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Date: Wed, 11 Jun 2003 11:55:24 -0400
Subject: [ChronicIllnessHouse] (HCV) has several important associations with autoimmune hepatitis


a.. The Hepatitis C Connection

Hepatitis C (HCV) has several important associations with autoimmune hepatitis. The prevalence rate of HCV infection in patients with autoimmune hepatitis is similar to that in the general population. This implies that HCV should not be an important factor in the etiology of autoimmune hepatitis; however, patients who are seropositive for anti–LKM-1 frequently are infected with HCV. These patients have predominant features of chronic viral hepatitis and frequently lack antibodies to P-450 IID6. Such patients respond to treatment with interferon. They should be distinguished from anti–LKM-1-positive patients who have a positive anti–P-450 IID6, are seronegative for anti-HCV, and are responsive to steroid therapy.

False-positive anti-HCV enzyme-linked immunoassay (ELISA) tests are described in the setting of hypergammaglobulinemia, including that observed in patients with autoimmune hepatitis. In patients with ANA and/or ASMA seropositivity and a positive anti-HCV, a false-positive reaction to HCV should be excluded by performing a test for HCV RNA, using the polymerase chain reaction (PCR). In general, patients with definite autoimmune hepatitis have median serum titers of ASMA and ANA of 1:160 and 1:320, respectively. In contrast, these titers may be in the range of 1:80 or less in patients with true chronic viral hepatitis.

Although autoimmune hepatitis and chronic HCV have similar histologic features, moderate-to-severe plasma cell infiltration of the portal tracts is more common in patients with autoimmune hepatitis. Portal lymphoid aggregates, steatosis, and bile duct damage are more common in patients with chronic HCV.

a.. Overlap syndromes: Patients with autoimmune hepatitis may present with features that overlap those classically associated to patients with primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC). Patients with disease that overlaps with PBC may have detectable AMA (usually in low titer), histologic findings of bile duct injury and/or destruction, and the presence of hepatic copper. These patients may improve with steroid therapy. Patients with disease that overlaps with PSC usually have concurrent inflammatory bowel disease, and the liver biopsy reveals bile duct injury. Findings from cholangiograms are abnormal. Such patients usually have mixed hepatocellular and cholestatic liver chemistries, and are typically resistant to steroid therapy.
a.. Autoimmune cholangitis is characterized by mixed hepatic and cholestatic liver chemistries, positive ANA and/or ASMA, negative AMA, antibodies to carbonic anhydrase, and histology that resembles PBC. Patients may have an unpredictable response to therapy with steroids or ursodeoxycholic acid.
a.. Cryptogenic autoimmune hepatitis is characterized by a clinical picture that is indistinguishable from autoimmune hepatitis. ANA, ASMA, and anti–LKM-1 are negative at disease onset and may appear late in the disease course, as might anti-SLA. The disease is usually responsive to steroid therapy.
Physical:

a.. Common findings at physical examination are as follows:
Hepatomegaly (83%)
Jaundice (69%)
Splenomegaly (32%)
Spider angiomata (58%)
Ascites (20%)
Encephalopathy (14%)

a.. All of these findings may be observed in patients with disease that has progressed to the point of cirrhosis with ensuing portal hypertension; however, hepatomegaly, jaundice, splenomegaly, and spider angiomata also may be observed in patients who do not have cirrhosis.
Causes: Autoimmune hepatitis is a chronic disease of unknown etiology

