ALCOHOLIC HEPATITIS

BY KEMBOI KIBET

  • Alcoholic liver disease (ALD) encompasses a spectrum of injury, ranging from simple steatosis to frank cirrhosis.
  • Alcohol remains amajor cause of liver disease worldwide
  • It is common for patients with ALD to share risk factors for simultaneous injury from other liver insults (e.g., coexisting nonalcoholic fatty liver disease, or chronic viral hepatitis).
  • The spectrum of alcohol-related liver injury varies from simple steatosis to cirrhosis.
  • These are not necessarily distinct stages of evolution of the disease, but rather, multiple stages that maybe present simultaneously in a given individual.
  • These are oft en grouped into three histological stages of ALD, including
    • fatty liver or simple steatosis.
    • alcoholic hepatitis (AH).
    • chronic hepatitis with hepatic fibrosis or cirrhosis.
  • The latter stages may also be associated with a number of histological changes, including
    • Mallory’s hyaline
    • megamitochondria
    • perivenular and perisinusoidal fibrosis
  • Alcoholic hepatitis is a syndrome of progressive inflammatory liver injury associated with long-term heavy intake of ethanol.
  • Alcoholic hepatitis (AH) remains a common and life threatening cause of liver failure, especially when it is severe.
  • Although the term “acute” is frequently used to describe this form of liver injury, it is usually subacute and has been developing for weeks to months before it becomes clinically apparent.

ETIOLOGY

  • Patients with this form of alcoholic liver disease usually have a history of drinking heavily for many years.
  • Observational studies have shown an increased risk of cirrhosis with ingestion of greater than
    • 10-20 g of alcohol per day in women and
    • more than 20-40 g/d in men.

RISK FACTORS

  • A variety of genetic,environmental and gender-related factors appear to independently influence the development of alcoholic liver disease.
  • Age, female gender, excess body weight [body mass index (BMI) > 27 kg/m2 in men, BMI > 25 kg/m2 in women have been identified as independent risk factors for development of liver disease. (Bruguera 2014)
  • In addition to a smaller volume of distribution, women are at higher risk due to a relative deficiency of gastric alcohol dehydrogenase compared to men.
  • several women have developed AH after gastric bypass, in which the amount of gastric mucosa available to metabolize alcohol was reduced.
  • More severe forms of AH are associated with consumption of large amounts of alcohol or binge drinking.
  • Not surprisingly concomitant malnutrition and the presence of coexisting hepatitis C has also been linked to a poorer prognosis.(Leslie, Pawloski et al. 2014)
  • The combination of hepatitis C virus and alcohol predisposes to moreadvanced liver injury than alcohol alone,76,77 with disease at a younger age, more severe histological features, and a decreased survival.(Stimac, Bradaric et al. 2013)
  • The risk of developing cirrhosis increases with the ingestion of > 60-80 g/day of alcohol for 10 years or longer in men, and >20g/day in women.6,50 Yet, even drinking at these levels, only 6%-41% develop cirrhosis.

EIDEMIOLOGY

  • The true prevalence of alcoholic hepatitis, especially of its milder forms, is unknown, because patients may be asymptomatic and never seek medical attention.
  • In the United States alone, alcoholic liver disease affects more than 2 million people (ie, approximately 1% of the population).
  • Although the exact prevalence is unknown, approximately 7.4% of adult Americans were estimated to meet DSM-IV criteria for the diagnosis of alcohol abuse and/or alcohol dependence in 1994
  • More recent data suggest 4.65% meet criteria for alcohol abuse and 3.81% for alcohol dependence. In 2003, 44% of all deaths from liver disease were attributed to alcohol.
  • Racial differences in incidence – no genetic predilection is noted for any particular race
  • Alcoholic hepatitis can develop at any age. However, its prevalence parallels the prevalence of ethanol abuse in the population, with a peak incidence in individuals aged 20-60 years.
  • Sexual differences in incidence – Women develop alcoholic hepatitis after a shorter period and smaller amounts of alcohol abuse than men, and alcoholic hepatitis progresses more rapidly in women than in men.

PATHOGENESIS

Ethanol metabolism

  • Most tissues of the body, including the skeletal muscles, contain the necessary enzymes for the oxidative or nonoxidative metabolism of ethanol.
  • However, the major site of ethanol metabolism is the liver.
  • Within the liver, 3 enzyme systems metabolise ethanol—
  1. Cytosolic ADH uses nicotinamide adenine dinucleotide (NAD) as an oxidizing agent. ADH exists in numerous isoenzyme forms in the human liver and is encoded by 3 separate genes, designated as ADH1, ADH2, and ADH3. Variations in ADH isoforms may account for significant differences in ethanol elimination rates.
  2. The microsomal ethanol-oxidizing system (MEOS) uses nicotinamide adenine dinucleotide phosphate (NADPH) and molecular oxygen. The central enzyme of MEOS is cytochrome P-450 2E1 (CYP2E1).
  • Peroxisomal catalase uses hydrogen peroxide as an oxidizing agent.
  • The product of all 3 reactions is acetaldehyde, which is then further metabolized to acetate by acetaldehyde dehydrogenase (ALDH).
  • Acetaldehyde is a reactive metabolite that can produce injury in a variety of ways.
  1. Toxic effects on cell membranes
  • Ethanol and its metabolite, acetaldehyde damage liver cell membranes.
  • Ethanol can alter the fluidity of cell membranes, thereby altering the activity of membrane-bound enzymes and transport proteins.
  • Ethanol damage to mitochondrial membranes may be responsible for the giant mitochondria (megamitochondria) observed in patients with alcoholic hepatitis.
  • Acetaldehyde-modified proteins and lipids on the cell surface may behave as neoantigens and trigger immunologic injury.
  1. Hypermetabolic state of the hepatocyte
  • Hepatic injury in alcoholic hepatitis is most prominent in the perivenular area (zone 3) of the hepatic lobule.
  • This zone is known to be sensitive to hypoxic damage.
  • Ethanol induces a hypermetabolic state in the hepatocytes, partially because ethanol metabolism via MEOS does not result in energy capture via formation of ATP.
  • Rather, this pathway leads to loss of energy in the form of heat.
  • In some studies, antithyroid drugs, such as propylthiouracil (PTU), that reduce the basal metabolic rate of the liver have shown to be beneficial in the treatment of alcoholic hepatitis.
  1. Generation of free radicals and oxidative injury
  • Free radicals, superoxides and hydroperoxides, are generated as byproducts of ethanol metabolism via the microsomal and peroxisomal pathways.
  • In addition, acetaldehyde reacts with glutathione and depletes this key element of the hepatocytic defense against free radicals.
  • Other antioxidant defenses, including selenium, zinc, and vitamin E, are often reduced in individuals with alcoholism.
  • Peroxidation of membrane lipids accompanies alcoholic liver injury and may be involved in cell death and inflammation.
  1. Steatosis
  • Oxidation of ethanol requires conversion of NAD to the reduced form NADH.
  • Because NAD is required for the oxidation of fat, its depletion inhibits fatty acid oxidation, thus causing accumulation of fat within the hepatocytes (steatosis).
  • Some of the excess NADH may be reoxidized in the conversion of pyruvate to lactate.
  • Accumulation of fat in hepatocytes may occur within days of alcohol ingestion;
  • with abstinence from alcohol, the normal redox state is restored, the lipid is mobilized, and steatosis resolves.
  • Although steatosis has generally been considered a benign and reversible condition, rupture of lipid-laden hepatocytes may lead to focal inflammation, granuloma formation, and fibrosis, and it may contribute to progressive liver injury
  • Nonoxidative metabolism of ethanol may lead to the formation of fatty acid ethyl esters, which may also be implicated in the pathogenesis of alcohol-induced liver damage.
  1. Formation of acetaldehyde adducts
  • Acetaldehyde may be the principal mediator of alcoholic liver injury.
  • The deleterious effects of acetaldehyde include
    • impairment of the mitochondrial beta-oxidation of fatty acids,
    • formation of oxygen-derived free radicals,
    • depletion of mitochondrial glutathione.
  • In addition, acetaldehyde may bind covalently with several hepatic macromolecules, such as amines and thiols, in cell membranes, enzymes, and microtubules to form acetaldehyde adducts.
  • This binding may trigger an immune response through
    • formation of neoantigens,
    • impair function of intracellular transport through precipitation of intermediate filaments and other cytoskeletal elements,
    • stimulation of hepatic stellate cells to produce collagen.
  • ALDH is downregulated by long-term ethanol abuse, with resultant acetaldehyde accumulation.
  1. Role of the immune system
  • Active alcoholic hepatitis often persists for months after cessation of drinking.
  • Its severity may worsen during the first few weeks of abstinence.
  • This observation suggests that an immunologic mechanism may be responsible for perpetuation of the injury.
  • levels of serum immunoglobulins, especially the immunoglobulin A (IgA) class, are increased in persons with alcoholic hepatitis.
  • Antibodies directed against acetaldehyde-modified cytoskeletal proteins can be demonstrated in some individuals.
  • Autoantibodies, including antinuclear and anti–single-stranded or anti–double-stranded DNA antibodies, have also been detected in some patients with alcoholic liver disease.
  • B and T lymphocytes are noted in the portal and periportal areas, and natural killer lymphocytes are noted around hyalin-containing hepatocytes.
  • Peripheral lymphocyte counts are decreased with an associated increase in the ratio of helper cells to suppressor cells, signifying that lymphocytes are involved in a cell-mediated inflammatory process.
  • Lymphocyte activation upon exposure to liver extracts has been demonstrated in patients with alcoholic hepatitis.
  • Immunosuppressive therapy with glucocorticoids appears to improve survival and accelerate recovery in patients with severe alcoholic hepatitis.
  1. Cytokines
  • Tumor necrosis factor-alpha (TNF-alpha) can induce programmed cellular death (apoptosis) in liver cells. (Marra and Tacke 2014)
  • Several studies have demonstrated extremely high levels of TNF and several TNF-inducible cytokines, such as interleukin (IL)–1, IL-6, and IL-8, in the sera of patients with alcoholic hepatitis. (Leake 2014)
  • Inflammatory cytokines (TNF, IL-1, IL-8) and hepatic acute-phase cytokines (IL-6) have been postulated to play a significant role in modulating certain metabolic complications in alcoholic hepatitis, and they are probably instrumental in the liver injury of alcoholic hepatitis and cirrhosis
  1. Role of concomitant viral disease
  • Alcohol consumption may exacerbate injury caused by other pathogenic factors, including hepatitis viruses.
  • Extensive epidemiologic studies suggest that the risk of cirrhosis in patients with chronic hepatitis C infection is greatly exacerbated by heavy alcohol ingestion.
  • Possible mechanisms include the impairment of immune-mediated viral killing or enhanced virus gene expression due to the interaction of alcohol and hepatitis C virus.

