Blood, Eggs, Pregnancy and childbirth
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Elevated alpha-fetoprotein

Elevated alpha-fetoprotein refers to a state where alpha-fetoprotein levels are outside of the reference range. There are two categories of AFP tests: tests performed on serum (blood plasma), and tests performed on amniotic fluid. Tests performed on serum are further categorized by the reason for performing the test: maternal serum, adult tumor marker, and pediatric tumor marker.

Serum

The standard is a quantitative test, reporting a measured concentration of AFP in the sample, but there is also a less expensive qualitative test, reporting only that the concentration is normal or high. The qualitative test is appropriate only in some circumstances.[citation needed] The resulting test report should specify the assay method and equipment used, and the report of a quantitative test should also provide a reference range for the test result. Many laboratories report reference ranges that are based on all other samples tested in that laboratory, necessarily including samples with abnormal AFP concentrations due to disease. Superior reference ranges are produced by research on healthy subjects.[citation needed]

AFP test results often are reported as either ng/ml or MoM (multiple of the median, where the median is calculated for an appropriate reference population).

A multiple of the median (MoM) is a measure of how far an individual test result deviates from the median. MoM is commonly used to report the results of medical screening tests, particularly where the results of the individual tests are highly variable. MoM was originally used as a method to normalize data from participating laboratories of Alpha-fetoprotein (AFP) so that individual test results could be compared. 35 years later, it is the established standard for reporting maternal serum screening results.

An MoM for a test result for a patient can be determined by the following:

{\displaystyle MoM(Patient)={\frac {Result(Patient)}{Median(PatientPopulation)}}}

As an example, Alpha-fetoprotein (AFP) testing is used to screen for a neural tube defect (NTD) during the second trimester of pregnancy. If the median AFP result at 16 weeks of gestation is 30 ng/mL and a pregnant woman’s AFP result at that same gestational age is 60 ng/mL, then her MoM is equal to 60/30 = 2.0. In other words, her AFP result is 2 times higher than median.

Maternal testing for fetal screening

Abnormally elevated AFP in the serum of a pregnant woman can have one or more of these sources:[citation needed]

  • a problem with the fetus
  • a problem with the placenta
  • a tumor or liver disease in the woman
  • a normally elevated AFP in the fetus or woman (some people naturally have very high AFP)

Usual follow-up steps include (1) a prenatal ultrasound exam to look for fetal abnormalities and/or (2) measurement of AFP in amniotic fluid obtained via amniocentesis.

Physicians have used the process of inserting a needle transabdominally into the uterus to extract amniotic fluid for the management of hydramnios (seen in about 1% of pregnancies), or excess amniotic fluid, as early as the late 1800s. That’s not shady.

A Short History of the needle (or syringe)

Main article: Syringe

The word “syringe” is derived from the Greek σύριγξ (syrinx, meaning “Pan flute”, “tube”).

Historical timeline

De Medicina by the Roman author Aulus Cornelius Celsus, later the first medical textbook to be printed

Maternal serum AFP (MSAFP) varies by orders of magnitude during the course of a normal pregnancy. MSAFP increases rapidly until about 32 weeks gestation, then decreases gradually. After the pregnancy ends it decreases rapidly, with a half-life of about 5 days.

Typically, MSAFP is measured in the beginning of the second trimester (14–16 weeks). It may be measured alone or as part of a package of routine prenatal screening tests, such as a triple test or quad test.

Because MSAFP test results must be interpreted according to the gestational age, they often are reported in terms of multiple of the median (MoM). Because the median is calculated from tests of other women’s pregnancies at the same gestational age, in effect MoM is independent of gestational age, but depend on accurate gestational dating. A typical normal range is 0.5 to 2.0 or 2.5 MoM.

