Inefficient Labor May Necessitate Ceasarian Section to Save the Baby. Courtesy Wikipedia.org
What Are Obstetrical Complications?
[dropcap]O[/dropcap]bstetrical complications are reproductive disorders during pregnancy, labor and delivery that endanger the mother and unborn infant.
Complications may result from prolonged constipation, malnutriton, hormonal imbalance, infection, systemic disease such as diabetes, obesity, tumors of the uterus, medication adverse effects, drug abuse, smoking, and alcohol abuse.
What Are Obstetrical Complications In Celiac Disease and/or Gluten Sensitivity?
[dropcap]D[/dropcap]ementia is the term used to describe a group of symptoms that show significant deterioration of an individual’s intellectual and social abilities.
The deterioration in intellectual function is progressive and is characterized by memory and cognitive impairment involving deficits in reasoning, judgment, abstract thought, comprehension, learning, use of language, and task execution.
Some types of dementia can be reversed, while most types of dementia are degenerative or nonreversible.
Q: What causes dementia?
A: There are many differing causes of dementia. Here are some causes according to nonreversible and reversible:
Nonreversible dementia may not be turned back due to these conditions:
Alzheimer’s disease is the most common type of degenerative dementia caused by abnormal protein structures in certain areas of the brain.
Lewy body disease is a leading cause of dementia in elderly adults.
Vascular dementia due to many small strokes.
Medical conditions: Huntington’s disease, multiple sclerosis, infections that can affect the brain, such as HIV/AIDS and Lyme disease, Parkinson’s disease, Pick’s disease, and progressive supranuclear palsy.
Reversible dementia may be stopped or reversed if these conditions are found soon enough:
Brain injury.
Brain tumors.
Chronic alcohol abuse.
Changes in blood sugar, sodium, and calcium levels.
Changes that can occur with celiac disease, diabetes, thyroid disease, and other metabolic disorders.
Nutritional deficiencies.
Use of certain medications, including cimetadine and some cholesterol-lowering medications.1
What Is Dementia In Celiac Disease and/or Gluten Sensitivity?
[dropcap]D[/dropcap]epression is a mood disorder characterized by absence of cheerfulness, dejection, and loss of interest or pleasure in living, making the person dysfunctional and unable to cope with or perform tasks of daily living.
More than a feeling, this negative psychological status can range from mild to profound and can involve other parts of the body, causing physical problems such as poor digestion, constipation, weight gain or weight loss, mentrual irregularities in females, and impotence in males.
Q: How is depression identified?
A: According to the American Psychiatric Association, depression is a psychic condition that lasts for more than a month and involves four or more of these symptoms:
Abnormal appetite.
Diminished ability to concentrate or think properly.
Feelings of worthlessness.
Low energy or fatigue.
Physical inactivity or hyperactivity.
Sleep disturbances.
Thoughts of death.
Grief or sadness at the loss of a loved one or a similar event or remorse for sin is normal. However, depression that is prolonged usually involves imbalances of nerve chemicals called neurotransmitters. Imbalances can result from health disorders such as hormonal imbalances, low blood sugar, stress, drug side effects, or nutrient deficiencies.
What Is Depression In Celiac Disease and/or Gluten Sensitivity?
Gluten sensitive enteropathy is active celiac disease characterized by inflammation of the small intestinal mucosa that results from an inherited immunologic intolerance to ingested gluten.
Q: What does the inflammation do to the mucosa in the small intestine?
A: Inflammation is a cell level immune response to gluten that has these effects on the mucosa:
Damages the barely visible villi (multitudinous finger-like structures) by causing atrophy or loss.
Likely affects the structural support and microcirculation of the villus, leading to collapse of the villus.
Elongates the crypts between villi. The thickening of the crypt is not so much a response to loss of surface enterocytes but represents inflammation of the mucosa.1
Increases round cells in the lamina propria and surface epithelial cells leaving few, irregular microvilli (brush border) on the surface of villi.
Damage is most intense in the duodenum and decreases toward the large intestine.
