Clinical manifestations of cirrhosis Symptoms Anorexia Weight loss Weakness Fatigue Muscle cramps Easy bruising Amenorrhea/oligomenorrhea/metrorrhagia (women) Impotence (men) Infertility Decreased libido (men) Jaundice* Dark or "cola-colored" urine* Pruritus* Hematemesis/melena/hematochezia* Abdominal distension* Lower extremity edema* Confusion or sleep disturbances* Physical examination Hepatomegaly Splenomegaly Spider angiomata/spider telangiectasias Palmar erythema Digital clubbing Hypertrophic osteoarthropathy Dupuytren's contracture Muehrcke nails Terry nails Parotid gland enlargement (likely due to alcohol use and not cirrhosis per se) Gynecomastia (men) Loss of chest or axillary hair (men) Testicular atrophy (men) Caput medusa Cruveilhier-Baumgarten murmur (venous hum heard best with the stethoscope over the epigastrium) Jaundice* Ascites (abdominal distension, shifting dullness, fluid wave)* Asterixis* Fetor hepaticus* Laboratory tests Moderately elevated aminotransferases (often with an AST:ALT ratio >1) Elevated alkaline phosphatase (2 to 3 times the ULN) Elevated gamma-glutamyl transpeptidase Thrombocytopenia Leukopenia/neutropenia Anemia Low serum albumin* Prolonged prothrombin time/elevated INR* Hyperbilirubinemia* Hyponatremia* Elevated serum creatinine* Imaging tests Surface nodularity Increased echogenicity (ultrasound) Atrophy of the right lobe Hypertrophy of the caudate or left lobes Small, nodular liver* Ascites* Hepatocellular carcinoma* Portal/splenic/superior mesenteric vein thrombosis* Portosystemic collaterals*
A meta-analysis found that the factors with the best ability to predict cirrhosis in adults with known or suspected liver disease included : ●Presence of ascites (likelihood ratio [LR] 7.2) ●Platelet count <160,000/mm3 (LR 6.3) ●Spider angiomata (LR 4.3) ●Bonacini cirrhosis discriminant score greater than 7 (LR 9.4) The Bonacini cirrhosis discriminant score is calculated by giving points for the following parameters : ●Platelets (x1000/mm3): •>340 – zero points •280 to 339 – one point •220 to 279 – two points •160 to 219 – three points •100 to 159 – four points •40 to 99 – five points •<40 – six points ●Alanine aminotransferase to aspartate aminotransferase (ALT/AST) ratio: •>1.7 – zero points •1.2 to 1.7 – one point •0.6 to 1.19 – two points •<0.6 – three points ●International normalized ratio (INR): •<1.1 – zero points •1.1 to 1.4 – one point •>1.4 – two points Factors associated with a low likelihood of cirrhosis included: ●Lok index <20 percent (LR 0.09) ●Platelet count of 160,000/mm3 or higher (LR 0.29) ●Absence of hepatomegaly (LR 0.37) The Lok index is calculated using the platelet count, AST, ALT, and INR . In a validation study, when a cutoff of <20 percent was used to exclude cirrhosis, the test had a specificity of 92 percent. When a cutoff of >50 percent was used to diagnose cirrhosis, the test had a sensitivity of 85 percent. Of note, the Lok index has only been validated in patients with hepatitis C virus.
In developed countries, common causes of cirrhosis include : ●Chronic viral hepatitis (hepatitis B, C) ●Alcoholic liver disease ●Hemochromatosis ●Nonalcoholic fatty liver disease Less common causes include: ●Autoimmune hepatitis ●Primary and secondary biliary cirrhosis ●Primary sclerosing cholangitis ●Medications (eg, methotrexate, isoniazid) ●Wilson disease ●Alpha-1 antitrypsin deficiency ●Celiac disease ●Idiopathic adulthood ductopenia ●Granulomatous liver disease ●Idiopathic portal fibrosis ●Polycystic liver disease ●Infection (eg, brucellosis, syphilis, echinococcosis) ●Right-sided heart failure ●Hereditary hemorrhagic telangiectasia ●Veno-occlusive disease
Referral to a hepatologist is recommended if the patient develops decompensated cirrhosis or major complications of cirrhosis. Patients with a MELD score ≥10 should be referred to a liver transplantation center for evaluation. In addition, referral to a hepatologist should be considered if the patient requires treatment for the underlying cause of the cirrhosis (eg, hepatitis C, autoimmune hepatitis) or if the clinician managing the patient would like the assistance of a hepatologist in the patient's general management.
Once these complications develop, patients are considered to have decompensated cirrhosis. Multiple factors can predispose to decompensation in a patient with cirrhosis. Risk factors for decompensation include bleeding, infection, alcohol intake, medications, dehydration, and constipation [3-5]. In addition, patients with obesity are at increased risk for decompensation . Once decompensation has developed, patients should be considered for liver transplantation.
The major goals of managing patients with cirrhosis include: ●Slowing or reversing the progression of liver disease ●Preventing superimposed insults to the liver ●Identifying medications that require dose adjustments or should be avoided entirely (table 2 and table 3) ●Managing symptoms and laboratory abnormalities ●Preventing, identifying, and treating the complications of cirrhosis ●Determining the appropriateness and optimal timing for liver transplantation
●Cirrhosis represents a late stage of progressive hepatic fibrosis characterized by distortion of the hepatic architecture and the formation of regenerative nodules. It is generally considered to be irreversible in its advanced stages. In earlier stages, specific treatments aimed at the underlying cause of liver disease may improve or even reverse cirrhosis.
Complications of portal hypertension include: ●Ascites ●Hepatic encephalopathy ●Variceal hemorrhage ●Spontaneous bacterial peritonitis ●Hepatorenal syndrome ●Portal hypertensive gastropathy ●Hepatic hydrothorax ●Hepatopulmonary syndrome ●Portopulmonary hypertension ●Cirrhotic cardiomyopathy
Common complications of cirrhosis Variceal hemorrhage Ascites Spontaneous bacterial peritonitis Hepatic encephalopathy Hepatocellular carcinoma Hepatorenal syndrome Hepatopulmonary syndrome Hepatic hydrothorax Portopulmonary hypertension Cirrhotic cardiomyopathy Portal vein thrombosis
Alcoholic liver cirrhosis .
