Search Results

You are looking at 1 - 10 of 32 items for :

  • Alanine aminotransferase x
Clear All
Open access

Takatoshi Anno, Hideaki Kaneto, Ryo Shigemoto, Fumiko Kawasaki, Yasuhiro Kawai, Noriyo Urata, Hirofumi Kawamoto, Kohei Kaku and Niro Okimoto

.93 Insulin-like growth factor 1 (ng/mL) ≤10 ≤10 Total Bilirubin (mg/dL) 0.4–1.5 1.7 2.2 Aspartate aminotransferase (U/L) 13–30 1102 2363 Alanine aminotransferase (U/L) 10–42 401 1797 Alkaline phosphatase (U

Open access

Carine Ghassan Richa, Khadija Jamal Saad, Ali Khaled Chaaban and Mohamad Souheil El Rawas

% neutrophils), alanine aminotransferase of 116 (normal range: 7–56 IU/L), aspartate aminotransferase of 60 (normal range: 5–40 IU/L), alkaline phosphatase of 140 IU/L (normal range: 44–147 IU/L), gamma-glutamyl transpeptidase of 62 (normal range: 9–48 IU

Open access

Charlotte S Schömig, Marie-Ève Robinson and Julia E von Oettingen

phosphatase (U/L) Alanine amino-transferase (U/L) 12 126.5 (H) 40.6 (H) 42 119.5 (H) 78.8 (H) 52 83.9 (H) 53.9 (H) 318 (H) 332 100 (H) 55 96.8 (H) 57.9 (H) 285 (H) 367 114 (H) 67 39

Open access

Yuri Tanaka, Taisuke Uchida, Hideki Yamaguchi, Yohei Kudo, Tadato Yonekawa and Masamitsu Nakazato

jugular veins, and bilateral pretibial pitting edema. Blood tests showed extremely high levels of aspartate transaminase and alanine aminotransferase (1458 and 555 U/L, respectively), renal failure, hypoglycemia, coagulopathy, and hyperammonemia ( Table 1

Open access

Baris Akinci, Rasimcan Meral, Diana Rus, Rita Hench, Adam H Neidert, Frank DiPaola, Maria Westerhoff, Simeon I Taylor and Elif A Oral

phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; CK, creatine kinase; FSH, follicle stimulating hormone; FT3, free triiodothyronine; FT4, free thyroxine; GAD, glutamic acid decarboxylase; GGTP, gamma-glutamyl transpeptidase; HDL

Open access

Snezana Burmazovic, Christoph Henzen, Lukas Brander and Luca Cioccari

 pO2 4.68 11.07–14.4 kPa  Bicarbonate 25.3 22–26 mmol/L  Lactate 1.3 0.5–1.6 mmol/L * Denotes abnormal values. ALT, alanine aminotransferase; INR, international normalized ratio; LDH, lactate dehydrogenase

Open access

Clarissa Ern Hui Fang, Mohammed Faraz Rafey, Aine Cunningham, Sean F Dinneen and Francis M Finucane

glomerular filtration rate of 26 mL/min 1.73/m 2 . Because of his altered level of consciousness, we performed CT and MRI brain and then lumbar puncture, all of which were normal. We noted an elevated alanine aminotransferase (ALT) level, most likely due to

Open access

Anthony Logaraj, Venessa H M Tsang, Shahrir Kabir and Julian C Y Ip

Summary

Adrenal haemorrhage is a rare cause of adrenal crisis, which requires rapid diagnosis, prompt initiation of parenteral hydrocortisone and haemodynamic monitoring to avoid hypotensive crises. We herein describe a case of bilateral adrenal haemorrhage after hemicolectomy in a 93-year-old female with high-grade colonic adenocarcinoma. This patient’s post-operative recovery was complicated by an acute hypotensive episode, hypoglycaemia and syncope, and subsequent computed tomography (CT) scan of the abdomen revealed bilateral adrenal haemorrhage. Given her labile blood pressure, intravenous hydrocortisone was commenced with rapid improvement of blood pressure, which had incompletely responded with fluids. A provisional diagnosis of hypocortisolism was made. Initial heparin-induced thrombocytopenic screen (HITTS) was positive, but platelet count and coagulation profile were both normal. The patient suffered a concurrent transient ischaemic attack with no neurological deficits. She was discharged on a reducing dose of oral steroids with normal serum cortisol levels at the time of discharge. She and her family were educated about lifelong steroids and the use of parenteral steroids should a hypoadrenal crisis eventuate.