CLINICAL PRESENTATION

Questions to ask patients with suspected alcoholic hepatitis

  1. When did you first start to drink alcohol?
  2. How many days per week do you usually drink?
  • How many years have you been drinking on a regular or daily basis?
  1. How many times have you been arrested for driving under the
  2. influence of alcohol?
  3. How many times have you been arrested for public intoxication?
  • What type of alcohol do you usually drink? Beer? Wine? Hard liquor?
  • How many drinks of each type of alcohol do you drink on an average
  1. day?
  2. Do you usually drink at home? Bars?
  3. Have you been through an alcohol rehabilitation program? What typeinpatient
  • or outpatient? How many times?
  • Have there been prolonged times when you drank no alcohol?
  • When was your last drink?

HISTORY

  • patients with AH have been drinking heavily for years and then report a dramatic increase in the amount of alcohol intake, usually relating to a major life stressor, such as death of a parent, loss of a job, divorce etc
  • patients have often stopped drinking alcohol days to weeks prior to presentation due to
    • Malaise,
    • Poor appetite,
    • The realization that their drinking finally“caught up” with them.
  • Most commonly patients present with nonspecific complaints such as
    • Anorexia (27-77%)
    • Nausea and vomiting (34-55%)
    • Abdominal pain (27-46%)
    • Weight loss (29-43%)

PHYSICAL EXAMINATION

  • Physical Examination Findings
    • Hepatomegaly (71-81%)
    • Ascites (35%)
    • Encephalopathy (from asterixis to coma) (18-23%)
    • Gastrointestinal bleeding requiring transfusion (23%)
    • Jaundice (37-100%)
    • Malnutrition (56-90%)
    • Hepatic bruit

LABORATORY DATA

Laboratory findings in AH are often nonspecific, but can on occasion provide clues to the diagnosis. These include

Liver Function Test

  • Mild to moderately elevated transaminases,
  • Ast: alt ratio above 1.5 with
  • Ast greater than 45 u/l but < 300 u/l.
  • However, an unusual variant of AH, known as alcoholic foamy degeneration, can lead to an AST as high as 730 U/L.
  • A serum bilirubin >2 mg/dl is often required to make a diagnosis,
  • Alkaline phosphatase (ALP) level elevations are typically mild in persons with alcoholic hepatitis.
  • The gamma-glutamyl transpeptidase (GGT) level is elevated markedly by alcohol use. (Although a normal value helps to exclude alcohol as a cause of liver disease, an elevated level is of no value in distinguishing between simple alcoholism and alcoholic hepatitis.)
  • Total blood cholesterol levels < 100 mg/dl can predict poor outcome; the lower the cholesterol, the worse the prognosis.

CBC Count

  • A complete blood cell (CBC) count commonly reveals some degree of neutrophilic leukocytosis with bandemia.
  • Usually, this is moderate; however, rarely, it is severe enough to provide a leukemoid picture.
  • Moderate anemia may be observed.
  • Alcohol use characteristically produces a moderate increase in MCV
  • Thrombocytosis may be observed as part of the inflammatory response;
  • Conversely, myelosuppression or portal hypertension with splenic sequestration may produce thrombocytopenia.

Screening Blood Tests

  • Screening blood tests to exclude other conditions (appropriate in any patient with alcoholic hepatitis) may include the following:
    • Hepatitis B surface antigen (hbsag) detects hepatitis B
    • Anti–hepatitis C virus by enzyme-linked immunosorbent assay (ELISA) detects hepatitis C
    • Ferritin and transferrin saturation detect hemochromatosis
    • Marked elevation of aminotransferase levels should raise concern for viral hepatitis or drug hepatotoxicity; in particular, people who are alcoholics may develop severe liver necrosis from standard therapeutic doses of acetaminophen
    • Alpha-fetoprotein (AFP) levels – Rapid deterioration of liver function should raise the possibility of hepatocellular carcinoma (HCC)
    • Alkaline phosphatase (ALP) Jaundice with fever can be caused by gallstones producing cholangitis

Liver Biopsy

  • Liver biopsy is not always required in the evaluation of alcoholic hepatitis,
  • but it may be useful in establishing the diagnosis, in determining the presence or absence of cirrhosis, and in excluding other causes of liver disease.
  • The risk of performing the biopsy should be weighed against the risk associated with the probable course of therapy, or the possible risk of an investigational treatment.
  • Percutaneous liver biopsy – should be avoided in the presence of severe thrombocytopenia or coagulopathy because of the risk of serious (possibly fatal) hemorrhage.
  • Transjugular liver biopsy – the risk of hemorrhage should be reduced. It can determine the transhepatic venous pressure gradient.
  • In alcoholic hepatitis, injury is characteristically most prominent in centrilobular (perivenular) areas (zone 3 of Rappaport).
  • Hepatocytes exhibit ballooning with necrosis.
  • Focal accumulation of polymorphonuclear leukocytes is noted in areas of injury.
  • Lymphocytes may also be present, especially in portal tracts.
  • Ropy eosinophilic hyaline inclusions- Mallory bodies may be observed in the perinuclear cytoplasm.
  • With electron microscopy, Mallory bodies may be observed to be composed of fibril clumps that histochemically are identifiable as intermediate filaments.
  • Mallory bodies are characteristic of alcoholic hepatitis, but they are not always present in this disease, and, occasionally, they can be observed in a variety of other disorders.
  • Macrovesicular steatosis, perivenular fibrosis, and frank cirrhosis commonly coexist with alcoholic hepatitis.