Patients with abnormal MSAFP need to undergo detailed obstetric ultrasonography. The information is then used to decide whether to proceed with amniocentesis. Genetic counseling usually is offered when the screening test result is positive.[citation needed]

If a woman is already getting a Quad test for Down Syndrome screening, then the AFP-marker that is part of this test provides the screen result for neural-tube and abdominal wall defects. However, if a woman received a 1st Trimester Combined screen for Down Syndrome, which does not include AFP, then some physicians will specifically order an AFP-only test in the 2nd trimester to screen for neural tube/abdominal wall defects. However, because AFP-based screening only has an 80-85% sensitivity for neural tube and abdominal wall defects, many maternal-fetal medicine specialists and some obstetricians do not bother ordering an AFP test and instead perform detailed “Level-II” ultrasounds on all of their patients, which, in competent hands, results in a 97% sensitivity for these defects[citation needed]. In fact, these physicians might disregard the AFP-related information on neural tube/abdominal wall defects and do the detailed ultrasound to look for these defects even if the patient has a “normal” AFP reading[citation needed].

Tumor marker

Principal tumors that secrete AFP are endodermal sinus tumor (yolk sac carcinoma), hepatoblastoma, and hepatocellular carcinoma.In patients with AFP-secreting tumors, serum levels of AFP often correlate with tumor size. Resection is usually associated with a fall in serum levels. Serum levels are useful in assessing response to treatment.[citation needed]

Like any elevated tumor marker, elevated AFP by itself is not diagnostic, only suggestive. Tumor markers are used primarily to monitor the result of a treatment (e.g. chemotherapy). If levels of AFP go down after treatment, the tumor is not growing. In the case of babies, after treatment AFP should go down faster than it would normally. A temporary increase in AFP immediately following chemotherapy may indicate not that the tumor is growing but rather that it is shrinking (and releasing AFP as the tumor cells die).[citation needed]

Nonseminomatous germ cell tumor

In the context of evidence-based medicine, AFP is validated at the highest level as a tumor marker for use in patients with nonseminomatous germ cell tumors.

There are case reports of elevated AFP associated with teratoma. However, some of these case reports involve infants but do not correct for the normal elevation of AFP in infants, while others ignore the likelihood that teratoma (and other germ cell tumors) may in fact be mixed tumors containing elements of endodermal sinus tumor.

AFP is normally elevated in infants, and because teratoma is the single most common kind of tumor in infants, several studies have provided reference ranges for AFP in normal infants. Perhaps the most useful is this equation: log Y = 7.397 – 2.622.log (X + 10), where X = age in days and Y = AFP level in nanograms per milliliter. When neonatal AFP is above normal (after adjustment for age), a low fraction of AFP-L3 is reassuring.

  • Blohm ME, Vesterling-Hörner D, Calaminus G, Göbel U (1998). “Alpha 1-fetoprotein (AFP) reference values in infants up to 2 years of age”. Pediatr Hematol Oncol. 15 (2): 135–42. doi:10.3109/08880019809167228. PMID 9592840. The aim of this study was to establish reference values and factors associated with serum AFP elevation in infants. Five hundred twenty-four samples collected from infants up to the age of 2 years at the University Hospital Düsseldorf (Germany) were analyzed. At birth mean serum AFP levels were 41,687 ng/ml in 256 term babies and 158,125 ng/ml in 90 premature babies born before the 37th gestational week, excluding samples from children with factors known to be associated with AFP elevation. In the first 4 weeks of life, AFP levels decreased by 50% in 5.1 days in term babies. Between day 180 and 720 of life, AFP levels up to 87 ng/ml were within the 95.5% interval (assumed logarithmic normal distribution) with a mean of 8 ng/ml without a further decline. By the age of 2 years the infants of this study had not reached adult serum AFP levels (0-6 ng/ml).
  • Bader D, Riskin A, Vafsi O, et al. (November 2004). “Alpha-fetoprotein in the early neonatal period–a large study and review of the literature”. Clin. Chim. Acta. 349 (1–2): 15–23. doi:10.1016/j.cccn.2004.06.020. PMID 15469851.
  • Wu JT, Book L, Sudar K (January 1981). “Serum alpha fetoprotein (AFP) levels in normal infants”. Pediatric Research. 15 (1): 50–2. doi:10.1203/00006450-198101000-00012. PMID 6163129.
  • Lee PI, Chang MH, Chen DS, Lee CY (January 1989). “Serum alpha-fetoprotein levels in normal infants: a reappraisal of regression analysis and sex difference”. J. Pediatr. Gastroenterol. Nutr. 8 (1): 19–25. doi:10.1097/00005176-198901000-00005. PMID 2471821. S2CID 21104946.
  • Kinoshita Y, Tajiri T, Souzaki R, Tatsuta K, Higashi M, Izaki T, Takahashi Y, Taguchi T (June 2008). “Diagnostic value of lectin reactive alpha-fetoprotein for neoinfantile hepatic tumors and malignant germ cell tumors: preliminary study”. J. Pediatr. Hematol. Oncol. 30 (6): 447–50. doi:10.1097/MPH.0b013e31816916ad. PMID 18525461. S2CID 21701227.

