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Open access

Usman Javaid, Vikram Lal, Catherine Napier, Alison Burbridge and Richard Quinton

hypernatraemia ( Fig. 1 ), profuse sweating, confusion, intermittent low-grade pyrexia and reduced conscious level, all of which were initially attributed to urosepsis. There was no spontaneous oral fluid intake, but nursing staff and family were able to briefly

Open access

Maria Tomkins, Roxana Maria Tudor, Diarmuid Smith and Amar Agha

examination, she had a low-grade pyrexia of 37.6°C, mild diffusely enlarged non-tender goitre with no evidence of retrosternal extension or thyroid eye disease. She had no signs of active vasculitis with no mouth ulcers, synovitis, rash or sensory deficit. She

Open access

S Hussain, S Keat and S V Gelding

(weight 58.9 kg), with a resting tachycardia (118 bpm), low grade pyrexia (37.8°C), reduced oxygen saturation (78% on room air) and normal blood pressure of 114/79 mmHg. Examination revealed an elevated jugular venous pressure (5 cm), left-sided chest wall

Open access

R Bou Khalil, M Abou Salbi, S Sissi, N El Kara, E Azar, M Khoury, G Abdallah, J Hreiki and S Farhat

Summary

Methimazole is an anti-thyroid drug commonly used to treat hyperthyroidism and is a relatively safe medication. Several side effects have been reported and usually develop within 3 months of therapy. Well-known adverse reactions include agranulocytosis, hepatitis, skin eruptions, and musculoskeletal complaints such as myalgia, arthralgia, and arthritis. So far, myositis secondary to carbimazole was described in the context of a lupus-like syndrome or other rare cases of anti-neutrophil cytoplasmic antibodies-associated vasculitis. Methimazole-induced myositis occurring independently of such reactions was rarely stated. We report a patient with hyperthyroidism who, early after therapy with methimazole, developed hepatitis, eosinophilia, and fever that resolved completely after stopping the medication as well as a delayed onset of biopsy-proven eosinophilic myositis and fasciitis of gluteal muscles that resolved eventually without any additional therapy. Therefore, we raise the awareness regarding a rare side effect of methimazole: myositis.

Learning points

  • Several differential diagnoses arise when managing a hyperthyroid patient with muscle complaints.
  • Both hyperthyroidism and methimazole are associated with myositis.
  • Methimazole-induced myositis is a rare clinical entity.
  • Resolution of symptoms may occur after stopping methimazole.

Open access

Punith Kempegowda, Eka Melson, Gerald Langman, Fady Khattar, Muhammad Karamat and Quratul-Ain Altaf

Summary

Diabetic myonecrosis, also known as diabetic muscle infarction is a rare complication of diabetes mellitus usually associated with longstanding suboptimal glycaemic control. Although theories of atherosclerosis, diabetic microangiopathy, vasculitis, ischaemia-reperfusion injury and hypercoagulable state have been proposed to explain the pathophysiology, none of these have been able to individually explain the pathophysiology in entirety. Diabetic renal disease is the most common risk factor for developing DMN and its recurrence. The diagnosis is often missed due to lack of awareness and the presentation mimicking other conditions associated with DM. The routine laboratory investigations are often non-specific and do not provide much value in the diagnosis as well. Muscle biopsy can provide a definite diagnosis but is not currently recommended due to its invasiveness and association with prolonged time to symptoms resolution. Magnetic resonance imaging, in combination with classic history and risk factors can clinch the diagnosis. Treatment is generally analgesia and rest, although the former’s use may be limited in the presence of renal disease.

