Harit Buch

Combination of insulin and thiazolidinedione therapy in massively obese patients with Type 2 diabetes.

Aims To evaluate the influence of addition of rosiglitazone to insulin therapy over a 24‐week period in massively obese patients with poorly controlled Type 2 diabetes taking large doses of insulin.

An assessment of care of paediatric and adolescent patients with diabetes in a large district general hospital.

Aims To assess the process of clinical care and outcomes of young patients with diabetes attending clinics at a large district general hospital.

Endocrine Hypertension: A Practical Approach

Elevated blood pressure resulting from few endocrine disorders (endocrine hypertension) accounts for a high proportion of cases of secondary hypertension. Although some features may be suggestive, many cases of endocrine hypertension remain silent until worked up for the disease. A majority of cases result from primary aldosteronism. Other conditions that can cause endocrine hypertension are: congenital adrenal hyperplasia, Liddle syndrome, pheochromocytomas, Cushings syndrome, acromegaly, thyroid diseases, primary hyperparathyroidism and iatrogenic hormone manipulation. Early identification and treatment of the cause of endocrine hypertension may help to reduce morbidity and mortality related to these disorders. This article gives a comprehensive and practical approach to the diagnosis and management of endocrine hypertension.

Seventh nerve palsy as a false localizing sign in benign intracranial hypertension

Rare clinical signs can pose a diagnostic conundrum to even the most experienced clinician. Most doctors feel safe in the knowledge that the myriad of clinical signs taught at medical school are key investigative tools in day-to-day practice. Clinical signs should be signposts to potentially altered anatomy or physiology, although in some cases, can lead even the good diagnostician down the wrong path.1 Even in the simplest cases, the diagnostic jigsaw puzzle can be complicated by rarely-seen (or taught) false localizing signs. The term ‘false localizing sign’ may be self-explanatory, but what is not always clear is the level of potential deviation from ‘normal’ pathology that can occur. False localizing signs can potentially waste valuable time and resources directing investigation at a disease that the patient does not have. Furthermore, patients can be labelled with an inappropriate diagnosis which can have serious psychological or social connotations for the rest of their lives. The differential diagnoses entertained in this case could have been significantly life-limiting and potentially life-threatening for a patient of such a young age. It is, therefore, important to highlight unusual false localizing signs in order to inform clinicians that certain conditions may present with rare but clinically vital false clinical signs. It is understood that sixth nerve palsies are a reasonably common occurrence in benign intracranial hypertension (BIH) (10–30% of cases)2 but there have been far less reported cases of seventh nerve palsy3–5 and only one case of facial diplegia documented.6 n nA 19-year-old woman was admitted with a 10-day history of left-sided headache and vomiting which worsened over five days and developed into diplopia on extreme left gaze (denoting lateral rectus palsy even on admission). The headache was associated with photophobia and general malaise although there was no rash, neck stiffness or fever. Her menstrual history was unremarkable with no association to the headache and she had no significant past medical history. n nHer BMI was >30 kg/m2. Opthalmoscopy revealed bilateral papillodema with normal visual acuity and visual fields. The rest of the neurological examination was normal on admission. The following day, she developed bilateral lateral rectus weakness that was more pronounced on the left with concurrent lower motor facial nerve palsy on the left side ( Figure 1). n n n nFigure 1 n nEvidence of left-sided seventh nerve palsy n n n nA diagnosis of BIH was made and an urgent CT brain/venogram was normal. Baseline biochemical, haematological and immunological investigations were within normal limits, and a lumbar puncture yielded a clear and colourless CSF with 3 WBC and 1 RBC. Microscopy and culture of the fluid showed no evidence of infection. The opening pressure was measured at 35 cmH20 and a closing pressure of 20 cmH20. n nShe was started on acetazolomide and within the next two days her signs were found to be completely resolved. Rapid resolution of her seventh nerve palsy within two days indicates the readily reversible nature of this lesion and is against concomitant Bells palsy or simple arterial or venous brainstem infarct involving the sixth and seventh nerve nuclei residing in the Pons.

