Hemostasis is the functional system of the body, providing, on the one hand, to stop and
prevent bleeding in violation of the integrity of the vascular wall, on the other - to save the liquid
state of circulating blood. In carrying out these two opposing goals (thrombosing at the broken
vessel and preventing thrombosis in systemic blood flow) involved three executives - vascular,
platelet and plasma. The clinical consequence is that not heavy damage or failure of one of
hemostatic mechanisms (inherited or acquired) can be compensated by enhanced functional
activity of another, and therefore clinically over a long period of life does not manifest bleeding
disorders. Only when there is an additional "disturbing factor" (an infectious disease and its
designees in connection with drugs, hypovitaminos and other nutritional deficiencies,
decompensated dysbacteriosis intestine, metabolic disorders, exacerbation of various chronic
diseases, adverse environmental impact, etc.) may appear hemorrhagic syndrome. For violations
of platelet disorders characterized by microcirculatory, petechial spotted (swelling) type of
bleeding disorders (spontaneous, mostly at night, emerging asymmetric hemorrhage into the skin
and mucous membranes, recurrent nosebleeds and microhematury; extended periods of bleeding
in women, melon, prolonged bleeding after a "small "surgery - removal of teeth, adeno-,
tonsillectomy, etc.); coagulation - gematomny (painful strained hemorrhage in the soft tissues,
joints, usually after a trauma, injection, prolonged bleeding from wounds). Vasculitic magenta
type observed in infectious and allergic vasculitis (often symmetrical, vegetative erythematous or
hemorrhagic rash, often combined with intestinal bleeding, often transforming into ICE
syndrome), and angiomatozny - with telangiectasia, angioma, arteriovenous shunts (persistent,
strictly localized and caused by local vascular pathology of bleeding). For some, hemorrhagic
diathesis and diseases typical of mixed-swell gematomny bleeding (von Willebrand disease, lack
of prothrombin complex factors and factor XIII, DVS-syndrome, overdose of anticoagulants and
thrombolytics, the appearance in the blood of immune inhibitors XIII and IV of the factors).
All primary hemorrhagic diathesis and the disease are divided into 3 groups:
coagulopathy, thrombocytopenia, and BPD, vazopathy.
Hereditary coagulopathy. Among all patients with hereditary coagulopathies from 9496% are diagnosed with hemophilia A and von Willebrand disease.
Hemophilia.
Hemophilia is a hereditary disease, transmitted by recessive, X-linked type, characterized
by a sharp slow blood clotting and bleeding disorders due to lack of coagulation activity VIII or
IX plasma factors of blood clotting. Hemophilia in the previously known disease Kristmass.
Pathogenesis. The concentration of factors VIII and IX in the blood plasma is not high
(respectively, 1 - 2 mg and 0.3 - 0.4 mg per 100 ml or one molecule of factor VIII per 1 million
molecules of albumin), but in the absence of one blood clotting in first of its phase along the
outer path of activation is dramatically slowed down or not occur.
Clinical picture. Characterized by:
1) prolonged bleeding after destroying the integrity of the skin and mucous membranes;
2) a tendency to focal massive hemorrhage (hematomy) into the subcutaneous tissue,
muscles, joints and internal organs after minimal trauma, shock, or even spontaneous bleeding.
Appears hemophilia more often in the second half of the 1-th - beginning of year 2 of life, in
sometimes later or already in the neonatal period. Bleeding in patients with hemophilia can occur
not immediately after the injury (eg, tooth extraction), and after 1 / 2 - 4 hours long bleeding,
usually do not stop at the local hemostatic therapy. Even procedures such as blood samples for
analysis, and subcutaneous injection within the muscle can cause the patient's bleeding continued
hours and even days. After intramuscular injection, a typical appearance of a very large
hematomy, which can cause compression of the nerves, causing the paralysis and paresis.
Bleeding into the joints is the most typical manifestation of hemophilia and the most frequent
cause of disability.
Diagnosis and differential diagnosis. Based on analysis of data pedigree (men on the
maternal side with bleeding disorders) and medical history, identifying the increasing duration of
withdrawal of venous blood by Lee - White (standard 8 minutes, while hemophilia dramatically
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lengthened) and violations in the first phase of blood clotting (when blood coagulation is not the
whole prothrombin goes into the clot, hence the low consumption of prothrombin; rate of 80100%), determination of activated partial time, low levels of factor VIII or IX.