Lab Studies:

a.. Autoantibodies: Autoimmune hepatitis is characterized by positive autoantibody tests . Autoimmune hepatitis type 1 is characterized by positive tests for ASMA and ANA. Type 2 disease is infrequently observed in the US but is well characterized in Europe. Type 2 disease is marked by a positive anti–LKM-1 antibody test. Type 3 disease also is infrequently observed in the US. Type 3 is marked by a positive anti-SLA antibody test.
a.. Serum protein electrophoresis and quantitative immunoglobulins
a.. An immunoglobulin G (IgG)-predominant polyclonal hypergammaglobulinemia is a common finding in patients with untreated autoimmune hepatitis. Gamma globulin values typically range from 3-4 g/dL and frequently are as high as 5-6 g/dL. Cases of hyperviscosity syndrome secondary to high IgG levels are reported. Autoimmune hepatitis is an unlikely diagnosis in patients who have acute hepatitis without hypergammaglobulinemia.
a.. The gamma globulin or the IgG level may be followed on a regular basis as a marker of disease responsiveness to therapy.
a.. Aminotransferases
a.. Serum aminotransferases (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]) are elevated in 100% of patients at initial presentation, with average values of 200-300 U/L. Aminotransferase values correlate poorly with the degree of hepatic necrosis; however, values in the thousands may indicate acute hepatitis or a severe flare of preexisting disease.
a.. Continued elevation of the aminotransferases in the face of ongoing therapy is a reliable marker for ongoing inflammatory activity in the liver. Normalization of the aminotransferases during therapy is an encouraging sign, but active liver inflammation is present in more than 50% of patients who normalize their liver chemistries. Indeed, biochemical remission may precede true histologic remission by 3-12 months; thus, patients should be treated for at least 1 year after documentation of normal liver chemistries. Liver biopsy may then be employed to determine whether the patient is in histologic remission. Drug withdrawal may be attempted at this time (see Treatment).
a.. Worsening of aminotransferases in a patient undergoing treatment or in a patient who is in remission may signal a resurgence of disease activity.
a.. Other liver chemistries
a.. Serum bilirubin and alkaline phosphatase values are mildly to moderately increased in 80-90% of patients. A sharp increase in the alkaline phosphatase values during the course of autoimmune disease might reflect the development of primary sclerosing cholangitis or the onset of hepatocellular carcinoma as a complication of cirrhosis.
a.. Hypoalbuminemia and prolongation of prothrombin time are markers of severe hepatic synthetic dysfunction, which may be observed in active disease or decompensated cirrhosis.
a.. Other common laboratory abnormalities
a.. Mild leukopenia
a.. Normochromic anemia
a.. Coombs-positive hemolytic anemia
a.. Thrombocytopenia
a.. Elevated sedimentation rate
a.. Eosinophilia (uncommon but counts ranging from 9-48% are described)
a.. Autoimmune hepatitis has even been described as the sole presenting feature of idiopathic hypereosinophilic syndrome.
Imaging Studies:


a.. Imaging studies, in general, are not helpful in making a definitive diagnosis of autoimmune hepatitis; however, the presence of heterogeneous echotexture on abdominal ultrasound or abnormal contrast enhancement on abdominal CT imaging may suggest the presence of active inflammation or necrosis. The appearance of an irregular nodular liver may confirm the presence of cirrhosis. Furthermore, these imaging studies may be used to rule out the presence of hepatocellular carcinoma, a potential complication of autoimmune hepatitis-induced cirrhosis.
Procedures:


a.. Liver biopsy
a.. Liver biopsy is the most important diagnostic procedure in patients with autoimmune hepatitis. This procedure can be performed percutaneously, with or without ultrasound guidance, or by the transjugular route. The latter is preferred if the patient has coagulopathy or severe thrombocytopenia. A transjugular liver biopsy also may be preferable if ascites is present or if the liver is small, shrunken, and difficult to reach percutaneously. Liver biopsy routinely is performed in the outpatient setting to investigate abnormal liver chemistries. Liver biopsy should be performed as early as possible in patients with acute hepatitis who are thought to have autoimmune hepatitis. Confirmation of the diagnosis enables initiation of treatment at an early stage in the disease process.
a.. The role of biopsy in patients presenting with well-established cirrhosis secondary to autoimmune hepatitis is less clear. As an example, the initiation of treatment in a patient with cirrhosis, normal aminotransferases, and a minimally elevated gamma globulin is not expected to influence the disease outcome.
a.. Endoscopic retrograde cholangiopancreatography: Occasionally, a patient with autoimmune hepatitis and ulcerative colitis may require endoscopic retrograde cholangiopancreatography (ERCP) to rule out coexisting primary sclerosing cholangitis.
Histologic Findings:

Autoimmune hepatitis is characterized by a chronic inflammatory cell infiltrate. Plasma cells are the prominent cell type. Biopsies may show evidence for interface hepatitis (piecemeal necrosis), bridging necrosis, and fibrosis. Lobular collapse, best identified by reticulin staining, is a common finding.

