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

Twenty-four hour urine and spot urine samples from 29 patients with metabolic acidosis were collected for evaluation of urine ammonium in relation to urine anion gap, urine osmolal gap (OG) and modified urine osmolal gap (MOG). Their underlying diseases included SLE in 8, RTA in 7, CRF in 6, RPGN in 2 (one with SLE), Lowe syndrome in 2, on acetazolamide in 2, gastroenteritis in 2, and CAH in one. Twenty-three patients had normal serum anion gap (< 14 mmol/L). Their mean CO2 was 13.77 (9.4-17.9) mmol/L, net acid excretion (NAE) was 33.18 +/- 35.36 mmol/24 hour, NH+4 excretion was 29.16 +/- 31.97 mmol/24 hour. Neither the 24-hour urine nor spot urine anion gap correlated with corresponding urine NH+4 with or without adding urine HCO-3 in the calculation. Spot urine NH+4 correlated well with urine OG (r2 = 0.82, p < 0.001) and less with MOG (r2 = 0.339, p < 0.006). The urine osmolality was well correlated with the sum of 2 (Na+ + K+ + NH+4) + urea for both spot (r2 = 0.990, p < 0.001) and 24 hour urine (r2 = 0.907, p < 0.001) collection. Twenty-four hour urine NH+4 did not correlate with the OG or the MOG. There was no correlation between spot urine NH4/Cr ratio and 24 hour urine NH4/Cr ratio (r2 = 0.243, p = 0.53) nor between spot NAE/Cr ratio and 24 hour urine NAE/Cr ratio (r2 = 0.380, p = 0.014). Therefore in the presence of low urine NH+4 (< 100 mmol/L), urine osmolal gap may be used to determine urine NH+4 indirectly with good correlation. Twenty-four hour urine collection is still necessary to assess renal acidification.
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PMID:Comparison of urine anion gap, urine osmolal gap and modified urine osmolal gap in assessing the urine ammonium in metabolic acidosis. 1073 May 27

Listeria meningitis, a rare but life-threatening infection in patients with systemic lupus erythematosus, often represents a diagnostic and therapeutic challenge because of its rarity and non-representative manifestations. L. monocytogenes is an intracellular pathogen capable of spreading directly from cell to cell without exposure to the extracellular humoral immune system. With the evolving trend of intense immunosuppressive therapy, patients with SLE usually have abnormal cell-mediated immunity and are susceptible to L. monocytogenes infections. The gastrointestinal tract is usually the portal of entry, and a transient gastroenteritis may precede the full-blown meningitides. Ampicillin and penicillin G are the drugs of choice. For patients who are allergic to penicillin, trimethoprim-sulfamethoxazole is an eligible alternative. Delay in diagnosis and inappropriate antibiotics are detrimental to the outcome. Herein, we report a young woman with systemic lupus erythematosus who developed listeria meningitis. Clinicians are advised to be aware of the clinical presentations of this disease.
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PMID:Listeria monocytogenes meningitis in a young woman with systemic lupus erythematosus. 2066 57

Increased susceptibility to infection has long been observed among patients with systemic lupus erythematosus, and still represents a chief cause of morbidity and mortality in these patients. This is due in part to the severity of infection and to the difficulty of early diagnosis owing to the similarity between SLE flares and infection. Epidural infection is an uncommon condition, and a most rare condition caused by salmonella, which accounts for a broad spectrum of human illnesses from gastroenteritis and typhoid fever to the asymptomatic carrier state. We report the first case of epidural abscess caused by Salmonella enteritidis in a female with SLE with protean manifestations treated by intravenous antibiotics and surgery with full recovery of neurological symptoms, illustrating the importance of performing an early diagnosis and prompt treatment.
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PMID:Epidural abscess due to Salmonella enteritidis in a patient with systemic lupus erythematosus. 2273 47

We describe a previously healthy 9-year-old girl who had multiple purpura several days after acute adenovirus gastroenteritis and mycoplasma pneumonia. Initial laboratory evaluation revealed a prolonged prothrombin time (PT) and APTT, low complement levels (C4, CH50), and positive immune complex (C1q) in her serum. Platelet count, fibrinogen, and other routine blood chemistry tests were normal. The prolonged APTT was not corrected by mixture of the patient's plus normal plasma. Clotting activities of factors II, V, VIII, IX, X, XI, and XII reduced. Further examinations revealed the presence of lupus anticoagulant (LA), phosphatidylserine-dependent anti-prothrombin antibodies (aPS/PT), and anticardiolipin antibodies. Mycoplasma pneumonia was treated by minocycline and the patient's skin lesions disappeared spontaneously within a week. During follow-up, she showed no other bleeding symptoms, and no signs of SLE or other autoimmune diseases. Four weeks after admission to our hospital, blood coagulation tests and serum complements normalized. Clotting activities of factors and antiphospholipid antibodies were not detected, half year later. The bleeding in this case was associated with acquired hypoprothrombinemia caused by antiphospholipid antibodies following acute adenovirus gastroenteritis and mycoplasma pneumonia.
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PMID:[A case of lupus anticoagulant hypoprothrombinemia syndrome following adenovirus gastroenteritis and mycoplasma pneumonia]. 2459 69

Hepatitis A virus is a common cause of acute viral hepatitis in India, due to lack of clean water and sanitation. Usual presentations include gastroenteritis or a viral respiratory infection. Hepatitis A has a variety of extra-hepatic manifestations which, if failed to be recognized, evades diagnosis. A 28-year-old lady presented with pain abdomen for 1 week, fever with rashes for 1 day. Patient was febrile at the time of examination. Rash was maculopapular with irregular edges, tender. On examining abdomen, tenderness noted in right hypochondrium and epigastrium with hepatomegaly. Patient was then admitted. Working diagnosis was Viral hepatitis for evaluation. Hepatitis A serology was sent which came positive for Ig M. Patient was treated with IV fluids, bile acid sequestrants, IV PPI, IV and oral antibiotics, antihistamines and 3 doses of injection Vit K. Calamine lotion was also given for skin care. Patient improved symptomatically in 2 days and was discharged after 3 days of hospital stay. In our case, the maculopapular rash spreading to the whole body was the major presenting symptom. The presentation of Hepatitis A with rashes maybe seen in around 10% of patients with extrahepatic manifestations along with arthralgia. Differential diagnosis in this case should be erythema multiforme which is the most common maculopapular eruptive rash. Other viral hepatitis causing agents (Hepatitis B&E) have been documented to present with rashes. SLE and Kawasaki disease rarely present with fever with rash with nonspecific multisystemic involvement. Borrelia, Leptospira also have icterus in their presentations. Early diagnosis and management in this case prevented complication such as autoimmune hepatitis, pleural effusion, ascites acute kidney injury. This case presentation urges the need to consider Hepatitis A to be an important differential diagnosis of fever with rash especially in tropical/sub-tropical countries with poor sanitation.
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PMID:Hepatitis A: A refreshing perspective through a rare symptom in a teaching hospital in south India. 3310 63