Ultrasonography

  • provides a good evaluation of the liver and other viscera, and it permits guided liver biopsy.
  • the liver appears enlarged and diffusely hyperechoic.
  • Features suggestive of coexistent portal hypertension and/or cirrhosis include the presence of varices, splenomegaly, and ascites.
  • helpful in excluding gallstones, bile duct obstruction, and hepatic or biliary neoplasms.
  • if stones are found or fever persists, cholangiography may be necessary.
  • Rapid deterioration of liver function should raise the possibility of hepatocellular carcinoma, which can be tested for by ultrasonography, computed tomography [CT] scanning, magnetic resonance imaging [MRI]) of the liver.

TREATMENT

MANAGEMENT

  • Cessation of alcohol consumption is the single most important treatment; without this all other therapies are of limited value.
  • Abstinence is even effective at preventing progression of liver disease and death when cirrhosis is present.
  • Life-long abstinence is the best advice and is essential for those with more severe liver disease.
  • Treatment for complications of cirrhosis, such as variceal bleeding, encephalopathy and ascites, may also be needed. (Raff and Singal 2014)

NUTRITION

  • Good nutrition is very important and enteral feeding via a fine-bore nasogastric tube may be needed in severely ill patients. (Koretz 2014)

ASCITES

  • Patients with pure severe AH in the absence of cirrhosishave relatively little problem with ascites.
  • They eat so little that they do not take in enough sodium to retain much fluid.
  • Maintenance intravenous fluids should be avoided to minimize fluid retention.
  • When cirrhosis is also present, they may have more problematic fluid retention. In this case, if blood urea nitrogen and creatinine are normal, spironolactone can be given.
  • This drug will increase urinary excretion of sodium and water, increase serum potassium, and decrease the need for potassium supplementation.
  • Once serum potassium is normal without supplementation, oral furosemide can be added, if needed.
  • If azotemia occurs, diuretics should be stopped and the patient should be evaluated for hepatorenal syndrome. (Israelsen, Gluud et al. 2014)
  • The first step is to give 1 g of 25% albumin/kg body weight (100 g maximum) intravenously daily for 2 d and to monitor creatinine.
  • If creatinine improves with albumin, the azotemia is probably diuretic-induced. If creatinine continues to rise, hepatorenal syndrome is probably present, as this commonly occurs in severe AH.

VARICEAL HEMORRHAGE

  • patients with pure severe AH in the absence of cirrhosis have relatively little problem with upper gut hemorrhage.
  • The relatively short duration of AH usually does not lead to formation of varices that are large enough to bleed.
  • However, patients with underlying cirrhosis can bleed from esophageal varices.
  • Urgent endoscopy with banding of varices is warranted when this occurs.
  • Patients with severe AH are very intolerant of hypotension and seldom survive shock superimposed on AH.(Li, Liu et al. 2013)

CORTICOSTEROIDS IN ALCOHOLIC HEPATITIS

  • In severe alcoholic hepatitis corticosteroids improve survival at 28 days from 65% to 85% Sepsis is the main side-effect of steroids, and existing sepsis and variceal haemorrhage are the main contraindication to their use.
  • If the bilirubin has not fallen 7 days after starting steroids, they are unlikely to reduce mortality and should be stopped

PENTOXIFYLLINE IN ALCOHOLIC HEPATITIS

  • In severe alcoholic hepatitis, oral pentoxifylline reduces inpatient mortality, particularly from hepatorenal failure, from 46% to 25% (Joshi, Manori et al. 2013)
  • Pentoxifylline, which has a weak anti-TNF action. It appears to reduce the incidence of hepatorenal failure and its use is not complicated by sepsis
  • Baclofen has recently been evaluated in terms of safety and efficacy in the setting of alcoholic cirrhosis.
  • Baclofen significantly reduced alcohol cravings and significantly lengthened time to relapse with no significant adverse effects noted after 12 wk of continuous use in a well run randomized, controlled trial
  • Discharge is considered as the bilirubi level approaches 10 mg/dL, and the clinician can use this to help plan initiation of baclofen

PRONOSIS

MADDREY’S SCORE(Forrest 2014)

  • Maddrey’s score, which enables the clinician to assess prognosis in alcoholic hepatitis
  • PT = prothrombin time. Serum bilirubin in μmol/l is divided by 17 to convert to mg/dl):

The Maddrey discriminant function (DF) = [4.6 × (prothrombin time (PT)  - control PT) + serum bilirubin (mg/dL)]

  • A cutoff value of 32 is used to identify patients with a mortality rate above 50% without pharmacologic therapy.

MODEL FOR END-STAGE LIVER DISEASE

  • MELD uses the patient’s values for serum bilirubin, serum creatinine, and the international normalized ratio for prothrombin time (INR) to predict survival. It is calculated according to the following formula

MELD = 3.78×ln[serum bilirubin (mg/dL)] + 11.2×ln[INR] + 9.57×ln[serum creatinine (mg/dL)] + 6.43×aetiology(0: cholestatic or alcoholic, 1- otherwise)

  • If the patient has been dialyzed twice within the last 7 days, then the value for serum creatinine used should be 4.0
  • Any value less than one is given a value of 1 (i.e. if bilirubin is 0.8, a value of 1.0 is used)
  • In interpreting the MELD Score in hospitalized patients, the 3 month mortality is:
    • 40 or more — 71.3% mortality
    • 30–39 — 52.6% mortality
    • 20–29 — 19.6% mortality
    • 10–19 — 6.0% mortality
    • <9 — 1.9% mortality

CHILD-PUGH SCORE

  • used to assess the prognosis of chronic liver disease
Measure 1 point 2 points 3 points
Total bilirubin, μmol/l (mg/dl) <34 (<2) 34-50 (2-3) >50 (>3)
Serum albumin, g/dl >3.5 2.8-3.5 <2.8
PT INR <1.7 1.71-2.30 > 2.30
Ascites None Mild Moderate to Severe
Hepatic encephalopathy None Grade I-II (or suppressed with medication) Grade III-IV (or refractory)
Points Class One year survival Two year survival
5-6 A 100% 85%
7-9 B 81% 57%
10-15 C 45% 35%

References

Bruguera, M. (2014). “[Liver diseases in the elderly.].” Gastroenterol Hepatol.

Liver diseases in the elderly have aroused less interest than diseases of other organs, since the liver plays a limited role in aging. There are no specific liver diseases of old age, but age-related anatomical and functional modifications of the liver cause changes in the frequency and clinical behavior of some liver diseases compared with those in younger patients. This review discusses the most important features of liver function in the healthy elderly population, as well as the features of the most prevalent liver diseases in this age group, especially the diagnostic approach to the most common liver problems in the elderly: asymptomatic elevation of serum transaminases and jaundice.

Forrest, E. (2014). “Letter: Prognostic scores in alcoholic hepatitis.” Aliment Pharmacol Ther 39(11): 1340-1341.

Israelsen, M. E., et al. (2014). “Acute kidney injury and hepatorenal syndrome in cirrhosis.” J Gastroenterol Hepatol.

Cirrhosis is the eighth leading cause of “years of lost life” in the US and accounts for approximately 1 to 2% of all deaths in Europe. Patients with cirrhosis have a high risk of developing acute kidney injury. The clinical characteristics of HRS are similar to prerenal uraemia, but the condition does not respond to volume expansion. HRS type 1 is rapidly progressive whereas HRS type 2 has a slower course often associated with refractory ascites. A number of factors can precipitate HRS such as infections, alcoholic hepatitis and bleeding. The monitoring, prevention, early detection and treatment of HRS are essential. This paper reviews the value of early evaluation of renal function based on two new sets of diagnostic criteria. Interventions for HRS type 1 include terlipressin combined with albumin. In HRS type 2 transjugular intrahepatic portosystemic shunt (TIPS) should be considered. For both types of HRS patients should be evaluated for liver transplantation.

Joshi, P., et al. (2013). “Pentoxifylline in severe alcoholic hepatitis: a prospective, randomised trial.” J Assoc Physicians India 61(5): 354.

Koretz, R. L. (2014). “The evidence for the use of nutritional support in liver disease.” Curr Opin Gastroenterol 30(2): 208-214.