Interface hepatitis does not predict a progressive disease course. By contrast, there is a strong likelihood that cirrhosis will develop when bridging necrosis is present. The presence or absence of cirrhosis on liver biopsy is an important determinant of the patient's prognosis.

Liver biopsy can help to differentiate autoimmune hepatitis from chronic HCV infection, alcohol-induced hepatitis, drug-induced liver disease, primary biliary cirrhosis, and primary sclerosing cholangitis.


Treatment

Medical Care:

For more than 3 decades, prednisone and azathioprine have been the mainstays of drug therapy for patients with autoimmune hepatitis. Considerable variation in practice style exists when it comes to answering the following common clinical questions:

How high a dose of prednisone should be used when initiating therapy?

When should azathioprine be added to the patient's treatment regimen? When should a reduction in steroid dosing be considered?

How long should treatment continue beyond a patient's biochemical remission?

Should liver biopsy be performed in order to document histologic remission, prior to attempting to withdraw immunosuppression? Should patients receive life-long low-dose maintenance therapy with azathioprine?

Approximately 65% of patients respond to initial therapy and enter histological remission; however, 80% of these patients relapse after drug withdrawal.

Albert Czaja has recently published his treatment recommendations for autoimmune hepatitis, which are as follows:

Absolute indication for treatment

a.. Incapacitating symptoms

b.. Relentless clinical progression

c.. AST greater than 10 times normal

d.. AST greater than 5 times normal and IgG greater than 2 times normal

e.. Bridging necrosis on histology

f.. Multilobular necrosis on histology


Relative indication for treatment

a.. Mild or no symptoms

b.. AST 3-9 times normal

c.. AST greater than 5 times normal and IgG less than 2 times normal

d.. Periportal hepatitis on histology


No indication

a.. Asymptomatic

b.. Previous intolerance to prednisone or azathioprine

c.. AST less than 3 times normal

d.. Severe cytopenia

e.. Inactive cirrhosis or mild portal hepatitis on histology

f.. Decompensated cirrhosis with variceal bleeding


Czaja's guidelines for single-drug therapy are as follows:

a.. Prednisone: 60 mg/d for 1 week, 40 mg/d for 1 week, 30 mg/d for 2 weeks, and 20 mg/d until reaching the treatment end point.

b.. Recommendations for combination drug therapy are prednisone: 30 mg/d for 1 week, 20 mg/d for 1 week, 15 mg/d for 2 weeks, and 10 mg/d until reaching the treatment endpoint with azathioprine: 50 mg/d until reaching the treatment end point.


Treatment endpoints: Patients may achieve 1 of 4 treatment endpoints.

a.. Complete remission is indicated by the absence of symptoms, a serum AST level less than 2 times normal, and histologic improvement to normal or minimal activity.

b.. Treatment failure is defined as a deterioration in patient condition during therapy.

c.. An incomplete patient response is defined as an improvement that is insufficient to satisfy remission criteria.

d.. Drug toxicity may occur.

e.. Patients with severe disease have a high short-term mortality rate if they fail to show normalization of at least 1 lab parameter or if pretreatment hyperbilirubinemia fails to improve during a 2-week treatment trial. In contrast, patients who improve by these parameters have an excellent immediate survival rate, and their treatment should be continued.

f.. Histologic remission tends to lag behind clinical and lab remission by 3-6 months. Follow-up liver biopsies can optimize management by avoiding medication withdrawal in patients who are not yet in histologic remission.


