Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A common reason for referring patients to hepatologists is persistently abnormal serum transaminase levels with vague constitutional symptoms. In the United Kingdom, these abnormalities are most often caused by a fatty liver either related to obesity or alcohol abuse; they are less commonly caused by chronic liver disease, particularly chronic viral hepatitis, autoimmune hepatitis, or chronic biliary disease. Endocrine disease is rarely a cause of these abnormalities, although hypothyroidism and hyperthyroidism are well-recognized causes. Addison's disease has been only reported once in the literature by R. G. Olsson as a cause of increased transaminase levels associated with constitutional symptoms; it is not mentioned in textbooks on hepatology. Three patients with Addison's disease are reported here, all of whom had increased serum transaminase levels for more than 6 months before the recognition of the hypoadrenalism with resolution to normal after steroid replacement. Hepatologists should consider subclinical Addison's disease as a cause of persistently increased transaminase levels with constitutional symptoms in the absence of evidence for fatty liver as well as viral and autoimmune markers.
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PMID:Subclinical Addison's disease: a cause of persistent abnormalities in transaminase values. 755 2

Seventy-two long-surviving liver transplant recipients were evaluated prospectively, including a baseline allograft biopsy for weaning off of immunosuppression. Thirteen were removed from candidacy because of chronic rejection (n = 4), hepatitis (n = 2), patient anxiety (n = 5), or lack of cooperation by the local physician (n = 2). The other 59, aged 12-68 years, had stepwise drug weaning with weekly or biweekly monitoring of liver function tests. Their original diagnoses were PBC (n = 9), HCC (n = 1), Wilson's disease (n = 4), hepatitides (n = 15), Laennec's cirrhosis (n = 1), biliary atresia (n = 16), cystic fibrosis (n = 1), hemochromatosis (n = 1), hepatic trauma (n = 1), alpha-1-antitrypsin deficiency (n = 9), and secondary biliary cirrhosis (n = 1). Most of the patients had complications of long-term immunosuppression, of which the most significant were renal dysfunction (n = 8), squamous cell carcinoma (n = 2) or verruca vulgaris of skin (n = 9), osteoporosis and/or arthritis (n = 12), obesity (n = 3), hypertension (n = 11), and opportunistic infections (n = 2). When azathioprine was a third drug, it was stopped first. Otherwise, weaning began with prednisone, using the results of corticotropin stimulation testing as a guide. If adrenal insufficiency was diagnosed, patients reduced to < 5 mg/day prednisone were considered off of steroids. The baseline agents (azathioprine, cyclosporine, or FK506) were then gradually reduced in monthly decrements. Complete weaning was accomplished in 16 patients (27.1%) with 3-19 months drug-free follow-up, is progressing in 28 (47.4%), and failed in 15 (25.4%) without graft losses or demonstrable loss of graft function from the rejections. This and our previous experience with self-weaned and other patients off of immunosuppression indicate that a significant percentage of appropriately selected long-surviving liver recipients can unknowingly achieve drug-free graft acceptance. Such attempts should not be contemplated until 5-10 years posttransplantation and then only with careful case selection, close monitoring, and prompt reinstitution of immunosuppression when necessary.
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PMID:Weaning of immunosuppression in long-term liver transplant recipients. 783 42

We report the first case of recurrent hepatitis secondary to a pituitary macroadenoma in a 55-year old man. Liver ischemia is thought to be the main consequence of episodes of acute adrenal insufficiency. Sudden acute adrenal insufficiency was due to enlargement of the sella content secondary to several microhemorrhages in the macroadenoma.
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PMID:[Hepatic ischemia and hypophyseal macroadenoma]. 1021 16

Two cases of young healthy males presenting with cardiac tamponade and developing clinical adrenal insufficiency within a few weeks are described. On presentation they had a brisk inflammatory response with complement activation. Both had signs of subclinical hepatitis, and both have later shown evidence of thyroid involvement. The possibility of a connection between pericarditis and adrenal insufficiency is discussed.
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PMID:Cardiac tamponade preceding adrenal insufficiency--an unusual presentation of Addison's disease: a report of two cases. 1049 30

Lisa Capaldini, a physician who treats patients with HIV-related fatigue, discusses symptoms, diagnosis techniques, and treatments of depression, anemia, and various other roots of fatigue in HIV-positive patients. Biochemical depression, caused by abnormal levels of serotonin and norepinephrine in the brain, is easily misdiagnosed or overlooked. Physical and emotional symptoms of depression mirror common effects of HIV such as exhaustion, anger, and irritability. Knowing the history of depression prior to HIV infection, including previous drug abuse and family history of depression, will help to diagnose fatigue. Dr. Capaldini recommends antidepressants provided the condition is properly diagnosed and the side effects are not harmful to the patient. Selective serotonin reuptake inhibitors (SSRI), the most frequently prescribed antidepressants, can cause short term sexual dysfunction. Bupropion and Wellbutrin can be prescribed to avoid this side effect. Psychotherapy can be effective if therapists are familiar with HIV disease and can distinguish between symptoms brought on by behavior, addictive habits, or pre-existing depression. Consideration also must be given to drug interactions, particularly with the antiretrovirals ritonavir and delavirdine, which can cause seizures or disturb cardiac rhythm. Anemia is most noticeable after physical exertion, and symptoms are more evident based on the increased rate that red blood cells move out of the normal range. To determine the course of treatment, physicians need to clarify the cause of anemia. Anemia can be caused by drugs, vitamin deficiencies, or other nutritional problems. Adrenal insufficiency, methemoglobinemia, and malnutrition are also causes of fatigue. Diagnosing fatigue due to hepatitis B or C, rather than HIV, can be achieved by measuring hepatitis levels and observing T cell counts and viral load. Dr. Capaldini suggests that proper diet and exercise prevent fatigue from getting worse.
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PMID:Fatigue and HIV: interview with Lisa Capaldini, M.D. Part II. Interview by John S. James. 1136 84