PURPOSE OF REVIEW: Although there is a well established association between malnutrition and poorer clinical outcomes in patients with liver disease, that fact alone does not prove that improving the malnutrition will improve outcome. The best way to determine if nutritional interventions are effective is to compare them to untreated control groups in well designed and executed randomized clinical trials. RECENT FINDINGS: A recent systematic review assessed 37 trials that compared parenteral nutrition, enteral nutrition, or nutritional supplements to no nutritional therapy in patients with a variety of liver diseases. Since the publication of that review, an additional three trials have become available. Whereas all but one of the trials did have methodologic shortcomings that may have allowed the introduction of bias (which usually results in an overestimation of benefit), the trials failed to show much, if any, benefit. In fact, the single trial at low risk of bias found that more deaths occurred in the recipients of the supplements. SUMMARY: Although malnutrition may be associated with a poor outcome, the current best evidence indicates that the provision of adjunctive nutritional support (parenteral or enteral nutrition, or nutritional supplements) to patients with a variety of liver diseases (alcoholic hepatitis, cirrhosis, hepatocellular carcinoma, liver surgery, liver transplantation, obstructive jaundice, hepatitis C antiviral treatment) does not improve clinical outcomes.

Leake, I. (2014). “Alcoholic hepatitis: potential role of cytokine CCL20 in alcoholic hepatitis.” Nat Rev Gastroenterol Hepatol 11(2): 76.

Leslie, T., et al. (2014). “Survey of health status, nutrition and geography of food selection of chronic liver disease patients.” Ann Hepatol 13(5): 533-540.

Background. Obesity, a complex disease determined both by genetic and environmental factors, is strongly associated with NAFLD, and has been demonstrated to have a negative impact on HCV and other chronic liver diseases (CLD). Rationale. This study assessed the association between type and location of food sources and chronic liver disease (CLD) using Geographic Information Systems (GIS). Results. CLD patients completed surveys [267 subjects, 56.5% female, age 55.8 +/- 12.0, type of CLD: 36.5% hepatitis C (HCV), 19.9% hepatitis B (HBV), 19.9% non-alcoholic fatty liver disease (NAFLD); primary food source (PFS): 80.8% grocery store, secondary: 26.2% bulk food store, tertiary: 20.5% restaurants; fresh food (FF): 83%, pre-packaged (PP) 8.7%, already prepared (AP) 8.3%]. FF consumers had significantly fewer UEH servings/month (p = 0.030) and lived further away from convenience stores (1.69 vs. 0.95 km, p = 0.0001). Stepwise regression reveals the lowest FF consumers were NAFLD patients, subjects with UEH or restaurants and ethnic food stores as their PFS (R = 0.557, p = 0.0001). Eating already-packaged foods and utilizing restaurants or ethnic food stores as the PFS positively correlated with NAFLD (R = 0.546, p = 0.0001). Conclusions. Environmental food source measures, including type and density, should be included when examining areas hyper-saturated with a variety of food options. In hyper-saturated food environments, NAFLD patients consume more prepared food and less FF. CLD patients with UEH also eat significantly more prepared food and frequent restaurants and ethnic food stores as their PFS.

Li, N., et al. (2013). “[A retrospective analysis of ectopic varices in gastrointestinal tract diagnosed by endoscopy].” Zhonghua Nei Ke Za Zhi 52(11): 936-939.

OBJECTIVE: To understand the incidence, causes, clinical manifestations and treatment of ectopic varices (EV) in gastrointestinal (GI) tract. METHODS: GI endoscopic examinations were carried out in 99 783 patients from January 2004 to October 2012 in General Hospital of PLA. Sixty-four cases of ectopic varices in GI tract were discovered. The clinical manifestations of EV patients and treatment were analyzed retrospectively. The literatures of EV were reviewed. RESULTS: The prevalence of EV in GI was 0.06% (64/99 783) in all patients undergoing endoscopic examinations, including 5 in the gastric antrum, 37 in the duodenum, 2 in the colon, 17 in the rectum, 1 in terminal ileum as well as whole colorectum, and 2 in the anastomotic stomas. The causes of EV included portal hypertension with cirrhosis in 52 cases (42 of hepatitis as dominant, 5 of alcoholic, 3 of biliary). Twenty-five cases had past history of endoscopic sclerotherapy, tissue adhesive injection or band ligation.Extrahepatic portal vein obstruction was seen in 4 cases (1 with pancreatic cancer, gastric cardia after surgery, pancreatic cancer after surgery, small intestine after partial hepatectomy respectively) and 8 cases uncertain. Nine cases accepted endoscopic tissue adhesive injection (no post-operative hemorrhage occurred in 9 cases and EV disappeared in 3 cases). Endoscopic band ligation was performed only for one patient. CONCLUSIONS: EV in GI tract is a rare condition, which occurs commonly in duodenum, colon, and rectum. Portal hypertension is the most common cause. Gastrointestinal hemorrhage is the main clinical manifestation. EV should be considered in GI bleeding, with gastroesophageal varices hemorrhage excluded. Endoscopic adhesive injection is an effective way to treat EV.

Marra, F. and F. Tacke (2014). “Roles for Chemokines in Liver Disease.” Gastroenterology 147(3): 577-594 e571.

Sustained hepatic inflammation is an important factor in progression of chronic liver diseases, including hepatitis C or non-alcoholic steatohepatitis. Liver inflammation is regulated by chemokines, which regulate the migration and activities of hepatocytes, Kupffer cells, hepatic stellate cells, endothelial cells, and circulating immune cells. However, the effects of the different chemokines and their receptors vary during pathogenesis of different liver diseases. During development of chronic viral hepatitis, CCL5 and CXCL10 regulate the cytopathic versus antiviral immune responses of T cells and natural killer cells. During development of nonalcoholic steatohepatitis, CCL2 and its receptor are up-regulated in the liver, where they promote macrophage accumulation, inflammation, fibrosis, and steatosis, as well as in adipose tissue. CCL2 signaling thereby links hepatic and systemic inflammation related to metabolic disorders and insulin resistance. Several chemokine signaling pathways also promote hepatic fibrosis. Recent studies have shown that other chemokines and immune cells have anti-inflammatory and antifibrotic activities. Chemokines and their receptors can also contribute to the pathogenesis of hepatocellular carcinoma, promoting proliferation of cancer cells, the inflammatory microenvironment of the tumor, evasion of the immune response, and angiogenesis. We review the roles of different chemokines in the pathogenesis of liver diseases and their potential use as biomarkers or therapeutic targets.

Raff, E. and A. K. Singal (2014). “Optimal management of alcoholic hepatitis.” Minerva Gastroenterol Dietol 60(1): 25-38.

Alcoholic hepatitis, a clinical syndrome among people with chronic and active alcohol abuse presents with with jaundice and liver failure with or without hepatic encephalopathy. In patients with severe episode, this condition has a potential for 40-50% mortality within a month of presentation. Corticosteroids and pentoxifylline, only available current treatment options provide only about 50% survival benefit. Response to corticosteroids can only be assessed at 1 week of initiation of these drugs using Lille score or documentation of improvement in bilirubin levels. Requirement of minimum 6 months abstinence for liver transplantation cannot be met for alcoholic hepatitis patients who fail to respond to steroids. Emerging data on the benefit of liver transplantation for select patients with first episode of severe AH with non-response to steroids are encouraging. There remains an unmet need for studies assessing newer therapeutic targets and drugs and for optimizing the currently available treatment options. In this regard, decision to promote clinical and translational research by the National Institute of Alcohol Abuse and Alcoholism will be helpful in improving survival of patients with alcoholic hepatitis.

Stimac, D., et al. (2013). “[Hepatitis C: who should be treated?].” Acta Med Croatica 67(4): 325-328.

Therapy is strongly recommended in patients with acute infection, patients with elevated ALT levels, patients with normal ALT level and F > or = 2 METAVIR score, in genotype 1 nonresponders and relapsers to antiviral therapy with triple therapy (pegylated interferon, ribavirin, bocaprevir or telaprevir), in patients with compensated cirrhosis and patients on hemodialysis. It is possible to treat patients with HBV and HIV co-infection, patients with severe HCV extrahepatic manifestations and patients with transplanted liver. Drug users and alcoholics can be treated after 6-month abstinence, but also with supportive therapy. This therapy is not recommended in patients with fulminant hepatitis, patients with persistent normal ALT levels and without fibrosis, in kidney transplant recipients and in pregnant women.