Treatment results

a.. Prednisone, alone or in combination with azathioprine, induces clinical, biochemical, and histologic remission in 65% of patients within 3 years. The average treatment interval until remission is 22 months. The fact that therapy improves survival rates is clear. The 10-year life expectancies for treated patients with and without cirrhosis at presentation are 89% and 90%, respectively.

b.. Patients with a histologic diagnosis of cirrhosis still may respond well to therapy and should be offered treatment in an attempt to slow disease progression.


Treatment failures and incomplete responses


a.. Nine percent of patients experience treatment failure with standard therapy. Treatment with high-dose prednisone (60 mg/d) alone or prednisone (30 mg/d) plus azathioprine (150 mg/d) is an alternative approach to therapy. Patients who are resistant to steroids can be treated with cyclosporine or tacrolimus.

b.. Thirteen percent of patients improve with standard therapy but do not achieve remission criteria. A low-dose, long-term prednisone schedule, similar to that used after relapse (10 mg/d), is reasonable. The goal of therapy is to control disease activity on the lowest dose of medication possible. Azathioprine may help to serve as a steroid-sparing agent.

c.. Patients should be referred for consideration of liver transplantation if they manifest signs of hepatic decompensation (eg, new onset of hypoalbuminemia or ascites).


Relapse

a.. Relapse occurs in 50% of patients within 6 months of treatment withdrawal and in 80% of patients within 3 years of treatment. Reinstitution of the original treatment regimen usually induces another remission; however, relapse commonly recurs after a second attempt at terminating therapy. The major consequence of relapse and retreatment is the development of drug-related complications, which occurs in 70% of patients.

b.. Patients who relapse twice require indefinite therapy with either prednisone or azathioprine. The dose is titrated as low as possible in order to prevent symptoms and to maintain AST below 5-fold normal. The median dose of prednisone required to achieve this is 7.5 mg/d. Recently, long-term therapy with azathioprine at a dose of 2 mg/kg/d was effective at maintaining remission in patients.


Treatment adverse effects

a.. Cushingoid features, acne, and hirsutism develop in 80% of patients after 2 years of treatment, irrespective of the treatment regimen. Osteoporosis with vertebral compression, diabetes, cataracts, severe emotional lability, and hypertension may develop in patients who are treated with prolonged courses of high-dose prednisone. Premature treatment withdrawal is justified in patients who develop intolerable obesity, cosmetic changes, or osteoporosis.

b.. Azathioprine can function as a steroid-sparing agent. The authors have had great success and minimal drug-related adverse effects using long-term therapy with prednisone 10 mg/d plus azathioprine 50 mg/d. Patients should be cotreated with calcium and vitamin D in order to prevent the development of steroid-induced osteoporosis. Regular exercise should be encouraged. Bone densitometry every 1-2 years should be used to monitor patients. Signs of early osteoporosis may warrant the institution of treatment with alendronate.

c.. Azathioprine therapy can be complicated by cholestatic hepatotoxicity, nausea, vomiting, rash, cytopenia, and pancreatitis. These complications occur in fewer than 10% of patients treated with azathioprine at 50 mg/d.

d.. Teratogenicity has been ascribed to treatment with azathioprine; however, the gastroenterology literature is replete with references that describe the safe use of azathioprine and 6-mercaptopurine in pregnant women with inflammatory bowel disease. Whether this observation can be extended to pregnant women with autoimmune hepatitis and whether azathioprine can be employed safely in these patients is unclear.

e.. Hematologic malignancy has been reported in patients undergoing treatment with azathioprine; however, the risk of malignancy is thought to be low in patients with autoimmune hepatitis who are treated with low doses of the drug.
The goals of pharmacotherapy are to reduce morbidity and prevent complications. Medications used include prednisone, prednisolone, and azathioprine.