Treatment. In hemophily has the following features:
1) intramuscular injections are forbidden (all products can only be assigned to either
intravenous inside);
2) any location and severity of bleeding, swelling and joint pain, suspicion of hemorrhage
in the internal organs - testimony to not slow ( even at night!) the introduction of concentrated
drugs;
3) should act similarly in injury in violation of the integrity of the skin;
4) the patient must be on a quarterly basis to visit a dentist with experience treating
children with hemophilia;
5) any surgical intervention is possible only after the introduction of drugs globulin. Used
for injections only superficial veins.
At present significant opportunities for improving the prognosis in the treatment of
hemophilia has made appearance in the treatment of antigemophilin factor (gemoctin STD),
which contains the active ingredient - coagulation factor VIII and factor Villibranta. Prepart used
for profilaction and treatment of bleeding in hemophily A.
Local therapy: the imposition of a tampon with a hemostatic sponge, thrombin, breast
milk in place of bleeding, the defect of the skin and mucous membranes. When Hemarthrosis 3 4 days immobilized joints, impose crepe bandage (but not longer). At very pronounced, painful
Hemarthrosis after transfusion of cryoprecipitate shown arthrocentesis and removal of blood (a
surgeon). The effectiveness of local application of cold (ice) is widely disputed.
Clinical supervision. Jointly haematologist specialized center and the district
pediatrician. A child is exempt from immunizations and physical education at school because of
the danger of injury. However, physical activity hemophiliac shown, since it increases the level
of factor VIII.
Willebrand disease.Von Willebrand disease (angiohemophily) hereditary disease usually
transmitted by an autosomal-dominant type, characterized by bleeding disorders, coupled with
increasing duration of bleeding, low levels of factor VIII in the blood and very low values (or
absence) of platelet adhesion to glass, platelet aggregation with ristocetine.
Clinical picture. In severe disease (factor VIII levels below 5% rule) does not differ
from the manifestations of hemophily. At a higher level of factor VIII to the forefront of
vascular-platelet type of bleeding: recurrent heavy bleeding skin, nasal, uterine, gastrointestinal
bleeding (and possibly bruising, particularly on the spot by intramuscular injection,
Hemarthrosis).
Diagnosis. Recognition of the disease is possible only with simultaneous and dynamic
study of the level of factor VIII and the properties of platelets, because even the most typical for
this disease defects may periodically disappear.
Typical defects include:
1) very sharp increase in bleeding time,
2) low platelet adhesion to fiber glass or glass beads, and
3) small amount of blood factor VIII,
4) low platelet aggregation with ristocetine.
The last defect is the most resistant. The platelet count is always normal. Endothelial
samples can be both positive and negative.
Treatment. In all forms of von Willebrand disease are highly effective as a hemostatic
remedy infusions of fresh frozen plasma (15 ml / kg) or cryoprecipitate, factor VIII concentrate
(20 IU / kg of patient weight) containing and VIII: vWF. Just as with hemophily A, shows the
appointment of aminocaproic acid (0,05 g / kg 4 times a day by mouth), ditsinona.
Thrombocytopenic purpura. Allocate primary and secondary thrombocytopenic
purpura. Refer to the primary idiopathic thrombocytopenic purpura (Idiopathic
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thrombocytopenic purpura), hereditary, isoimmune (congenital - incompatibility with the fetus
and the mother of platelet antigens, posttransfusion - after blood transfusions and platelet mass),
congenital transimmun (transient thrombocytopeny of newborns from mothers, patients with
idiopathic thrombocytopenic purpura, lupus erythematosus). Secondary (symptomatic),
thrombocytopeny in children develop more primary and may occur in acute infectious diseases
(particularly common in the perinatal viral infections), allergic reactions and illnesses that occur
with hyperreactivity of immediate type, collagen and other autoimmune disorders, DIC
syndrome, malignant blood diseases (leukemia, hypoplastic and vitamin B12-deficient anemia)
disease are accompanied by splenomegaly and dissplenizmom (portal hypertension in liver
cirrhosis, etc.), congenital anomalies of the blood vessels (hemangiomas) and metabolism
(Gaucher's, Nieman Pick, and others ).