Kwashiorkor

BY KEMBOI KIBET

Kwashiorkor is a form of malnutrition. It occurs when you don’t have enough protein in your diet. It is the most common nutritional disorder in developing countries. Children with Kwashiorkor may not grow or develop properly. It may be life threatening if not treated .

CAUSES

It is caused by not having enough protein in your diet. It is common in children in Africa and Central America. It is also common in developing countries where there is

  • famine
  • limited food supply
  • low levels of eduction

It usually occurs during political unrest, natural disasters or drought. Thee conditions may lead to lack of food which in turn leads to malnutrition.

Kwashiorkor is very rare in the united states. If it does occur, it is usually a sign  of child abuse or severe neglect.

SYMPTOMS

Symptoms of kwashiorkor includes the following :

  • large belly that sticks out
  • failure to grow or gain eight
  • fatigue
  • changes in skin pigment
  • diarrhea
  • hair changes
  • irritability
  • flaky rash
  • loss of muscle mass
  • swelling
  • lethargy
  • shock which occurs in the latter stages of kwashiorkor

TEST AND DIAGNOSIS

A physical exam may reveal an enlarged liver and well as edema (swelling). Your doctor may also order the following tests.

TREATMENT

Kwashiorkor can be corrected by including more protein and calories in your diet. This is helpful if treatment is started early. You will be given more calories in the form of carbohydrates, sugar and fats to give you energy. You will then be given protein rich foods. Giving of calories is done slowly because your body needs to adjust since you have been without food for a while.

Your doctor may also recommend vitamin and mineral supplements.

COMPLICATIONS

Possible complication of kwashiorkor includes

  • coma
  • permanent and physical disability
  • shock

PREVENTION

You can prevent kwashiorkor by eating enough carbohydrates and protein rich foods. These  include fat (at least 10 percent of total calories) and protein (12 percent of total calories).

REFERENCESMedlinePlus.http://www.nlm.nih.gov/medlineplus/ency/article/001604.htm.

What is kwashiorkor. Healthline Networks.http://www.healthline.com/health/kwashiorkor#Causes.

Kwashiorkor. NHS choices.http://www.nhs.uk/conditions/kwashiorkor/Pages/Introduction.aspx

The American Heritage® Stedman’s Medical Dictionary. Retrieved April 2014 from Dictionary.com website.http://dictionary.reference.com.

The Difference Between Men And Women

 

Let’s say a guy named Fred is attracted to a woman named Martha. He asks her out to a movie; she accepts; they have a pretty good time. A few nights later he asks her out to dinner, and again they enjoy themselves. They continue to see each other regularly, and after a while neither one of them is seeing anybody else.

And then, one evening when they’re driving home, a thought occurs to Martha, and, without really thinking, she says it aloud: “Do you realize that, as of tonight, we’ve been seeing each other for exactly six months?”

And then, there is silence in the car.

To Martha, it seems like a very loud silence. She thinks to herself: I wonder if it bothers him that I said that. Maybe he’s been feeling confined by our relationship; maybe he thinks I’m trying to push him into some kind of obligation that he doesn’t want, or isn’t sure of.

And Fred is thinking: Gosh. Six months.

And Martha is thinking: But, hey, I’m not so sure I want this kind of relationship either. Sometimes I wish I had a little more space, so I’d have time to think about whether I really want us to keep going the way we are, moving steadily towards, I mean, where are we going? Are we just going to keep seeing each other at this level of intimacy? Are we heading toward marriage? Toward children? Toward a lifetime together? Am I ready for that level of commitment? Do I really even know this person?

And Fred is thinking: …so that means it was…let’s see…February when we started going out, which was right after I had the car at the dealer’s, which means…lemme check the odometer…Whoa! I am way overdue for an oil change here.

And Martha is thinking: He’s upset. I can see it on his face. Maybe I’m reading this completely wrong. Maybe he wants more from our relationship, more intimacy, more commitment; maybe he has sensed – even before I sensed it – that I was feeling some reservations. Yes, I bet that’s it. That’s why he’s so reluctant to say anything about his own feelings. He’s afraid of being rejected.

And Fred is thinking: And I’m gonna have them look at the transmission again. I don’t care what those morons say, it’s still not shifting right. And they better not try to blame it on the cold weather this time. What cold weather? It’s 87 degrees out, and this thing is shifting like a garbage truck, and I paid those incompetent thieves $600.

And Martha is thinking: He’s angry. And I don’t blame him. I’d be angry, too. I feel so guilty, putting him through this, but I can’t help the way I feel. I’m just not sure.

And Fred is thinking: They’ll probably say it’s only a 90-day warranty…scumballs.

And Martha is thinking: Maybe I’m just too idealistic, waiting for a knight to come riding up on his white horse, when I’m sitting right next to a perfectly good person, a person I enjoy being with, a person I truly do care about, a person who seems to truly care about me. A person who is in pain because of my self-centered, schoolgirl romantic fantasy.

And Fred is thinking: Warranty? They want a warranty? I’ll give them a warranty. I’ll take their warranty and stick it right up their…

“Fred,” Martha says aloud.

“What?” says Fred, startled.

“Please don’t torture yourself like this,” she says, her eyes beginning to brim with tears. “Maybe I should never have…oh dear, I feel so…”(She breaks down, sobbing.)

“What?” says Fred.

“I’m such a fool,” Martha sobs. “I mean, I know there’s no knight. I really know that. It’s silly. There’s no knight, and there’s no horse.”

“There’s no horse?” says Fred.

“You think I’m a fool, don’t you?” Martha says.

“No!” says Fred, glad to finally know the correct answer.

“It’s just that…it’s that I…I need some time,” Martha says.

(There is a 15-second pause while Fred, thinking as fast as he can, tries to come up with a safe response. Finally he comes up with one that he thinks might work.)

“Yes,” he says. (Martha, deeply moved, touches his hand.)

“Oh, Fred, do you really feel that way?” she says.

“What way?” says Fred.

“That way about time,” says Martha.

“Oh,” says Fred. “Yes.” (Martha turns to face him and gazes deeply into his eyes, causing him to become very nervous about what she might say next, especially if it involves a horse. At last she speaks.)

“Thank you, Fred,” she says.

“Thank you,” says Fred.

Then he takes her home, and she lies on her bed, a conflicted, tortured soul, and weeps until dawn, whereas when Fred gets back to his place, he opens a bag of Doritos, turns on the TV, and immediately becomes deeply involved in a rerun of a college basketball game between two South Dakota junior colleges that he has never heard of. A tiny voice in the far recesses of his mind tells him that something major was going on back there in the car, but he is pretty sure there is no way he would ever understand what, and so he figures it’s better if he doesn’t think about it.

The next day Martha will call her closest friend, or perhaps two of them, and they will talk about this situation for six straight hours. In painstaking detail, they will analyze everything she said and everything he said, going over it time and time again, exploring every word, expression, and gesture for nuances of meaning, considering every possible ramification.

They will continue to discuss this subject, off and on, for weeks, maybe months, never reaching any definite conclusions, but never getting bored with it either.

Meanwhile, Fred, while playing racquetball one day with a mutual friend of his and Martha’s, will pause just before serving, frown, and say: “Norm, did Martha ever own a horse?”

And that’s the difference between men and women.

 

Adapted from withalittlehelp

Nonalcoholic Fatty Liver Disease

 

 

INTRODUCTION

Nonalcoholic fatty liver disease is fat accumulation in the liver of people who don’t drink or drink little alcohol. This disease is common and may cause no complications . A more serious form of nonalcoholic fatty liver disease is called nonalcoholic steatohepatitis (NASH). This can cause inflammation and scarring of liver and eventual death of liver tissue.

CAUSES

The exact cause of nonalcoholic fatty liver disease in not clear but it occurs as a result of failure of the liver to breakdown fat resulting in its accumulation  in the liver tissue.

