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The focus on metabolic conditions in serious mental illness dates from the switch to atypical antipsychotics starting in the late 1990s. Metabolic adverse effects of antipsychotics have been the subject of litigation and the focus of much media attention.1,2 There is considerable public awareness that compels clinicians to pay attention to these issues when prescribing antipsychotics. While there has been agreement about the importance of metabolic monitoring for close to a decade, practice audits consistently show low rates of adherence to monitoring guidelines. One of the most concerning consequences of this is that clinical decisions are based on limited data. Hypothyroidism is a risk factor for new onset diabetes mellitus (DM), in particular for those who take statins. Universal Viewers Offer Freedom from Platform and Format Limitations Putting Clinical Insights within Reach; Is Your Image Viewer as Universal as You Think? Patients with type 2 AIP usually do not show the immune-mediated diseases, that are observed in about 20 to 40 % of patients with IgG4-related disease (6,9,10).
The subtypes of AIP differ in their clinical features such as gender and mean age at diagnosis (6). Long time follow-up in patients with AIP after pancreatic resection revealed that recurrence of the disease is often observed in type 1 AIP, but is very rare in type 2 AIP (1,6,19).
Among the autoantibodies that may be detected are antibodies against antigens from the pancreatic ducts and acini such as lactoferrin, carbonic anhydrase type II, SPINK1 and trypsinogen (13,17).
The pathogenesis of AIP is still not known, but several findings, common to both types of AIP, are suggestive of an immune-related etiopathogenesis. A clear difference between the AIP subtypes concerns the amount of IgG4-positive plasma cells in the pancreatic tissue, a finding that often correlates with the serum IgG4 levels in patients. Detlefsen S, Zamboni G, Frulloni L, Feyerabend B, Braun F, Gerke O, Schlitter AM, Esposito I, Kloppel G. Lohr JM, Faissner R, Koczan D, Bewerunge P, Bassi C, Brors B, Eils R, Frulloni L, Funk A, Halangk W, Jesnowski R, Kaderali L, Kleef J, Kruger B, Lerch M, Losel R, Magnani M, Neumaier M, Nittka S, Sahintoth M, Sanger J, Serafini S, Schnolzer M, Thierse H-J, Wandschneider S, Zamboni G, Kloppel G.
Saito T, Tanaka S, Yoshida H, Imamura T, Ukegawa J, Seki T, Ikegami A, Yamamura F, Mikami T, Aoyagi Y, Niikawa J, Mitamura K. Taniguchi T, Okazaki K, Okamoto M, Seko S, Tanaka J, Uchida K, Nagashima K, Kurose T, Yamada Y, Chiba T, Seino Y.
Zamboni G, Luttges J, Capelli P, Frulloni L, Cavallini G, Pederzoli P, Leins A, Longnecker D, Kloppel G.
Metabolic conditions may include type 2 diabetes mellitus, hyperlipidemia, weight gain, obesity, metabolic syndrome, and associated coronary heart disease.
Metabolic adverse effects have clearly overtaken neurological adverse effects as a major concern in treating psychosis. In a recent international review of guideline-concordant monitoring for metabolic risk in patients treated with antipsychotics, adherence was “concerningly low” in routine clinical practice.3 Monitoring rates remained low even after the widespread introduction of local and national guidelines starting from 2004. For example, is monitoring the responsibility of the psychiatrist or of a primary care physician?
For example, a patient is found to have diabetes well into the course of antipsychotic treatment. Severe hypoglycemia is significantly associated with the severity of depressive symptoms among type 2 DM patients. The region that seems to be most often affected is the pancreatic head including the pancreatic portion of the distal bile duct. In approximately 80% they present as a tumorous mass in the head of the pancreas mimicking ductal adenocarcinoma (14,19). Instead they commonly suffer from chronic inflammatory bowel disease such as ulcerative colitis or Crohn’s disease (10,19).
Many patients complain of abdominal pain, although the frequency and intensity of pain attacks tend to be lower in patients with type 1 AIP than type 2 AIP (10).
Another interesting question is whether pancreatic ductal adenocarcinoma (PDAC), which has recently been described in association with AIP, has a predilection for one of the two AIP types.