Congenital isoimmune thrombocytopenic purpura usually occurs in the presence of fetal
platelet antigen RLA I and the absence of his mother (in a population of individuals 2-5%),
which leads to sensitization of the mother, the synthesis of its antiplatelet antibodies, which
penetrates through the placenta to cause trombotsitoliz fetus. Thrombocytopeny is held from 2 to
12 weeks, and sometimes even longer, although the increase in hemorrhagic syndrome docked at
rational therapy in the first days of life. Congenital transimmunny thrombocytopeny in the
neonatal period occurs in 30-50% of children from their mothers, patients with idiopathic
thrombocytopenic purpura. In half the cases is not accompanied by hemorrhagic disorders.
Genesis of thrombocytopeny associated with penetration from mother to fetus antiplatelet
antibodies and sensibilizovanny maternal lymphocytes. Clinical symptoms usually develop in the
first days of life: small ecchymosis on his back, chest, extremities, and rarely hemorrhage on the
mucous membranes, melena, epistaxis. Typically, mild bleeding, but described cases of
intracranial hemorrhage. Diagnosis is based on anamnestic, clinical and laboratory data with the
discovery of his mother antiplatelet autoantibodies, and the mother and child - to
autotrombotsitam sensitized lymphocytes.
Idiopathic thrombocytopenic purpura (ITP) is the primary hemorrhagic diathesis due to
lack of quantitative and qualitative platelet disorders. Characteristic signs of the disease are
purpura (hemorrhage in the thickness of the skin and mucous membranes) and bleeding of
mucous membranes and low platelet count in peripheral blood, normal or increased number of
megakaryocytes in the bone marrow, spleen and the absence of systemic diseases, for which may
be complicated thrombocytopenia.
Etiology and pathogenesis. ITP is a disease with a hereditary predisposition, is the
presence of BPD in patients with hereditary and therefore the viral infection (ARI, measles,
rubella, etc.), immunizations, physical and psychological trauma, and other external factors
could lead to a breach of the digestive function of macrophages continue to rise
immunopathological process - proliferation of sensitized lymphocytes to autotrombotsitam, the
synthesis of antiplatelet autoantibodies. According to modern concepts, the TPI always leads
immunopathological process. The formal genesis of thrombocytopeny in ITP is not in doubt increased destruction of platelets in the spleen, which is also the site of synthesis of antiplatelet
antibodies. Thrombocytopoiesis with ITP increased, as indicated by the large number of
megatrombotsitov in the blood. Bleeding in patients with ITP is caused by quantitative
(thrombocytopeny) and qualitative (BPD), deficiency of platelet hemostasis. The vascular
endothelium, devoid platelet function undergoes degeneration, leading to increased vascular
permeability, spontaneous hemorrhages.
Clinical picture. ATP in most cases develops in childhood, mainly in preschoolers.
Before puberty among patients with ITP, boys and girls occur with equal frequency, but among
older students girls have 2 times more. In the early and preschool age ITP usually develops
within 2-4 weeks after viral infection: cutaneous appear hemorrhage, bleeding in the mucous
membranes, bleeding.
Characteristic features of purpura in children are:
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1) polychrome (both on the skin can detect hemorrhages of different colors - from red to bluishgreen and yellow),
2) polymorphism (along with various sizes are available ecchymosis petechy), and
3) asymmetry,
4) the spontaneity origin, mainly at night.
Diagnosis. The most characteristic abnormalities in laboratory examination of patients
with ITP were thrombocytopeny (average platelet count in peripheral blood of 150-400 109 / l),
an increase in bleeding time after a standard injury, a positive test for resistance capillaries
(tourniquet, cupping, etc.), increasing the number of " inactive "megakaryocytes in the bone
marrow.
Treatment. Depends on the genesis of thrombocytopenia. Infants and isoimmune
transimmunnymi purpura within 2 weeks fed donor breast milk, and then put to the mother's
breast (with control number of platelets in peripheral blood of the child). In other
thrombocytopenic purpura of children fed normally, in accordance with age. Regime restrictions
usually needed only during hemorrhagic crisis. At any thrombocytopenic purpura (if we exclude
DIC-syndrome) showed the appointment of epsilon-aminocaproic acid (0,05-0,1 g / kg 4 times a
day) and other products that will improve the adhesive-platelet aggregation (adrokson, etamzilat,
ditsinon, calcium pantothenate, chlorophyllin sodium, ATP intramuscularly in combination with
magnesium inside, herbal medicine). During hemorrhagic crisis epsilon-aminocaproic acid
should be 1-2 times a day to enter intravenous drip. Immunoglobulin intravenous (only product
specially made) infusion at a dose of 0.5 g / kg body weight (10 ml / kg 5% solution) daily for 4
days leads to a rise in platelet counts at the end of treatment at 2/3-3 / 4 patients with ITP,
although only in 25-30% of patients achieved stable clinical remission.