Learning points:

  • Diabetic myonecrosis is a rare complication of diabetes mellitus associated with longstanding suboptimal glycaemic control.
  • Diabetic renal disease is a known risk factor, although the evidence is merely observational.
  • Although muscle biopsy could provide a definite diagnosis, it is not recommended as it can prolong the disease process and should be reserved only for cases not responding to conventional treatment.
  • Typical MRI findings in combination with classic symptoms and risk factors can clinch the diagnosis
  • Current treatment recommendations include NSAIDs and/or aspirin (if not contraindicated) alongside bed rest. Physiotherapy is not recommended in the acute phase but should be started as soon as patient is discharged from hospital.
  • Optimal glycaemic control is key to prevent recurrence.
Open access

Melissa Katz, Simon Smith, Luke Conway and Ashim Sinha

Summary

Diabetes mellitus is a well-recognised risk factor for melioidosis, the disease caused by Burkholderia pseudomallei, which is endemic in northern Australia and Southeast Asia. We present the initial diagnostic dilemma of a febrile patient from northern Australia with type 1 diabetes mellitus and negative blood cultures. After a 6-week history of fevers and undifferentiated abdominal pain, MRI of her spine revealed a psoas abscess. She underwent drainage of the abscess which cultured B. pseudomallei. She completed 6 weeks of intravenous (IV) ceftazidime and oral trimethoprim/sulphamethoxazole (TMP/SMX) followed by a 12-week course of oral TMP/SMX. We postulate that the likely route of infection was inoculation via her skin, the integrity of which was compromised from her insulin pump insertion sites and an underlying dermatological condition.

Learning points:

  • Diabetes mellitus is the strongest risk factor for developing melioidosis.
  • Atypical infections need to be considered in individuals with diabetes mellitus who are febrile, even if blood cultures are negative.
  • There is heterogeneity in the clinical presentation of melioidosis due to variable organ involvement.
  • Consider melioidosis in febrile patients who have travelled to northern Australia, Asia and other endemic areas.
Open access

Ernesto Solá, Carmen Rivera, Michelle Mangual, José Martinez, Kelvin Rivera and Ricardo Fernandez

Summary

Diabetes mellitus was identified as a risk factor for developing tuberculosis (TB) infection, and relapse after therapy. The risk of acquiring TB is described as comparable to that of HIV population. The fact that diabetics are 3× times more prone to develop pulmonary TB than nondiabetics cannot be overlooked. With DM recognized as global epidemic, and TB affecting one-third of the world population, physicians must remain vigilant. We present a 45-year-old woman born in Dominican Republic (DR), with 10-year history of T2DM treated with metformin, arrived to our Urgency Room complaining of dry cough for the past 3months. Interview unveiled unintentional 15lbs weight loss, night sweats, occasional unquantified fever, and general malaise but denied bloody sputum. She traveled to DR 2years before, with no known ill exposure. Physical examination showed a thin body habitus, otherwise well appearing woman with stable vital signs, presenting solely right middle lung field ronchi. LDH, ESR, hsCRP and Hg A1C were elevated. Imaging revealed a right middle lobe cavitation. Sputum for AFB disclosed active pulmonary TB. Our case portrays that the consideration of TB as differential diagnosis in diabetics should be exercised with the same strength, as it is undertaken during the evaluation of HIV patients with lung cavitation. Inability to recognize TB will endanger the patient, hospital dwellers and staff, and perpetuate this global public health menace.

Learning points

  • Diabetes mellitus should be considered an important risk factor for the reactivation of pulmonary tuberculosis.
  • High clinical suspicious should be taken into consideration as radiological findings for pulmonary tuberculosis in patients with diabetes mellitus may be atypical, involving middle and lower lobes.
  • Inability to recognize pulmonary tuberculosis will endanger the patient, hospital dwellers and staff, and perpetuate this global public health menace.