RISK FACTORS

Certain factors and conditions may increase your risk of getting nonalcoholic fatty liver disease. These include :

  • rapid weight loss
  • obesity
  • Wilson’s disease
  • certain medications
  • high levels of cholesterol and triglycerides
  • malnutrition
  • viral hepatitis
  • inherited or autoimmune liver disease
  • metabolic syndrome
  • type 2 diabetes

SYMPTOMS

This disease is mostly asymptomatic especially in it’s early stages. As disease progressed however it may exhibit symptoms such as

  • weight loss
  • fatigue
  • nausea
  • weakness
  • pain in the upper right abdomen
  • impaired judgement
  • enlarged liver

TEST AND DIAGNOSIS

Nonalcoholic fatty liver disease is usually diagnosed during a routine medical exam. Doctor may also suspect you have it  after asking for your medical history and doing a physical exam. Doctor may then perform these test to conform the disease.

Blood test : Liver function test is done to evaluate liver enzymes and help with diagnosis.

Imaging tests : Imaging tests such as abdominal ultrasound, computerized tomography (CT) scan and magnetic resonance imaging (MRI) are used to diagnose fatty liver disease.

Liver biopsy : This confirmatory test involves taking  a sample of liver tissue  to the lab  to look for signs of inflammation and scarring.

TREATMENT

There is no specific treatment for Nonalcoholic fatty liver disease. Treatment  means taking care of underlying medical conditions such as diabetes and obesity . These include losing weight if you are obese, managing blood sugar level if you have diabetes and changing medications if it is the cause.

PREVENTION

Takes these steps to prevent this disease.

Maintain a healthy weight.

Eat healthy such as including more fruits and vegetables in your diet.

Take medication for disease that can cause fatty liver disease such as diabetes and high cholesterol. You can also reduce your cholesterol using home remedies.

Cirrhosis

by Kemboi Kibet

Cirrhosis is a liver disease which involves irreversible scarring of the liver. Some of the common causes of cirrhosis includes alcohol abuse, hepatitis B and hepatitis C. Early treatment of cirrhosis can limit further damage to the liver. This disease can be life threatening.

CAUSES

This disease is caused by long-term liver damage as a result of liver diseases and other conditions. Diseases and conditions that can cause cirrhosis includes the following

alcohol abuse
chronic viral hepatitis
bile duct disease such as biliary atresia
cystic fibrosis
genetic diseases such as glycogen storage diseases, Alpha-1 antitrypsin deficiency, autoimmune hepatitis and Wilson’s disease
schistosomiasis
accumulation of fat in the liver

SYMPTOMS

Cirrhosis can be asymptomatic but when symptoms do appear, they usually include the following

itching skin
jaundice
fatigue
loss of appetite
easy bruising and bleeding
weight loss
Fluid build up and painful swelling of the legs (edema) and abdomen (ascites)
abdominal pain

TEST AND DIAGNOSIS

To diagnose cirrhosis, your doctor will do a physical exam. He may also ask you about your medical history. Other tests that will be done to confirm this diagnosis include :

Liver function test : This blood test is done to checked for excess bilirubin and certain enzymes that may indicate liver damage.

Imaging tests : These include MRI, CT scan and ultrasound to check for liver damage.

Biopsy :A sample liver tissue is taken and examined for the cause and severity of liver damage.

TREATMENT

Treatment of cirrhosis depends on the cause and extent of damage to the liver. The goal of treatment is to prevent further damage and avoid complications.It is also important to treat any underlying cause of the disease such as losing weight, stop drinking and medications of hepatitis. Any associated complications will also be treated. In advanced stages when the liver loses it’s function,liver transplant is necessary.

LIFESTYLE CHANGES THAT CAN HELP YOU MANAGE CIRRHOSIS

Stop drinking alcohol.
Maintain a healthy weight
Limit salt intake to reduce fluid buildup
Avoid raw shellfish
Get vaccinated for hepatitis A and B, influenza, and pneumonia.
Ask your doctor before using any over the counter medications, vitamins or supplement.
Practice safe sex to avoid any infections.
Do not share needles, razors, toothbrushes or other personal items with others

SYMPTOMS YOU SHOULD NEVER IGNORE

How do you know if a symptom is serious or not. Symptoms that develop all of a sudden and with increasing intensity should not be taken for granted. Here are some symptoms you should not ignore.

SHORTNESS OF BREATH
If you are unable to catch your breath or gasping for breath, then you need to be evaluated or you must seek emergency care. Shortness of breath could be a sign of severe underlying diseases like asthma, bronchitis, pulmonary embolism, lung and heart disease.

SUDDEN INTENSE HEADACHE
If you are experiencing headache like you’ve never had before. If it happened suddenly and keeps getting worse with no relief, you need to seek urgent care. It could be a sign serious conditions like of ruptured aneurysm, a condition in which a blood vessel in your brain suddenly bursts. It could also be a sign of meningitis.

UNEXPLAINED WEIGHT LOSS
I f you are losing weight without trying, it might be more of a curse than a blessing. If you lose about 10% of your total weight in about 6 months without putting in any effort, you should consult your doctor. Unexplained weight loss could be an indication of diabetes if it is accompanied by frequent urination and extreme thirst, hyperthyroidism if you also experience restlessness and increased appetite, some types of cancers and liver disease. Gastrointestinal diseases like inflammatory bowel movement could also be the cause if you having diarrhea and abdominal pain.

LOWER BACK PAIN
Lower back pain can be from muscle pull or some physical exertion on the back. Persistent back pain accompanied with fever and weight loss and especially if pain is radiating down the leg, could be a sign of some cancers like breast and lung cancers. Aggressive forms of these cancers may spread to the bone and cause lower back pain.

HEAVY PERIODS
Heavy periods known as menorrhagia happens to some women. However if you experience heavy periods during pregnancy it could be a sign of ectopic pregnancy. Fibroid tumors and ovarian cyst may cause heavy periods. Seek medical help.

CHEST PAIN
Chest discomfort, heaviness and pressure may be a signs of heart attack especially if it is accompanied by pain radiating down the arm, shortness of breath, nausea and vomiting and sweating. Women especially experience other symptoms like upper abdominal discomfort and fatigue. Severe upper back pain may be due to tear in the aorta. Other non life threatening conditions such as acid reflux or a peptic ulcer may also cause chest pain. Get to emergency room if you experience these signs.

FAINTING
This is due to transient drop in blood pressure which can happen as a result of the brain not getting enough blood. This usually happens when you sick , tired or scared. Experiencing fainting spells after exercising or lifting heavy things may require medical attention. It could be a sign of stroke or heart problem.

FEVER
Having fever is nothing to worry about so much. Fever is your body’s way of fighting infection. However fever of about 103 degrees and higher may be a source of serious infection like meningitis, endocarditis and so one. Persistent fever may also be a sign of some forms of cancers like lymphoma or sinus infection. Urgent medical care is therefore essential in such cases.

CHANGE IN BOWEL MOVEMENT
Normal bowel habits depends on each person. What is normal for one person might not be normal for anther. When you notice any change in your bowel habits such as persistent diarrhea or constipation, change in shape and color of stool or bloody stool, it is time to contact your physician. It might be a sign of serious infection

UNUSUAL BLEEDING
If you see blood where it’s not suppose to be, then its time to talk to your doctor. Blood in vomit may be a sign of gastric or esophageal cancer. Rectal bleeding may be a sign of colon or rectal cancer and vaginal bleeding may be linked to gynecological cancer. Unusual bleeding can also be linked to non life threatening conditions like hemorrhoids and stomach ulcers. Seek immediate medical care if you experience any of these conditions.

EARLY SATIETY
If you consistently feel full earlier than normal or after having a small meal ,you need to get checked out. If it is accompanied by symptoms such as weight loss or gain bloating, nausea or vomiting ,it could be a sign of reflux disease, commonly known as GERD or life threatening diseases like pancreatic cancer.

SUDDEN CONFUSION
Sudden confusion or inability to concentrate are conditions that need immediate medical care. It could be as a result of brain bleeding or brain tumor. If this condition is accompanied by slurred speech, numbness in face hand or leg and difficulty finding words, then stroke is imminent. Seek medical care immediately to avoid irreversible brain damage.

EDEMA
Swelling in the extremities such as legs warrants medical check up. When heart cannot pump enough blood that the body needs, blood backs up in veins causing accumulation of body fluids. Doctor fear heart failure when both legs are affected and especially when one is experiencing other symptoms like shortness of breath, fatigue and numbness.