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✍️✍️Late Effects Of Blood And Marrow Transplantation ___________________________________________ Abstract Hematopoietic cell transplantation is a curative treatment for a variety of hematologic diseases. Advances in transplantation technology have reduced early transplant-relatedmortality and expanded application of transplantation to older patients and to a wider variety of diseases. Management of late effects after transplantation is increasingly important for a growing number of long-term survivors that is estimated to be half a million worldwide. Many studies have shown that transplant survivors suffer from significant late effects that adversely affect morbidity, mortality, working status and quality of life. Late effects include diseases of the cardiovascular, pulmonary, and endocrine systems, dysfunction of the thyroid gland, gonads, liver and kidneys, infertility, iron overload, bone diseases, infection, solid cancer, and neuropsychological effects. The leading causes of late mortality include recurrent malignancy, lung diseases, infection, secondary cancers and chronic graft-versus-host disease. The aim of this review is to facilitate better care of adult transplant survivors by summarizing accumulated evidence, new insights, and practical information about individual late effects. Further research is needed to understand the biology of late effects allowing better prevention and treatment strategies to be developed. Introduction Hematopoietic cell transplantation (HCT) is a curative treatment for a variety of hematologic diseases.1 The safety of HCT has improved over the decades,2 indications for HCT have expanded to older patients,3 and almost all patients are able to find suitable allogeneic donors by the growing use of cord blood4 and haploidentical transplantation.5 These current conditions have contributed to a growing number of HCT survivors, estimated to be half a million worldwide.6 Patients who are disease-free at two or five years after HCT have a greater than 80% subsequent 10-year survival rate,7–10 but many studies show that HCT survivors suffer from significant late effects that adversely affect morbidity, mortality, working status and quality of life.7–13 A prospective observational study of 1022 survivors who underwent HCT between 1974 and 1998 showed that 66% of the survivors had at least one chronic condition and 18% had severe or life-threatening conditions.14 A retrospective study of 1087 contemporary survivors also showed that the cumulative incidence of any non-malignant late effect at five years after HCT was 45% among autologous and 79% among allogeneic recipients, and 2.5% of autologous and 26% of allogeneic recipients had three or more late effects.15 Life expectancy among 5-year survivors remained 30% lower compared with the general population, regardless of their current ages and years since HCT.9 The leading causes of excess deaths in 5-year survivors included secondary malignancies (27%) and recurrent disease (14%), followed by infections (12%), chronic graft-versus-host disease (GvHD) (11%), cardiovascular diseases (11%), and respiratory diseases (7%).9 The aim of this review is to facilitate better care of adult HCT survivors by summarizing accumulated evidence, new insights, and practical information about individual late effects (Figure 1). Recurrent disease and chronic GvHD are not discussed and readers are referred to other reviews.16–20 Figure 1. Download figure Open in new tab Download powerpoint Figure 1. Late effects of blood and marrow transplantation. Cardiovascular diseases Cardiovascular diseases (CVD) after HCT include cardiomyopathy, congestive heart failure, valvular dysfunction, arrhythmia, pericarditis, and coronary artery disease.21 Their cumulative incidences were 5%–10% at ten years after HCT,22–24 accounting for 2%–11% of mortality among long-term survivors.8,9,25 The incidence of CVD and its associated mortality were 1.4–3.5-fold higher compared with the general population.8,9,24,25 HCT survivors are more likely to have conventional risk factors such as dyslipidemia and diabetes than the general population.26 Early diagnosis and treatment of modifiable risk factors is important. We usually treat hypertension more than 140/90 mmHg on 2 separate visits or more than 130/80 mmHg for patients with diabetes or renal disease.27 The first step is lifestyle modification including weight reduction, dietary sodium reduction and regular physical activity, followed by initiating antihypertensive drugs such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs). Anthracycline exposure and chest radiation are the major risk factors for CVD after HCT.21 Several studies showed that dexrazoxane, ACE inhibitors, ARBs and beta-blockers can prevent anthracycline-related cardiomyopathy in the non-HCT setting.28–32 Once cardiomyopathy is established, it is important to initiate appropriate treatment. ACE inhibitors and beta-blockers have been effective in improving left ventricular function.33 Pulmonary diseases Non-infectious late complications of the lung include bronchiolitis obliterans syndrome (BOS), cryptogenic organizing pneumonia (COP) and pulmonary hypertension. BOS represents chronic GvHD of the lung, and is characterized by the new onset of fixed airflow obstruction after allogeneic HCT.34 According to the strict 2005 National Institutes of Health (NIH) diagnostic criteria for chronic GvHD, incidence of BOS was 5.5% and its prevalence was 15% among patients with chronic GvHD.35 Symptoms of BOS include dyspnea on exertion, cough and wheezing, but early BOS may be asymptomatic until significant lung function is lost.36 One study showed rapid decline in %FEV1 during the six months before BOS diagnosis, with a lower %FEV1 at diagnosis associated with worse survival.37 In our practice, we perform pulmonary function tests every three months including %FEV1 and FEV1/FVC among patients with active chronic GvHD. When testing shows significant new airflow obstruction, we repeat testing every month until stability is confirmed.38 Plasma matrix metalloproteinase 3 levels39 and parametric response mapping from CT scans40 might be useful diagnostic tests for BOS but these have not yet entered clinical practice. Standard treatment of BOS is prednisone at 1 mg/kg per day, followed by a taper to reach a lower, alternate-day regimen.38 A multicenter prospective study showed that addition of FAM (inhaled fluticasone propionate at 440 μg twice a day, azithromycin at 250 mg taken 3 days per week, and montelukast at 10 mg nightly) to prednisone treatment stabilized pulmonary function in 70% of patients with newly diagnosed BOS and permitted systemic steroid exposure to be reduced.41 Cryptogenic organizing pneumonia is a disorder involving bronchioles, alveolar ducts, and alveoli, the lumen of which become filled with buds of granulation tissue consisting of fibroblasts.42 Clinical symptoms include dry cough, shortness of breath, and fever. Bronchoalveolar lavage is performed to exclude infection. Lung biopsy is required for definitive diagnosis, but an empiric diagnosis is often based on radiographic findings of diffuse, peripheral, fluffy infiltrates consistent with airspace consolidation. Pulmonary function testing shows restrictive changes and low diffusing capacity of the lungs for carbon monoxide. The incidence of COP is 2%–10%,43,44 and it is strongly associated with acute and chronic GvHD.45 COP usually responds within 5–7 days to prednisone at 1 mg/kg per day, which is continued for one month followed by a slow taper over five months because COP can often recur. Small case series suggest potential benefits of macrolides for treatment of COP.46 Pulmonary hypertension is an uncommon but potentially fatal complication after HCT, with a reported prevalence of 2.4%.47 The most common symptoms are hypoxia, tachypnea, dyspnea, and acute respiratory failure,48 and if untreated, pulmonary hypertension can result in a progressive increase in pulmonary vascular resistance, right ventricular failure and death. Since initial symptoms are non-specific, it is likely to be underdiagnosed after HCT. Although cardiac catheterization is the gold standard for diagnosis of pulmonary hypertension, high-resolution chest computed tomography and echocardiography are non-invasive and useful diagnostic modalities. The most common types are pulmonary arterial hypertension and pulmonary veno-occlusive disease, sometimes associated with transplant-associated microangiopathy and inherited or acquired hemolytic anemia.48 First-line therapies are supplemental oxygen and phosphodiesterase-5 inhibitors, followed by inhaled nitric oxide, diuretics, bipyridine inotropes and after-load reducing agents.48 Endocrine diseases Major late