Learning points:

  • Adrenal haemorrhage is a rare cause of hypoadrenalism, and thus requires prompt diagnosis and management to prevent death from primary adrenocortical insufficiency.
  • Mechanisms of adrenal haemorrhage include reduced adrenal vascular bed capillary resistance, adrenal vein thrombosis, catecholamine-related increased adrenal blood flow and adrenal vein spasm.
  • Standard diagnostic assessment is a non-contrast CT abdomen.
  • Intravenous hydrocortisone and intravenous substitution of fluids are the initial management.
  • A formal diagnosis of primary adrenal insufficiency should never delay treatment, but should be made afterwards.
Open access

V Larouche and M Tamilia

Summary

Enteroviruses, including coxsackieviruses and Echovirus, are well known pathogens responsible for the development of thyroiditis. We describe the case of a 49-year-old woman with no personal or family history of thyroid disease who presented to the emergency room with a two-week history of daily fevers up to 39°C, a sore throat, occasional palpitations and diaphoresis, decreased appetite and an unintentional 10 kg weight loss over the same time course Physical examination revealed mild tachycardia, an intention tremor and a normal-sized, nontender thyroid gland without palpable nodules. The remainder of the physical examination was unremarkable and without stigmata of Graves’ disease. Her initial blood tests revealed overt thyrotoxicosis, elevated liver enzymes, an elevated C-reactive protein, a negative monospot and a positive CMV IgM antibody. Thyroid sonography revealed areas of hypoechogenicity and relatively low vascularity. Fine-needle biopsy showed a lymphocytic infiltrate. The patient was treated symptomatically with propranolol. On follow-up, the patient became euthyroid, and her liver enzymes normalised. Previous cases of CMV-induced thyroiditis occurred in immunosuppressed patients. This is the first reported case of a CMV-mononucleosis-induced thyroiditis in an immunocompetent adult patient and serves as a reminder that viral illnesses are a common cause of thyroiditis with abnormal liver enzymes.

Learning points:

  • The differential diagnosis of thyrotoxicosis with abnormal liver enzymes includes severe hyperthyroidism and thyroid storm caused by Graves’ disease as well as the thyrotoxic phase of a thyroiditis, usually caused by a virus such as coxsackievirus or, in this case, cytomegalovirus.
  • Cytomegalovirus appears to be a recently recognized causal agent for thyroiditis, both in immunosuppressed and immunocompetent patients.
  • Careful follow-up of thyroid function tests in patients with thyroiditis allows clinicians to determine if patients’ thyroid hormone secretion normalizes or if they remain hypothyroid.
Open access

Nobuhiro Miyamura, Shuhei Nishida, Mina Itasaka, Hirofumi Matsuda, Takeshi Ohtou, Yasuhiro Yamaguchi, Daisuke Inaba, Sadahiro Tamiya and Tetsuo Nakano

Summary

Hepatitis C-associated osteosclerosis (HCAO), a very rare disorder in which an extremely rapid bone turnover occurs and results in osteosclerosis, was acknowledged in 1990s as a new clinical entity with the unique bone disorder and definite link to chronic type C hepatitis, although the pathogenesis still remains unknown. Affected patients suffer from excruciating deep bone pains. We report the 19th case of HCAO with diagnosis confirmed by bone biopsy, and treated initially with a bisphosphonate, next with corticosteroids and finally with direct acting antivirals (DAA: sofosbuvir and ribavirin) for HCV infection. Risedronate, 17.5 mg/day for 38 days, did not improve the patient’s symptoms or extremely elevated levels of bone markers, which indicated hyper-bone-formation and coexisting hyper-bone-resorption in the patient. Next, intravenous methylprednisolone pulse therapy followed by high-dose oral administration of prednisolone evidently improved them. DAA therapy initiated after steroid therapy successfully achieved sustained virological response, but no additional therapeutic effect on them was observed. Our results strongly suggested that the underlying immunological alteration is the crucial key to clarify the pathogenesis of HCAO. Bone mineral density of lumbar vertebrae of the patient was increased by 14% in four-month period of observation. Clarification of the mechanisms that develop osteosclerosis in HCAO might lead to a new therapeutic perspective for osteoporosis.

Learning points:

  • HCAO is an extremely rare bone disorder, which occurs exclusively in patients affected with HCV, of which only 18 cases have been reported since 1992 and pathogenesis still remains unclear.
  • Pathophysiology of HCAO is highly accelerated rates of both bone formation and bone resorption, with higher rate of formation than that of resorption, which occur in general skeletal leading to the diffuse osteosclerosis with severe bone pains.
  • Steroid therapy including intravenous pulse administration in our patient evidently ameliorated his bone pains and reduced elevated values of bone markers. This was the first successful treatment for HCAO among cases reported so far and seemed to propose a key to solve the question for its pathogenesis.
  • The speed of increase in the bone mineral content of the patient was very high, suggesting that clarification of the mechanism(s) might lead to the development of a novel therapy for osteoporosis.