Date d'application 1er Février 2013 Version en vigueur Prise en charge médico-chirurgicale des infections osseuses Référence(s) Ce protocole décrit la prise en charge des infections osseuses SPILF 2009, CRIOGO 2011, HAS. Références 8.g « Maitrise du risque infectieux » et Chap II. « Prise en charge du patient » Médecin, Chirurgien
Gonococcus see Neisseria gonorrhoeae
GPT see Alanine Aminotransferase (ALT), Serum
Growth Hormone (HGH, STH) see Somatotropin
Haloperidol, Serum or Plasma
Lithium (Li), Serum Synonyms:
Dozic®; Fortunan®; Haldol®; Haloneural®; Background: Antipsychotic drug, used in the therapy of Tourette syndrome, sedation of agi-
tated or delirious patients.
Sign of overdose: cardiovascular alterations such as EKG changes (depressed T or ST waves), arrhythmias; hyperglycemia; exacerbation of myasthenia gravis.
Bioavaliability 40%-80%; urinary excretion 1%; plasma binding 90%-94% increased in cirrhosis; volume of distribution 11-25 L/kg; half life time 13-23h decreased in children; peak time im: 0.6h, oral: 1.5-5h; peak concentration im: 5-40 ng/mL after a 10 mg single dose, oral: 5-14 ng/mL after a single 20 mg dose.
Haloperidol undergoes reversible metabolism to the reduced, less active form with a half life time of 16-120h. Slow reconversion to the parent drug may be responsible for prolonged half life time in 7 days samples of 70h.
Sampling: 2 mL serum
Therapeutic values: Hantavirus, Serology see Bunyaviruses, Serology
Haptoglobin (Hp), Serum
C-Reactive Protein, Serum Blood Count, Complete Myoglobin, Blood or Serum or Plasma Myoglobin Qualitative, Urine Background: Haptoglobin is a plasma glycoprotein with alpha electrophoretic mobility that
binds irreversibly to free hemoglobin, which can be removed by the liver saving hemoglobin from
renal loss. Two major genetic variants Hp1 and Hp2 are known.
Haptoglobin is a sensitive marker for hemolysis which is decreasing haptoglobin levels. If the red blood cells half life is decreased from 26 days to less than 17 days haptoglobin plasma levels are undetectable. Disease causing ineffective erythropoiesis, soft tissue hemorrhage and drug induced hemolytic anemia decrease haptoglobin levels. Increase may occur in acute infl ammation (acute phase reactant) counteracting concurrent he- molysis. Corticosteroids and nephrotic syndrome may elevate haptoglobin levels.
Decreased levels occur in liver disease and during estrogen therapy.
Sampling: 2 mL serum
10 days – 60 years Helicobacter pylori
Background: Helicobacter organisms are gram negative, spirale shaped, terminal fl agellated,
microaerophilic, urease positive bacilli (Campylobacter in contrast is urease negative), fi rst iso- lated in 1982. The natural habitat of H. pylori is the human stomach. Epidemiology: The infection rate decreases with increasing socio-economic level. Infection oc- curs in childhood and is likely to persist life long. Due to poor sanitation; the rate of infection in developing countries is high. In western countries in young individuals prevalence is up to 20%. The mode of infection is uncertain but likely to be fecal-oral or oral-oral.
Helicobacter pylori cause chronic gastritis and peptic ulcer and is considered a risk factor for gastric carcinoma. H. pylori is fragile, biopsies must be kept in transport medium and cultured within 24h. Cultures will be kept for up to 10 days.
Therapy: Clarithromycin plus amoxicillin or clarithromycin plus metronidazole.
Sampling: Serology: 2 mL serum
Antigen detection: approx. 2 g stool Culture and resistance testing: Gastric biopsy in Portagerm pylori transport medium Antibody of the IgG class IgG antibody Validation by immunoblot Antigen detection: Negative Culture: Report on diagnostic fi nding
Helminths, Microscopy, Feces
Ancylostoma duodenale (old world hookworm) Diphyllobothrium (fi sh tapeworm) Enterobius vermicularis (pinworm) Fasciola hepatica (sheep liver fl uke) Hymenolepis nana (dwarf tapeworm) Necator americanus (new world hookworm) Nemathelminthes (Nematodes, roundworms) Paragonimus westermani (lung fl uke) Taenia solium (pork tapeworm) Taenia saginata (beef tapeworm) Trichuris trichiura (whipworm) Strongyloides stercoralis (small roundworm) Background: The multicellular metazoan or helminthes are subdivided in two phyla: the Platy-
helminthes (fl atworms) and the Nemathelminthes. The phylum Platyhelminthes contains two medical important classes: Cestoda (tapeworms) and Trematoda (fl ukes). The tapeworms consist of two parts, a scolex (head) and multiple proglottids, which repli- cate from the germinal center next to the scolex to grow worm, the distal end contain gravid proglottids, which are excreted with the feces. The intermitted hosts are pigs, cattle, and fi sh. Infection of the human is by larvae ingestion or in case of cysticercosis and hydatid disease by egg ingestion.
Taenia solium (pork tapeworm) The adult worm causes taeniasis. The infection occurs after ingesting uncooked pork con- taining the larvae. The larvae take 3 months to grow into the adult worm measuring up to several meters. Cysticercosis occurs, if the egg is digested by the defi nitive host, the hu- man, not by the pig as intermediate host. The egg hatches in the small intestine and the oncosphere disseminate by the circulation system especially into the eye and brain, where they encysted to form cysticerci.
Laboratory diagnosis is made by identifying gravid proglottids with 5-10 primary uterine
branches in the stool. T. saginata proglottides have 10-15 uterine branches. Cysticercosis is diagnosed by fi nding cysts in tissue after surgical removal. Treatment: Praziquantel, for cysticercosis in addition surgical.
Taenia saginata (beef tapeworm) Infection is acquired by humans eating undercooked beef containing the larvae which at- tach in the small intestine and grow in 3 month to the adult, several meters long worm. Detached proglottides passed with the feces infect cattle. The oncosphere emerge from the egg and are carried to the muscle to develop in cysticerci. Laboratory diagnosis: T. saginata has, in contrast to T. solium, no hooklets at the scolex but also 4 suckers. Treatment: Praziquantel Diphyllobothrium latum (fi sh tapeworm) After ingestion raw or undercooked fi sh containing the larvae (plerocercoid or sparganum), the larvae develop in the human gut to the adult worm, releasing eggs, which develop in fresh water into embryos to be ingested by copepod Crustacea's as the fi rst intermediate host. When the copepod is eaten by the second intermediate host, (pike, trout, and perch) the larvae differentiate into plerocercoids in the fi sh muscle.