Drug Category: Corticosteroids --

Drug Name

Prednisone (Deltasone, Orasone, Meticorten) -- Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and also suppresses lymphocytes and antibody production.
Adult Dose 5-60 mg/d PO qd or divided bid/qid; taper over 2 wk, as symptoms resolve
Pediatric Dose 4-5 mg/m2/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2 wk, as symptoms resolve
Contraindications Documented hypersensitivity; viral, fungal or tubercular infections, peptic ulcer disease, osteoporosis
Interactions Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin, may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteoporosis and osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use
Drug Name

Azathioprine (Imuran) -- Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, which results in lower autoimmune activity.
Adult Dose 1 mg/kg/d PO for 6-8 wk; increase by 0.5 mg/kg q4wk until response or dose reaches 2.5 mg/kg/d
Pediatric Dose Initial dose: 2-5 mg/kg/d PO/IV
Maintenance dose: 1-2 mg/kg/d PO/IV
Contraindications Documented hypersensitivity; low levels of serum thiopurine methyl transferase (TPMT)
Interactions Toxicity increases with allopurinol; concurrent use with ACE inhibitors may induce severe leukopenia; may increase levels of methotrexate metabolites and decrease effects of anticoagulants, neuromuscular blockers, and cyclosporine

Pregnancy D - Unsafe in pregnancy
Precautions Increases risk of neoplasia; caution with liver disease and renal impairment; hematologic toxicities may occur; check TPMT level prior to therapy and follow liver, renal, and hematologic function; pancreatitis rarely associated

Drug Name

Prednisolone (Delta-Cortef, Econopred, Articulose-50) -- Decreases autoimmune reactions, possibly by suppressing key components of immune system.
Adult Dose 5-60 mg/d PO/IV/IM in divided doses
Pediatric Dose 0.1-2 mg/kg/d PO/IV/IM qd or divided tid/qid
Contraindications Documented hypersensitivity; viral, fungal or tubercular infections, peptic ulcer disease, osteoporosis
Interactions Decreases effects of salicylates and toxoids (for immunizations); phenytoin, carbamazepine, barbiturates, and rifampin decrease the effect of corticosteroids

Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Caution in hyperthyroidism, osteoporosis, cirrhosis, nonspecific ulcerative colitis, peptic ulcer, diabetes, and myasthenia gravis



Generic Name
Brand Name(S)

Azathioprine
Imuran

Corticosteroids

Chlorphenirahine
Piriton

Cyclosporin
Neoral, Sandimmun, SangCya

Diuretics

Mycophenolate
CellCept

Omeprazole
Losec

Phytomenadione (Vit K)
Konakion

Prednisolone
Precortisyl Forte, Prednesol

Ranitidine
Zantac

Spironolactone
Aldactone

Sucralfate
Antepsin

Tacrolimus
Prograf

Ursodeoxycholic Acid
Destolit, Urdox, Ursofalk, Ursogal

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Azathioprine

Explanation: It is a powerful CYTOTOXIC and IMMUNOSUPPRESSANT drug. It is mainly used to reduce tissue rejection in transplant patients, but it can also be used to treat myasthenia gravis, rheumatoid arthritis, ulcerative colitis and several autoimmune diseases.
Possible Side-Effects: Hypersensitivity reactions including dizziness, malaise, vomiting, fever, muscular pains and shivering, joint pain, jaundice, heart arrhythmias, low blood pressure (requiring withdrawal of treatment), symptoms of bone marrow suppression, which should be reported (eg bleeding or bruising), hair loss, increased susceptibility to infections, nausea, pneumonia and pancreatitis.