SEVERE ABDOMINAL PAIN
This could be as a result of aortic aneurysm which happens in the abdominal area. It could also mean a hole in the stomach or intestines as a result of an ulcer. Another condition that causes this is Intestinal ischemia which is when blood flow to the intestines is stopped or slowed down resulting tissues being oxygen deprived. All these conditions are life threatening and should be taken seriously.

HYPERHIDROSIS- ARE YOU A SWEATY

By Kemboi Kibet

Excessive sweating also known as hyperhidrosis is sweating for no apparent reason and occurs even when you are not exercising or when temperature is not hot. This condition can be very embarrassing and usually affects palms, soles, feet and underarms.

I SWEAT A LOT??? NOW WHAT!!!!

There are a number of home remedies than can help curb this condition by reducing the sweating.

Antiperspirants : The first step to solving hyperhidrosis is using antiperspirants. Antiperspirants contain aluminium salts which when rolled on the skin can form plugs which block perspiration. It should be noted that deodorant unlike antiperspirants control odor produced by sweating but does not in itself reduce or block perspiration. You can get antiperspirants from over the counter in which case it is less irritating or by prescription from a doctor if the over the counter ones dont work.

Apple Cider Vinegar: This can be applied directly to areas of excessive sweating or it can be taken orally. Apply a combination of apple cider vinegar and lemon juice to the skin at areas of excessive sweating . It can also be taken orally by drinking three glasses of water a day mixed with two teaspoon of cider vinegar and two teaspoons of honey. It is most effective when taken on empty stomach. You can also soak cotton balls in apple cider vinegar or white vinegar and rub underarms to get rid of underarm odor. For sweaty feet apply apple cider vinegar to feet after washing and drying feet.

Tomato Juice : Drink a glass of fresh home-made tomato juice for at least a week. If you see progress you can continue drinking it everyday or every other day.

Bathe Regularly : Bathing frequently helps keep the number of bacteria on the skin low. Bathing with antibacterial soap can also control the bacteria that inhabit areas of the skin prone to hyperhidrosis and cause odor.

Reduce Stress : Stress can trigger perspiration. It is important to engage in relaxation exercises such as yoga and meditation.

Herbal Tea: Sage herbal tea is particularly essential in curbing hyperhidrosis. Sage contains vitamin B and magnesium which reduces sweat gland activity and thereby reduces sweating. Boil a teaspoon of dried sage leaves and set it aside to cool down. Apply the mixture to feet , sole , palms and underarm after thoroughly washing and drying. You can also add the herb to diet such as soup. It is also known that having green tea everyday can also eliminate hyperhidrosis.

Potato Slices : Slice potato and rub them underarm to get rid of excessive sweating. This is an effective way of getting rid of hyperhidrosis.

Wheat Grass Juice : Wheat grass extract is effective in reducing excessive sweating. One glass a day of this juice helps neutralize and dilute toxins in the blood. It is also a very good source of protein, vitamin C, vitamin B-12, folic acid, and vitamin B-6.

Witch Hazel : This is a natural perspirant for the face . It gently dries skin and prevents infection.

Tea Tree Oil : Apply oil directly to affected areas such as foot, armpit and hands to reduce hyperhidrosis.

Tea Bag : Tannic acid in tea has astringent properties that act as a natural antiperspirant. Soak about 5 tea bags in hot water and let it cool. Soak hands and feet in it for about 30 minutes and notice the difference.

Cornstarch and Baking Soda : Clean underarm thoroughly then apply cornstarch and baking soda. Wait for about 30 minutes and then wash off.

Anti Sweat Diet : Foods such as strawberries, almonds and onions contain silicon which is effective in reducing hyperhidrosis. It is also important to stay well hydrated because water removes the toxins that causes odor from sweat.Vitamin B rich foods also reduces sweating. It should also be noted that spicy foods and alcohol makes you sweat and so does hot drinks like tea and coffee. Magnesium deficiency is also known to cause hyperhidrosis. Taking magnesium supplement daily can get rid of this condition.

Wear Breathable Clothing : Choose fabrics such as cotton wool or silk which makes your skin breathe. It is also crucial to wear wool and cotton soaks. These absorb moisture and keep the feet dry.

Kemboi Kibet

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Down Syndrome – Your Health Is Your Wealth

 

Down syndrome is also known as Trisomy 21. It is a genetic disorder in which an extra copy of chromosome 21 causes life long mental retardation, developmental delays and other problems. It is the most common genetic cause of learning disabilities in children. It affects 1 in every 800 babies born in the United States. Severity of the disease range from mild or  moderate to serious with some children needing more medical attention than others. People with Down Syndrome may have other health issues like heart disease, intestinal abnormalities, seizure disorders, respiratory problems, obesity and  an increased susceptibility to infections. There is no way of preventing this disease but research shows that the chance of having a child with down syndrome increases with age. This disease cannot be cured but resources are available to make life comfortable for both victims and caregivers. Down syndrome is not inherited. It is caused by abnormal cell division during egg cell and sperm cell development.

CAUSES

Babies normally inherit  genetic material from both parents. Human cells have 23 pairs of chromosomes. One chromosome in each pair comes from the mother and the other from the father. In some cases a baby may inherit an extra copy of chromosome 21 and this results in the baby having the disease thus the name trisomy 21.

TYPES

Down syndrome may be divided into three types depending on how the extra genetic material is acquired.

Trisomy 21 : This is the most common affecting about 95% of individuals. The child has 3 copies of chromosome 21 instead of the usual 2. It is caused by abnormal division during egg cell and sperm cell division.

Mosaic down syndrome : This is a rare form. It occurs when a child inherits an extra copy of chromosome 21 in some cells but not others.  These individuals may not have all the typical features of people with trisomy 21 and their condition may not be as severe. This type is caused by abnormal division after fertilization.

Translocation down syndrome : These individuals do not inherit the entire chromosome 21. They just inherit some extra chromosome 21 attached to another chromosome usually chromosome 14. This type is uncommon.

RISK FACTORS

Some people are at a higher risk of having children with Down Syndrome than others.

The main risk factor of having a child with the disease is advanced maternal age. A woman’s risk of having a baby with Down Syndrome increases because older eggs  are more likely to experience improper chromosomal cell division.

  • 25 years 1 in 1,250
  • 30  years 1 in 1,000
  • 35 years 1 in 400
  • 40 years 1 in 100
  • 45 years 1 in 30

If you already have a child with Down Syndrome, there is the likelihood of having  another baby with the disease. Also parents can pass on the genetic translocation for Down Syndrome to their children if they are carriers.

SYMPTOMS

Most children with Down Syndrome have distinct physical characteristics. These include the following :

  • flattened facial features
  • short neck
  • protruding tongue
  • upward slanting eyes that may have small skin folds at the inner corner
  • unusually shaped ears
  • small head
  • poor muscle tone and loose ligaments
  • relatively short fingers
  • broad short hands with a single crease in the palm
  • white spots on the colored part of the eye
  • excessive flexibility

Development and growth may usually be delayed. They are usually shorter than children of the same age. They usually reach  milestones such as sitting, crawling and walking later than other children. They have delays in speech and self-care such as feeding, toileting and dressing.

TEST AND DIANGONSIS

The  American Congress of Obstetrician and Gynecologists recommends offering various screening tests for Down Syndrome to all pregnant women regardless of their age. This helps parents make important decisions and prepare for caring for a child with special needs. It should be noted that these tests are not 100 % accurate. Some of these tests may also cause a miscarriage.

Ultrasound : It is used to measure a  specific region on the back of a baby’s neck. More fluid than usual tends to collect in these tissues when abnormalities exist. This test is known as nuchal translucency screening test.

Blood Test : It measures the  levels of pregnancy-associated plasma protein-A (PAPP-A)  and human chorionic gonadotropin (HCG). Abnormal levels may indicate a problem with the baby.

Amniocentesis : It is performed between 16 and 20 weeks of pregnancy. A thin needle is inserted through the abdominal wall and a small  sample of amniotic fluid is taken. The sample is then used to analyze the chromosomes of the fetus. This procedure carries a  risk of miscarriage.

Chorionic villus sampling (CVS) : This is usually done at 11-12 weeks of pregnancy. Collection  of  chorionic villus cell sample from the placenta  is done to  analyze fetal chromosome deviations. This test also carries a risk of miscarriage.

