike Field, the author, contradicts this statement
• Chronology, Nursing school
• The Institutional Records of The Johns Hopkins Hospital Colored Orphan
• Abstract Johns Hopkins Dream for a Model of its Kind: The JHH Colored Orphans Asylum" By Dr. P. Reynolds
• "If He Could See Us Now: Mr. Johns Hopkins' Legacy Strong University, Hospital Benefactor Turned 200 on May 19, 1995" by Mike Field a writer for the Johns Hopkins Gazette. Field, Thom, and Jacob called Johns Hopkins an abolitionist. See also The Racial Record of Johns Hopkins University in the Journal of Blacks in Higher Education, No. 25, Autumn, 1999, pp. 42-43/ JSTOR
• Johns Hopkins, Maryland State Archives
• "The History of African Americans @ Johns Hopkins University" See in particular the chronology and the paper by Danton Rodriguez.