Laboratory diagnosis is made by demonstrating in feces the typical eggs or typical parts of the worm: 2 elongated sucking grooves with no hooks at the scolex, eggs are oval with an operculum at one end, proglottides are wider then long, which differentiates the organism from the other cestodes.
Hymenolepis nana (dwarf tapeworm) The 3-5 cm long worm does not need an intermediate host and eggs can infect humans directly. In the duodenum, hatched eggs develop into cysticercoid larvae and into adult worms, reaching by autoinfection several hundreds of parasites in the gut.
Laboratory diagnosis is made by demonstrating eggs which 6 hooked larvae and 8-10 fi laments lying between the membrane of the larvae and the outer shell. Trematodes (fl ukes)
including Schistosomia species, Clonorchis sinensis and Paragonimus westermani, Fas- ciola hepatica, Fasciolopsis buski and Heterophyes heterophyes.
Three species are known: S. mansoni and S. japonicum live in the mesenteric veins, S. hae- matobium in the veins of the urinary bladder. Infection occurs by free swimming cercariae, penetrating the skin. The larvae enter the circulation system, enter the liver for maturation into the fl uke and migrate into the typical veins system thereafter. The female fl ukes pro- duce eggs to enter the gut or bladder lumen and eggs can be diagnosed in stool or urine. The egg hatches in fresh water to penetrate snails and develop into cercariae. S. mansoni is endemic in Africa and Latin America, S. haematobium in Africa and Middle East, S. japonicum in Asia.
Clinically, transient eosinophilia, gastrointestinal hemorrhage, liver granulomas may occur with fi brosis and hepatomegaly, portal hypertension with splenomegaly and esophageal varices. Liver function remains unaltered. In chronic S. haematobium infection, carcinoma of the bladder may occur.
Laboratory diagnosis is made according to the egg form: S. mansoni eggs have prominent lateral spine, S. japonicum small lateral spine and S. haematobium eggs have terminal Therapy: Praziquantel Clonorchis sinensis (and closely related Opisthorchis viverrini, Opisthorchis felineus) also named human liver fl ukes.
Aquatic snails are infected by human feces containing ova to differentiate to the rediae and further to free swimming cercaria are released from the snails encyst to the stage of metacercariae under the scales of freshwater fi sh and are capable to infect humans if eaten undercooked. Passing through the duodenum, the metacercariae encyst and enter the biliary ducts and differentiate to the adult hermaphroditic fl uke producing eggs which are excreted by the feces. The geographical region is restricted to eastern Asia ans some areas in Siberia. Prevalence in endemic regions up to 35%.There is an association between O. viverrini and cholangiocarcinoma in high endemic areas. Laboratory diagnosis is made by fi nding in the stool typical small, brown, operculated eggs. Paragonimus westermani (lung fl uke) Infection occurs by eating undercooked metacercariae containing crab or crayfi sh. The larvae encysted in the small intestine and migrate through the mucosa and diaphragma into the lung to differentiate into hermaphroditic adult fl ukes. Eggs produced are either swal- lowed or coughed, reaching fresh water and hatch into miracidia, entering snails as the fi rst intermediate host. There, fi rst redia develops and then cercariae which encyst in freshwater crabs as the second intermediate host. Paragonimiasis is endemic in eastern Asia and central and Western Africa and occasionally in other tropical areas.
Laboratory Diagnosis is made by fi nding typical operculated eggs in sputum or feces.
Treatment: Praziquantel Fasciola Hepatica (sheep liver fl uke) causes diseases primary in sheep and other domestic animals. Humans are infected by watercress contaminated with the larvae, they excyst in the duodenum and reach the liver to mature into the adult. Eggs shed into the bile tract are shed by the feces, hatch in fresh water and enter snails as an intermediate host, develop into cercariae which are shed and encyst on aquatic vegetation.
Laboratory diagnosis is made by identifi cation of eggs in the feces.
Therapy: Praziquantel and bithionol Fasciolopsis buski is endemic in Asia and India. Aquatic vegetation is the source of infection when carrying eggs. Attached to the gut mucosa, the fl uke differentiate into the adult. Eggs are shed with feces and a snail is necessary as an intermediate host. Laboratory diagnosis is made by demonstrating characteristic eggs in the feces.
Heterophyes heterophyes is endemic in Africa, Middle East, Asia. Infection occurs by eating raw fi sh containing cysts. Mucosa attached larvae produce eggs in the small intestine, passed in the feces and are ingested by snails in brackish water. Cercariae are produced that encyst in certain fi sh Laboratory diagnosis is made by fi nding characteristic eggs in the feces.
Nematodes have cylindrical bodies covered with a highly resistant cuticle. The male has a coiled tail, the female is usually larger. The intestinal nematodes include Enterobius (pin- worm), Trichuris (whipworm), Ascaris (roundworm), Necator, Ancylostoma (hookworms), and Strongyloides (small roundworm). Diagnosis of Trichinella and Anisakiasis (infection with the third-stage larvae of the round worm Anisakis marinae) is not made by stool exami- nation. Two larvae forms are known: the noninfectious rhabditiform larvae and the infectious fi lariform larvae. Symptoms: Itching in the perianal skin area is caused by Enterobius infections, rectal pro- lapse may occur in Trichuris infection and migrating larvae of Ascaris may cause pneumo- nia. Anemia occurs in Ancylostoma and Necator infection, Strongyloides may disseminate in various tissues in immunocompromised patients. Enterobius vermicularis (pinworm) After ingestion, eggs hatch in the small intestine, differentiate into adult worms and migrate to the colon, where mating occurs releasing eggs which become infectious larvae within 6 h at the anus which may reinfect the host when carried to the mouth. Enterobius is found worldwide and affects children most commonly.
Laboratory diagnosis is made by recovered eggs from the perianal skin by tape technique. They are not recovered from the feces.
Treatment: Mebendazole or pyrantel pamoate. Trichuris trichiura Humans are infected by ingesting eggs in contaminated water or food. Hatching in the small intestine the larvae differentiate in adults who migrate to the colon to mature and pro- duce thousands of eggs daily. Eggs are passed with the feces and form embryos in moist warm soil. Ingestion of eggs completes the cycle.
Laboratory diagnosis is made by demonstrating barrel-shaped (lemon shaped) eggs with a plug at each end in the feces.
Ascaris lumbricoides Infection occurs via egg contaminated food or water. Eggs hatches in the small intestine and the larvae migrate through the intestinal mucosa and bloodstream into the lungs, pass- ing through the trachea and are swallowed. In the intestine they develop into adult worms which are up to 25 cm long. Eggs are passed through the feces and form embryos in warm moist soil. Ascariasis is common in the tropics ans in the southeastern US states. Lab. Diagnosis is made microscopically by detecting oval, irregular surfaced eggs.