Percutaneous umbilical blood sampling (PUBS) : Fetal blood is taken from  the umbilical cord. The procedure is done by  inserting a needle  through the abdominal wall. The procedure is usually done around 18 weeks of pregnancy. It carries a greater risk of miscarriage than amniocentesis and CVS. It is done when previous test results are not clear.

At birth, the initial diagnosis of Down Syndrome is usually based on baby’s facial appearance. You  doctor will order chromosomal karyotype to confirm Down Syndrome.

TREATMENT

There is no cure for Down Syndrome. Early intervention programs and regular medical check-ups for associated health issues may help one manage the disease well.

Children with the disease should be enrolled in specialized programs that will  help  them develop their sensory, motor and cognitive skills .  Early intervention programs  include physical  therapy, occupational therapy and speech therapy. They should also be included in family activities.

Corrective surgery may be done for heart defects and other associated health issues that  the child may have.

Regular check-ups to screen the child for other diseases is also essential.

COMPLICATIONS

People with Down Syndrome may have a wide variety of complications, some of which include the following :

  • heart defects
  • leukemia
  • obesity
  • dementia
  • infectious disease
  • respiratory infections
  • sleep apnea
  • seizures
  • hearing loss
  • poor vision

PREVENTION

There is no way of preventing Down Syndrome. If you fall into the high risk category of having a child with the disease, it is better to consult a genetic counselor before getting pregnant. The genetic counselor will explain to you prenatal testing available for the  disease and what to expects when you have a child with the disease

Morning Sickness

  By Kemboi Kibet

Morning sickness is nausea that occurs during pregnancy. Though it is called morning sickness, it can occur at any time of the day. This condition is more common during the first trimester but in some cases it may linger throughout the whole pregnancy. Treatment is not necessary but there are certain tips that can help you contain the condition better.In severe cases of morning sickness known as hyperemesis gravidarum, patient may need to be hospitalized  and treated with intravenous (IV) fluids and medications. This however is very rare.

TIPS TO EASE MORNING SICKNESS

There is no guarantee that you can prevent morning sickness altogether. There are however steps you can take to reduce the frequency and severity of this condition.

Keep some snacks such as crackers by your bedside. Before you get out of bed in the morning, nibble on some crackers. This will prevent your blood sugar from getting low and absorb your stomach acid.

Get out of bed slowly and then nibble on some more crackers slowly. This will help your stomach settle and prevent queasiness when you walk around.

Eat small meals about every two to three hours instead of eating three large meals. This helps to prevent your blood sugar from going low. You need to always have some kind of food in your stomach otherwise your stomach acid will work on your stomach wall causing nausea.

Keep snacks such as crackers, vegetables sticks, fruits and Cheerios by you all day and snack on them to keep your blood sugar up.

Avoid foods that trigger morning sickness such as fried and greasy foods, sweets and caffeine.

Drink lot of fluids such as water and or ginger ale. It helps also helps suck on some ice chips.Staying hydrated is also essential for baby’s growth.

Avoid foods and smells that make your nausea worse.

If taking prenatal vitamins makes you queasy, it will be better to take them at night with food . If that doesn’t help, ask your doctor for chewable prenatals.

Avoid large amounts of water and beverages during a meal.

Make time to rest. Fatigue, worry and stress exacerbate morning sickness symptoms. Try taking naps during the day.

Fresh air may help. Take short walks or sleep with windows open if  weather permits.

Eating or drinking something sour like lemon may also help.

Fresh ginger is used to battle morning sickness. Add  a 2-inch piece of ginger root, peeled and sliced to tea and boiling water and let it stand for about 15-20 minutes. strain and then drink.

After eating sit down so that the gravity helps to keep food in your stomach.

Dont brush your teeth immediately after eating because this can cause you to vomit.

Avoid fatty or spicy foods. Avoid alcohol as well.

Wear lose and comfortable clothing. Tight clothing may exacerbate the symptoms of morning sickness.

Food Poisoning

by Kemboi Kibet  

Food poisoning happens after consuming a contaminated food or drink. It also called food borne disease. Different types of organisms such as different types of bacteria, viruses and parasites and their toxins usually cause food poisoning. Food poisoning can be mild or deadly and depending on the organisms that cause it. Victims may be symptom free or have symptoms such as diarrhea, nausea , vomiting, cramping, fever and chills. Food contamination can occur  during food processing and production or can even happen at home when food is manhandled.

 

CAUSES

Food poisoning can be caused by infectious agents such as viruses, bacteria and parasites or toxic agents such as pesticides on fruits. Food contamination can happen from growing, harvesting, processing, storing, shipping or preparing.

Some of the most common bacteria  that cause food poisoning  are:

  • Salmonella
  • Listeria
  • Campylobacter
  • E. coli

 

SYMPTOMS

Symptoms of food poisoning vary depending the type of contaminant but most  types present one or more of these common symptoms. They include the following :

  • nausea
  • vomiting
  • fever
  • watery diarrhea
  • abdominal pain and cramps

Food poisoning is usually mild and may run its course for 24-48 hours .In severe cases however symptoms may last longer and patient may need to be hospitalised. Symptoms can develop quickly within an hour or may be slow and worsen with time.

 

RISK FACTORS

Groups of people or conditions that put one at a higher risk of getting food poisoning include the following:

Pregnant Women : Changes in metabolism and increased circulation may increase your risk of catching food poisoning. Their symptoms may be severe. It is however rare for your baby to get sick from it.

Children : These group face the risk of getting food poisoning because their immune system is not fully developed.

Elderly : The elderly usually have compromised immune system due to their age or illness making it difficult for them to fight infection.

People With Chronic Diseases : Diseases such as HIV and diabetes reduces the effect of your immune system to fight diseases.

 

TEST AND DIAGNOSIS

Your doctor will ask you detailed questions to help diagnose food poisoning. These include what your symptoms are, how long you’ve been sick, what foods you’ve eaten and so on.Doctor may also check you for dehydration and may also check your blood pressure, pulse, breathing rate and temperature. In some cases stool samples will be sent to the lab to identify the toxin causing symptoms. Blood test may also be done to check for seriousness of the sickness.

 

TREATMENT

Most cases of food poisoning may resolve on its own but some may need to be treated. Treatment depends on severity of disease and organism causing the symptoms.

Replacing Lost Fluids : During diarrhea the body loses essential electrolytes and fluids and these need to be replaced to avoid dehydration. Patients may need to be hospitalised and nutrients and fluid replaced through an IV. Giving fluid and electrolyte through an IV is faster than oral hydration.

 

Antibiotics : Pregnant women with food poisoning may need to be treated with antibiotics to prevent baby from getting infected. Some organisms like listeria need to be treated with antibiotics.

Doctor may also treat fever with medications and may also give anti vomiting medication to control vomiting. He may also treat diarrhea with medications

 

SELF CARE

These self-care or home remedies makes patients more comfortable and prevent dehydration.

Let your stomach settle. Do not eat or drink for a few hours.

Small frequent sips of water helps keep you hydrated.

Avoid alcoholic, caffeinated, or sugary drinks.

Get enough rest.

Gradually begin to eat bland, easy-to-digest foods, such as soda crackers and banana.

Don’t use anti-diarrheal medications.They may slow elimination of toxins from the body.

 

PREVENTION

Cook foods to a safe temperature. Use meat themometer.

  • Cook ground meats to 160 F (71 C)
  • Cook ground poultry to 165 F (74 C)
  • Cook beef, veal, and lamb steaks, roasts and chops to 145 F (63 C)
  • Cook all cuts of fresh pork to 160 F (71 C).
  • Whole poultry should reach 180 F (82 C) in the thigh; breasts 170 F (76.6 C).

Defrost food safely. Safe way to defrost food is to use refrigerator or microwave.

Never leave food out for more than two hours.

Keep hot foods hot and cold foods cold.

Wash before and after handling raw food.

keep raw foods such as poultry away from other foods to prevent cross contamination.

keep surfaces and cooking items clean.

Store perishable foods immediately in refrigerator.

When not sure of food safety, throw away.

 

COMPLICATIONS

Food poisoning can cause dehydration which can be fatal. It is essential to stay hydrated by taking frequent sips of water or getting hydrated through IV if need be.

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