Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017160 (gastroenteritis)
11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 75-year-old man, with a long history of recurrent lymphoplasmacytoid lymphoma, presented with diffuse large-cell lymphoma affecting adrenal glands and causing severe hypoadrenalism. The lymphoma responded to rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone (R-CHOP) chemotherapy. Seven months postcompletion of chemotherapy, he developed signs of gastroenteritis and septicaemia. He deteriorated 24 h postadmission with a significant fall in Glasgow Coma Scale Score. Polymerase chain reaction testing of cerebrospinal fluid suggested enteroviral encephalitis. He responded symptomatically to intravenous immunoglobulins. His immunoglobulin levels were monitored weekly and supplemented to maintain immunoglobulin G level at 10 g/l, but in spite of this, his neurological condition deteriorated and he died after 14 weeks. Rituximab can cause prolonged B-cell deficiency. We speculate that profound immunosuppression induced by rituximab, together with previous chemotherapy, predisposed this patient to fatal enteroviral meningoencephalitis.
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PMID:Enteroviral meningoencephalitis in a patient with non-Hodgkin's lymphoma treated previously with rituximab. 1643 Apr 65

As copper sulphate pentahydrate (CSP) is a common compound used in agriculture and industry, chronic occupational exposures to CSP are well known, but acute poisoning is rare in the Western world. This case report describes acute poisoning of a 33-year-old woman who attempted suicide by ingesting an unknown amount of CSP. On admission to the hospital, she had symptoms and signs of severe hemorrhagic gastroenteritis, dehydration, renal dysfunction and methaemoglobinaemia with normal serum copper level. Therapy included early gastric lavage, fluid replacement, vasoactive drugs, furosemide, antiemetic drugs, ranitidine, and antidotes methylene blue and 2,3-dimercaptopropane-1-sulphonate (DMPS). However, the patient developed severe intravascular haemolysis, acute severe hepatic and renal failure, as well as adrenal insufficiency. After prolonged, but successful hospital treatment, including haemodialysis and IV hydrocortisone, the patient was discharged with signs of mild renal and liver impairment. Our conclusion is that in severe cases of copper poisoning early supportive measures are essential. In addition, antidotes such as methylene blue for methaemoglobinaemia and chelating agent such as DMPS improve morbidity and survival of severely poisoned victims.
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PMID:Severe acute copper sulphate poisoning: a case report. 1840 69

In patients known to have adrenal insufficiency, inadequate adjustment of the glucocorticoid dosage during intercurrent illness can be life threatening. We describe two patients with adrenal insufficiency who died after their glucocorticoid dosage was insufficiently increased during an episode of gastroenteritis and pneumonia, respectively. Another patient died after a few days of fever and vomiting of unknown origin, after a period of refusing her medication. To prevent unnecessary death from Addisonian crisis, we have developed a protocol. Patients with known adrenal insufficiency, as well as their relatives and general practitioners, should repeatedly receive verbal and written instructions on how to deal with physical and severe psychic stress. We teach the patients and their relatives how to use an emergency injection of hydrocortisone, and the patients can consult the on-call endocrinologist by telephone 24 hours a day.
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PMID:[Addisonian crisis in patients with known adrenal insufficiency: the importance of early intervention]. 1868 56

Kidney transplant patients (KTPs), and particularly those with advanced chronic kidney rejection, may be affected by opportunistic infections, metabolic alterations and vascular and oncologic diseases that promote clinical conditions that require a variety of treatments, the combinations of which may predispose them to hyponatremia. Salt and water imbalance can induce abnormalities in volemia and/or serum sodium depending on the nature of this alteration (increase or decrease), its absolute magnitude (mild or severe) and its relative magnitude (body sodium:water ratio). Hyponatremia appears when the body sodium:water ratio is reduced due to an increase in body water or a reduction in body sodium. Additionally, hyponatremia is classified as normotonic, hypertonic and hypotonic and while hypotonic hyponatremia is classified in hyponatremia with normal, high or low extracellular fluid. The main causes of hyponatremia in KTPs are hypotonic hyponatremia secondary to water and salt contraction with oral hydration (gastroenteritis, sepsis), free water retention (severe renal failure, syndrome of inappropriate antidiuretic hormone release, hypothyroidism), chronic hypokalemia (rapamycin, malnutrition), sodium loss (tubular dysfunction secondary to nephrocalcinosis, acute tubular necrosis, tubulitis/rejection, interstitial nephritis, adrenal insufficiency, aldosterone resistance, pancreatic drainage, kidney-pancreas transplant) and hyponatremia induced by medication (opioids, cyclophosphamide, psychoactive, potent diuretics and calcineurinic inhibitors). In conclusion, KTPs are predisposed to develop hyponatremia since they are exposed to immunologic, infectious, pharmacologic and oncologic disorders, the combinations of which alter their salt and water homeostatic capacity.
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PMID:Hyponatremia in kidney transplant patients: its pathophysiologic mechanisms. 3009 23

The diagnosis of adrenal insufficiency is often delayed, as the presenting symptoms of fatigue, abdominal pain, and anorexia are vague and nonspecific. However, timely diagnosis and treatment with replacement steroids are needed to prevent fatal adrenal crisis. While the most common cause of primary adrenal insufficiency in childhood is congenital adrenal hyperplasia, a significant minority (13-23%) is caused by autoimmune destruction of the gland. We present a case of a 4-year-old, previously healthy child who had a one-day history of nausea and vomiting, and was found unresponsive by her caretaker. Despite emergency rescue and transport to the hospital, she was pronounced dead. At autopsy, the adrenal glands were atrophied. Histologic examination revealed lymphocytic infiltration of the adrenal glands consistent with autoimmune adrenal insufficiency. Fecal viral antigen testing was positive for rotavirus. The cause of death was determined to be adrenal crisis in the setting of rotavirus gastroenteritis due to adrenal insufficiency (Addison disease).
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PMID:Fatal Rotavirus Infection in a 4-Year-Old with Unsuspected Autoimmune Adrenal Insufficiency. 3123 65