Indications for the purpose of glucocorticoids to children with ITP are: generalized
cutaneous hemorrhagic syndrome, combined with the bleeding of mucous membranes, bleeding
in the sclera and retina, "wet" purpura complicated by hemorrhagic anemia, hemorrhages in
internal organs. Prednisolone appointed for 2 - 3 weeks at a dose of 2 mg / kg per day with a
further reduction in dose and the abolition of the drug. Long term, many months of
glucocorticoid therapy is ineffective and leads to several complications. Indications for
splenectomy in patients with ITP: "wet" purpura, which lasts more than 6 months and requiring
the appointment of repeated courses of glucocorticoids, acute purple in the presence of heavy
bleeding is not docked in the background, a modern complex therapy of suspected brain
haemorrhage.
PD. BPD is disorders of hemostasis caused by qualitative deficiency of blood platelets in
their normal number. There are hereditary and acquired BPD. Among the primary hereditary
platelet dysfunction most often occurs trombasteny. Secondary hereditary BPD typical for vWD.
Acquired BPD with hemorrhagic syndrome with or without typical of many blood diseases
(leukemy, hypoplastic and megaloblastic anemia), uremia, DIC-syndrome, immunocomplex
disease (hemorrhagic vasculitis, lupus erythematosus, diffuse glomerulonephritis and others),
drug-disease while taking salicylates, xanthine, Carbenicillin, etc.
Clinical picture. In different variants of platelet deficiency disease severity varies from
mild bleeding syndrome (a tendency to "swelling" with minor injuries, skin hemorrhage with
"rubbing" the body of clothing, on-site compression of the rubber bands or with the strong
pressure on the limb, slim recurrent nosebleeds, "family" prolonged menstrual bleeding in
women, etc.) to heavy nasal, uterine, gastrointestinal bleeding, a common skin purpura. Often
such patients have a small surgery (tooth extraction, adenotomy, tonsillectomy, etc.) cause a
heavy and prolonged bleeding, leading to anemia. Cutaneous hemorrhagic syndrome may be in
the form of petechiae, ecchymosis, less bruising. Often the "minimal bleeding" so prevalent
among the relatives that this is explained by "family weakness of the vessels", "family sensitive,"
etc.
Diagnosis and differential diagnosis.
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The final diagnosis is only possible if the laboratory study of the properties of platelets:
their adhesive ability to glass and collagen retention in their Ranke, aggregation with different
doses of ADP, collagen, ristocetine, estimating the "release reaction". This survey should be
conducted in the dynamics (preventing accidental changes in the properties of platelets) and not
necessarily only the child but also his parents, as well as "bleeding" of relatives.
Treatment. Drugs that contribute to the improvement of adhesive-aggregative function
of platelets: aminocaproic acid, ditsinon, adrokson, calcium pantothenate and ATP
intramuscularly in combination with magnesium inside, chlorophyllin sodium, lithium
preparations. All of these medications are used in normal age-dose rates. We also demonstrate
that herbal medicine.
Hemorrhagic vasculitis (HV). HV (Henoch - Schonlein syndrome, anaphylactic
purpura, kapillyarotoksikoz) is an allergic disease characterized by systemic vasculitis and
manifests itself symmetrical, often petechial hemorrhages on the skin, usually in combination
with pain and swelling of joints, abdominal pain, kidney damage.
Etiology and pathogenesis. The cause of the disease has not been established, but some
of the children is awarded its connection with the development replaced acute viral diseases,
bacterial infections (most often streptococcal), preventive vaccinations, injections of gamma
globulin, drug allergy, helminthiasis. Specific hereditary predisposition (ie, the presence of a
similar illness in the family) has only a small number of patients, while burdening pedigree
allergic diseases are available to most children. Many patients can detect foci of chronic
infection. It is believed that the leading role in the pathogenesis of immune deposit may play a
defeat.