Other autoantibodies associated with AIP are antinuclear antibody, rheumatoid factor and anti-smooth muscle antibody. This assumption is based on the general histopathological features of both AIP types, their frequent association with immune-related disorders such as the systemic manifestations of IgG4-related disease on one hand and idiopathic inflammatory bowel diseases on the other, and the response to steroid treatment.

Diagnosis of autoimmune pancreatitis by core needle biopsy: application of six microscopic criteria. Deposition of complement C3c, immunoglobulin (Ig)G4 and IgG at the basement membrane of pancreatic ducts and acini in autoimmune pancreatitis.
Clinical features and relapse rates after surgery in type 1 autoimmune pancreatitis differ from type 2: a study of 114 surgically treated European patients. Autoimmune pancreatitis: the clinicopathological characteristics of the subtype with granulocytic epithelial lesions. Autoantibodies against the exocrine pancreas in autoimmune pancreatitis: gene and protein expression profiling and immunoassays identify pancreatic enzymes as a major target of the inflammatory process. Idiopathic chronic pancreatitis with periductal lymphoplasmacytic infiltration: clinicopathologic features of 35 cases.
High prevalence of autoantibodies against carbonic anhydrase II and lactoferrin in type 1 diabetes: concept of autoimmune exocrinopathy and endocrinopathy of the pancreas. Histopathological features of diagnostic and clinical relevance in autoimmune pancreatitis: a study on 53 resection specimens and 9 biopsy specimens. Type 2 diabetes can be due to increased peripheral resistance to insulin or to reduced secretion of insulin.
The rationale for monitoring metabolic parameters during the course of antipsychotic treatment is clear.
As clinicians, we need to incorporate metabolic monitoring into clinical practice and to understand the significance of metabolic changes that develop during antipsychotic treatment. In a comparison of pre- and post-guideline practices, only glucose monitoring showed a statistically significant incremental increase. Mental health practitioners may not be up-to-date or comfortable assessing and interpreting metabolic parameters.
Time-updated hemoglobin A1c (HbA1c) variables have a stronger association with myocardial infarction (MI) than baseline HbA1c. As in type 1 AIP, the outstanding histologic feature is a periductal lymphoplasmacytic infiltrate usually affecting some or all of the medium sized ducts (Figure 1). The inflammatory infiltration of the pancreas head and the wall of the extrahepatic bile duct can cause narrowing of the distal bile duct and main pancreatic duct. Moreover, these patients mostly fail to exhibit elevated IgG4 serum levels and increased IgG4 positive plasma cells.
While in Europe each subtype can be expected in about 40-60% of the cases (in biopsy series they amount to 38% and 45%, respectively), type 2 AIP seems to be rare in East Asia (11). Whether the demonstrated circulating autoantibodies against carbonic anhydrase II, lactoferrin and nuclear and smooth muscle antigens as well as SPINK1  are found in the same frequency in type 1 AIP as in type 2 AIP is unknown. Patients with serious mental illness may not have access to primary care and may not follow through with laboratory testing or medical appointments. Without systematic monitoring, it is unclear how long the patient has had diabetes and what the relationship was to the prescribed antipsychotic. It is often accompanied by a collar-like periductal fibrosis, with narrowing of the affected duct. Immunostaining for CD3, CD4 and CD8 positive lymphocytes, CD79a positive plasma cells and CD68 positive macrophages often reveals a higher number of these cells in type 1 AIP compared to type 2 AIP (12,20). Corticosteroid treatment resolves strictures of the extrahepatic bile ducts and main pancreatic duct, as well as the pancreatic mass and focal lesions in the lungs, kidneys and retroperitoneal inflammatory pseudotumors. On the basis of these findings it may be hypothesized that IgG4 could play a role in the deposition of immune complexes at pancreatic structures that seem to be the target of the fibroinflammatory process characterizing AIP. Or, clozapine is not prescribed for a diabetic patient with refractory psychosis because the clinician is convinced that there will be further weight gain and worsening of diabetes. In order to clarify whether this hypothesis is only valid in IgG4 positive patients with type 1 AIP, a patient was included in the study whose clinical features were indistinguishable from those of the other six patients of the series, but whose immunohistochemical staining was more consistent with type 2 AIP (very low numbers of IgG4-positive plasma cells in the pancreatic tissue). Clinicians are busy and, thus, often systematic metabolic monitoring is not completed or sustained during the course of treatment. With careful metabolic monitoring, this may well not be the case, and if there is worsening glucose control, diabetes medication can be easily adjusted.