Treatment: Mebendazole and pyrantel pamoate.
Ancylostoma duodenale (old world hookworm) and Necator americanus (new world hookworm) Infection occurs when fi lariform larvae living in a moist soil penetrate the skin, and are car- ried to the lungs, migrate to the trachea and are swallowed. In the small intestine they de- velop into adult worms attached to the mucosa. Eggs are passed in the feces and develop fi rst into feeding, rhabditiform larvae and then into infectious, non feeding fi lariform larvae. Hookworms are distributed worldwide in tropical areas.
Laboratory diagnosis is made microscopically by observing typical eggs in the stool, frequently occult blood in the stool and eosinophilia.
Treatment: Mebendazole and pyrantel pamoate.
Infection occurs by penetration of the skin by infectious (fi lariform) larvae which migrate to the lung. After entering the trachea they are swallowed. In the small intestine the larvae differentiate to adult worms, enter the mucosa and produce eggs, which hatch within the mucosa forming rhabditiform larvae which are passed with the feces. Some larvae form fi larial larvae which auto-infect the host by penetrating the mucosa and migrate to the lung. In immunocompromised patients, massive autoinfection may occur with dissemination into organs. The rhabditiform larvae passed with the stool, molt through stages in warm moist soil to form adult female and male worms. The entire life cycle can occur in the soil, but after several free living cycles fi larial larvae are formed which are capable to enter the parasitic cycle in humans.
Strongyloidiasis is endemic in the tropics, particularly in south eastern Asia. Prevalence in Laboratory diagnosis is made by fi nding the larvae form in stool and massive eosinophilia.
Sampling: approx. 2 g of fresh stool.
Optimum for obtaining specimens: Ascaris lumbricoides, hookworms, Trichuris trichiura occur are constantly in feces but Diphyl- lobothrium latum and Schistosomia species are seen on an irregular base.
Report on diagnostic fi nding Hemochromatosis DNA Testing
Ferritin, Serum or Plasma Transferrin and Total Iron Binding Capacity, Serum Synonyms:
Hereditary Hemochromatosis; HFE Genotyping Test Includes: Detection of C282, H 63D, S65C mutation
Background: Hereditary hematochromatosis (HH) is an autosomal recessive disease. It is com-
mon in Europe and among Caucasians; the prevalence in Caucasians is 1:400 and 1:10 for carriers. Siblings have a 1:4 risk of developing the disease. Caucasian parents and offspring's have a 1:20 risk of being affected. The HFE gene is located in the HLA region on chromosome 6p21, encoding a cell surface protein which is similar to HLA class I molecules. The normal heterodimer modulates the affi nity of the transferrin receptor for transferrin, the mutation prevents expression of the protein at the position at the cell surface.
Clinically, patients in late stage HH present with arthropathy, cardiomyopathy, hypothyrosis, tes- ticular atrophy, abnormalities of the anterior pituitary gland, pancreas, cirrhosis, diabetes mellitus and skin bronzing, which may be preventable by early diagnosis and treatment.
Useful test in the evaluation of patients with persistent elevated AST or ALT or elevated serum transferrin iron saturation in at least two fasting blood samples. Liver biopsy is a complementary procedure particularly in patients to develop cirrhosis. Used also in risk assessment in families with hemochromatosis. For northern Europe 90% of the patients have a mutation at C282Y in the HLA lined HFE gene, in 40%-60% of non C282Y cases a mutation at H63D occurs with lower penetrance. Only 2% of C282Y/H63D or homozygote H63D patients develop clinically signifi cant signs. Limitations: Expression of heterozygosis of C282Y mutation does not invariably indicate clinical signs of HH. Fibrosis usually does not occur before the age of 40 years. The test is not diagnostic for neonatal and juvenile hemochromatosis since different genes are Sampling: 2 mL EDTA blood, do not freeze, ship to laboratory within 5 days. Please provide
clinical diagnosis, ethic background, serum iron, ferritin level, family history of HH.
absence of detectable mutation one mutation detected Hereditary hemochromatosis or predisposition for disease: two or more mutations Hemoglobin Electrophoresis
Background: HbA is the predominant hemoglobin (Hb) in the human body, other normal Hb
types are HbA , which is gene encoded and modifi ed forms such as Hb A , HbA , HbA . During week 5-8 of gestation, HbF replaces precursor Hb forms (HbGower and Portland), new- borns still have 80% HbF, which is replaced by adult Hb during the fi rst 12 month of life.
HbA and HbF are composed of four chains out of two classes (alpha, beta, delta, gamma globulin). For HbA the chains are alpha and beta , for HbA alpha and delta , for HbF alpha The electrophoresis method separates Hb into the normal forms HbA or HbF and abnormal forms such as HbC, HbS, and others. The parameter is used in the diagnosis of hemoglobinopathies (incidence worldwide 0.17%) such as thalassemia, sickling hemoglobulinemias and structural chain abnormalities and in the evaluation of hemolytic anemias. Cord blood is suitable to detect alpha chain variants (HbF, HbG) and HbS or HbC. Thalassemia is caused by a defi cient synthesis of alpha or beta or rarely delta or gamma chain. Patients present increased levels of HbA , HbF, HbH (four beta chains) or HbBarts (four gamma Other forms of hemoglobinopathies are due to abnormal structures of the alpha, beta delta or gamma globulin, there are approx 900 types known so far. HbA is elevated in beta thalassemia, sickle cell disease, megaloblastic anemias, and hyperthy- roidism. HbA is decreased in alpha thalassemia, beta delta thalassemia, delta thalassemia, iron defi ciency, and sideroblastic anemias.
Limitations: Avoid test after blood transfusions. Sampling: 3 mL EDTA whole blood
Children 1-2 years Hemopexin, Serum
Background: Hemopexin is a beta-migrating single chain polypeptide with a MW 70 kDa and
with 20% carbohydrates. Hemopexin binds heme released by degeneration of hemoglobin, contributing by protecting the iron from escaping from the porphyrin molecule and preserving body iron stores.
Deceased to a lesser extend during decreased production in liver failure; a major decrease is caused by intravascular hemolysis, when the amount of free hemoglobin exceeds haptoglobin binding capacity. Heme-hemopexin complexes are cleared by hepatocytes, lowering hemopexin levels in the circulation. Heme subsequently binds to albumin but is redistributed to hemopexin which is newly synthesized by the liver. Therefore depressed levels of free hemopexin are a long term marker for previous hemolysis after haptoglobin levels have returned to normal.
