Diagnosis and Treatment > Signs and Symptoms
Search for other papers by S Hussain in
Google Scholar
PubMed
Search for other papers by S Keat in
Google Scholar
PubMed
Search for other papers by S V Gelding in
Google Scholar
PubMed
Summary
We describe the case of an African woman who was diagnosed with ketosis-prone diabetes with diabetes-associated autoantibodies, after being admitted for diabetic ketoacidosis (DKA) precipitated by her first presentation of systemic lupus erythematosus (SLE). She had a seven-year history of recurrent gestational diabetes (GDM) not requiring insulin therapy, with return to normoglycaemia after each pregnancy. This might have suggested that she had now developed type 2 diabetes (T2D). However, the diagnosis of SLE prompted testing for an autoimmune aetiology for the diabetes, and she was found to have a very high titre of GAD antibodies. Typical type 1 diabetes (T1D) was thought unlikely due to the long preceding history of GDM. Latent autoimmune diabetes of adults (LADA) was considered, but ruled out as she required insulin therapy from diagnosis. The challenge of identifying the type of diabetes when clinical features overlap the various diabetes categories is discussed. This is the first report of autoimmune ketosis-prone diabetes (KPD) presenting with new onset of SLE.
Learning points:
-
DKA may be the first presentation of a multi-system condition and a precipitating cause should always be sought, particularly in women with a history of GDM or suspected T2D.
-
All women with GDM should undergo repeat glucose tolerance testing postpartum to exclude frank diabetes, even when post-delivery capillary blood glucose (CBG) tests are normal. They should also be advised to continue CBG monitoring during acute illness in case of new onset diabetes.
-
KPD comprises a spectrum of diabetes syndromes that present with DKA, but subsequently have a variable course depending on the presence or absence of beta cell failure and/or diabetes autoantibodies.
-
KPD should be considered in a patient with presumed T2D presenting with DKA, especially if there is a personal or family history of autoimmune diabetes.
-
LADA should be suspected in adults presumed to have T2D, who do not require insulin therapy for at least six months after diagnosis and have anti-GAD antibodies.
-
Patients with autoimmune diabetes have an increased risk of other autoimmune diseases and screening for thyroid, parietal cell, coeliac and antinuclear antibodies should be considered.
Search for other papers by Ernesto Solá in
Google Scholar
PubMed
Search for other papers by Carmen Rivera in
Google Scholar
PubMed
Search for other papers by Michelle Mangual in
Google Scholar
PubMed
Search for other papers by José Martinez in
Google Scholar
PubMed
Search for other papers by Kelvin Rivera in
Google Scholar
PubMed
Search for other papers by Ricardo Fernandez in
Google Scholar
PubMed
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.
Search for other papers by Huanyu Ding in
Google Scholar
PubMed
Search for other papers by Yang Li in
Google Scholar
PubMed
Search for other papers by Caishun Ruan in
Google Scholar
PubMed
Search for other papers by Yuan Gao in
Google Scholar
PubMed
Search for other papers by Hehua Wang in
Google Scholar
PubMed
Search for other papers by Xiangsong Zhang in
Google Scholar
PubMed
Search for other papers by Zhihong Liao in
Google Scholar
PubMed
Summary
Erdheim-Chester disease (ECD), one type of systemic non-Langerhans cell histiocytosis, has been rarely seen and is characterized by the accumulation of foamy CD68+CD1a- histiocytes. We reported a case of ECD and reviewed the clinical features of 13 cases of ECD reported so far in China. A 53-year-old male was diagnosed with central diabetes insipidus in March 2014, followed by fever, splenomegaly and anemia in July 2014. His initial pituitary magnetic resonance imaging (MRI) revealed the absence of high signal at T1-weighted image in posterior pituitary without any lesion. A further positron emission tomography/computer tomography (PET/CT) images showed elevated metabolic activity of 18F-2-fluro-D-deoxy-glucose (FDG) and low 13N-NH3 uptake in the posterior pituitary, and multi-organ involvement. Biopsy at right femur lesion revealed that granulomatous infiltration of foamy histiocytes and Touton giant cells surrounded by fibrosis tissues. Immunohistochemistry stain was positive for CD68, negative for CD207/Langerin and S-100. The diagnosis of ECD was confirmed and the treatment with pegylated interferon was effective. ECD was a possible immune-related disorder concluding from the IgG4 immunohistochemistry results. We summarized the pathological manifestations for ECD and its differential diagnosis from Langerhans cell histiocytosis (LCH) and Rosai-Dorfman disease (RDD). ECD should be considered by both pathologists and clinicians in the differential diagnosis when central diabetes insipidus is accompanied with multi-organ involvement, especially skeletal system involvement, or recurrent fever.
Learning points
-
ECD should be considered when central diabetes insipidus is accompanied with multisystem involvement, especially symmetric/asymmetric bone lesions, or recurrent fever.
-
PET/CT scanning was helpful for locating pituitary lesion, discovering multiple system involvement and indicating the biopsy sites.
-
Conducting proper immunohistochemistry stains was important for diagnosing ECD. ECD might be correlated with immune disorder.
Search for other papers by Durgesh Gowda in
Google Scholar
PubMed
Search for other papers by Vasant Shenoy in
Google Scholar
PubMed
Search for other papers by Usman Malabu in
Google Scholar
PubMed
Search for other papers by Donald Cameron in
Google Scholar
PubMed
Search for other papers by Kunwarjit Sangla in
Google Scholar
PubMed
Summary
Our patient had drainage of a large amoebic liver abscess. This got complicated by a severe degree of hypotension, which required aggressive fluid resuscitation and hydrocortisone support. Computerised tomography (CT) of the abdomen revealed bilateral adrenal gland haemorrhage (BAH) resulting in primary adrenal gland failure, which was the cause for hypotension. Patient was on long-term warfarin for provoked deep vein thrombosis of lower limb, which was discontinued before the procedure. Thrombophilia profile indicated the presence of lupus anticoagulant factor with prolonged activated partial thromboplastin time (aPTT). Patient was discharged on lifelong warfarin. This case emphasises the need for strong clinical suspicion for diagnosing BAH, rare but life-threatening condition, and its association with amoebic liver abscess and anti-phospholipid antibody syndrome (APLS).
Learning points
-
Recognition of BAH as a rare complication of sepsis.
-
APLS can rarely cause BAH.