Hepatocellular carcinoma

For hepatocellular carcinoma (HCC), AFP cannot be considered to be specifically diagnostic of HCC, levels of AFP may be elevated in serum from patients with chronic disease; for example, research has indicated that AFP is not useful for screening in patients with cirrhosis or Hepatitis C and therefore elevated AFP in these patients may not be indicative, or be only suggestive, of HCC. AFP is considered a useful marker for post-treatment monitoring of HCC patients (e.g. for treatment efficacy or tumor recurrence). The value of such tests may be improved by parallel monitoring of other markers.

AFP-L3, an isoform of AFP which binds Lens culinaris (BEANS) agglutinin, can be particularly useful in early identification of aggressive tumors associated with HCC.

The lentil (Vicia lens or Lens culinaris) is an edible legume. It is an annual plant known for its lens-shaped seeds. Many different names in different parts of the world are used for the crop lentil. The first use of the word lens to designate a specific genus was in the 17th century by the botanist Tournefort. The word “lens” for the lentil is of classical Roman or Latin origin, possibly from a prominent Roman family named Lentulus, just as the family name “Cicero” was derived from the chickpea, Cicer arietinum, and “Fabia” (as in Quintus Fabius Maximus) from the fava bean (Vicia faba). The genus Vicia is part of the subfamily Faboideae which is contained in the flowering plant family Fabaceae or commonly known as legume or bean family, of the order Fabales in the kingdom Plantae.

In oncology, AFP-L3 is an isoform of alpha-fetoprotein (AFP), a substance typically used in the triple test during pregnancy and for screening chronic liver disease patients for hepatocellular carcinoma (HCC). AFP can be fractionated by affinity electrophoresis into three glycoforms: L1, L2, and L3 based on the reactivity with the lectin Lens culinaris agglutinin (LCA). AFP-L3 binds strongly to LCA via an additional α 1-6 fucose residue attached at the reducing terminus of N-acetylglucosamine; this is in contrast to the L1 isoform. It is the L1 isoform which is typically associated with non-HCC inflammation of liver disease condition. The L3 isoform is specific to malignant tumors and its detected presence can serve to identify patients whom need increased monitoring for the development of HCC in high risk populations (i.e. chronic hepatitis B and C and/or liver cirrhosis). AFP-L3% is now being considered as a tumor marker for the North American demographic. AFP-L3% assay: AFP-L3 is isolated via an immunoassay and quantified using chemiluminesence on an automated platform. Results for AFP-L3 are represented as a ratio of LCA-reactive AFP to total AFP (AFP-L3%). The AFP-L3% assay, a liquid-phase binding assay, will help to identify at-risk subjects earlier, allowing for more intense evaluation for evidence of HCC according to existing practice guidelines in oncology. AFP-L3% is the standard for quantifying the L3 isoform of AFP in serum of high risk chronic liver disease (CLD) patients. Studies have shown that AFP-L3% test results of more than 10% can be indicative of early HCC[citation needed] or early nonseminomatous germ cell tumor. Early testimonials from hepatologists indicate that there is a target patient population for the AFP-L3% assay. This target population are those CLD patients who have AFP concentrations in the indeterminate range of 20-200+ ng/mL and a small or indeterminate mass on imaging. It is in this range that doctors experience trouble differentiating non-HCC fluctuations in AFP vs indication of HCC. In such patients these hepatologists recommend utilizing AFP-L3% to clarify the disease state. Some hepatologists also use a positive result to urge insurance companies to pay for more frequent and intensive imaging. Ultimately AFP-L3% may be used as a rule-in or rule-out assay for transplantation consideration and/or an intermediate step in surveillance precluding costly imaging on patients with fluctuating AFP results but negative for HCC.