Sampling: 1 mL serum
Hepatitis A Antibodies, IgG and IgM (IgG anti-HAV, IgM anti-HAV)
Alanine Aminotransferase (ALT), Serum Alkaline Phosphatase, Serum Aspartate Aminotransferase (AST), Serum Bilirubin, Fractionated, Serum Hepatitis B (HBV), Serology and Antigen Detection Hepatitis B Virus DNA Detection (HBV-DNA) Hepatitis C Genotyping Hepatitis C Virus RNA Quantifi cation (HCV-RNA) Hepatitis D Serology Hepatitis E Antibody (Anti-HEV Background: Transmission of hepatitis A virus occurs via the fecal oral route. Traveling in en-
demic areas or consumption of contaminated food are major risk factors. After an incubation period of 2-7 weeks the self limiting disease manifests with fever, jaundice, anorexia, and diar- rhea. Fecal excretion peaks before the symptoms develop. Specifi c IgM antibodies appear in acute hepatitis A infection within a week of the clinical onset and persist for 3-6 month with a peak at 3 month and up to one year in 20% of the patients. IgG specifi c antibodies persist life long and 50% of the adult population of Western countries have IgG type antibodies. Hepatitis A does not become chronic, subclinical courses, particularly in children are common. Rarely, a fulminant Hepatitis A infection is seen. A vaccine is available.
Sampling: 1 mL serum, EDTA or citrate plasma
Hepatitis A IgG antibody (IgG anti-HAV): IgG positive: Immunity protective for at least 5 years. Hepatitis A IgM antibody (IgM anti-HAV): negative Hepatitis B (HBV), Serology and Antigen Detection
Alanine Aminotransferase (ALT), Serum Alkaline Phosphatase, Serum Aspartate Aminotransferase (AST), Serum Bilirubin, Fractionated, Serum Hepatitis A Antibodies, IgG and IgM (IgG anti-HAV, IgM anti-HAV) Hepatitis B Virus DNA Detection (HBV-DNA) Hepatitis C Genotyping Hepatitis C Virus RNA Quantifi cation (HCV-RNA) Hepatitis D Serology Hepatitis E Antibody (Anti-HEV) Background: HBV is a partially double stranded DNA, enveloped virus of the hepadnavirus
family. The major proteins are: The surface antigen (HBsAg), which is part of the envelope, the core antigen (HBeAg) which is located together with the e antigen(HBeAg), a proteolytic prod- uct, in the nucleocapsid protein. There are four serologic subtypes of the HBsAg, adw, adr, ayw and ayr for epidemiological use. The only natural hosts are humans. HBV is distributed worldwide with a high prevalence in Asia. Mode of transmission are via blood, sexual intercourse and perinatally. About 5% of HBV infected patients become chronic carriers defi ned as HBsAg persisting for more than 6 month. Chronic carriers are more likely to develop in newborns (up to 90%) than in adults, and subse- quently with a high risk of developing hepatocellular carcinoma. Immunity lasts lifelong when antibodies directed against HBsAg are produced.
Clinically, many HBV infections are asymptomatic but fulminant courses may occur particularly in patients coinfected with HIV or with preexisting liver damage. The Incubation period varies between 1 and 6 month (usually 4-12 weeks) Staging of HBV infection: (early) positive negative negative positive positive positive or negative positive or negative HBs Antigen can be detected 1-7 weeks before liver enzymes levels rise, 50% of the patients are positive 3 weeks after onset of the acute hepatitis, at week 17 only 10 % are still positive. Markers for infectivity are HBs Antigen and HBe Antigen. HBe Antigen usually convert to negative within 3-6 weeks, persistence for more than 10 weeks suggests risk for development of chronic Hepatitis B. Infectivity is approx. 5 fold as high if HBe Antigen and HBs Antigen are co-present as compared to HBs Antigen alone. In chronic carriers HBeAg may become negative and HBe Antibodies may develop after more than 6 month, but HBs Antigen persists.
A quantifi cation of HBs Antibodies is useful in the assessment of the immune status after vaccination. Sampling: 1 mL serum citrate plasma or EDTA plasma for each test
Hepatitis B core Antibody (Anti-HBc) Reference Interval: negative
Hepatitis B core IgM Antibody (IgM anti-HBc) Reference Interval: negative
Hepatitis Be Antigen (HBeAg) Reference Interval: negative
Hepatitis Be Antibody (Anti-HBe) Reference Interval: negative
Hepatitis Bs (surface) Antigen (HbsAg) Reference Interval: negative
Hepatitis Bs (surface) Antibody quantitative (Anti-HBs) Reference Interval:
negative < 10 IU/L Quantifi cation for immune status assessment: Recommendations for vaccination: immunity not suffi cient, immunization necessary Immunity present booster within weeks 1001–7500 IU/L check in 2–3 years Hepatitis B Virus DNA Detection (HBV-DNA)
Alanine Aminotransferase (ALT), Serum Alkaline Phosphatase, Serum Aspartate Aminotransferase (AST), Serum Bilirubin, Fractionated, Serum Hepatitis A Antibodies, IgG and IgM (IgG anti-HAV, IgM anti-HAV) Hepatitis B (HBV), Serology and Antigen Detection Hepatitis C Serology Hepatitis C Virus RNA Quantifi cation (HCV-RNA) Hepatitis D Serology Hepatitis E Antibody (Anti-HEV Background: Chronic viral hepatitis is caused by Hepatitis B virus (HBV) or Hepatitis C virus.
In most of the HBV infected patients, antibody response to HBs Antigen occurs and persists lifelong. 10% of the HBV infections are characterized by the absence of HBs Antibodies and the presence of HBs Antigen and HBc Antigen. Determination of HBV DNA is a supplement test to determine carrier state and quantifi cation provides information of the infectivity and is of prog- nostic relevance. It is useful for the measurement of the response to antiviral therapy.
Sampling: 2 mL serum or EDTA blood, (heparinized blood is not accepted)
Determination of the HB virus load DNA not detectable: < 1000 Virus particles (VP) / mL Hepatitis C Antibody (Anti-HCV)
Alanine Aminotransferase (ALT), Serum Alkaline Phosphatase, Serum Aspartate Aminotransferase (AST), Serum Bilirubin, Fractionated, Serum Hepatitis A Antibodies, IgG and IgM (IgG anti-HAV, IgM anti-HAV) Hepatitis B Virus DNA Detection (HBV-DNA) Hepatitis B (HBV), Serology and Antigen Detection Hepatitis C Genotyping Hepatitis C Virus RNA Quantifi cation (HCV-RNA) Hepatitis D Serology Hepatitis E Antibody (Anti-HEV) Background: Hepatitis C is a single stranded RNA enveloped virus causing a slowly progres-
sive and often asymptomatic hepatitis. Worldwide 180 million people are chronic carriers. About 30-50% of the patients recover; in 70-50% the infection becomes chronic. Cirrhosis develops in 20% of the patients after more than 20 years. HCV contribute to the prevalence of acute forms of hepatitis 20%, 60% to the cases of chronic hepatitis and 20-30% for cirrhosis of which 1-4% annually may develop hepatocellular carcinoma, whereas alcoholism enhances the rate of carcinoma. Antibody titer rises after 4-10 weeks post exposure. 80% of the infected become positive within 15 weeks post exposure.
