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hepatitis serology 321 herpes gestationis (HG) antibodies
hepatitis serology
Hepatitis B antigens and antibodies against them. Core
antigen is designated HBc. The HBc particle is comprised
of double-stranded DNA and DNA polymerase. It has an
association with HBe antigens. Core antigen signifies persistence
of replicating hepatitis B virus. Anti-HBc antibody is a
serologic indicator of hepatitis B. It is an immunoglobulin M
(IgM) antibody that increases early and is still detectable 20
years post-infection. The IgM anti-HBc antibody assay is the
best for acute hepatitis B. The HBe antigen (HBeAG) follows
the same pattern as HBsAg antigen. When found, it signifies
a carrier state. Anti-HBe increases as HBe decreases.
Anti-HBe appears in patients who are recovering and may
last for years after the hepatitis is resolved. The first antigen
detectable following hepatitis B infection is surface antigen
(HBsAg). It is detectable a few weeks before clinical disease
and is highest with the first appearance of symptoms. It disappears
6 months from infection. Antibody to HBs increases
as the HBsAg levels diminish. Anti-HBs is often detectable
for the lifetime of the individual.
hepatitis vaccines
The vaccine used to actively immunize subjects against
hepatitis B virus contains purified hepatitis B surface
antigen. Current practice uses an immunogen prepared by
recombinant DNA technology (Recombivax). The antigen
preparation is administered in three sequential intramuscular
injections to individuals such as physicians, nurses, and
other medical personnel who are at risk. Temporary protection
against hepatitis A is induced by the passive administration
of pooled normal human serum immunoglobulin, which
protects against hepatitis A virus for a brief time. Antibody
for passive protection against hepatitis must be derived from
the blood sera of specifically immune individuals.
hepatocyte-stimulating factor
A substance indistinguishable from interleukin-6 (IL6),
classified as a monokine, that stimulates hepatocytes to
produce acute phase reactants.
hepatosplenomegaly
Liver and spleen enlargement attributable to an expanded
lymphocyte population.
herbimycin A
An inhibitor of T cell activation. Its target is the Sre family
of protein tyrosine kinases.
Herceptin ®
Refer to trastuzumab.
herd immunity
Nonspecific factors along with specific immunity may have
a significant role in resistance of a group (herd) of humans
or other animals against an infectious disease agent.
Elimination of reservoirs of the disease agent may be as
important as specific immunity in diminishing disease incidence
among individuals. Herd immunity also means that
an epidemic will not follow infection of a single member
of the herd or group if other members are immune to that
particular infectious agent. The successful vaccination of
most members of a population against a selected pathogen
may protect nonimmune individuals in the group, whose
vulnerability is diminished because the pathogen cannot
become established in the vaccinated population.
hereditary angioedema (HAE)
A disorder in which recurrent attacks of edema persisting
for 48 to 72 hours occur in the skin and gastrointestinal
and respiratory tracts. It is nonpitting and life-threatening
if laryngeal edema becomes severe enough to obstruct the
airway. Swelling of the epiglottis may lead to suffocation.
Edema in the jejunum may be associated with abdominal
cramps and bilious vomiting. Edema of the colon may
lead to watery diarrhea. No redness or itching is associated
with edema of the skin. Tissue trauma of no apparent
initiating cause may induce an attack. HAE is due to
decreased or absent C1 inhibitor (C1 INH). It is inherited
in an autosomal-dominant fashion. Heterozygotes for the
defect develop the disorder. Greatly diminished C1 INH
levels (5 to 30% of normal) are found in affected individuals.
Activation of C1 leads to increased cleavage of C4
and C2, decreasing their serum levels during an attack.
C1 INH is also a kinin system inactivator. The C1 INH
deficiency in HAE permits a kinin-like peptide produced
from C2b to increase vascular permeability, leading to
the manifestations of HAE. Some have proposed that
bradykinin may represent the vasopermeability factor.
Hereditary angioedema has been treated with ε aminocaproic
acid and transexamic acid, but they do not elevate C1
INH or C4 levels. Anabolic steroids such as danazol and
stanozolol, which activate C1 INH synthesis in affected
individuals, represent the treatment of choice.
hereditary angioneurotic edema (HANE)
Refer to hereditary angioedema.
hereditary ataxia telangiectasia
Refer to ataxic telangiectasia.
hereditary complement deficiencies
Associated with defects in activation of the classical pathway
that lead to increased susceptibility to pyogenic infections.
A deficiency of C3 produces a defect in activation of
both the classical and alternative pathways that leads to an
increased frequency of pyogenic infections that may prove
fatal. Other characteristics are defective opsonization and
phagocytosis. Defects of alternate pathway factors D and P
lead to impaired activation of the alternative pathway with
increased susceptibility to pyogenic infections. Deficiencies
of C5 through C9 are associated with defective membrane
attack complex (MAC) formation and lysis of cells, including
bacteria. This produces increased susceptibility to
disseminated Neisseria infection.
herpes gestationis (HG)
A very pruritic blistering condition of the skin characterized
by vesicles and bullae that develop in rare cases of
pregnancy. HG is rare in black subjects and is associated
with HLA-DR3 and DR4. By light microscopy, a subepidermal
bulla with eosinophils may be identified in a few
cases. Edema of the papillary dermis, lymphohistiocytic
infiltrate with eosinophils in perivascular regions, spongiosis,
liquefactive degeneration, and possible necrosis in
the epidermis are present. The eruption occurs usually in
the second or third trimester of pregnancy and appears as
hive-like plaques, blisters, or vesicles. Immunofluorescence
reveals C3 at the dermal–epidermal junction in nearly all
cases, and IgG in 25% of biopsies. Circulating IgG antibody
binds to the herpes gestationis antigen, a 180-kDa epidermal
protein in the skin basement membrane.
herpes gestationis (HG) antibodies
Antibodies present in 89% of HG sera that are incomplete
Freund’s adjuvant (IFA)-positive and in sera of 47% of
patients with bullous pemphigoid. These antibodies are not
H