This report describes a 60-yr-old white male presenting with decompensated liver cirrhosis. He had a history of Addison's disease for 36 yr, primary hypothyroidism for 5 yr, and moderate alcohol consumption. His laboratory studies and a liver biopsy supported the diagnosis of autoimmune hepatitis. Furthermore, he was found to be heterozygous for the piZ allele of the alpha1-antitrypsin gene with normal serum alpha1-antitrypsin levels and absence of pulmonary affection. Mucosal biopsies revealed moderately severe atrophic gastritis; however, signs of pernicious anemia were missing. An association of autoimmune hepatitis with endocrine disorders and atrophic gastritis has been described. Long term hydrocortisone therapy for his adrenal insufficiency may have prevented a faster course of the liver disease, whereas the heterozygous alpha1-antitrypsin deficiency and moderate alcohol consumption constituted additional risk factors ultimately leading to the development of cirrhosis.
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PMID:A patient with autoimmune hepatitis type I, Addison's disease, atrophic thyroiditis, atrophic gastritis, exocrine pancreatic insufficiency, and heterozygous alpha1-antitrypsin deficiency. 1200 88

A 56 year old man was admitted cause he had increasing symptoms as weakness, lethargy, disorientation. The total eosinophil count was 3000/mm3, the serum sodium concentration was 120 mmol per litre. In spite of severe hyponatriemia, urinary sodium excretion was not suppressed and serum osmolality (240 mOsm/Kg was lower than urine osmolality (488 mOsm/Kg). SIADH and Idiopathic Hypereosinophilic Syndrome was diagnosed because we found systemic failure signs due to hypereosinophilia (hepatitis, gastritis, pulmonary hypertension, and encefalopathy). Cortisonic treatment was started with symptoms improving, natriemia, eosynophil count and hepatitis signs normalization. After treatment stopping, reappeared asymptomatic hypereosinophilia, than we choosed Idrossiurea but, non-standing hypereosinophilia disappeared, appeared signs of preexisting adrenal insufficiency, emphasized by stopping cortisone therapy. A RMN showed an hypofiseal adenoma. Many cases of SIADH and Hypereosinophilia hiding adrenocortical insufficiency are reported with severe and unusual hypereosinophilia.
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PMID:[Association of hyponatremia and eosinophilia: correlated idiopathic hypereosinophilic syndrome and SIADH or adrenal insufficiency with secondary eosinophilia]. 1285 64

Autoimmune polyglandular syndrome type 1 (APS-1) is an autosomal recessive disorder characterized by chronic mucocutaneous candidiasis, autoimmune hypoparathyroidism, and primary adrenal insufficiency. It has recently been associated with mutations of a single gene found on chromosome 21, designated AutoImmune Regulator (AIRE). We report two patients with APS-1 referred to our hospital for evaluation. The first patient was an 11-year-old girl with hypoparathyroidism, infectious or immunological malabsorption, and autoimmune hepatitis. Hypoparathyroidism associated with other processes with a probable autoimmune origin suggested APS-1. Genetic study was performed revealing deletion of 13 base pairs in exon 8 of the AIRE gene. The second patient was a 17-year-old girl with autoimmune hepatitis, hypoparathyroidism, mucocutaneous candidiasis, nail dystrophy, and obliterating bronchiolitis with a probable autoimmune origin. We suspected APS-1 and genetic study was performed. The only finding was an AIRE gene polymorphism. In conclusion, the presence of a single disease criterion is sufficient to suspect APS-1 and to indicate genetic study. Further studies are required to confirm the involvement of other genes in the development of this disease.
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PMID:[AIRE gene mutation in polyglandular syndrome type 1]. 1679 67

Cholestatic hepatitis is identified as one of the features of hypopituitarism in the newborn, but the exact etiology of cholestasis in these cases has not been well established yet. We report here two infants, one with isolated glucocorticoid deficiency and the other with multiple pituitary hormone deficiency, indicating primary and central adrenal insufficiency, respectively, who presented with recurrent hypoglycemic seizures and cholestatic hepatitis. Severe cortisol deficiency in these cases was suggested to be the cause of cholestatic hepatitis. Review of the literature and our cases showed that the cortisol deficiency in both primary and central adrenal insufficiency occurring only during neonatal and early infancy period cause cholestatic hepatitis. The severity and the age of onset of cortisol deficiency are suggested to be the important predictors of cholestatic hepatitis in childhood.
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PMID:Cholestatic hepatitis as a result of severe cortisol deficiency in early infancy: report of two cases and review of literature. 1729 May 78

The large hyperaemic foetal adrenal gland is vulnerable to vascular damage. This may occur in the neonatal period as a consequence of difficult labour, or its aetiology may not be apparent. The spectrum of presentation is considerable, ranging from asymptomatic to severe life-threatening intra-abdominal haemorrhage. The presentation of adrenal insufficiency may be delayed but the regenerative capacity of the adrenal is great, and most adrenal haemorrhage is not associated with significantly impaired function. Some reports showed that cholestatic hepatopathy with congenital hypopituitarism reversed by hydrocortisone treatment is considered in the context of the endocrine syndrome, probably as a consequence of the adrenal failure. We describe a case of bilateral adrenal haemorrhage with hepatitis syndrome and persistent hypoglycaemia in a newborn male with striking features of neonatal cholestasis and adrenal crisis.
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PMID:Adrenal haemorrhage with cholestasis and adrenal crisis in a newborn of a diabetic mother. 1745 Oct 84


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