Classification. There are simple (skin), skin and joints, skin, abdominal and mixed
(cutaneous articular-abdominal) forms of purpura, as well as complications: nephropathy,
appendicitis, intussusception, necrosis of the intestinal wall with the development of peritonitis,
etc.
Clinic. The most typical symptom is skin lesions. In the absence of skin changes do not
make a diagnosis. The beginning of the disease (usually within 1-2 weeks after an acute
respiratory illness) may be acute with the simultaneous appearance of several syndromes, but the
lesions sometimes occur and later articular or abdominal syndrome. Typically, the changes
appear on the skin of the lower extremities, then on the buttocks, upper extremities, chest, back,
face and neck. In typical cases, the first is a small (about 2-W mm in diameter), erythematous
patches or makulopapuly. Pressing the elements become pale, but subsequently lose this ability.
Sometimes the initial stage of the disease in the appointment of heparin rash may disappear
within a few hours. Usually a rash after a while becomes haemorrhagic and elements of a redpurple color. Then a rash fades, becoming brown, and then with a yellowish tinge, but usually
not "bloom".
Cutaneous lesions usually symmetrical, clustered around the joints, on the buttocks, inner
thighs, extensor surfaces of extremities. Skin lesions can be polymorphic at the expense of
further "podsypany. Undulating "podsypany" - a typical symptom. In addition, patients can
sometimes be the phenomenon multiforme or nodose (nodular), erythema, angioedema, and
swelling of the hands, moaning, legs, eyelids, face. Elements of the rash may be as high as 3 5
cm in diameter. Because of concomitant secondary BPD (especially on the background on the
values of non-steroidal anti-inflammatory drugs) may epistaxis, ecchymosis. Itching for HBV
atypical. In more serious possible necrotic purpura, preceded by bullous eruption. Necroses after
themselves can leave scars.
Articular syndrome is swelling, tenderness, hyperemia - occurs in 2 / 3 patients in the
large joints (knees, elbows, ankles, etc.). The most common lesion is asymmetrical. Arthritis in
HBV usually passes quickly and resistant strains of joints does not cause.
Abdominal syndrome develops in approximately 2 / 3 HBV patients, and is characterized
by sudden cramping, a very sharp pain, which often are located around the navel may be
accompanied by a chair in black or scarlet (melena), nausea, vomiting, re (gematemezis).
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Abdomen slightly distended, but the tension of the abdominal wall in uncomplicated usually
absent. Stool can become more frequent. X-ray of the gastrointestinal tract exhibit decrease the
mobility of the intestine, segmental narrowing, probably due to edema and hemorrhages.
Dysmotility may lead to obstruction, intussusception, infarction, bowel perforation and
peritonitis (2-3% of patients). An analysis of occult blood in the stool (reaction Gregersen) is
positive in serial studies ing 80% of patients.
Nephritic syndrome occurs in 1/3-1/2 of patients in the form of focal or segmental,
diffuse glomerulonephritis, subacute extracapillary proliferative nephritis. Usually 2 / 3 of
patients with renal damage manifested short microhematuria and albuminuria, assessed as focal
nephritis. Some children microchanges in the urine or even gross hematuria without extrarenal
symptoms and gross violations of renal function are kept long enough for several weeks or
months and even years. In these cases it is probably a segmental nephritis. At 1 / 3 of patients
with nephropathy is a typical clinical acute nephritis with clear extrarenal symptoms and
syndromes. The flow of this type of nephropathy were also more likely benign, but can lead to
chronic nephritis. The most serious complication - Subacute nephritis, acute renal failure.
Diagnosis. Is based on clinical data and does not require additional studies to confirm. In
the analysis of peripheral blood exhibit varying degrees of severity of leukocytosis (moderate),
increased ESR, neutrophilia, eosinophilia. Given the frequent involvement of the kidneys, all
patients should be systematically make urine. When there are changes in urine produced a study
to assess renal function.
Treatment. Specific therapy HV does not exist. If a connection with the transferred
bacterial infection or the patient has decompensated focus of chronic infection, fever, a course of
antibiotics. A careful analysis of history must bring to mind the food or drug allergens that
should be eliminated from the diet and treatment. However, it is better to cancel all medicines,
against which there was purpura. The diet in the acute period with a restriction of animal protein,
salt, extractives, products containing a lot of histamine or are his Liberator. Undesirable as
products of industrial canning. Milk products are useful.