Post-radioiodine De Novo Onset Graves’ Ophthalmopathy: Case Reports and a Review of the Literature

ABSTRACT New-onset Graves’ ophthalmopathy (GO) following radioiodine treatment (RAI) and worsening of existing GO are well-described in the endocrinology literature. These phenomena are recognized by ophthalmologists, yet poorly documented in the ophthalmology literature. Two male patients, aged 43 and 62 years, respectively, with Graves’ disease without GO, received RAI. Four months later, one patient developed acute GO with unilateral reduction in visual acuity, conjunctival chemosis, lagophthalmos, bilateral severely restricted ocular motility, and lid retraction. High-dose intravenous steroids, followed by oral steroids, led to a dramatic clinical improvement. The second patient received a second dose of RAI for persistent hyperthyroidism and subsequently developed acute GO-comprising restricted ocular motility, peri-orbital swelling, and conjunctival chemosis. Symptoms gradually resolved on continued carbimazole treatment. Neither patient received pre-RAI prophylactic glucocorticoids, as currently they are only recommended for patients with pre-existing GO or multiple risk factors. We discuss the limitations of using this risk-based approach in preventing new-onset GO following RAI therapy.

Consultant delivered seven‐day health care: results from a medical model on a diabetes base ward

There is increasing emphasis on consultant delivered health care outside normal working hours, although its impact on outcomes away from emergency assessment units is not well known. We introduced structured seven‐day working for consultants on a 28 bedded diabetes base ward. Subsequent evaluation of its impact on patient throughput measures is presented.There is increasing emphasis on consultant delivered health care outside normal working hours, although its impact on outcomes away from emergency assessment units is not well known. We introduced structured seven-day working for consultants on a 28 bedded diabetes base ward. Subsequent evaluation of its impact on patient throughput measures is presented. n n n nWe measured discharge patterns and rates, length of stay and 30-day readmission following the introduction of seven-day consultant working including weekend ward rounds. Data collected over an identical seven-month period before and after the introduction of weekend consultant ward rounds were compared. n n n nSixty percent of discharged patients in both periods compared had diabetes. The number of discharges during the study period (seven months) increased from 459 to 496 almost entirely owing to increase in weekend discharges (45 to 83). The overall length of stay (LoS) was largely unchanged (11.3±15.4 vs 10.5±7.9), although there was a significant reduction in the LoS of weekend discharges (11.2±10.3 vs 7.9±6.4, p<0.01). Thirty-day emergency readmission fell from 132 to 107. Effectively this translated to 625 potential bed days gained over a seven-month period representing an annual saving of approximately £123 000 at basic tariff. n n n nWe concluded that consultant seven-day working is effective in facilitating increased discharges with reductions in LoS and readmissions, and has significant economic benefit. Additional work is needed to evaluate the impact on quality measures, especially with regard to specialty specific outcomes. Copyright

Sphenoid mucocele: an uncommon complication of a rare condition.

A 58-year-old white woman presented with sudden onset of diplopia, headache and vomiting with a history of tiredness and lethargy over the past four to six months. She had smooth, pale, hairless skin and on examination she was found to have left-sided third and sixth nerve palsy. Laboratory tests confirmed pan-anterior hypopituitarism. Computerized tomography scan of head and magnetic resonance imaging appearances were consistent with those of a sphenoid sinus mucocoele. Following adequate replacement with hydrocortisone and thyroxine she underwent sphenoid mucocoele drainage and endoscopic left sphenoethmoidectomy. Her symptoms were relieved over the next few days and she had a near-total recovery of ophthalmoplegia over the following three months. Pituitary function tests showed partial resolution of hypopituitarism with recovery of hypothalamic–pituitary–adrenal axis and hydrocortisone therapy was withdrawn, but she continued to require thyroxine.

The price of a 15-year delay in diagnosis of Sheehan's syndrome.