Hepatitis C is transmitted by contact with human blood. There is no insect vector in opposite to the other fl avivirus the yellow fever virus. 60% of HCV infections are due to shared needles in IV drug abusers and rarely by sexual contact. The risk of acquiring HCV by sexual contact however increase with coinfectoion with other sexual transmitted diseases. The risk of mother to child transmission is less than 5%, for needlestick infections less than 0.1%.
Limitations: False positive results may occur in pregnant women (0.2%), in recent immunized individuals against infl uenza virus, hypergammaglobulinemia, positive rheumatoid factor, con- nective tissue diseases. False negative results occur in patients with essential mixed cryoglobu- linemias, hemodialysis, and immunodefi cient patients. Sampling: 1 mL serum EDTA or citrate plasma
Reference Interval: Antibody
Validation by Immunoblot Hepatitis C Genotyping
Alanine Aminotransferase (ALT), Serum Alkaline Phosphatase, Serum Aspartate Aminotransferase (AST), Serum Bilirubin, Fractionated, Serum Hepatitis A Antibodies, IgG and IgM (IgG anti-HAV, IgM anti-HAV) Hepatitis B Virus DNA Detection (HBV-DNA) Hepatitis B (HBV), Serology and Antigen Detection Hepatitis C Serology Hepatitis C Virus RNA Quantifi cation (HCV-RNA) Hepatitis D Serology Hepatitis E Antibody (Anti-HEV) Background: There are 6 HCV genotypes and 50 subtypes known. The genotypes are based
on differences of the genes that encode one of the two envelope proteins. Genotype 1,2,3 are found worldwide, genotype 4 mainly in Egypt and Zaire, genotype 5 in South Africa, genotype 6 in Asia. Subtypes are described with letters. There is an association between disease progres- sion and genotype: Genotype 1 b and genotype 4 causes a more aggressive form of hepatitis, Sampling: 5 mL EDTA blood kept at 4˚C and ship as soon as possible or freeze to -20˚C.
Report on diagnostic fi ndings: Genotypes 1, 2, 3 Determination of subtype a, b Hepatitis C Virus RNA Quantifi cation (HCV-RNA)
Alanine Aminotransferase (ALT), Serum Alkaline Phosphatase, Serum Aspartate Aminotransferase (AST), Serum Bilirubin, Fractionated, Serum Hepatitis A Antibodies, IgG and IgM (IgG anti-HAV, IgM anti-HAV) Hepatitis B Virus DNA Detection (HBV-DNA) Hepatitis B (HBV), Serology and Antigen Detection Hepatitis C Serology Hepatitis C Genotyping Hepatitis D Serology Hepatitis E Antibody (Anti-HEV) Background: Hepatitis C is a member of the fl avivirus family. It is an enveloped virus with a
single stranded positive polarity RNA. The onset of Hepatitis C is usually slow; the mean incu- bation time is 8 weeks. Patients without receiving treatment remain in 80% chronic carriers for at least one year. Chronic active hepatitis occurs in 10% of theses patients. About 20% of the chronic carriers develop cirrhosis. HCV–RNA assay becomes positive within days of exposure before ALT or AST becomes usually moderate elevated. The assay is useful in early diagnosis and therapy monitoring.
Sampling: 3 mL EDTA blood kept at 4˚C and ship as soon as possible or freeze to -20˚C.
RNA not detectable: < 100 VP/mL Hepatitis D Antibody (Anti-Delta), Serology
Aspartate Aminotransferase (AST), Serum Bilirubin, Fractionated, Serum Hepatitis A Antibodies, IgG and IgM (IgG anti-HAV, IgM anti-HAV) Hepatitis B Virus DNA Detection (HBV-DNA) Hepatitis B (HBV), Serology and Antigen Detection Hepatitis C Antibody (Anti-HCV) Hepatitis C Genotyping Hepatitis C Virus RNA Quantifi cation (HCV-RNA) Hepatitis E Antibody (Anti-HEV) Background: Hepatitis delta agent (HDV), a RNA virus, occurs only in patients already infected
with Hepatitis B virus. Coinfection increases the risk of fulminant and to develop chronic hepati- tis with cirrhosis and carcinoma. Mode of transmission is more likely by i.v. drug use than sexual transmitted. Up to 20% of HBV positive individuals may carry in endemic areas HDV, in chronic liver disease patients up to 60%. Antibodies develop 5-7 weeks after infection.
Limitations: Patients with rheumatoid factors or lipemia may have false positive results.
Sampling: 1 mL serum or EDTA plasma
Negative for IgG and IgM Hepatitis E Antibody (Anti-HEV)
Aspartate Aminotransferase (AST), Serum Bilirubin, Fractionated, Serum Hepatitis B Virus DNA Detection (HBV-DNA) Hepatitis B (HBV), Serology and Antigen Detection Hepatitis C Antibody (Anti-HCV) Hepatitis C Genotyping Hepatitis C Virus RNA Quantifi cation (HCV-RNA) Background: Hepatitis E is a self limiting hepatitis comparable to Hepatitis A. Route of trans-
mission: Fecal-oral, particularly by contaminated water. The disease is endemic in India, Middle East, Southeast and Central Asia with seroprevalence between 2% and 30%. Acquisition of antibodies occurs predominantly during the fi rst 2 decades of life. Incubation period is 15-60 days; no chronic infection has been described.
Serology: IgM antibodies are detectable 1-4 weeks after exposure, IgG can persist for 2 years. PCR is of limited use since no chronic state is known.
Sampling: 1 mL serum or EDTA plasma
Herpes Simplex Virus Type 1, 2 (HSV), DNA Detection
Herpes Simplex Virus Type 1, 2 (HSV), Serology Background: The test detects nucleic acid of HSV-1 and HSV-2 in blood, CSF or swaps.