effects in the endocrine system include thyroid dysfunction, diabetes, dyslipidemia, and adrenal insufficiency. Hypothyroidism occurs in 30% of patients by 25 years after HCT.49 Risk factors include age under ten years, conditioning containing radiation, busulfan or cyclophosphamide, and hematologic malignancies.49,50 The international guidelines recommend checking serum thyroid-stimulating hormone and free thyroxine levels every year.21 For patients who received radiolabeled iodine antibody therapy, thyroid function should be checked earlier starting at three and six months after HCT, and other times as clinically indicated. Standard criteria are used to initiate replacement therapy for hypothyroidism. Some patients develop hyperthyroidism after HCT as a rare complication.51 Diabetes occurs in 8%–41% of patients after allogeneic HCT and in 3% of patients after autologous HCT.15,52,53 Its incidence after allogeneic HCT is 3.65 times higher compared with their siblings.54 Initial treatment is therapeutic lifestyle counseling, but many patients require hypoglycemic agents or insulin. Dyslipidemia occurs in 9%–61% of HCT survivors.53,55 Despite no established consensus for management of dyslipidemia after HCT, our practice is to initiate therapeutic lifestyle counseling followed by statin therapy when LDL cholesterol exceeds 130–190 mg/dL according to the estimated risk of CVD, based on the National Cholesterol Education Program Adult Treatment Panel III guidelines56 and the recently suggested approach after allogeneic HCT.57 The 2013 ACC/AHA guidelines do not specify the targeted levels for LDL cholesterol, and addition of statin therapy is based on calculated risk for future cardiovascular events.58 Addition of omega-3-acid ethyl esters or fibrate is considered when fasting triglycerides exceed 200–499 mg/dL. Adrenal insufficiency occurs in 13% of patients after allogeneic HCT and 1% of patients after autologous HCT,15 and can be confirmed by a cortisol-stimulation test. Once adrenal insufficiency is diagnosed, physiological glucocorticoid replacement and a very slow terminal taper is needed. Patients should carry notification that they have adrenal insufficiency to alert emergency medical providers. For chronic GvHD therapy, the risk of adrenal insufficiency is lower with alternate-day administration of corticosteroids than with daily dosing,59 although patients with brittle diabetes need daily dosing to allow for optimal glucose control. Male gonadal dysfunction and infertility Hypogonadism is common after HCT. Impaired spermatogenesis, erectile dysfunction, low testosterone, and low libido occur in male patients. Erectile dysfunction and low libido have been associated with both physical and psychosocial factors.60,61 Testosterone replacement may be considered for patients with low testosterone levels and has improved sexual function, libido and bone mass, although monitoring prostate-specific antigen and testosterone levels is necessary.62,63 Azoospermia occurred in 70% of male patients, and spermatogenesis recovered in 90% of patients conditioned with cyclophosphamide alone, in 50% of patients conditioned with cyclophosphamide plus busulfan or thiotepa, and in 17% of patients conditioned with total body irradiation (TBI).64 Semen banking or cryopreservation of testicular tissue should be discussed before HCT with patients desiring fertility. Female gonadal dysfunction, infertility and pregnancy Ovarian insufficiency, vaginal changes and low libido occur in female patients. A historical study showed that ovarian failure occurred in more than 90% of female patients after HCT and recovered in 92% of patients conditioned with cyclophosphamide alone, but only in 24% of patients conditioned with cyclophosphamide and TBI.65 A pilot study showed that only 10% of patients had ovarian failure after reduced-intensity allogeneic HCT.66 The use of hormone replacement therapy for premature ovarian failure should be individualized based on the patient age, severity of menopausal symptoms, low bone density, risk of breast cancer, clotting predisposition and liver abnormalities.67 Since efficacy of gonadotropin-releasing hormone agonists in preserving fertility in cancer patients is controversial,68,69 cryopreservation of oocytes, ovarian tissue, or embryos should be discussed with patients desiring fertility.70 The largest study of pregnancy after HCT showed that 0.87% of patients or their partners had pregnancies after allogeneic HCT, and 0.36% of those after autologous HCT.71 We generally recommend that women wait 2–5 years after HCT before attempting conception since rates of relapse are generally highest in the first two years after HCT. Another concern is the theoretical risk of recurrent malignancy because of disturbance of the graft-versus-leukemia effect, and some cases of recurrent chronic myeloid leukemia after conception have been reported.71 Pregnancy outcomes are generally good with no increase in the risk of fetal malformations, although these pregnancies are considered high risk because of higher maternal risks of pregnancy complications.71 Iron overload Iron overload is rare after autologous HCT72 but common after allogeneic HCT.73,74 Previous prospective studies showed that 30%–60% of long-term survivors of allogeneic HCT had elevated serum ferritin levels and 25%–50% had elevated liver iron concentration on T2* magnetic resonance imaging (MRI).73,74 Since serum ferritin does not specifically reflect iron overload and can be elevated in hepatic and systemic inflammation, additional testing is required if the ferritin is elevated. We favor transferrin saturation, which is widely available and defined as the ratio of serum iron concentration divided by total iron-binding capacity.75 Normal transferrin saturation is less than 50% in males and less than 45% in females. Patients with iron overload usually have saturation more than 60%. HFE genotyping is considered in patients with a family history of hemochromatosis and in patients of Northern or Western European ethnicity. When saturation is not elevated, other etiologies for an elevated ferritin including inflammation, metabolic syndrome, and alcoholism should be ruled out. The most accurate test of tissue iron concentration is liver biopsy, but the procedure is invasive and may cause serious complications. Thus, T2* MRI and other modalities (FerriScan and superconducting quantum interference device) have been increasingly used.76 Importantly, liver tests are often normal among long-term survivors with iron overload, so hepatitis and GvHD should also be considered when results of liver tests are elevated.77 Iron overload may cause cardiomyopathy. Studies of thalassemia patients showed that cardiomyopathy typically took more than ten years to be clinically evident,78 and that many patients improved with intensive chelation therapy.79 Although a prospective study and a meta-analysis showed no statistical association of liver iron concentration with mortality after allogeneic HCT,80,81 our practice is to start phlebotomy of 5 mL/kg or 250–300 mL every 3–4 weeks as long as hematocrit is more than 35% until serum ferritin falls below 1000 ng/mL. Deferasirox, an oral chelating agent, is considered for patients with anemia precluding phlebotomy. Liver diseases Late liver diseases include chronic hepatitis B, chronic hepatitis C, liver cirrhosis, nodular regenerative hyperplasia and focal nodular hyperplasia.77 Hepatitis B-infected patients have an increased risk of fulminant liver failure. One study reported a 35% risk of HBV reactivation after HCT even among patients with isolated anti-HBc antibodies, mostly during steroid treatment for GvHD.82 Patients treated with anti-CD20 antibodies have an increased risk of HBV reactivation. Antiviral prophylaxis using entecavir or lamivudine will prevent almost all fulminant cases if initiated before the start of conditioning regimens in patients with positive blood HBV DNA levels.83 Patients with latent HBV (i.e. anti-HBc+/HBV DNA−) should be monitored monthly with HBV DNA levels after HCT and antiviral treatment should be initiated when viremia is detected.83 Hepatitis C virus infection in HCT survivors almost always results in chronic hepatitis.84,85 Typically, asymptomatic elevation of alanine aminotransferase occurs 2–4 months after HCT, coinciding with tapering of immunosuppressive medications. There may be little liver-related mortality in the first ten years after HCT,84 but liver cirrhosis occurs later with a cumulative incidence of 4%–24% at 20 years.85,86 A large retrospective study showed that hepatitis C-infected patients had an increased risk of 2-year non-relapse mortality due to hepatic problems and bacterial infection.87 Antiviral therapy for HCV has not been given early after HCT, but may