The extent of the damage to the intestine determines the malabsorptive consequences of the disease. Both gastric and small intestinal permeability are disrupted in patients with celiac disease.2
Relationship between active celiac disease and intestinal permeability: There is a clear association between degree of mucosal damage and the intestinal-permeability ratio, and a normal ratio generally implies near-normal small intestinal structure. A raised intestinal permeability of the mucosal lining (leaky gut) could predispose to a high absorption of gluten and exacerbate an existing lesion and hence convert a latent to an overt enteropathy.3
Relationship between active celiac disease and tight junction proteins: A study of intestinal permeability showed that the expression of all junction proteins of the small intestinal lining (occludin, claudin 3, zonula occludens 1, and E-cadherin) was already decreased in early stage celiac disease when compared with non-celiac controls, showing leaky gut and confirming the above earlier study by Johnston et al. Junction protein expression correlated positively with mucosal villus structure and negatively with the number of intraepithelial lymphocytes (IELs), the intensity of small-intestinal autoantibody deposits, and serum autoantibodies. The expression of claudin 3 showed a negative correlation with diarrheal score.4
Relationship between active celiac disease and inflammation. In celiac disease there is an over production of inflammatory interleukin-15 (IL-15) which inhibits the correct removal of damaged intraepithelial lymphocytes caused by the reaction to gluten. Serum levels of IL-15 are directly correlated with the seriousness of tissue damage.5
Relationship between active celiac disease and gut microbiota. Results of a study investigating intestinal microbiota (normal bacterial residents) in patients with celiac disease suggest that with lower levels of the genus bifidobacteria, celiac patients have an imbalance in the intestinal microbiota even while on a gluten-free diet. This fact could favor the pathological process of the disorder. The concentration of bifidobacteria per gram of feces was significantly higher in healthy subjects (2.5 ± 1.5 x107 CFU/g) when compared to celiac patients (1.5 ± 0.63 x108 CFU/g).6
Relationship between active celiac disease and endoscopy technique. The most severe degree of villous atrophy was detected when distal duodenal biopsy specimens were taken in addition to a duodenal bulb biopsy specimen from either the 9- or 12-o’clock position (96.4% sensitivity; 95% CI, 79.7%-100%). The difference between the 12-o’clock position biopsy and the 3-o’clock position biopsy in detecting the most severe villous atrophy was 92% (24/26 patients) versus 65% (17/26 patients).7
Relationship between active celiac disease and diet adherence. Patients with consistent gluten free diet adherence experience symptomatic responses to dietary gluten (SRDG) faster and more severe in comparison to their prior gluten exposure possibly demonstrating an adept immunological response. Anxiety and depression also enhance the speed of symptom onset and co-existing visceral hypersensitivity is a risk factor for severe reactions to dietary gluten.8
Relationship between active celiac disease and atrial fibrillation: Patients with celiac disease, verified by intestinal biopsy, are at increased risk of atrial fibrillation. This observation is consistent with previous findings that elevation of inflammatory markers predicts atrial fibrillation.9
How Prevalent Is Gluten Sensitive Enteropathy?
Sources:
Murray JA, the widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999; 69(3):354-365. [↩]
Murray JA, the widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999; 69(3):354-365. [↩]
Johnston SD, Smye M, Watson RGP. Intestinal permeability and morphometric recovery in coeliac disease. Lancet. Jul 28, 2001;358(9278):259, 2p. [↩]
Rauhavirta T, Lindfors K, Koskinen O, Laurila K, Kurppa K, Saavalainen P, Mäki M, Collin P, Kaukinen K. Impaired epithelial integrity in the duodenal mucosa in early stages of celiac disease. Transl Res. 2014 Sep;164(3):223-31. doi: 10.1016/j.trsl.2014.02.006 [↩]
Stazi AV, Trinti B. Selenium status and over-expression of interleukin-15 in celiac disease and autoimmune thyroid diseases. Ann Ist Super Sanita. 2010;46(4):389-99.DOI: 10.4415/ANN_10_04_06. [↩]
Golfetto L, de Senna FD, Hermes J, Beserra BT, França Fda S, Martinello F. Lower bifidobacteria counts in adult patients with celiac disease on a gluten-free diet. Arq Gastroenterol. 2014 Apr-Jun;51(2):139-43. [↩]
Kurien M, Evans KE, Hopper AD, Hale MF, Cross SS, Sanders DS. Duodenal bulb biopsies for diagnosing adult celiac disease: is there an optimal biopsy site? Gastrointest Endosc. 2012 Jun;75(6):1190-6. doi: 10.1016/j.gie.2012.02.025. [↩]
Barratt SM, Leeds JS, Sanders DS. Factors influencing the type, timing and severity of symptomatic responses to dietary gluten in patients with biopsy-proven coeliac disease. J Gastrointestin Liver Dis. 2013 Dec;22(4):391-6. [↩]
Emilsson L, Smith JG, West J, Melander O, Ludvigsson JF. Increased risk of atrial fibrillation in patients with coeliac disease: a nationwide cohort study. Eur Heart J. 2011 Oct;32(19):2430-7. doi: 10.1093/eurheartj/ehr167. [↩]
What Is Peripheral Neuropathy? [dropcap]P[/dropcap]eripheral neuropathy is a syndrome involving damage to one or more peripheral nerves characterized by impaired nerve transmission. Peripheral nerves are nerves of the body outside the brain and spinal cord. Q:…
Child with autism stacking cans. Courtesy Wikimedia.
What Is Autism and Learning Disabilities?
[dropcap]A[/dropcap]utism and learning disabilities constititute a non-progressive psychiatric syndrome appearing in childhood characterized by withdrawal from communication with others often accompanied by repetitive or primitive behaviors.