In culture methods sensitivities are 40%-70% for genital ulcers and 40%-70% for neonatal encephalitis, the PCR improves the sensitivity substantially. PCR is considered as the test of choice for CNS HSV infection due the rapid and sensitive performance, however, a negative result cannot rule out HSV infection. HSV encephalitis is caused in most of the cases by HSV-1, HSV meningitis, which is more frequent, by HSV-2. Sampling: Swap or vesicle fl uid: Cytobrush in transport buffer
CSF/liquor: 2 mL EDTA blood: 2 mL Bronchial lavage fl uid Rapid transport to laboratory required, if more than 2h transit time expected, keep at 4˚C, if 8h expected, freeze. Do not use heparinized tubes.
HSV-1 or HSV-2 DNA not detected Herpes Simplex Virus Type 1, 2 (HSV), Serology
Herpes Simplex Virus Type 1, 2 (HSV), DNA Detection Background: Herpes simplex virus (HSV)-1 and Herpes simplex virus (HSV)-2 also ICTV named
as Human herpesvirus-1 and -2 are members of the subfamily Alphaherpesviridae in the genus Herpesviridae have an icosahedral core surrounded by a lipoprotein obtained when budding from the nuclear membrane, a large seize of 120 – 200 nm, and a double stranded DNA. HSV-1 peak incidence of primary infection occurs in childhood, for HSV-2 during adolescence. Adult seroprevalence in HSV-1 is 75% to 100%, for HSV-2 5%-95%. Main route of transmission for HSV are oral secretions, for HSV-2 genital secretions. Herpes simplex virus types 1 and 2 and varicella viruses causes vesicular rash, HSV-1 causes lesion appears above the waist, HSV-2 below. HSV-1 causes acute gingivostomatitis, recurrent herpes labialis, keratoconjunctivitis, and temporal lobe encephalitis. HSV-2 causes neonatal disseminated disease, aseptic meningitis, recurrent genital herpes; HSV-1 is transmitted by respiratory secretions and saliva, HSV-2 via sexual contact and perinatal infection. Nearly all of the HSV-2 seropositive individuals shed virus intermittently from the mucosa.
Herpes simplex -1 or HSV-2 encephalitis, although rare with an incidence of 1 case per 250 000 population per year is the most common form of sporadic fatal encephalitis. 95% of HSV encephalitis is caused by HSV-1. One third of the adults developing herpes encephalitis have a primary infection, and those who have antibodies to HSV at the onset of encephalitis, 90% did not have had recurrent HSV-2 infection.
Neonatal herpes infection occurs if the mother has a primary infection during delivery. Infants born to seronegative mothers have an increased risk to acquire HSV-2 during delivery than infants born by seropositive mothers. More than 50% of the newborns become infected, mortal- ity in disseminated infection in newborns exceed 70%. Prompt initiation of antiviral therapy may prevent development of neurologic impairment.
Therapy: For HSV -1 and-2 the DNA polymerase inhibitors acyclovir, valaciclovir, famciclovir, and in case of resistance foscarnet or cidofovir are available. Theses drugs have been shown to reduce duration of viral shedding, time of healing of lesions, duration of pain, complication rate. Intravenous administration of acyclovir is indicated even before laboratory confi rmation in patients suspected systemic disease or herpes encephalitis.
Sampling: 1 mL serum
Differentiation of immunoglobulin classes IgG differentiation to IgG-HSV-1 and IgG-HSV-2 type IgM antibodies are produced in primary infection and to a lesser extend during recurrent dis- ease. Unspecifi c reactivity occurs. Increased IgA antibodies support the diagnosis of recent or Herpes-Zoster see Varicella-Zoster Virus, Serology
High Density Lipoprotein Cholesterol, Serum or Plasma
Apolipoprotein A-1 and B-100, Serum Cholesterol, Total, Serum or Plasma Lipoprotein (a), Serum Low Density Lipoprotein Cholesterol Triglycerides, Serum or Plasma Synonyms:
Alpha1 Lipoprotein Cholesterol ; HDL ; HDLC ; HDL Cholesterol Background: The HDL fraction summarizes a heterogenous class of lipoprotein particles. The
level of HDL is considered as a major risk factor for coronary heart diseases (CHD) in an inverse CHD risk increases 2%-3% for every 1 mg/dL decrease in HDL. Increase in HDL is seen in physical exercise, weight loss, and moderate alcohol consumption as well in medications as niacin, fi brates, statins, resins, estrogens. A decrease is associated with smoking, obesity, pregnancy, stress, hospitalization, and medications as probucol, corticoste- roids, androgens, progestins, diuretics, propanolol. Decrease also occurs during chronic renal failure, type II diabetes, myocardial infarction, thyroid dysfunction.
Hereditary defects of metabolism are: Familial hyperalphalipoproteinemia which is a defi ciency of the cholesterol ester transfer protein, causing an increase in HDL and decrease in LDLC and Tangier disease, apolipoprotein A-I defi ciency, lecithin–cholesterol acyltransferase defi ciency and fi sh eye disease are further types of genetic disorders affecting HDL. Sampling: 1 mL serum or plasma. For optimal results, the patient should be on a stable diet for
2-3 weeks, stable body weight and fasting for 10h. Reference Interval:
Male standard risk favorable or protective Female standard risk favorable or protective Histamine, Urine or Plasma
Related Information: Immunoglobulin
Background: Histamine is a mediator of anaphylaxis or other allergic states such as urticaria,
fl ushing, asthma, and tachycardia. Histamine is released by basophil cells and mast cells via IgE receptor mediation. May also be elevated in myeloproliferative diseases and in carcinoid tumors (gastric origin).
Limitations: False positive during urinary tract infections.
2 mL of EDTA plasma, freeze immediately and ship frozen.
ship a 10 ml aliquot of a 24h urine collected in a clean container. Keep cool.
Note total quantity.
10-35 ng/mL or < 45 µg/g creatinine Related Information:
Antinuclear Antibody, Antibodies, dsDNA, Antibodies, ssDNA, Smith (Sm) Antibody Background: Histones are tetrameric proteins located at the nucleolus. The tetramers are
composed of H2A-H2B and H3-H4. Useful test in drug induced systemic lupus erythematosus (SLE). Relevant antibodies are of the IgG and IgA type, IgM antibodies are present in healthy individuals and are directed against complexed DNA with H2A-H2B. In drug induced systemic lupus erythematosus antibodies di- rected against histones are present in 95% in high levels, and in 20%-70% in non-drug induced systemic lupus erythematosus. Absence of SLE antibodies such as Antinuclear Antibody, native ds-DNA Antibody, Smith (Sm) Antibody and high levels of Histone Antibodies favor the diag- nosis of drug induced SLE. Clinically the drug induced SLE is characterized by skin and joint symptoms without renal involvement. Antibodies to ssDNA are present in 70%-90%, but no antibodies to dsDNA.