Corticosteroids

Explantion: Steroid hormone secreted by the cortex (outer part) of the adrenal glands, or are synthetic substances that closely resemble the natural forms. There are two main types, glucocorticoids and mineralocorticoids. The latter assist in maintaining the salt-and water balance of the body. Corticosteroids such as the glucocorticoid HYDROCORTISONE and the mineralocorticoid FLUDROCORTISONE ACETATE can be given to patients for replacement therapy where there is a deficiency, or in Addison's disease, or following adrenalectomy or hypopituitarism. The glucocorticoids are potent ANTI-INFLAMMATORY and ANTI-ALLERGIC drugs and are frequently used to treat inflammatory and/or allergic reactions of the skin, airways and elsewhere. COMPOUND PREPARATIONS are available that contain both an ANTIBACTERIAL or ANTIFUNGAL drug with an anti-inflammatory corticosteroid and can be used in conditions where an infection is also present. However, these preparations must be used with caution because the corticosteroid component diminishes the patient's natural immune response to the infective agent. Absorption of a high dose of corticosteroid over a period of time may also cause undesirable, systemic side-effects.
Possible Side-Effects: Mineralocorticoid adverse effects include hypertension, sodium and water retention and potassium loss. Glucocorticoid adverse effects include diabetes, osteoporosis, avascular necrosis, mental disturbances, euphoria, muscle wasting and possibly peptic ulceration. Corticosteroids may also cause Cushing's syndrome, suppressed growth in children and adrenal atrophy. If administered during pregnancy, they may affect adrenal gland development in the child. Suppression of the sympoms of infection may occuR.



Chlorphenirahine

Explantion: Is an ANTIHISTAMINE drug. It is used to treat the symptoms of allergic conditions such as hay fever and urticaria (itchy skin rash) and is also occasionally used in emergencies to treat anaphylactic shock. Administration is either oral as tables or a syrup, or by injection.
Side-effects: Because of its sedative side-effects, the performance of skilled tasks such as driving may be impaired. Injections may be irritant and cause short-lasting hypotension and stimulation of the central nervous system.



Cyclosporin

Explantion: It is an IMMUNOSUPPRESSANT drug, which is particularly to limit tissue rejection during and following organ transplant surgery. It can also be used to treat severe, active rheumatoid arthritis and some skin conditions such as severe, resistant atopic dermatitis and) under special supervision) psoriasis. It has very little effect on the blood-cell producing capacity of the bone marrow, but does have liver toxicity.
Possible Side-Effects: Include changes in blood enzymes, disturbances in liver, kidney and cardiovascular function, excessive hair growth, gastrointestinal disturbances, tremor, gum growth, oedema (accumulation of fluid in the tissues), fatigue and burning sensations in the hands and feet.



Duretics

Explantion: Drugs used to reduce fluid in the body by increasing the excretion of water and mineral salts by the kidney, so increasing urine production.



Mycophenolate

Explantion: see Cyclosporin
Possible Side-Effects: Diarrhoea, vomiting, constipation, nausea, dyspepsia, abdominal pain, dizziness, insomnia, headache, tremor.



Omeprazole

Explantion: Is an ulcer-healing drug. It works by being a proton-pump inhibitor and so interferes with the secretion of gastric acid from the parietal cells of the stomach lining. It is used for the treatment of benign gastric and duodenal ulcers.
Possible Side-Effects: Diarrhoea or constipation, nausea, flatulence; dizziness, headaches, sleep disorders, disturbances of vision, hair loss, skin and mood disorders (some of these last side-effects occur only in the very ill).



Phytomenadione (Vit K)
Explantion: Is a natural form of Vitamin K and is normally obtained from vegetables and dairy products. Phytomenadione can be used to treat Vit K deficiency, but not a deficiency caused by malabsorption states. Administration is either oral in the form of tables or by slow intravenous injection.
Possible Side-effects: there may be liver damage if high doses are taken for a long period.