This patient did not have any IgG4-positive deposits at the basement membranes of the ducts and acini, but remained positive for C3c and IgG.

These histological changes can also be found in type 1 AIP, but are usually less pronounced in type 2 AIP. If this unique finding is confirmed in future studies, it would imply that in type 2 AIP the mechanisms leading to the changes in the ducts and acini and the fibrosis are independent of the effects of IgG4. Glucose is then stored as glycogen in liver and muscle.Insulin also inhibits the release of glucagon and so blocks fat being used as an energy source.
Conversely, the finding of the so called granulocytic epithelial lesion (GEL) is specific to AIP 2 (19).
This lesion is characterized by focal disruption and destruction of the duct epithelium due to the invasion of neutrophilic granulocytes. There are one million to three million islets of Langerhans (pancreatic islets) and beta cells constitute 60-80% of all the cells. GELs affect medium sized and small ducts (Figure 2), and may also be recognized in the acinar tissue. Insulin is synthesised from the proinsulin precursor molecule by the action of proteolytic enzymes, known as prohormone convertases, as well as the exoprotease carboxypeptidase E. If a GEL is included in a biopsy specimen from the pancreas it is diagnostic for type 2 AIP (4). There are a family of four specialised transporter proteins that carry glucose across the membrane. GLUT4 carries glucose into muscle and adipose tissue after the insulin receptor has been stimulated - see diagram above. This treats insulin resistance.Sulfonylureas (gliclazide) bind to an ATP-dependent potassium channel on the cell membrane of pancreatic beta cells.
This depolarisation opens voltage-gated calcium channels which leads to increased fusion of insulin granulae with the cell membrane, and increased secretion of (pro)insulin.Glitazones also treat insulin resistance. They bind to peroxisome proliferator-activated receptor gamma (a nuclear regulatory protein) which influences insulin-sensitive genes, which enhance production of mRNAs of insulin-dependent enzymes.
It should be remembered that there is a temporary increased risk of lactic acidosis in situations where increased tissue hypoxia occurs, e.g.
This is increased in older age groups, mild-to-moderate hepatic impairment, and renal impairment. The trials that have been done indicate that the incidence of hypoglycaemia is equivalent to that of the older sulphonylureas.18ThiazolidinedionesThiazolidinediones (TDZs) or 'glitazones' - pioglitazone19 is the only one currently licensed in the UK.
Its mechanism of action is still subject to debate but is thought to act in a similar manner to metformin, increasing hepatic sensitivity to insulin, and enhancing glucose clearance. They also slow the rate of absorption of nutrients into the bloodstream by reducing gastric emptying, and may directly reduce food intake.
Both are rapidly deactivated by dipeptydyl peptidase-4 (DPP4) GLP1 is not useful in diabetes treatment, as it has a very short half-life and must be given as a continuous subcutaneous (SC) injection.
Inhibiting the enzyme that inactivates GLP1 is more successful and several oral DPP4 inhibitors are available for type 2 diabetes management, e.g. Updated 3rd November 2008, accessed 29 Dec 2009Klip A, Leiter LA; Cellular mechanism of action of metformin. Updated September 2005, accessed 29 Dec 2009Landgraf R, Bilo HJ, Muller PG; A comparison of repaglinide and glibenclamide in the treatment of type 2 diabetic patients previously treated with sulphonylureas. Updated 24 Feb 2009, accessed 29 Dec 2009Wada K, Nakajima A, Katayama K, et al; Peroxisome proliferator-activated receptor gamma-mediated regulation of neural stem cell proliferation and differentiation. Updated 10 November 2009, accessed 29 Dec 2009Sitagliptin, New Drug Evaluation No 45, Regional Drug and Therapeutic Centre, (Aug 2007)Summary of Product Characteristics (SPC) - Galvus® 50 mg tablets (vildagliptin), Novartis Pharmaceuticals UK Ltd, electronic Medicines Compendium. Updated Aug 2009, accessed 29 Dec 2009Summary of Product Characteristics (SPC) - Byetta® (exenatide), (5 micrograms and 10 micrograms solution for injection, prefilled pens), Eli Lilly and Company Limited, electronic Medicines Compendium.

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