The regime of bed for 2-3 weeks, then it gradually expanded because of possible
recurrences of purpura, explains how the "tilt" purpura. All the children appropriate to the
appointment of activated charcoal, enterosorbent and (or) cholestyramine polyphepan inside.
Applied also stomach drops, antihistamines, calcium pantothenate, rutin, moderate doses of
ascorbic acid, herbal medicine, although their effectiveness and questionable. When abdominal
pain, do not pass after taking the stomach drops, prescribed painkillers - but, silos baralgin etc.
Pronounced activity of the process of rapid abdominal, cutaneous and articular syndrome indication for combined use of prednisolone and heparin. Isolated appointment of prednisolone is
dangerous because it contributes to hypercoagulation and the propensity for the development of
DIC-syndrome in this disease there (even if there are no clear signs of its presence). Prednisone
is usually prescribed in doses of 1 mg / kg, and heparin 200-300 IU / kg per day, divided into 4-6
injections under the skin of the abdomen. If the background of heparin therapy of venous blood
clotting time continues to be shortened (less than 8 minutes), then the dose can be increased to 1
1 / 2 times. Heparin should not be administered 2 or 3 times a day, Because it provokes the
development of intravascular thrombi. Cancellation of heparin should be gradual, but by
reducing the dose rather than reducing the number of injections. Sometimes stormy clinical
picture has to resort to infusion therapy, and in this case, you can achieve optimal administration
of heparin - intravenously with the uniform of his entrance into the body within days. With the
rapidly progressing forms of the positive effect was obtained from hemosorption and course of
plasmapheresis with fresh frozen plasma.
At any thrombocytopenic purpura (if we exclude DIC-syndrome) showed the
appointment of epsilon-aminocaproic acid (0,05-0,1 g / kg 4 times a day) and other products that
will improve the adhesive-platelet aggregation (adrokson, etamzilat, ditsinon, calcium
pantothenate, chlorophyllin sodium, ATP intramuscularly in combination with magnesium
inside, herbal medicine). During hemorrhagic crisis epsilon-aminocaproic acid should be 1-2
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times a day to enter intravenous drip. Immunoglobulin intravenous (only product specially made)
infusion at a dose of 0.5 g / kg body weight (10 ml / kg 5% solution) daily for 4 days leads to a
rise in platelet counts at the end of treatment at 2/3-3 / 4 patients with ITP, although only in 2530% of patients achieved stable clinical remission.
Indications for the purpose of glucocorticoids to children with ITP are: generalized
cutaneous hemorrhagic syndrome, combined with the bleeding of mucous membranes, bleeding
in the sclera and retina, "wet" purpura complicated by hemorrhagic anemia, hemorrhages in
internal organs. Prednisolone appointed for 2 - 3 weeks at a dose of 2 mg / kg per day with a
further reduction in dose and the abolition of the drug. Long term, many months of
glucocorticoid therapy is ineffective and leads to several complications. Indications for
splenectomy in patients with ITP: "wet" purpura, which lasts more than 6 months and requiring
the appointment of repeated courses of glucocorticoids, acute purple in the presence of heavy
bleeding is not docked in the background, a modern complex therapy of suspected brain
haemorrhage. Articular syndrome is swelling, tenderness, hyperemia - occurs in 2 / 3 patients in
the large joints (knees, elbows, ankles, etc.). The most common lesion is asymmetrical. Arthritis
in HBV usually passes quickly and resistant strains of joints does not cause.
Abdominal syndrome develops in approximately 2 / 3 HBV patients, and is characterized
by sudden cramping, a very sharp pain, which often are located around the navel may be
accompanied by a chair in black or scarlet (melena), nausea, vomiting, re (gematemezis).
Abdomen slightly distended, but the tension of the abdominal wall in uncomplicated usually
absent. Stool can become more frequent. X-ray of the gastrointestinal tract exhibit decrease the
mobility of the intestine, segmental narrowing, probably due to edema and hemorrhages.
Dysmotility may lead to obstruction, intussusception, infarction, bowel perforation and
peritonitis (2-3% of patients). An analysis of occult blood in the stool (reaction Gregersen) is
positive in serial studies ing 80% of patients.
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