improve both oncological and hepatic outcomes after HCT.88 Ribavirin and interferon-based therapy have been used for patients who have discontinued all immunosuppressive medications without active GvHD, but it can cause pancytopenia and GvHD. Recently, highly effective and well tolerated direct acting antiviral agents with more than 90% rates of sustained virological response have been developed, and interferon-free regimens are now the treatments of choice.89,90 Nodular regenerative hyperplasia is a rare liver condition characterized by a widespread benign transformation of the hepatic parenchyma into small regenerative nodules.77 This process is usually asymptomatic unless portal hypertension develops. Focal nodular hyperplasia occurs in 12% of HCT survivors, and possibly reflects sinusoidal injury caused by myeloablative conditioning regimens.91 Kidney diseases Chronic kidney disease (CKD) is defined as an elevated serum creatinine level, or a decreased glomerular filtration rate (GFR) less than 60 mL/min/1.73 m2 for three months or longer.92 CKD occurs in approximately 20% of HCT recipients.93–95 There are three major etiologies of CKD after HCT: thrombotic microangiopathy (TMA), nephrotic syndrome and idiopathic CKD. Other etiologies include persistent acute kidney injury and BK virus nephropathy.96 Whenever possible, renal biopsy should be considered to accurately diagnose the etiology of CKD and to provide appropriate management.97 Thrombotic microangiopathy occurs in 2%–21% of patients after HCT, and is characterized by renal dysfunction, thrombocytopenia, neurological dysfunction, hemolytic anemia with schistocytes, elevated lactate dehydrogenase and decreased haptoglobin.98,99 Risk factors of TMA include TBI, calcineurin inhibitors, and acute and chronic GvHD.100–102 TMA-related kidney injury often improves with tapering or stopping calcineurin inhibitors, but full renal function is rarely restored.103 In some cases TMA did not improve until GvHD was treated.104 Efficacy of plasma exchange is limited.105 Nephrotic syndrome occurs in 6%–8% of patients after allogeneic HCT.106,107 Membranous nephropathy comprised 61% of cases, and minimal change disease comprised 22% of cases, with a median onset of 14 months and eight months after HCT, respectively.108 Mechanisms of membranous nephropathy are thought to be formation of immune complexes through allo- or auto-antibodies recognizing antigens expressed by the podocyte, while T cells are implicated with minimal change disease.109 Nephrotic syndrome after HCT is often associated with chronic GvHD and tapering of immunosuppressive medications. Initial treatment is prednisone 1 mg/kg/day in addition to calcineurin inhibitors. Complete response was observed in 90% of patients with minimal change in disease, but only in 27% of patients with membranous nephropathy.108 Refractory cases may be treated with rituximab or mycophenolate mofetil.110 Idiopathic CKD comprises most cases of CKD. Risk factors include acute GvHD, chronic GvHD, acute kidney injury, long-term use of calcineurin inhibitors and previous autologous HCT,94,111 suggesting that GvHD, accompanying treatment and inflammatory conditions may have pathogenic roles in this entity. Associations of TBI with risk of CKD have been controversial.94,112 ACE inhibitors and ARBs have been used to treat CKD and hypertension associated with CKD.113 Bone diseases Late complications of bone include osteopenia, osteoporosis and avascular necrosis (AVN).114 Osteoporosis has been reported in as many as 50% of HCT recipients.115,116 The diagnoses of osteopenia and osteoporosis are made by measuring T-scores with dual-energy X-ray absorptiometry. A T-score between −1.0 and −2.5 indicates osteopenia, and a T-score less than −2.5 or presence of a fragility fracture indicates osteoporosis.117 Multiple risk factors are implicated including chemotherapy, radiation, corticosteroids, calcineurin inhibitors, vitamin D deficiency, and gonadal failure.116,118 Bone loss occurs within 6–12 months after HCT, and recovery of bone mineral density (BMD) begins from the lumber spine, followed by a slower recovery in the femoral neck. The use of corticosteroids is the strongest risk factor for osteoporosis. General preventative recommendations include adequate intake of calcium of 1200 mg per day or over and vitamin D of 1000 IU (25 μg) per day or over, regular weight-bearing exercise, and avoidance of smoking and excessive alcohol. Bisphosphonates are the primary treatment for bone loss.119 Patients who are taking 5 mg or more daily prednisone-equivalent steroids for three months or more should have screening BMD tests for osteoporosis, and bisphosphonate treatment may be indicated until corticosteroid treatment is discontinued or for up to five years.120 Second-line treatment includes calcitonin, raloxifene, denusomab, romosozumab, and blosozumab, though their reported use in HCT recipients is limited and adverse effects may be more prominent than with the bisphosphonates. Avascular necrosis occurs in 4%–19% of HCT survivors with a cumulative incidence of 3%–10% at five years after HCT.121,122 AVN causes severe bone pain and bone destruction, causing significant impairment in quality of life. AVN typically affects the femoral heads, but sometimes affects other joints such as the knee and shoulders.21 Risk factors for AVN include corticosteroids, calcineurin inhibitors, older age and TBI conditioning.114 When AVN is suspected, diagnostic MRI should be performed. Early involvement of an orthopedic specialist is important for management of AVN, including conservative treatment, joint-preserving surgery and joint replacement surgery.21,114 Infectious diseases All HCT survivors have some degree of immunodeficiency, particularly during the first year after HCT.123 If patients are able to stop immunosuppressive medications without GvHD or recurrent disease, many recover adequate immune function by one year after HCT. Patients with chronic GvHD, however, remain immunodeficient and have a high risk of infections. Common late infections are caused by Pneumocystis jirovecii, encapsulated bacteria, fungi, varicella-zoster virus (VZV), cytomegalovirus, and respiratory viruses. Patients may report more frequent episodes of upper respiratory infections and sinusitis. All patients should receive prophylaxis against Pneumocystis jirovecii for at least one year after HCT or until 3–6 months after all immunosuppressive medication is discontinued, whichever occurs later. The preferred drug is trimethoprim-sulfamethoxazole, but dapsone or atovaquone could be substituted for patients who are allergic to or intolerant of trimethoprim-sulfamethoxazole. In particular, patients with chronic GvHD are highly susceptible to encapsulated bacteria such as Streptococcus pneumoniae, Haemophilus influenzae and Neisseria meningitidis due to low levels of opsonizing antibodies, low CD4+ T-cell counts, poor reticuloendothelial function and suppressive effects of immunosuppressive medications on phagocytosis. Vaccination against these bacteria is recommended.124 Efficacy of vaccination in increasing antibody levels has been shown in several prospective studies.125,126 Chemoprophylaxis is always recommended due to the unpredictable protection provided by vaccination. The first-line drug is trimethoprim-sulfamethoxazole, but if it is not tolerated, penicillin or azithromycin is substituted until 3–6 months after discontinuation of all immunosuppressive medications. Invasive fungal infection occurs in 1% of patients after autologous HCT and in 6%–8% of patients after allogeneic HCT.127 GvHD and long-term use of corticosteroids have been a major risk factor associated with onset of invasive fungal infection.128 As recommended in the European guidelines, mold prophylaxis with posaconazole or voriconazole may be considered for patients with GvHD requiring high-dose corticosteroid treatment.129 Varicella-zoster virus-seropositive patients should receive prophylaxis with acyclovir or valacyclovir during the first year after HCT or until six months after discontinuation of immunosuppressive medications. A standard dose of acyclovir is 800 mg twice daily,130 but some studies showed that 200 mg once daily was effective in preventing VZV reactivation.131 Acyclovir should be started empirically if the patient presents with an acute abdomen or hepatitis typical of fulminant visceral VZV infection.132 CMV monitoring in blood is continued beyond 100 days after HCT until one year for patients at risk of late CMV disease, including CMV-seropositive patients receiving high-dose corticosteroids, those who have already experienced CMV reactivation, and cord blood transplantation.133 Pre-emptive therapy is usually considered for CMV levels of 250 IU/mL or more (equivalent