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hemolytic system 318 hepatitis A (inactivated, injection)
hemolytic system
The visible phase of a complement fixation test in which
sheep red blood cells (SRBCs) combine with their homologous
antibody and are added to a system in which antigen
is mixed with patient serum, presumed to contain specific
antibody, followed by complement. If antibody is present
in the patient’s serum and combines with the antigen, the
added complement is fixed and is no longer available to
react with antibody-coated sheep red cells, which are added
as the second phase or visible reaction. Lysis indicates the
presence of free complement from the first phase of the
reaction, indicating that antibody against the antigen in
question is not present in the patient’s serum. By contrast,
no hemolysis indicates the presence of the antibody. The
hemolytic system may also be used to describe a reaction
in which erythrocytes are combined with their homologous
antibody. The addition of all nine components of complement
together with calcium and magnesium ions followed
by incubation at 37°C results in immune lysis (hemolysis).
hemophagocytic syndrome (HPS)
A primary immunodeficiency attributable mainly to
a granule exocytosis pathway defect of cytotoxic T
lymphocytes. Also referred to as hemophagocytic
lymphohistiocytosis.
hemophilia
An inherited coagulation defect attributable to blood
clotting factor VIII, factor IX, or factor XI deficiency.
Hemophilia A patients are successfully maintained by the
administration of exogenous factor VIII, which is now
safe. Before mid-1985, factor products transmitted several
cases of AIDS when factor VIII was accidentally extracted
from the blood of HIV-positive subjects. Hemophilia B
patients are treated with factor IX. Hemophilia A and B are
X-linked; hemophilia C is autosomal.
Hemophilus influenzae vaccine
Refer to Hib.
hemopoietic resistance (HR)
Transplantation of allogeneic, parental, or xenogeneic
bone marrow or leukemia cells into animals exposed to
total body irradiation often results in the destruction of the
transplanted cells. The mechanism causing the failure of the
transplant appears similar for all three types of cells. This
phenomenon, designated hemopoietic resistance (HR), has
a genetic basis and mechanism different from conventional
transplantation reactions against solid tumor allografts. It
does not require prior sensitization and apparently involves
the cooperation of natural killer (NK) cells and macrophages,
both resistant to irradiation. The NK cells have
the characteristics of null cells; macrophages play an accessory
cell role. The cooperative activity seems to represent in
vivo surveillance against leukemogenesis.
hemostatic plug
The immediate response to a vessel wall injury is the adhesion
of platelets to the injury site and the growth by further
aggregation of platelets of a mass that tends to obstruct
(often incompletely) the lumen of the damaged vessel. This
platelet mass is called a hemostatic plug. The exposed basement
membranes at the sites of injury are the substrate for
platelet adhesion, but deeper tissue components may have
a similar effect. Far from being static, the hemostatic plug
has a continuous tendency to break up with new masses
re-formed immediately at the original site.
Henoch–Schoenlein purpura
A systemic form of small vessel vasculitis that is characterized
by arthralgias, nonthrombocytopenic purpuric skin
lesions, abdominal pain with bleeding, and renal disease.
Immunologically, immune complexes containing IgA
activate the alternate pathway of complement. Patients may
present with upper respiratory infections preceding onset of
the disease. Certain drugs, food, and immunizations have
also been suspected as etiologic agents. The disease usually
occurs in children 4 to 7 years of age, although it can occur
in adults. Histopathologically, diffuse leukocytoclastic vasculitis
involves small vessels. The submucosa and subserosa
of the bowel may be sites of hemorrhage. There may be focal
or diffuse glomerulonephritis in the kidneys. Children may
manifest lesions associated with the skin, gastrointestinal
tract, or joints, whereas in adults the disease is usually associated
with skin findings. The skin lesions begin as a pruritic
urticarial lesion that develops into a pink maculopapular spot,
which matures into a raised and darkened lesion. The maculopapular
lesion may ultimately resolve in 2 weeks without
leaving a scar. Patients may also have arthralgias associated
with the large joints of the lower extremities. Skin biopsy
reveals the vasculitis, and immunofluorescence examination
shows immunoglobulin A (IgA) deposits in vessel walls, in
accord with a diagnosis of Henoch–Schoenlein purpura.
HEP
Acronym for high egg passage, which signifies multiple passages
of rabies virus through eggs to achieve attenuation for preparation
of a vaccine appropriate for use in immunizing cattle.
heparan sulfate
A glycosaminoglycan that resembles heparin and is
comprised of the same disaccharide repeating unit; it is a
smaller molecule and less sulfated than heparin. An extracellular
substance, heparin sulfate is present in the lungs
and arterial walls and on numerous cell surfaces.
heparin
A glycosaminoglycan comprised of two types of disaccharide
repeating units. One is composed of d-glucosamine and
d-glucuronic acid, and the other is composed of d-glucosamine
and l-iduronic acid. Heparin is extensively sulfated
and is an anticoagulant. It unites with an antithrombin
III, which can unite with and block numerous coagulation
factors. It is produced by mast cells and endothelial cells.
It is found in the lungs, liver, skin, and gastrointestinal
mucosa. Based on its anticoagulant properties, heparin is
useful for treatment of thrombosis and phlebitis.
hepatitis A
A picornavirus, also called enterovirus 72. It is spread from
person to person via the fecal–oral route or by consumption
of contaminated water or food.
hepatitis A (inactivated, injection)
For active immunization of individuals 12 months of age
and older against disease caused by hepatitis A virus (HAV).
Primary immunization should be administered at least 2
weeks before expected exposure to HAV. Primary immunization
of children and adolescents (12 months to 18 years)
consists of a single dose of 720 enzyme-linked immunosorbent
assay (ELISA) units in 7.5 mL and a booster dose (720
units in 0.5 mL) should be administered 6 to 12 months later.
For adults, primary immunization consists of a single dose of
1440 ELISA units in 1 mL and a booster dose (1440 units in
1 mL) should be administered 6 to 12 months later.