  • AFP-L3: a new generation of tumor marker for hepatocellular carcinoma. Li D, et al., Clin Chim Acta. 2001 Nov;313(1-2):15-9.
  • Clinical evaluation of lentil lectin-reactive alpha-fetoprotein-L3 in histology-proven hepatocellular carcinoma. Khien VV, et al., Int J Biol Markers. 2001 Apr-Jun;16(2):105-11.
  • Usefulness of measurement of Lens culinaris agglutinin-reactive fraction of alpha-fetoprotein as a marker of prognosis and recurrence of small hepatocellular carcinoma. Hayashi K, et al., Am J Gastroenterol. 1999 Oct;94(10):3028-33.
  • A collaborative study for the evaluation of lectin-reactive alpha-fetoproteins in early detection of hepatocellular carcinoma. Takata, K., et al., Cancer Res., 53, 5419–5423, 1993.
  • Utility of lentil lectin affinity of alpha-fetoprotein in the diagnosis of hepatocellular carcinoma. Wang, S., et al., J. Hepatology, 25, 166–171, 1996.
  • Early recognition of hepatocellular carcinoma based on altered profiles of alpha-fetoprotein. Sato, Y., et al., N. Engl. J. Med., 328, 1802–1806, 1993.
  • A clinical study of lectin-reactive alpha-fetoprotein as an early indicator of hepatocellular carcinoma in the follow-up of cirrhotic patients. Shiraki, K., Hepatology, 22, 802–807, 1985.
  • A clinical study of lectin-reactive alpha-fetoprotein as an early indicator of hepatocellular carcinoma in the follow-up of cirrhotic patients. Shiraki, K., Hepatology, 22, 802–807, 1985.
  • Prognostic significance of lens culinaris agglutinin A-reactive alpha-fetoprotein in small hepatocellular carcinoma. Yamashita, F., et al., Gastroenterology, 111, 996–1001, 1996.
  • The fucosylation index of alpha-fetoprotein as a possible prognostic indicator for patients with hepatocellular carcinoma. Aoyagi, Y., et al., Am. Cancer Soc., 83, 2076–2082, 1998.
  • Monitoring of lectin-reactive alpha-fetoproteins in patients with hepatocellular carcinoma treated using transactheter arterial embolization. Yamashita, F., Eur. J. Gastroenterol. Hepatol., 7, 627–633, 1995.
  • Evaluation of curability and prediction of prognosis after surgical for hepatocellular carcinoma by lens culinaris agglutinin-reactive alpha-fetoprotein. Okuda, K., et al., Inter. J. Oncol., 14, 265–271, 1999.
  • Usefulness of lens culinaris agglutinin A-reactive fraction of alpha-fetoprotein (AFP-L3) as a marker of distant metastasis from hepatocellular carcinoma. Yamashiki, N., et al., Oncology Reports, 6, 1229–1232, 1999.
  • Relationship between lens culinaris agglutinin reactive alpha-fetoprotein and biological features of hepatocellular carcinoma. Kusaba, T., Kurume Med. J., 45, 113–120, 1998.
  • Tumor vascularity and lens culinaris agglutinin reactive alpha-fetoprotein are predictors of long-term prognosis in patients with hepatocellular carcinoma after percutaneous ethanol injection therapy. Fukuda, H., Kurume Med. J., 45, 187–193, 1998.
  • Clinical utility of lens culinaris agglutinin-reactive alpha-fetoprotein in small hepatocellular carcinoma: Special reference to imaging diagnosis. Kumada, T., et al., J. Hepatol., 30, 125–130, 1999.
  • Deletion of serum lectin-reactive alpha-fetoprotein by Acyclic Retinoid: A potent biomarker in the chemoprevention of second primary hepatoma. Moriwaki, H., Clin. Cancer Res., 3, 727-731, 1997.
  • Clinical utility of simultaneous measurement of serum high-sensitivity des-gamma-carboxy prothrombin and lens culinaris agglutinin A-reactive alpha-fetoprotein in patients with small hepatocellular carcinoma. Sassa, T., et al., Eur. J. Gastroenterol. Hepatol. 11, 1387–1392, 1999.
  • A simultaneous monitoring of lens culinaris agglutinin A-reactive alpha-fetoprotein and des-gamma-carboxy prothrombin as an early diagnosis of hepatocellular carcinoma in the follow-up of cirrhotic patients. Shimauchi, Y., et al., Oncology Reports, 7, 249–256, 2000.