Prednisolone

Explantion: It is a synthetic, glucocorticoid CORTICOSTEROID with ANTI-INFLAMMATORY properties. It is used in the treatment of a number of rheumatic and allergic conditions (particularly those affecting the joints or lungs) and collagen disorders. It is also an effective treatment for ulcerative colitis, inflammatory bowel disease, Crohn's disease, rectal or anal inflammation, haemorrhoids and as an IMMUNOSUPPRESSANT in the treatment of myasthenia gravis. It may also be used for systemic corticosteroid therapy.
Possible Side-Effects: See Corticosteroids


Ranitidine

Explantion: Is an effective and extensively prescribed H2-antagonist and ulcer-healing drug. It is used to assist in the treatment of benign peptic (gastric and duodenal) ulcers, to relieve heartburn in cases of reflux oesophagitis (caused by regurgitation of acid and enzymes into the oesophagus).
Possible Side-Effects: Tiredness, rash, dizziness, headache or confusion.


Spironolactone

Explantion: Is a diuretic drug of the aldosterone-antagonist type. It is also potassium-sparing and so can be used in conjunction with other types of diuretic, such as the thiazides, which cause loss of potassium, to obtain a more beneficisal action. It can be used to treat oedema (accumulation of fluid in the tissues) associated with aldosteronism (abnormal production of aldosterone by the adrenal gland), in congestive heart failure treatment, kidney disease and fluid retention and ascites caused by liver disease.
Possible Side-Effects: Gastrointestinal disturbances, impotence and gynaecomastia (enlargements of breats) in men; irregular periods in women; skin rashes, raised blood potassium and lowered blood sodium levels.



Sucralfate

Explantion: Is a drug that is a complex of aluminium hydroxide and sulphated sucrose. It can be used as a long-term treatment of gastric and duodenal ulcers. It has very little antacid action, but is thought to work as a cytoprotectant by forming a barrier over an ulcer, so protecting it from acid and the enzyme pepsin and allowing it to heal.
Possible Side-Effects: Constipation, diarrhoea, nausea, indigestion, gastric discomfort, dry mouth, skin rash and itching.



Tacrolimus

Explantion: It is a IMMUNOSUPPRESSANT drug (a MACROLIDE ANTIBIOTIC) that is used particularly to limit tissue rejection during and following organ transplant surgery (particularly of liver or kidney).
Possible Side-Effects: See Cyclosporin



Ursodeoxycholic Acid

Explantion: A drug that can dissolve some gallstones in situ. Administration is oral in the form of capsules or tablets.
Possible Side-Effects: Diarrhoea and itching, mid liver dysfunction and changes in blood enzymes.




Surgical Care:

a.. Liver transplantation

a.. This procedure is an effective form of therapy for patients with decompensated cirrhosis caused by autoimmune hepatitis. This procedure also may be used to rescue patients who present with fulminant hepatic failure secondary to autoimmune hepatitis.
a.. The long-term outlook after liver transplantation is excellent, with 5-year survival rates reported at 90% or more. Positive autoantibodies and hypergammaglobulinemia tend to disappear within 2 years of transplantation.
a.. Recurrence of autoimmune hepatitis is uncommon after liver transplantation. It has been reported primarily in inadequately immunosuppressed patients and HLA DR3-positive recipients of HLA DR3-negative donors.
Diet:

a.. Patients with acute autoimmune hepatitis and symptoms of nausea and vomiting may require intravenous fluids and even total parenteral nutrition; however, most patients can tolerate a regular diet. A high caloric intake is desirable.
a.. Patients with cirrhosis secondary to autoimmune hepatitis may develop ascites. A low salt diet (generally <2000 mg of sodium per d) is mandatory in these individuals. Patients should continue to consume protein (ie, >1.1 g protein/kg body weight), given the catabolic nature of the disease and patients' high risk for developing muscle wasting.
Activity: Most patients do not need hospitalization, although this may be required for clinically severe illness. Forced and prolonged bed rest is unnecessary, but patients may feel better with restricted physical








DHEA is a natural hormone, and it is produced in our body by the adrenal glands. DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells. Our body produces less DHEA as we get older. DHEA dietary supplements have been used for a variety of health benefits: To deter aging, improve sexual function/erectile dysfunction, treat cognitive decline, enhance athletic performance, facilitate weight loss, improve strength, prevent osteoporosis, enhance immunomodulation for rheumatic conditions, and treat depression.



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