Felty syndrome is associated in up to 85% with high level histone antibodies, 5%-15% of pa- tients with rheumatoid arthritis or primary biliary cirrhosis have elevated histone antibody levels as well as in autoimmune hepatitis, scleroderma, and neoplastic diseases. Sampling: 1 mL serum
Negative: < 20 U/mL HIV-1/HIV-2 Serology
Test includes: HIV antibody detection by ELISA, confi rmation of ELISA positives by Western
Blotting, p-24 Antigen detection on request Background: Human immunodefi ciency virus (HIV) is the etiologic agent of AIDS. Acute infec-
tion is either symptome free or presents with fl u-like disease. During the stage of acute infection at week 2-3 post infection virus can be detected in the plasma by p24 antigen assay or by PCR based viral DNA test. After 3 weeks, antibodies can be detected in serum or plasma.
Screening for HIV is performed by highly sensitive and specifi c ELISA (EIA) method; positive results have to be repeated by a second sample due to serious consequences of the diagnoses to rule out switched samples or contaminations and subsequently has to be confi rmed by the Western blot method. HIV-2 is closely related to HIV-1, endemic in West Africa causing the same clinical disease, but time to develop AIDS may be longer.
Limitations: A positive HIV EIA must be confi rmed by a second method that has to be based on an alternative principle of antibody detection. Cross reactivities in the screening EIA based test have been rarely described. Cross-reactions may be due to histocompatibility antigen mis- matches or very rare in other viral diseases such as infl uenza.
Serology cannot be used in infants born to an HIV positive mother due to maternal antibody transfer by the placenta. Virus cultivation or DNA detection are more appropriate.
Sampling: 1 mL serum
p-24 antigen detection: negative HIV1/HIV-2 antibody detection: negative Related Information: C4Complement
Rheumatoid Factor, Serum or Body Fluid Yersinia enterocolitica and Yersinia pseudotuberculosis, Culture and Serology Background: HLA-B27 is an allele of the HLA-B locus. It is predictive marker for ankylosing
spondylitis (AS). A patient tested positive has a 100 times greater like hood to develop AS than a negative patient.
Epidemiology: HLA B-27 allele is present in 3%-4% of African-Americans, in 6%-8% of Cauca- sians, and in 1% of Asians.
Sensitivity and specifi city: 90% of patients with ankylosing spondylitis (AS) are positive. 10% of normal subjects are HLAB27 positive. Most of the HLAB27 subtypes are associated with AS. The antigens is also associated, but to a lesser extend with Reiter syndrome, psoriatic arthritis, juvenile rheumatoid arthritis, or post infectious arthritis as well as congenital defi ciency of C4 and C2, adrenal hyperplasia.
Sampling: 3 mL EDTA or ACD blood
Reference Interval: Negative
Homocyst(e)ine Total, Plasma
Cholesterol, Total, Serum or Plasma Factor V Mutation (Leiden Mutation), Folic Acid, Serum Methylmalonic Acid, Serum, Plasma or Urine Vitamin B 12 , Plasma or Serum Background: 80%-90% of the homocysteine is protein bound in the plasma, 5%-10% circu-
lates as homocysteine, 5%-10% is bound to mixed disulfi des, 2% is unbound (free). Metabolized from the essential amino acid methionine, it undergoes either remethylation to methionine, transsulfuration to cysteine and glutathione (vitamin B 6 and ribofl avin needed) or oxidation to homocysteine and mixed disulfi des.
Useful as an independent risk factor for atherosclerosis. An increased value is a marker for thrombophilic state on risk for thrombosis (arteria and venous).
When increased a marker for vitamin defi ciency (B6, B12 ribofl avin) and folic acid. Raised levels in newborns may indicate inborn errors of cobalamin and folate metabolism and the rare autosomal recessive disorder of homocystinuria. Elevated levels are found in patients with renal insuffi ciency and hypothyroidism. Highly prevalent, in 10%-15% of the population, a thermolabile variant of 5,10-methylenetetra hydrofolate reductase present with raised blood homocysteine levels and require higher folic Sampling: Optimal is fasting 2 mL serum and immediately centrifuged.
10% increase per hour if not separated, slowed by placing on ice.
Alternative: overall 95 th percentile 5-15 µmol/L Homovanillic Acid (HVA), Urine
Catecholamines, Fractionation, Plasma Catecholamines, Fractionation, Urine Vanillylmandelic Acid, Urine Background: HVA is a major terminal metabolite of dopamine.
Patients with neuroblastoma excrete dopamine and vanillylmandelic acid. Neuroblastomas are third (7%-11%) among malignancies during childhood, behind leukemia and gliomas. Diagnos- tic sensitivity depends on the tumor stage, in early stages 60%-70% stage I/II and 80% for stage II increasing to 98% in stage IV.
In pheochromocytoma sensitivity of urinary excretion for tumor detection is 96% for catechol- amines, 96% for metanephrine, and 89% for vanillylmandelic acid.
Sampling: Ship an aliquot of 10 mL of a 24h urine, collected in a container prefi lled with of 10 ml
of a 20% hydrochloric acid solution. Ph should be between 2 and 4. Note total quantity! Avoid aspirin, disulfi ram, reserpine, pyridoxine 2 days prior to collection; avoid levodopa 2 weeks prior to the testing.
mg/g creatinine, 95% percentile Alternative value for adults: < 6.9 mg/24 h Human Herpesvirus Typ 6, Serology
HHV-6; Herpesvirus-Typ 6 Background: HHV-6 is a member of the subfamily beta-Herpesviridae and in the genus Ro-
seolovirus. HHV-6 was originally isolated from T cell cultures derived from the blood of patients with AIDS. In contrast to CD4 T cell infection with HIV, HHV-6 infection is rapidly controlled by the immune system. HHV-6 is closely related to cytomegalovirus and HHV-7 viruses. There are two HHV-6 variants; HHV-6 B is the primary etiologic agent of exanthema subitum, for HHV-6 A (and HHV-7) no single disease has been associated with. HHV-6 (and HHV-7) infection occurs early in life, virus is present in saliva of most adults. Virus replicate in CD4 and in CD8 T cells, in natural killer cells, monocytes, epithelial cells and in brain cells. Exanthema subitum (roseola infantum) in young children is characterized by fever, sometimes associated with a mild respiratory illness and lymphadenopathy, followed by the appearance of a fi ne maculopapular rash spreading from the trunk to the extremities. High fever for 3-4 days and infl ammation of the tympanic membranes may occur, but rash may be present in only 10% of the patients. It was estimated that up to 25% of all hospital admissions of children under the age of 3 years with acute febrile illness is due to HHV-6 infection. Primary HHV-6 infection may also cause seizures in infants which accounts for up to 30% of all febrile seizures under the age of 3 years. Rarely, serve courses have been described such as meningoencephalitis, fulminant hepatitis or pancytopenia. In adolescents, HHV-6 may cause mononucleosis like illness. A defi nite role in Multiple sclerosis and lymphoproliferative disorders has not been established and is still under investigation.