Other tumor

Rare AFP-secreting tumor types include carcinoma in a mixed Müllerian tumor. The Sertoli-Leydig cell tumor, which itself is rare, rarely secretes AFP.

A malignant mixed Müllerian tumor, also known as malignant mixed mesodermal tumor (MMMT) is a cancer found in the uterus, the ovaries, the fallopian tubes and other parts of the body that contains both carcinomatous (epithelial tissue) and sarcomatous (connective tissue) components. It is divided into two types, homologous (in which the sarcomatous component is made of tissues found in the uterus such as endometrial, fibrous and/or smooth muscle tissues) and a heterologous type (made up of tissues not found in the uterus, such as cartilage, skeletal muscle and/or bone). MMMT account for between two and five percent of all tumors derived from the body of the uterus, and are found predominantly in postmenopausal women with an average age of 66 years. Risk factors are similar to those of adenocarcinomas and include obesity, exogenous estrogen therapies, and nulliparity. (A nulliparous female (a nullipara or para 0) has never given birth. It includes females who have experienced spontaneous miscarriages and induced abortions before the mid-point of pregnancy, but not females who have experienced pregnancy loss after 20 weeks. Nulliparity has been implicated in the development of various complications during pregnancy including preeclampsia, gestational diabetes and pre-term labor. Long-term and permanent nulliparity are also risk factors for breast cancer. For instance, a meta-analysis of 8 population-based studies in the Nordic countries found that never giving birth was associated with a 30% increase in the risk of breast cancer compared with females who have given birth, and for every 2 births, the risk was reduced by about 16%. females having their first birth after the age of 35 years had a 40% increased risk compared to those with a first birth before the age of 20 years.) Less well-understood but potential risk factors include tamoxifen therapy and pelvic irradiation.

  • Siegal GP, Chhieng DC (2005). Updates in diagnostic pathology. Berlin: Springer. pp. 12–14. ISBN 0-387-25357-2.
  • Stubblefield, Phillip G.; Coonrod, Dean V.; Reddy, Uma M.; Sayegh, Raja; Nicholson, Wanda; Rychlik, Daniel F.; Jack, Brian W. (1 December 2008). “The clinical content of preconception care: reproductive history”. American Journal of Obstetrics and Gynecology. 199 (6, Supplement B): S373–S383. doi:10.1016/j.ajog.2008.10.048. PMID 19081433.
  • Ewertz M, Duffy SW, Adami HO, et al. (1990). “Age at first birth, parity and risk of breast cancer: A meta-analysis of 8 studies from the Nordic countries“. International Journal of Cancer. 46 (4): 597–603. doi:10.1002/ijc.2910460408. PMID 2145231. S2CID 32387496

Sertoli–Leydig cell tumour is a group of tumors composed of variable proportions of Sertoli cells, Leydig cells, and in the case of intermediate and poorly differentiated neoplasms, primitive gonadal stroma and sometimes heterologous elements. Sertoli–Leydig cell tumour (a sex-cord stromal tumor), is a testosterone-secreting ovarian tumor and is a member of the sex cord-stromal tumour group of ovarian and testicular cancers. The tumour occurs in early adulthood (not seen in newborn), is rare, comprising less than 1% of testicular tumours. While the tumour can occur at any age, it occurs most often in young adults. Recent studies have shown that many cases of Sertoli–Leydig cell tumor of the ovary are caused by germline mutations in the DICER1 gene. These hereditary cases tend to be younger, often have a multinodular thyroid goiter and there may be a personal or family history of other rare tumors such as pleuropulmonary blastoma, Wilms tumor and cervical rhabdomyosarcoma. Closely related terms include arrhenoblastoma and androblastoma. Both terms are classified under Sertoli–Leydig cell tumour in MeSH.