We describe a case of a 48-year-old woman who presented with a 15-year history of recurrent episodes of hypoglycemia and hyponatremia leading to altered behavior and generalized seizures. She underwent full clinical assessment, endocrine tests, and a pituitary magnetic resonance scan that showed pananterior hypopituitarism secondary to postpartum pituitary necrosis (Sheehans syndrome). She was commenced on appropriate hormone replacement therapy, which led to significant improvement in lethargy, anorexia, muscle weakness, and episodes of hypoglycemia. In addition to the alleviation of her physical symptoms, she experienced a significant improvement in her psychological well-being and reduction in hospital visits. This case illustrates the impact of delay in diagnosis of an easily treatable medical condition and its socioeconomic implications, especially for the population of a developing country like India.

Interaction of interferon alpha therapy with thyroid function tests in the management of hepatitis C: a case report

BackgroundInterferon alpha is a widely used therapeutic agent in the treatment of hepatitis C virus infection. Clinical thyroid disease is seen in nearly 15 % of patients receiving interferon alpha for hepatitis C virus infection. The mechanism of thyroid dysfunction with interferon alpha is either autoimmune or inflammatory. We report a case of young woman who developed biphasic thyroid dysfunction posing a diagnostic challenge, while receiving interferon alpha treatment for hepatitis C virus infection.Case presentationA 29-year-old, Caucasian woman with type 1 diabetes and hepatitis C virus infection was referred with hyperthyroidism, while she was at 17 weeks of a planned 24-week course of interferon alpha therapy. A laboratory investigation revealed a thyroid stimulation hormone level of 0.005 mU/L (0.350–4.94), free thyroxine of 45.6 pmol/L (9.0–19.0) and free tri-iodothyronine of 12.6 pmol/L (2.6–5.7). She had a mild neutropenia and alanine aminotransferase at double the reference value. Her thyroid peroxidase antibody level was 497 ku/L (<5.6) and thyroid inhibitory factor 7 IU/L (>1.8 iu/l is positive). Thyroid scintigraphy with technetium99 scan confirmed a normal-sized thyroid gland with diffuse but normal overall uptake. A diagnosis of interferon alpha-triggered autoimmune hyperthyroidism as opposed to an inflammatory thyroiditis was made. She was offered radioactive iodine therapy, as thionamides were considered inappropriate in view of her liver disease and mild neutropenia. Due to our patient’s personal circumstances, radioactive iodine therapy was delayed by 8 weeks and her thyrotoxic symptoms were controlled with beta-blockers alone. A repeat thyroid function test, 4 weeks post treatment with interferon alpha, indicated spontaneous conversion to hypothyroidism with a thyroid stimulation hormone level of 100 mU/L, free thyroxine of 5.2 pmol/L and free tri-iodothyronine of 1.7 pmol/L. She subsequently received levothyroxine for 4 months only and had remained euthyroid for the last 3 months without any treatment.ConclusionsInitial investigations favored the autoimmune nature of hyperthyroidism but follow-up of the case, interestingly, was more consistent with inflammatory thyroiditis. We propose that this can be explained either on the basis of autoimmune subacute thyroiditis or a change in the nature of thyroid stimulation hormone receptor antibody production from stimulating-type to blocking-type antibodies, with disappearance of the latter on discontinuation of interferon alpha.

Mortality rates in hospital patients with hyperglycaemia and MRSA bacteraemia

Methicillin Resistant Staphylococcus Aureus (MRSA) infections in the hospital population have shown a dramatic increase. This pilot study determined whether random/fasting blood glucose measurements were performed on patients admitted to hospital with MRSA bacteraemia. We also examined mortality in relationship to hyperglycaemia, defined as random glucose ≥ 11 mmol/L. Retrospective data for all in-patients aged ≥ 16 years for the three years; 2000—2002 identified 309 patients with MRSA bacteraemia and all of them had laboratory blood glucose concentrations recorded on admission in all cases. A random blood glucose ≥ 11 mmol/L was noted in 129 (42%) patients of whom 82 (64%) died. The mortality was significantly more likely to be in the highest tertile (p<0.05) of blood glucose distributions.