to ≥1000 copies/mL) or a positive antigenemia test. Community-acquired respiratory virus infections are an important cause of morbidity and mortality after HCT. The most frequent viruses include rhinovirus, respiratory syncytial virus (RSV), parainfluenza viruses (PIV), human metapneumovirus, and influenza viruses as these frequently cause lower respiratory tract disease associated with 12%–100% mortality.134 An immunodeficiency scoring index can predict severity of RSV infection.135 Aerosolized ribavirin showed efficacy in treating lower tract RSV after HCT.136 Combination therapy with immunomodulators such as intravenous immunoglobulin or palivizumab has been seen to have variable success.137 Treatment for PIV infection has not been established. Efficacy of ribavirin has been limited for patients with lower respiratory tract infection of PIV.138 Novel drugs such as a recombinant sialidase fusion protein and a hemagglutinin-neuraminidase inhibitor are under investigation.138 Solid cancers There is an increased risk of solid cancers following both autologous and allogeneic HCT compared with the general population. The cumulative incidence is 1%–6% at ten years after HCT, and continues to rise over time without a plateau.139–142 The most common sites include oral cavity, skin, breast and thyroid, but rates are also elevated in esophagus, liver, nervous system, bone and connective tissues compared with the general population.143 Myeloablative TBI, young age at HCT, chronic GvHD and prolonged immunosuppressive medications beyond two years are well-documented risk factors for many types of cancers.143 All HCT recipients should be advised of the risk of second cancers and should be encouraged to undergo recommended screening tests based on their predisposition.143 The 5-year overall survival rates after diagnosis of solid cancers varied by cancer site, with 88%–100% for thyroid, testis and melanoma, approximately 50% for breast, mouth, soft tissue and female reproductive organs, and 20% or less for bone, lower gastrointestinal tract, and central nervous system.144 These rates were similar to those of de novo cancers, except that rates were lower for female reproductive organs, bone, colorectum, and central nervous system, although further studies are warranted to confirm this observation. There is emerging evidence that human papilloma virus (HPV) is involved in the pathogenesis of squamous cell cancer after HCT.145,146 The efficacy of HPV vaccination in preventing squamous cell cancer after HCT remains to be determined in prospective studies.147 Neuropsychological effects Neuropsychological effects after HCT are being increasingly recognized and include, among others, depression, post-traumatic stress disorder, and neurocognitive deficits. Depression occurs in 12%–30% of HCT survivors and is more frequent in female patients, younger patients and those with poor social support, history of recurrent disease, chronic pain, and chronic GvHD.148 Post-traumatic stress disorder occurs in 28% of patients at six months after HCT and may persist for 5%–13% of cases, although its risk factors are not yet clear.148–150 Neurocognitive deficits, so called “chemo brain”, have adverse functional impacts on HCT survivors who return to work and daily activities that require short-term memory, information-processing speed, multitasking and co-ordination.151 Neuropsychological tests can help identify neurocognitive deficits. Most evidence is derived from studies of breast cancer survivors, with estimated rates of deficits ranging from 16% to 50% up to ten years after treatment.152,153 Potential mechanisms for chemotherapy-induced neurocognitive changes include cytokine and immune dysregulation, damage to DNA and telomere length through cytotoxic agents, oxidative stress and hormonal changes.154 In cases of HCT survivors, there may be additional deficits derived from neurological complications including nervous system infection (HHV-6, fungi, etc.), immune-mediated damage, and toxicities of calcineurin inhibitors such as TMA and posterior reversible encephalopathy syndrome. A prospective observational study showed that neurocognitive function declined substantially at 80 days after HCT, returned to pre-transplantation levels at one year, and continued to improve between one and five years after HCT, except for motor dexterity and verbal learning and retention.155 Mostly mild, neurocognitive dysfunction according to the Global Deficit Score persisted at five years in 42% of long-term survivors.155 Rehabilitation programs have succeeded in improving neurocognitive functions,156 and methylphenidate and modafinil have demonstrated variable efficacies to improve neurocognitive function in non-HCT cancer patients.157,158 Efficacies of these interventions remaine to be determined among HCT survivors. Influence of newer practices on late effects An understanding of the influence of newer practices such as cord blood transplantation, non-TBI or reduced-intensity conditioning regimens and older patients on the incidence and severity of late effects awaits longer follow up. For example, TBI is associated with an increased risk of many late effects such as cardiovascular diseases, COP, hypothyroidism, diabetes, dyslipidemia, infertility, TMA-related kidney injury, bone density loss, avascular necrosis, and secondary solid cancer.49,54,100,102,114,118,143,159,160 The use of non-TBI conditioning regimens might reduce the burden of these late effects among HCT survivors. Some studies found that cumulative incidences of late effects did not differ much after reduced-intensity regimens compared with myeloablative regimens,15,161 and reduced-intensity conditioning was associated with a higher risk of recurrent malignancy among patients with myeloid malignancy.162 One study showed that the risk of AVN was elevated after cord blood transplantation, but graft source had a limited influence on other long-term health status and QOL.163 Consensus guidelines for late effects and prevention behaviors Incidence, mortality, morbidity and management of individual late effects are summarized in Tables 1 and 2. Recognizing the importance of managing late effects after HCT, the Center for International Blood and Marrow Transplant Research (CIBMTR), the European Group for Blood and Marrow Transplantation (EBMT), and the American Society for Bone Marrow Transplantation (ASBMT) developed recommendations in 2006 for screening and prevention practices for HCT survivors.164 Consensus recommendations were up-dated in 2011 including other international transplant communities.21 The NIH convened working groups to formulate late effects initiatives in 2015.148,165–169 View inlineDownload powerpoint Table 1. Late effects after blood and marrow transplantation View inlineDownload powerpoint Table 2. Tests, preventive approaches and treatment of late effects. Despite higher levels of engagement with health care providers, HCT survivors had similar health and prevention behaviors as matched untransplanted controls, suggesting the need for further education of both HCT survivors and health practitioners.170 Major modifiable predictors of lower adherence to preventive care practices were concerns about medical costs and lack of knowledge.171 Conclusion While the number of HCT survivors is growing, there is no evidence that the burden of late effects is lessening. HCT survivors face myriad late effects that can limit their functioning, require prolonged or life-long medical treatment, reduce their quality of life and also shorten their survival. To the extent that the HCT procedure itself causes these late effects, the transplant community has a responsibility to appropriately monitor, treat and ultimately try to prevent late effects. Given the dispersion of survivors and the varied structure of health care, hematologists, oncologists, primary care physicians and medical subspecialists are all involved in providing this care. Further research is needed to understand the biology of late effects to help identify better prevention and treatment strategiesDr. Ved Srivastava3 Likes4 Answers