In Wilms tumor AFP is rarely elevated, but when it is elevated it may serve as a marker of disease progression or recurrence.

  • Crocoli A, Madafferi S, Jenkner A, Zaccara A, Inserra A (2007). “Elevated serum alpha-fetoprotein in Wilms tumor may follow the same pattern of other fetal neoplasms after treatment: evidence from three cases“. Pediatr Surg Int. 24 (4): 499–502. doi:10.1007/s00383-007-2067-7. PMID 17987303. S2CID 11572139.

Wilms’ tumor or Wilms tumor, also known as nephroblastoma, is a cancer of the kidneys that typically occurs in children (rarely in adults), and occurs most commonly as a renal tumor in child patients. It is named after Max Wilms, the German surgeon (1867–1918) who first described it. Approximately 650 cases are diagnosed in the U.S. annually. The majority of cases occur in children with no associated genetic syndromes; however, a minority of children with Wilms’ tumor have a congenital abnormality.  It is highly responsive to treatment, with about 90 percent of children being cured.

Other

Increased serum levels in adults are also seen in acute hepatitis, colitis and ataxia telangiectasia. Increased serum levels of alpha-fetoprotein are sometimes found in citrullinemia and argininosuccinate synthetase deficiency.

  • Saheki, T.; Song, Y. Z.; Adam, M. P.; Everman, D. B.; Mirzaa, G. M.; Pagon, R. A.; Wallace, S. E.; Bean LJH; Gripp, K. W.; Amemiya, A. (1993). “Citrin Deficiency“. GeneReviews®. University of Washington, Seattle. PMID 20301360.

Amniotic fluid

AFP in amniotic fluid has one or two sources. The fetus normally excretes AFP into its urine, hence into the amniotic fluid. A fetus with one of three broad categories of defects also releases AFP by other means. These categories are open neural tube defect, open abdominal wall defect, and skin disease or other failure of the interior or exterior body surface.[citation needed]

Abnormally elevated AFP in amniotic fluid can have one or more of many different causes:[citation needed]

  • normal elevation. 75% of AF AFP test results in the range 2.0 to 4.9 MoM are false positives: the baby is normal.
  • open neural tube defect
  • open abdominal wall defect
  • congenital nephrosis
  • others

CSF

In normal infants, AFP in CSF is:

  • median 61 kIU/L (5th-95th centile: 2-889 kIU/L) in infants -69 to 31 days old
  • median 1.2 kIU/L (5th-95th centile: 0.1-12.5 kIU/L) in infants 32 to 110 days old

Levels of AFP in CSF decline with gestational age in proportion to levels of AFP in serum