In immunocompromised patients, HHV-6 has been associated with intestinal pneumonia and Serology: IGM antibody is the fi rst antibody to be produced in response to acute (primary) as well as in recurrent disease, although the amount of produced IgM is generally higher during pri- mary infection. Paired samples 10-20 days apart are recommended for serological diagnosis. Therapy: Some effect was seen with Foscarnet and Cidofovir Sampling: 1 mL serum
Differentiation of immunoglobulin class IgG antibody negative: IgM antibody negative: Human Papillomavirus (HPV) DNA
HPV, HPV Test, HPV screen Background: HPV primarily infects keratinizing mucosal squamous epithelium. HPV is a mem-
ber of the family of Papovaviruses, which are double stranded, circular, supercoiled DNA viruses with an icosahedral nucleocapsid. Carcinogenesis by HPV involves two proteins encoded by gene E6 and E7, interfering with the tumor suppressor gene p53 and Rb. More than 100 types of papilloma viruses are known, some highly correlated to carcinoma of the cervix.
Although prevalence of HPV infection as a sexual transmitted disease (STD) among women is high, only a faction develops high grade squamous intraepithelial lesions with few progressions to cervical carcinoma. Co-risk factors are smoking, oral contraceptives, nullipara, and other STDs. Immunocompetent women are able to clear the infection within 1-2 years. The test is useful in monitoring patients demonstrating minor cytological abnormalities by Pap test or any abnormal cytologic results or clinical fi nding such as koilocytosis, condyloma acuminatum, low grade squamous intraepithelial lesions, high grade squamous intraepithelial lesions, invasive cervical squamous cell carcinomas and adenocarcinomas.
Of the 30 known anogenital HPV types, 13 types are implicated in the pathogeneses of cer- vical cancer: 16,18,31,33,35,39,45,52,58,59,68. The most common high risk types are: 16,18,31,33,35,45. Low risk types are: 6,11,42,43,44. Sampling: Cytobrush in special transport medium on request to obtain from MEDLAB
Report on diagnostic fi nding Humoral Immunoglobulin Production, Liquor see Cerebrospinal Fluid (CSF, Liquor)
Hydantoins see Phenytoin, Serum
5-Hydroxyindoleacetic Acid (5-HIAA) Quantitative, Urine
Related Information: Serotonin,
Background: 5-HIAA is a serotonin metabolite excreted in larger amounts by carcinoid neo-
plasms of the gastrointestinal tract or respiratory tract and other sites. Used in the diagnosis and monitoring of carcinoid tumors. Urinary excretion > 24 mg/24h favors the diagnosis, particularly if clinical signs are present as fl ushing, hepatomegaly, diarrhea, and bronchospasm.
Limitations: However, some tumors release non-hydroxylated indole acid which is not mea- sured in the assay. Renal diseases may lower urinary secretion.
Increase in patients with malabsorption, (celiac disease, tropical sprue), chronic obstruction. Urinary increase after ingestion of food rich in serotonin such as avocados, bananas, canta- loupe, chocolate, eggplants, dates, kiwi, melon, nuts, pineapples, plantain, plums, tomatoes. Drugs increasing 5-HIAA are acetaminophen, salicylates, phenacetin, naproxen, methocarba- mol, imipramine, isoniazid, MAO-inhibitors, methenamine, methyldopa, reserpine, phenothi- Sampling: 10 mL aliquot of a 24h urine, collect in a prefi lled container with 10 mL of 20% hy-
drochloric acid, note total quantity.
0.6 – 8.2 mg/24h Related Information:
Adrenocorticotropic Hormone, ACTH, Plasma Androstenedione, Cortisol, Serum or Plasma Background: 17-OHP is a precursor of cortisol and synthesized by the adrenal cortex, ovaries,
testes, and placenta.
It is a marker for patients with congenital adrenal hyperplasia (CAH), characterized as an auto- somal recessive disorder by defi ciency of cortisol due to 21 hydroxylase defi ciency (90% of the cases) which leads to ACTH induced adrenal hyperplasia. Patients present with virilization and mineralocorticoid defi ciency, increased 17-ketosteroid and pregnanetriol urine values.
The test is used - In CAH newborn screening and diagnosis and therapy monitoring on cortisol medication.
- In the evaluation of hirsutism, infertility, hermaphroditism which may be caused by 17-hydrolase defi ciency.
- In the diagnosis of endocrine active tumors.
Limitations: 17-OHP is elevated to a lesser extend in 11 beta hydroxylase defi ciency. To differen- tiate both 11-deoxycortisol and desoxycorticosterone have to be determined. Sampling: 2 mL serum or heparin plasma, peak level in the morning. Separate serum or plasma
within 6h. Newborn screening at the age of 2-4 days recommended, not earlier than day 2.
3 days to 60 days 0.1-9.4 3 month to 11 years Newborn screening (ng/dL) (dryed whole blood spot) congenital adrenal hyperplasia suggested Hydroxyproline, Total, Urine
Alkaline Phosphatase, Serum Alkaline Phosphatase, Liver-Intestine-Bone-Isoenzymes, Serum Calcium (Ca), Total, Serum Osteocalcin, Serum or Plasma Test includes: Creatinine, Total, Urine
Background: A marker for bone metabolism and bone turnover. Elevated in Paget s disease,
healing phase after fractures, primary and secondary hyperparathyroidism. The parameter is sensitive to diet, low dose gelatin were used for establishing reference intervals. For best results avoid foods containing gelatine (cooked collagen) and meat for 1-2 days prior to collection. Ice cream, candies, desserts may contain gelatine as well. Avoid aspirin.
Sampling: Ship to the laboratory a 10 ml aliquot of a 24h urine, collect in container pre fi lled
with 1 mL glacial acetic acid. Note total quantity.
2000 µmol/g creatinine 1500 µmol/g creatinine 1000 µmol/g creatinine 200 µmol/g creatinine 30 µmol/g creatinine Ident Card see Paternity Testing
Architecture Paradigms and Programming Languages for Efficient programming of multiple COREs Specific Targeted Research Project (STReP) C2µTC/SL - C Paralellizing Compiler targeting SVP Deliverable D3.4, Issue 1.1 Dissemination level: Purpose: Describe the 1st version of C2µT C/SL compiler.Results: A detailed description of the compiler, implementation details and evaluation results.Conclusion: C2µT C/SL can extract sufficient parallelism from C programs and produce reli-able and efficient code targeting the SVP parallel programming model.