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Hi every one Today we discuss about Liver.... The liver is a large, meaty organ that sits on the right side of the belly. Weighing about 3 pounds, the liver is reddish-brown in color and feels rubbery to the touch. Normally you can't feel the liver, because it's protected by the rib cage. The liver has two large sections, called the right and the left lobes. The gallbladder sits under the liver, along with parts of the pancreas and intestines. The liver and these organs work together to digest, absorb, and process food. The liver's main job is to filter the blood coming from the digestive tract, before passing it to the rest of the body. The liver also detoxifies chemicals and metabolizes drugs. As it does so, the liver secretes bile that ends up back in the intestines. The liver also makes proteins important for blood clotting and other functions. Liver Conditions Hepatitis: Inflammation of the liver, usually caused by viruses like hepatitis A, B, and C. Hepatitis can have non-infectious causes too, including heavy drinking, drugs, allergic reactions, or obesity. Cirrhosis: Long-term damage to the liver from any cause can lead to permanent scarring, called cirrhosis. The liver then becomes unable to function well. Liver cancer: The most common type of liver cancer, hepatocellular carcinoma, almost always occurs after cirrhosis is present. Liver failure: Liver failure has many causes including infection, genetic diseases, and excessive alcohol. Ascites: As cirrhosis results, the liver leaks fluid (ascites) into the belly, which becomes distended and heavy. Gallstones: If a gallstone becomes stuck in the bile duct draining the liver, hepatitis and bile duct infection (cholangitis) can result. Hemochromatosis: Hemochromatosis allows iron to deposit in the liver, damaging it. The iron also deposits throughout the body, causing multiple other health problems. Primary sclerosing cholangitis: A rare disease with unknown causes, primary sclerosing cholangitis causes inflammation and scarring in the bile ducts in the liver. Primary biliary cirrhosis: In this rare disorder, an unclear process slowly destroys the bile ducts in the liver. Permanent liver scarring (cirrhosis) eventually develops. Liver Tests Blood Tests: Liver function panel: A liver function panel checks how well the liver is working and consists of many different blood tests. ALT (Alanine Aminotransferase): An elevated ALT helps identify liver disease or damage from any number of causes, including hepatitis. AST (Aspartate Aminotransferase): Along with an elevated ALT, the AST checks for liver damage. Alkaline phosphatase: Alkaline phosphatase is present in bile-secreting cells in the liver; it's also in bones. High levels often mean bile flow out of the liver is blocked. Bilirubin: High bilirubin levels suggest a problem with the liver. Albumin: As part of total protein levels, albumin helps determine how well the liver is working. Ammonia: Ammonia levels in the blood rise when the liver is not functioning properly. Hepatitis A tests: If hepatitis A is suspected, the doctor will test liver function as well as antibodies to detect the hepatitis A virus. Hepatitis B tests: Your doctor can test antibody levels to determine if you have been infected with the hepatitis B virus. Hepatitis C tests: In addition to checking liver function, blood tests can determine if you have been infected with the hepatitis C virus. Prothrombin Time (PT): A prothrombin time, or PT, is commonly done to see if someone is taking the correct dose of the blood thinner warfarin (Coumadin). It also checks for blood clotting problems. Partial Thromboplastin Time (PTT): A PTT is done to check for blood clotting problems. Imaging Tests: Ultrasound: An abdominal ultrasound can test for many liver conditions, including cancer, cirrhosis, or problems from gallstones. CT scan (computed tomography): A CT scan of the abdomen gives detailed pictures of the liver and other abdominal organs. Thank you all hope u enjoy the reading Tomarow I will come with the treatment of different liver diseases ... So join again with me tomarow Till than have a good time and a healthy life Regards Dr BakshiDr. Kousar Bakshi14 Likes11 Answers
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Friends today I am discussing about Hepatitis. Hepatitis Hepatitis is the inflammation of the liver. The most common cause for hepatitis is viruses. Other causes may include excessive alcohol use, certain medications, toxins, other infections, and autoimmune diseases. Types of Hepatitis Hepatitis is mainly of five types that are caused by a virus, A, B, C, D, and E. These can be commonly determined by a laboratory test. Hepatitis types A, C, D, and E is caused by viruses that have a core of ribonucleic acid (RNA). While virus responsible for hepatitis B has a DNA core. Causes of Hepatitis • Hepatitis A and E are mainly spread by contaminated food and water. Hepatitis A is also called infectious hepatitis as it is very highly contagious disease, but it is rarely fatal. • Hepatitis B spreads through sexually transmission, but may also be passed from mother to baby during pregnancy or childbirth. Hepatitis B is also called as viral hepatitis. It can be severe and often leads to liver cirrhosis. Hepatitis B may commonly transmit through transfusions of contaminated blood. • Both hepatitis B and hepatitis C are commonly spread through infected blood like during sharing of the needle by intravenous drug users. Complications of Hepatitis C can lead to chronic hepatitis, cirrhosis, or liver failure. • Hepatitis D can only infect people already infected with hepatitis B. Hepatitis D is the most serious and also the rarest form of viral hepatitis. Many cases of hepatitis D are fatal, and most chronic cases lead to cirrhosis. • Hepatitis E often occurs in epidemics that can be linked to poor hygiene and contaminated water. Pregnant women can be at risk due to infection by Hepatitis E. The disease has been reported almost exclusively in developing countries. Symptoms of hepatitis Many people with hepatitis experience either mild symptoms or none at all. Symptoms may not occur until liver damage occurs. Acute hepatitis - The initial phase of hepatitis is called the acute phase. The symptoms may include: • Diarrhea • Fatigue • Loss of appetite • Mild fever and flu-like symptoms • Muscle or joint aches • Nausea & Vomiting • Pain in abdominal • Unexplained Weight loss. Chronic hepatitis-- The acute phase is not usually dangerous, but it may develop into the fulminant type of hepatitis which is a very serious stage and can lead to death. As the patient gets worse, these symptoms may follow: • Portal Circulation problems • Dark urine • Dizziness & Drowsiness (only toxic/drug-induced hepatitis) • Enlarged spleen (only alcoholic hepatitis) • Headache • Hives with or without Itching of skin • Clay-colored stool, which may contain pus • Yellow skin, whites of eyes, tongue (jaundice). Complications of Hepatitis Fibrosis - One of the most common complications of chronic hepatitis is fibrosis, which is a type of scarring of the liver. Due to constant inflammation, the liver is damaged and creates the scar tissue to repair itself. Cirrhosis of the liver - Extensive fibrosis is called cirrhosis. There are many causes for Liver cirrhosis, but alcoholic hepatitis and Hepatitis C is the common. Cancer of the Liver - One of the complications of cirrhosis is liver cancer, which are usually two types. First is hepatocellular carcinoma, where liver cells are affected. The other type is cholangiolar carcinoma, which affects the bile ducts. Liver Failure - Liver failure is a serious, but uncommon, complication of hepatitis. In this condition, function of the liver stopped and this leads to the body shutting down, and eventually, death. Glomerulonephritis - Glomerulonephritis is a kidney disorder caused by inflammation of nephrons and is seen in chronic hepatitis B and hepatitis C infections. Cryoglobulinemia - Seen in chronic hepatitis B and hepatitis C infection, cryoglobulinemia is an uncommon disease caused by an abnormal cluster of a kind of protein that blocks small blood vessels leading to circulation problems. Hepatic Encephalopathy - Severe loss of liver function, such as liver failure, can lead to inflammation in the brain called encephalopathy. This causes mental problems, like confusion, and can lead to coma. Portal Hypertension - One of the liver's important jobs is to filter blood. When this portal system is blocked due to liver cirrhosis and other problems, blood can't return to the liver from the digestive system and pressure increases. This is called portal hypertension and it is a serious complication and can be fatal. Porphyria - Porphyria is a group of diseases caused by problems processing important chemicals in the body called porphyrins. One type, called porphyria cutanea tara, leads to blistering of the hands and face and is a rare complication of chronic hepatitis C infection. Viral Co-Infection - A challenging complication of hepatitis is the possibility of having two viral infections at the same time. A common with co-infection with hepatitis is the human immunodeficiency virus (HIV). Other common co-infections are with the hepatotropic viruses, named A through E. This type of Co-infections can be fatal. Diagnosis • Complete blood count • Liver function Test • Laboratory test to identify virus in blood • Bleeding time • Clotting