Open access

Nicola Tufton, Nazhri Hashim, Candy Sze and Mona Waterhouse

Summary

A 57-year-old female presented 17 days after treatment with radioactive iodine (RAI) for difficult-to-control hyperthyroidism. She was febrile, had a sinus tachycardia, and was clinically thyrotoxic. Her thyroid function tests showed a suppressed TSH <0.02 mU/l, with free thyroxine (FT4) >75 pmol/l and total triiodothyronine (TT3) 6.0 nmol/l. She was diagnosed with thyroid storm and was managed with i.v. fluids, propylthiouracil (PTU) 200 mg four times a day, prednisolone 30 mg once daily and propanolol 10 mg three times a day. She gradually improved over 2 weeks and was discharged home on PTU with β blockade. On clinic review 10 days later, it was noted that, although she was starting to feel better, she had grossly abnormal liver function (alanine transaminase (ALT) 852 U/l, bilirubin 46 μmol/l, alkaline phosphatase (ALP) 303 U/l, international normalized ratio (INR) 0.9, platelets 195×109/l). She was still mildly thyrotoxic (TSH <0.02 mU/l, FT4 31 pmol/l, TT3 1.3 nmol/l). She was diagnosed with acute hepatitis secondary to treatment with PTU. Ultrasound showed mild hepatic steatosis. PTU was stopped and she was managed with fluids and prednisolone 60 mg once daily and continued β blockade. Her liver function gradually improved over 10 days (bilirubin 9 μmol/l, ALT 164 U/l, ALP 195 U/l, INR 0.9, platelets 323×109/l) with conservative management and had normalised by clinic review 3 weeks later. This case highlights the potentially fatal, but rare, complications associated with both RAI and PTU, namely, thyroid storm and acute hepatitis respectively.

Learning points

  • Thyroid storm is an important, albeit rare, endocrinological emergency.
  • Thyroid storm following RAI treatment is extremely rare.
  • Management is with i.v. fluids, β blockade, anti-thyroid drugs and steroids.
  • High dose glucocorticoid steroids can block the peripheral conversion of T4 to active T3.
  • Liver dysfunction, acute hepatitis and potential hepatic failure are significant adverse drug reactions known to occur with PTU treatment. Supervising clinicians should be vigilant for evidence of this developing and intervene accordingly.
  • Clinicians need to be aware of possible interactions between regular paracetamol use and PTU in predisposing to liver impairment.

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

Junji Kawashima, Hideaki Naoe, Yutaka Sasaki and Eiichi Araki

Summary

Anti-tumor necrosis factor (TNF)-α therapy is established as a new standard for the treatment of various autoimmune inflammatory diseases. We report the first case showing subacute thyroiditis-like symptoms with an amyloid goiter after anti-TNF-α therapy. A 56-year-old man with Crohn's disease presented with fever and a diffuse, tender goiter. To control the diarrhea, anti-TNF therapy (infliximab) was administered 4 weeks before the thyroid symptoms emerged. The patient reported a swollen neck with tenderness on the right side and fever 4 days after the second infliximab injection. An elevated serum C-reactive protein (CRP) and serum thyroid hormone level with suppressed serum thyrotropin were observed. The thyroid-stimulating antibody was not elevated. An ultrasonograph of the thyroid revealed an enlarged goiter with posterior echogenicity attenuation and a low echoic region that was tender. The thyroid uptake value on technetium-99m scintigraphy was near the lower limit of the normal range. The patient was initially diagnosed with thyrotoxicosis resulting from subacute thyroiditis. Administration of oral prednisolone improved the fever, thyroid pain, and thyroid function, but his thyroid remained swollen. The patient developed diarrhea after prednisolone withdrawal; therefore, adalimumab, another TNF inhibitor, was administered. After three injections, his abdominal symptoms were alleviated, but the thyroid pain and fever recurred. Elevated serum CRP levels in the absence of thyroid dysfunction were observed. The patient's symptoms resolved after prednisolone retreatment, but an elastic, firm goiter persisted. A fine-needle biopsy revealed amyloid deposition in the thyroid.

Learning points

  • Many cases with thyroid dysfunction accompanied by amyloid goiter have been reported.
  • There are cases that develop amyloid goiter with subacute thyroiditis-like symptoms after anti-TNF therapy.
  • When the thyroid remains swollen after improvement of thyrotoxicosis following treatment with prednisolone, it should be assessed to differentiate between an amyloid goiter and common subacute thyroiditis.