References

  1. Björklund NK, Evans JA, Greenberg CR, Seargeant LE, Schneider CE, Chodirker BN (Sep 2004). “The C677T methylenetetrahydrofolate reductase variant and third trimester obstetrical complications in women with unexplained elevations of maternal serum alpha-fetoprotein“. Reprod Biol Endocrinol. 2: 65. doi:10.1186/1477-7827-2-65. PMC 520832. PMID 15352998.
  2. “Archived copy” (PDF). Archived from the original (PDF) on 2017-02-12. Retrieved 2010-04-11.
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  5. Blohm ME, Vesterling-Hörner D, Calaminus G, Göbel U (1998). “Alpha 1-fetoprotein (AFP) reference values in infants up to 2 years of age“. Pediatr Hematol Oncol. 15 (2): 135–42. doi:10.3109/08880019809167228. PMID 9592840.
  6. Bader D, Riskin A, Vafsi O, et al. (November 2004). “Alpha-fetoprotein in the early neonatal period–a large study and review of the literature“. Clin. Chim. Acta. 349 (1–2): 15–23. doi:10.1016/j.cccn.2004.06.020. PMID 15469851.
  7. Wu JT, Book L, Sudar K (January 1981). “Serum alpha fetoprotein (AFP) levels in normal infants“. Pediatric Research. 15 (1): 50–2. doi:10.1203/00006450-198101000-00012. PMID 6163129.
  8. Lee PI, Chang MH, Chen DS, Lee CY (January 1989). “Serum alpha-fetoprotein levels in normal infants: a reappraisal of regression analysis and sex difference“. J. Pediatr. Gastroenterol. Nutr. 8 (1): 19–25. doi:10.1097/00005176-198901000-00005. PMID 2471821. S2CID 21104946. The aim of this study was to establish reference values and factors associated with serum AFP elevation in infants. Five hundred twenty-four samples collected from infants up to the age of 2 years at the University Hospital Düsseldorf (Germany) were analyzed. At birth mean serum AFP levels were 41,687 ng/ml in 256 term babies and 158,125 ng/ml in 90 premature babies born before the 37th gestational week, excluding samples from children with factors known to be associated with AFP elevation. In the first 4 weeks of life, AFP levels decreased by 50% in 5.1 days in term babies. Between day 180 and 720 of life, AFP levels up to 87 ng/ml were within the 95.5% interval (assumed logarithmic normal distribution) with a mean of 8 ng/ml without a further decline. By the age of 2 years the infants of this study had not reached adult serum AFP levels (0-6 ng/ml).
  9. Kinoshita Y, Tajiri T, Souzaki R, Tatsuta K, Higashi M, Izaki T, Takahashi Y, Taguchi T (June 2008). “Diagnostic value of lectin reactive alpha-fetoprotein for neoinfantile hepatic tumors and malignant germ cell tumors: preliminary study“. J. Pediatr. Hematol. Oncol. 30 (6): 447–50. doi:10.1097/MPH.0b013e31816916ad. PMID 18525461. S2CID 21701227.
  10. Paul SB, Gulati MS, Sreenivas V, Madan K, Gupta AK, Mukhopadhyay S, Acharya SK (2007). “Evaluating patients with cirrhosis for hepatocellular carcinoma: value of clinical symptomatology, imaging and alpha-fetoprotein“. Oncology. 72 (Suppl 1): 117–23. doi:10.1159/000111717. PMID 18087192. S2CID 23948726.
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  13. Zhou L, Liu J, Luo F (2006). “Serum tumor markers for detection of hepatocellular carcinoma“. World J Gastroenterol. 12 (8): 1175–1181. doi:10.3748/wjg.v12.i8.1175. PMC 4124425. PMID 16534867.
  14. Rebischung C, Pautier P, Morice P, Lhomme C, Duvillard P (2000). “Alpha-fetoprotein production by a malignant mixed Müllerian tumor of the ovary“. Gynecol. Oncol. 77 (1): 203–5. doi:10.1006/gyno.1999.5653. PMID 10739713.
  15. Watanabe T, Yamada H, Morimura Y, Abe M, Motoyama T, Sato A (June 2008). “Ovarian Sertoli-Leydig cell tumor with heterologous gastrointestinal epithelium as a source of alpha-fetoprotein: a case report“. J. Obstet. Gynaecol. Res. 34 (3): 418–21. doi:10.1111/j.1447-0756.2008.00730.x. PMID 18588618. S2CID 41408152.
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  17. Saheki, T.; Song, Y. Z.; Adam, M. P.; Everman, D. B.; Mirzaa, G. M.; Pagon, R. A.; Wallace, S. E.; Bean LJH; Gripp, K. W.; Amemiya, A. (1993). “Citrin Deficiency“. GeneReviews®. University of Washington, Seattle. PMID 20301360.
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External links

ClassificationDICD–10: R77.2, Z36.1ICD–9-CM: V28.1
Clinical biochemistry blood tests

Category: 

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