time • Imaging- Ultrasonography, CT- scan, MRI • Liver biopsy Homoeopathy in the treatment of Hepatitis and other liver problem Homeopathy provides a very effective and safe treatment for Hepatitis and other liver disorders. It relieves the discoloration of the skin, mucous membrane, and sclera. These medicines strengthen the liver and metabolic system. The aim of homeopathy is not only to treat Hepatitis infection but It works by treating the underlying cause and not just the symptoms. The treatment is gentle and the relief obtained is usually long term. There are many homoeopathic medicines that have the potential to cure Jaundice. Out of them, few are – Andrographis Paniculata - Useful in resistant jaundice. Useful in Hepatitis B and C. It is found useful when Chelidonium Majus does not help. Arsenic Album - Where hepatitis results from bad food or food poisoning, Arsenic Album is the best Homeopathic medicine. There is burning pain in the liver which gets better with warm drinks. Aurum Metallicum - Very effective for jaundice during pregnancy. Distension of epigastrium with increased thirst and appetite, followed by burning sensation and hot eructations. Carduuas Marianus - Carduus Marianus is a very effective remedy for liver cirrhosis with general edema. There is engorged and laterally swollen liver, which gets worse from pressure. Jaundice. Carica Papaya - Hepatomegaly and splenomegaly associated with fever, dyspepsia and indigestion. Constipation is marked feature of this remedy. Intolerance to milk even small amount may lead to pain. Chelidonium - Chelidonium is very effective in treating an enlarged liver with tenderness. Hepatomegaly with bilious complications. Dull, throbbing pain in the region of the liver is also best treated with Chelidonium. Jaundice due to hepatic and gallbladder obstruction. Pain aggravation on eating. Marked desire for hot food and drinks Chionanthus - Chionanthus is very effective in chronic cases of jaundice, which recur every summer. The symptoms include an enlarged liver, constipation, clay-coloured stools and very yellow skin. Crotalus Horridus - Crotalus Horridus is used to treat jaundice cases where the entire body has gone yellow. Pain in the liver, coldness, Constant nausea and vomiting. Jaundice with haemorrhagic manifestations. Atonic dyspepsia. Complications arise from a blood transfusion. Lachesis - Lachesis is very effective for liver complaints largely among alcoholics. In cases where the liver region is very sensitive and a person can’t bear anything around the waist, Lachesis is one of the most effective Homeopathic medicines for fatty liver. Sensitiveness of right hypochondrium, hazards of blood transfusion. Lycopodium - Hepatitis, the atrophic form of nutmeg liver. Shooting pain across lower abdomen from right to left. Excessive flatulence. Bread aggravates. The desire for sweet and warm things. Natrum Sulpuricum - Natrum Sulphuricum is one of the great Homeopathic medicines for liver problems like jaundice where the symptoms include a liver region that is sensitive, tender and sore to the touch. Vomiting bile is another indicator. Nux Vomica - Hepatitis associated with constipation. Liver enlarged with stitches and soreness. Alcoholic liver. Phosphorus - Acute hepatitis. Fatty degeneration of liver, cirrhosis, and jaundice associated with the pancreatic disease. Suppuration with hectic night sweats, enlargement, and marked soreness. Podophyllum - Chronic relapsing hepatitis. History of repeated jaundice. Pain in right hypochondrium. Not well since the first attack of hepatitis. Irritable temperament with suicidal tendency.Dr. Rajesh Gupta4 Likes6 Answers
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four years male present with anasarca bilateral pitting oedema fluid thrill and shifting dullness positive umbilicus everted periorbital puffiness icterus positive hepatosplenomegaly with attached report. rk 39 and Australia antigen is negative. usg report suggestive of ascites and hepatosplenomegaly.is there possibility of autoimmune hepatitis because SGPT IS NOT MUCH ELEVSTED IN COMPARISION TO SERUM BILIRUBIN ELEVATION. HISTORY of blood TRANFUSION one time. history of casualty of sister three months ago. sister suffering from same problem according to patient father. father is migrant worker. chest X-RAYS suggestive of cardiomegaly. further investigation and treatment.Dr. Rajeev Gupta2 Likes16 Answers
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Hepatitis *Hepatitis* refers to an inflammatory condition of the liver. It’s commonly caused by a viral infection, but there are other possible causes of hepatitis. These include autoimmune hepatitis and hepatitis that occurs as a secondary result of medications, drugs, toxins, and alcohol. Autoimmune hepatitis is a disease that occurs when your body makes antibodies against your liver tissue. ￼ Timeline 8th Century: Infectious Nature of HBV suggested 17th-19th Centuries: Outbreaks of epidemics of jaundice in military and civilian populations during wars 1883: Lurman reports outbreaks of serum hepatitis follwing vaccination of dockers 1908: McDonald postulates that the infectious jaundice is caused by a virus 1939-1945: WWII-A series of outbreaks after vaccination for measles and yellow fever 1947: MacCallum classifies viral hepatitis into two types- Viral hepatitis A—> Infectious hepatitisViral hepatitis B—> Serum hepatitis 1965: Blumberg discovers Australia antigen (HBsAg) in aborigines and shows presence of antigen at high frequency in patients with leukemia and children with Down’s syndrome 1970: Dane discovers the Dane particle (complete HBV particle) 1972: Discovers HBeAg 1973: Feinstone and Purcell identifies HAV 1977: Rizzetto describes delta antigen HDV 1983: Recovery of HEV 1988: Chiron group (Choo, Kuo, Houghton) closes and identifies HCV. 1995: Abbot group reports GB Virus-C (GBV-C) and Genelabs group reports in 1996 hepatitis G virus (HGV)—GBV-C=HGV 1996: Chang’s group at NTUH reports in JAMA the successful prevention of HBV infection by nation-wide vaccination on newborn babies launched in 1984 in Taiwan. 1997: Chang’s group at NTUH reports in NEJM a decrease in annual incidence rate of hepatocellular carcinoma in children ascribed to nation-wide vaccination against HBV on newborn babies launched in 1984 in Taiwan. Epidemiology Globally, viral It was the seventh leading cause of death in 2013, up from the 10th leading cause in 1990. Worldwide, HAV is responsible for an estimated 1.4 million infections annually. About 2 billion people in the world have evidence of past or current HBV infection, with 240 million chronic carriers of HBsAg. HBV, along with the associated infection by the hepatitis D virus, is one of the most common pathogens afflicting humans. HBV leads to 650,000 deaths annually as a result of viral hepatitis–induced liver disease. The worldwide annual incidence of acute HCV infection is not easily estimated, because patients are often asymptomatic. An estimated 71 million people are chronically infected with HCV worldwide. About 55-85% of these people infected progress to chronic HCV infection, with a 15-30% risk of developing liver cirrhosis within two decades. China, the United States, and Russia have the largest populations of anti-HCV positive injection drug users (IDUs). It is estimated that 6.4 million IDUs worldwide are positive for antibody to hepatitis B core antigen (HBcAg) (anti-HBc), and 1.2 million are HBsAg-positive. Types and causes Viral infections of the liver that are classified as hepatitis include hepatitis A, B, C, D, and E. A different virus is responsible for each type of virally transmitted hepatitis. Hepatitis A is always an acute, short-term disease, while hepatitis B, C, and D are most likely to become ongoing and chronic. Hepatitis E is usually acute but can be particularly dangerous in pregnant women. Hepatitis A Hepatitis A is caused by an infection with the hepatitis A virus (HAV). This type of hepatitis is most commonly transmitted by consuming food or water contaminated by feces from a person infected with hepatitis A. Hepatitis B Hepatitis B is transmitted through contact with infectious body fluids, such as blood, vaginal secretions, or semen, containing the hepatitis B virus (HBV). Injection drug use, having sex with an infected partner, or sharing razors with an infected person increase your risk of getting hepatitis B. It’s estimated by the CDC that 1.2 million people in the United States and 350 million people worldwide live with this chronic disease. Hepatitis C Hepatitis C comes from the hepatitis C virus (HCV). Hepatitis C is transmitted through direct contact with infected body fluids, typically through injection drug use and sexual contact. HCV is among the most common bloodborne viral infections in the United