Primary gastrointestinal pathology may play an important role in the inception and clinical expression of autism.
Autistic children often manifest complex biochemical and immunological abnormalities.1 Following are four main features involving the digestive tract:
1) Brain dysfunction from an abnormal gut. Common characteristics of hepatic encephalopathy (brain dysfunction caused by liver disease) and a form of autism associated with developmental regression and immune caused gastrointestinal pathology (abnormal) in an apparently healthy child, have led to the proposal that there may be similar mechanisms of toxic brain dysfunction caused by gluten and casein proteins.
Gluten in wheat and casein in cow milk are called exomorphines because they act like morphine (opioid) in the brain. Aberrations in opioid biochemistry are common in autism.
2) Characteristic intestinal pathology. Many autistic children with gut symptoms have ileocolonoic lymphoid nodular hyperplasia and inflammation of the intestinal lining. The colon lesion consisting of a mucosal infiltrate of yo T cells and Celiac Disease8+ T cells and crypt cell proliferation is enhanced significantly, and the basement membrane is thicker than in normal or disease groups. Neutrophil and eosinophil mucosal infiltration and absence on colonic epithelium of HLA-DR antigen suggests a T-helper -2 dominated immune response.
The corresponding small intestinal lesion also shows a distinct inflammatory reaction in which immune-mediated epithelial cell damage is predominant and blood anitibodies of the IgG type colonizes with complement.
3) Intestinal permeability abnormalities. A subset of children with autism were found to display increased immune reactivity to gluten, the mechanism of which appears to be distinct from that in celiac disease. The increased anti-gliadin antibody response and its association with gastrointestinal symptoms points to a potential mechanism involving immunologic and/or intestinal permeability abnormalities in affected children.2
4) Secondary dysbiosis. Anaerobic dysbiosis develops in the colon caused by fermentation of the overload of undigested food arriving from the small intestine. Billions of microbes in the colon normally breakdown undigested food, however, in autism, the process is dysfunctional and produces byproducts that are toxic to the brain resulting in encephalopathy.
What Is Autism and Learning Disabilities In Celiac Disease and/or Gluten Sensitivity?
Sources:
Wakefield AJ, Puleston M, Montgomery SM, Anthony A, O’Leary JJ, Murch SH. Review Article: the concept of entero-colonic encephalopathy, autism, and opioid receptor ligands. Aliment Parmacol Ther. 2002; 16:663-674. [↩]
Lau NM, Green PH, Taylor AK, Hellberg D, Ajamian M, Tan CZ, Kosofsky BE, Higgins JJ, Rajadhyaksha AM, Alaedini A. Markers of Celiac Disease and Gluten Sensitivity in Children with Autism. PLoS One. 2013 Jun 18;8(6):e66155. Print 2013. [↩]
[dropcap]F[/dropcap]olic acid deficiency anemia, also called folate deficiency anemia, is a macrocytic anemia characterized by defective DNA synthesis of red blood cells that results from a lack of folate in the body.
Q: How does folate deficiency cause anemia?
A: Folates are a family of B vitamins and folic acid is an active form.
Folate is required for the formation of both red and white blood cells in the bone marrow and for their maturation.
Also, folate serves as a carrier in the formation of heme, which contains iron, and is the non-protein part of the hemoglobin molecule.1
Red blood cells provide oxygen to body tissues. When there are not enough red blood cells or when they cannot properly carry oxygen, the condition is called anemia. In folic acid deficiency anemia, the red blood cells are abnormally large. Such cells are called macrocytes (macro size cells). They are also called megaloblasts (mega size cells) as seen in the bone marrow where they are produced. This is why this macrocytic anemia is also called megaloblastic anemia.2
Tests that may be done to determine folate adequacy are complete blood count (CBC), red blood cell folate level, methylmalonic acid level, and homocysteine level. Folic acid deficiency anemia shows a decrease in red blood cell folate and/or serum folate levels and normal plasma methylmalonic acid level with elevated homocysteine blood level. These levels distinguish folic acid deficiency anemia from vitamin B12 deficiency anemia.3
What Is Folate Deficiency Anemia In Celiac Disease and/or Gluten Sensitivity?
[dropcap]A[/dropcap]pathy is an abnormal emotional state that is characterized by indifference to things which others find interesting, moving or exciting, and diminished motivation to perform regular daily activities.
The neural mechanisms of apathy are postulated to involve the brainstem and forebrain circuits that regulate goal-directed behavior.1
What Is Apathy In Celiac Disease and/or Gluten Sensitivity?
[dropcap]M[/dropcap]iscarriage, or spontaneous abortion, is a reproductive failure characterized by loss of an unborn baby before the 20th week of pregnancy.
What Is Miscarriage In Celiac Disease and/or Gluten Sensitivity?