States. Approximately 2.7 to 3.9 million Americans are currently living with a chronic form of this infection. Hepatitis D Also called delta hepatitis, hepatitis D is a serious liver disease caused by the hepatitis D virus (HDV). HDV is contracted through direct contact with infected blood. Hepatitis D is a rare form of hepatitis that only occurs in conjunction with hepatitis B infection. The hepatitis D virus can’t multiply without the presence of hepatitis B. It’s very uncommon in the United States. Hepatitis E Hepatitis E is a waterborne disease caused by the hepatitis E virus (HEV). Hepatitis E is mainly found in areas with poor sanitation and typically results from ingesting fecal matter that contaminates the water supply. This disease is uncommon in the United States. However, cases of hepatitis E have been reported in the Middle East, Asia, Central America, and Africa, according to the CDC. Autoimmune Hepatitis Autoimmune hepatitis is a rare form of chronic hepatitis. Like other autoimmune disorders, its exact cause is unknown. Autoimmune hepatitis may develop on its own or it may be associated with other autoimmune disorders, such as systemic lupus erythematosus. In autoimmune disorders, a misdirected immune system attacks the body’s own cells and organs (in this case the liver). Symptoms When symptoms occur, they can include: Jaundice (a yellowing of the skin and eyes)Abdominal painLoss of appetiteNausea and vomitingDiarrheaFeverClay-colored bowel movementsPainful joints ￼ Yellowing of skin and eye ￼ Complications of hepatitis Chronic hepatitis B or C can often lead to more serious health problems. Because the virus affects the liver, people with chronic hepatitis B or C are at risk for: Chronic liver diseaseCirrhosisLiver cancer When your liver stops functioning normally, liver failure can occur. Complications of liver failure include: Bleeding disordersA buildup of fluid in your abdomen, known as ascitesIncreased blood pressure in portal veins that enter your liver, known as portal hypertensionKidney failureHepatic encephalopathy , which can involve fatigue, memory loss, and diminished mental abilities due to the buildup of toxins, like ammonia, that affect brain functionHepatocellular carcinoma, which is a form of liver cancerDeath People with chronic hepatitis B and C are encouraged to avoid alcohol because it can accelerate liver disease and failure. Certain supplements and medications can also affect liver function. If you have chronic hepatitis B or C, check with your doctor before taking any new medications. Diagnosis and test History and physical exam To diagnose hepatitis, first your doctor will take your history to determine any risk factors you may have for infectious or noninfectious hepatitis. During a physical examination, your doctor may press down gently on your abdomen to see if there’s pain or tenderness. Your doctor may also feel to see if your liver is enlarged. If your skin or eyes are yellow, your doctor will note this during the exam. Liver function tests Liver function tests use blood samples to determine how efficiently your liver works. Abnormal results of these tests may be the first indication that there is a problem, especially if you don’t show any signs on a physical exam of liver disease. High liver enzyme levels may indicate that your liver is stressed, damaged, or not functioning properly. Other blood tests If your liver function tests are abnormal, your doctor will likely order other blood tests to detect the source of the problem. These tests can check for the viruses that cause hepatitis. They can also be used to check for antibodies that are common in conditions like autoimmune hepatitis. Ultrasound An abdominal ultrasound uses ultrasound waves to create an image of the organs within your abdomen. This test allows your doctor to take a close at your liver and nearby organs. It can reveal: Fluid in your abdomenLiver damage or enlargementLiver tumoursAbnormalities of your gallbladder Sometimes the pancreas shows up on ultrasound images as well. This can be a useful test in determining the cause of your abnormal liver function. Liver biopsy A liver biopsy is an invasive procedure that involves your doctor taking a sample of tissue from your liver. It can be done through your skin with a needle and doesn’t require surgery. Typically, an ultrasound is used to guide your doctor when taking the biopsy sample. This test allows your doctor to determine how infection or inflammation has affected your liver. It can also be used to sample any areas in your liver that appear abnormal. Treatment and medications Treatment options are determined by which type of hepatitis you have and whether the infection is acute or chronic. Hepatitis A Hepatitis A usually doesn’t require treatment because it’s a short-term illness. Bed rest may be recommended if symptoms cause a great deal of discomfort. If you experience vomiting or diarrhea , follow your doctor’s orders for hydration and nutrition. The hepatitis A vaccine is available to prevent this infection. Most children begin vaccination between ages 12 and 18 months. It’s a series of two vaccines. Vaccination for hepatitis A is also available for adults and can be combined with the hepatitis B vaccine. Hepatitis B Acute hepatitis B doesn’t require specific treatment. Chronic hepatitis B is treated with antiviral medications. This form of treatment can be costly because it must be continued for several months or years. Treatment for chronic hepatitis B also requires regular medical evaluations and monitoring to determine if the virus is responding to treatment. Hepatitis B can be prevented with vaccination. The CDC recommends hepatitis B vaccinations for all newborns. The series of three vaccines is typically completed over the first six months of childhood. The vaccine is also recommended for all healthcare and medical personnel. Hepatitis C Antiviral medications are used to treat both acute and chronic forms of hepatitis C. People who develop chronic hepatitis C are typically treated with a combination of antiviral drug therapies. They may also need further testing to determine the best form of treatment. People who develop cirrhosis (scarring of the liver) or liver disease as a result of chronic hepatitis C may be candidates for a liver transplant . Currently, there is no vaccination for hepatitis C. Hepatitis D No antiviral medications exist for the treatment of hepatitis D at this time. According to a 2013 study , a drug called alpha interferon can be used to treat hepatitis D, but it only shows improvement in about 25 to 30 percent of people. Hepatitis D can be prevented by getting the vaccination for hepatitis B, as infection with hepatitis B is necessary for hepatitis D to develop. Hepatitis E Currently, no specific medical therapies are available to treat hepatitis E. Because the infection is often acute, it typically resolves on its own. People with this type of infection are often advised to get adequate rest, drink plenty of fluids, get enough nutrients, and avoid alcohol. However, pregnant women who develop this infection require close monitoring and care. Autoimmune hepatitis Corticosteroids, like prednisone or budesonide, are extremely important in the early treatment of autoimmune hepatitis. They’re effective in about 80 percent of people with this condition.Azothioprine ( Imuran ), a drug that suppresses the immune system, is often included in treatment. It can be used with or without steroids.Other immune suppressing drugs like mycophenolate (CellCept), tacrolimus (Prograf) and cyclosporine (Neoral) can also be used as alternatives to azathioprine for treatment. Prevention There are many steps you can take to reduce the risk of viral hepatitis: Consider getting vaccinated against hepatitis A and B if you weren’t vaccinated as a child. This is the number one way to prevent these illnesses.Wash your hands with soap and water after using the bathroom or changing a baby’s diaper and before handling food.When traveling in developing countries, avoid unpeeled or raw foods. Drink only bottled, boiled or chemically treated water.Practice safe sex. Hepatitis B is about 50–100 times more transmissible during sex than HIV. Condoms and other barrier methods greatly reduce the risk.Never share syringes, shaving razors, toothbrushes or tattooing or piercing supplies.Wear gloves when performing first aid.Disinfect blood spills (including dried ones) with diluted bleach and wear gloves during clean-up.Follow all occupational safety precautions in your workplace.If you are pregnant, seek early and regular prenatal care. To reduce the risk of non-viral hepatitis, avoid excessive alcohol consumption and consult with a healthcare professional about medications and supplements.Dr. Shailendra Kawtikwar5 Likes21 Answers